Mann's Surgery of The Foot and Ankle

MANN’S SURGERY OF THE FOOT AND ANKLE

Volume 1

MANN’S SURGERY OF THE FOOT AND ANKLE NINTH EDITION Michael J. Coughlin, MD Director, Saint Alphonsus Foot and Ankle Clinic, Boise, Idaho Clinical Professor, Department of Orthopaedic Surgery University of California, San Francisco, San Francisco, California Past-president, American Orthopedic, Foot and Ankle Society Past-president, International Federation of Foot and Ankle Societies

Charles L. Saltzman, MD Chairman, Department of Orthopaedics Louis S. Peery MD Endowed Presidential Professor, University of Utah University Orthopaedic Center, Salt Lake City, Utah Past-president, American Orthopaedic Foot and Ankle Society Vice President, International Federation of Foot and Ankle Societies

Robert B. Anderson, MD Chief, Foot and Ankle Service Vice-chair, Department of Orthopaedic Surgery, Carolinas Medical Center OrthoCarolina Foot and Ankle Institute, Charlotte, North Carolina Past-president, American Orthopaedic Foot and Ankle Society

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

MANN’S SURGERY OF THE FOOT AND ANKLE

ISBN: 978-0-323-07242-7 Volume 1 Part Number: 9996074684 Volume 2 Part Number: 9996074749

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Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Copyright

Library of Congress Cataloging-in-Publication Data Mann’s surgery of the foot and ankle / [edited by] Michael J. Coughlin, Charles Saltzman, Robert B. Anderson.—Ninth edition. p. ; cm. Surgery of the foot and ankle Preceded by Surgery of the foot and ankle / edited by Michael J. Coughlin, Roger A. Mann, Charles L. Salzmann. 8th ed. c2007. Includes bibliographical references and index. ISBN 978-0-323-07242-7 (set : hardcover : alk. paper) I. Coughlin, Michael J., editor of compilation. II. Saltzman, Charles L., editor of compilation. III. Anderson, Robert B. (Robert Bentley), 1957- editor of compilation. IV. Title: Surgery of the foot and ankle. [DNLM: 1. Ankle—surgery. 2. Foot—surgery. 3. Ankle Injuries—surgery. 4. Foot Diseases— surgery. WE 880] RD563 617.5’85059—dc23 2013017557 Executive Content Strategist: Dolores Meloni Content Development Manager: Lucia Gunzel Publishing Services Manager: Anne Altepeter Project Manager: Cindy Thoms Design Direction: Louis Forgione Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

To our parents— Martha and Jim, Abraham and Ruth, and Dottie and Dick, for the opportunities they presented to us; to our wives— Kirsten, Ingrid, and Jean, for their support and encouragement; and to our children— Erin and Elizabeth; Hanna and Erik; and Ryan, Tyler, and Michael, for the happiness, enthusiasm, and joy that they bring to our families

Contributors

Richard G. Alvarez, MD Professor and Chair Department of Orthopaedic Surgery Director of Foot and Ankle University of Tennessee College of Medicine Chattanooga, Tennessee Chapter 11: Toenail Abnormalities John G. Anderson, MD Associate Professor Department of Orthopaedic Surgery Michigan State University College of Human Medicine Chairman, Spectrum Health Hospitals Department of Orthopaedic Surgery Co-Director, Grand Rapids Orthopaedic Foot and Ankle Fellowship Co-Director, Grand Rapids Orthopaedic Residency Program Grand Rapids, Michigan Chapter 37: Ankle Fractures Robert B. Anderson, MD Chief, Foot and Ankle Service Vice-chair, Department of Orthopaedic Surgery Carolinas Medical Center OrthoCarolina Foot and Ankle Institute Charlotte, North Carolina Chapter 2: Principles of the Physical Examination of the Foot and Ankle Chapter 6: Hallux Valgus Chapter 31: Stress Fractures of the Foot and Ankle Chapter 40: Fractures of the Midfoot and Forefoot Rahul Banerjee, MD Assistant Professor Department of Orthopaedic Surgery University of Texas Southwestern Medical Center Dallas, Texas Chapter 39: Fractures and Fracture-Dislocations of the Talus

Alexej Barg, MD Attending Surgeon Orthopaedic Department University Hospital of Basel Basel, Switzerland; Research Fellow Harold K. Dunn Orthopaedic Research Laboratory University Orthopaedic Center University of Utah Salt Lake City, Utah Chapter 22: Ankle Replacement Judith F. Baumhauer, MD, MPH Professor and Associate Chair of Academic Affairs Department of Orthopaedic Surgery Foot and Ankle Division University of Rochester Rochester, New York Chapter 13: Plantar Heel Pain Timothy C. Beals, MD Associate Professor Director of Foot and Ankle Fellowship Department of Orthopaedics University of Utah Salt Lake City, Utah Rosenberg Cooley Metcalf Clinic Park City, Utah Chapter 34: Congenital and Acquired Neurologic Disorders Douglas Beaman, MD Summit Orthopaedics, LLP Portland, Oregon Chapter 23: Ring External Fixation in the Foot and Ankle James H. Beaty, MD Professor of Orthopaedics Department of Orthopaedic Surgery University of Tennessee-Campbell Clinic Memphis, Tennessee Chapter 33: Congenital Foot Deformities vii

Contributors

Alireza Behboudi, DO Orthopaedics East Texas Medical Center Tyler, Texas Chapter 37: Ankle Fractures Gary M. Berke, MS, CP Adjunct Clinical Assistant Professor Department of Orthopaedic Surgery Stanford University Palo Alto, California Private Practitioner Gary M. Berke Prosthetics/Orthotics Redwood City, California Chapter 29: Lower Limb Prosthetics Mark J. Berkowitz, MD Associate Staff Orthopaedic Surgeon Orthopaedic and Rheumatologic Institute Cleveland Clinic Foundation Cleveland, Ohio Chapter 35: Dislocations of the Foot Brad D. Blankenhorn, MD Assistant Professor Department of Orthopaedic Surgery University of New Mexico Albuquerque, New Mexico Chapter 21: Ankle Arthritis Donald R. Bohay, MD, FACS Professor Department of Orthopaedic Surgery Michigan State University College of Human Medicine Director, Grand Rapids Orthopaedic Foot and Ankle Fellowship Program Grand Rapids, Michigan Chapter 37: Ankle Fractures James W. Brodsky, MD Clinical Professor of Orthopaedic Surgery University of Texas Southwestern Medical School Director, Foot and Ankle Surgery Fellowship Program Baylor University Medical Center Professor of Orthopaedic Surgery Texas A&M University, College of Medicine Dallas, Texas Chapter 27: Diabetes Chapter 28: Amputations of the Foot and Ankle George T. Calvert, MD Assistant Professor Division of Orthopaedic Surgery City of Hope National Medical Center Duarte, California Chapter 18: Soft Tissue and Bone Tumors

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Loretta B. Chou, MD Professor and Chief of Foot and Ankle Surgery Department of Orthopaedic Surgery Stanford University Stanford, California Chapter 4: Conservative Treatment of the Foot Thomas O. Clanton, MD Director, Foot and Ankle Sports Medicine The Steadman Clinic Vail, Colorado Chapter 30: Athletic Injuries to the Soft Tissue of the Foot and Ankle J. Chris Coetzee, MD Orthopedic Foot and Ankle Surgeon Twin Cities Orthopedics Minneapolis, Minnesota Chapter 20: Treatment of Hindfoot and Midfoot Arthritis Bruce E. Cohen, MD Assistant Residency Program Director Department of Orthopaedic Surgery Carolinas Medical Center; Fellowship Director, OrthoCarolina Foot and Ankle Institute Charlotte, North Carolina Chapter 31: Stress Fractures of the Foot and Ankle Michael J. Coughlin, MD Director, Saint Alphonsus Foot and Ankle Clinic Boise, Idaho Clinical Professor, Department of Orthopaedic Surgery University of California, San Francisco San Francisco, California Chapter 6: Hallux Valgus Chapter 7: Lesser Toe Deformities Chapter 9: Bunionettes Chapter 10: Sesamoids and Accessory Bones of the Foot Chapter 11: Toenail Abnormalities Chapter 19: Arthritis of the Foot and Ankle Chapter 24: Disorders of Tendons Jennifer J. Davis, MD Associate Professor Department of Anesthesiology University of Utah Salt Lake City, Utah Chapter 5: Anesthesia W. Hodges Davis, MD OrthoCarolina Foot and Ankle Institute Charlotte, North Carolina Chapter 2: Principles of the Physical Examination of the Foot and Ankle

Contributors

Laura K. Dawson, MD Orthopaedic Foot and Ankle Fellow Department of Orthopaedics and Rehabilitation University of Rochester Rochester, New York Chapter 13: Plantar Heel Pain Jonathan T. Deland, MD Chief, Foot and Ankle Service Hospital for Special Surgery New York, New York Chapter 25: Pes Planus Brian D. Dierckman, MD Attending Surgeon American Health Network Bone and Spine Carmel, Indiana Chapter 32: Arthroscopy of the Foot and Ankle Benedict F. DiGiovanni, MD Professor Department of Orthopaedics and Rehabilitation Director, Musculoskeletal Curriculum University of Rochester Rochester, New York Chapter 13: Plantar Heel Pain Matthew B. Dobbs, MD Department of Orthopaedic Surgery Barnes-Jewish Hospital at Washington University School of Medicine Saint Louis Shriners Hospital Saint Louis, Missouri Chapter 33: Congenital Foot Deformities Jesse F. Doty, MD Clinical Instructor Department of Orthopaedic Surgery University of Tennessee College of Medicine Chattanooga, Tennessee Chapter 11: Toenail Abnormalities J. Kent Ellington, MD OrthoCarolina Foot and Ankle Institute Charlotte, North Carolina Chapter 40: Fractures of the Midfoot and Forefoot Richard D. Ferkel, MD Assistant Clinical Professor of Orthopedic Surgery UCLA Center for the Health Sciences Director of Sports Medicine Fellowship Southern California Orthopedic Institute Van Nuys, California Chapter 32: Arthroscopy of the Foot and Ankle

Richard E. Gellman, MD Summit Orthopaedics, LLP Portland, Oregon Chapter 23: Ring External Fixation in the Foot and Ankle J. Speight Grimes Jr., MD Assistant Professor Department of Orthopaedics Texas Tech Health Sciences Center Lubbock, Texas Chapter 15: Infections of the Foot Gregory P. Guyton, MD Attending Orthopaedic Surgeon Department of Orthopaedic Surgery Medstar Union Memorial Hospital Baltimore, Maryland Chapter 26: Pes Cavus Steven L. Haddad, MD Senior Attending Illinois Bone and Joint Institute, LLC Glenview, Illinois Chapter 25: Pes Planus Andrew Haskell, MD Department of Orthopaedics Palo Alto Medical Clinic Palo Alto, California Assistant Clinical Professor Department of Orthopaedic Surgery University of California, San Francisco San Francisco, California Chapter 1: Biomechanics of the Foot and Ankle Catherine L. Hayter, MBBS, FRANZCR Radiologist Castlereagh Sports Imaging St Leonards, New South Wales, Australia Chapter 3: Imaging of the Foot and Ankle Christopher B. Hirose, MD Private Practice of Orthopaedic Foot and Ankle Surgery Coughlin Clinic Saint Alphonsus Regional Medical Center Boise, Idaho Chapter 19: Arthritis of the Foot and Ankle Kenneth J. Hunt, MD Assistant Professor Department of Orthopaedic Surgery Stanford University Palo Alto, California Chapter 34: Congenital and Acquired Neurologic Disorders

Contributors

Todd A. Irwin, MD Assistant Professor Department of Orthopaedic Surgery University of Michigan Ann Arbor, Michigan Chapter 2: Principles of the Physical Examination of the Foot and Ankle

Stephen J. Kovach, MD Assistant Professor Department of Surgery—Plastic Surgery University of Pennsylvania Health System Philadelphia, Pennsylvania Chapter 17: Soft Tissue Reconstruction for the Foot and Ankle

J. Benjamin Jackson III, MD Chief Resident Carolinas Medical Center OrthoCarolina Foot and Ankle Institute Charlotte, North Carolina Chapter 40: Fractures of the Midfoot and Forefoot

Fabian G. Krause, MD Assistant Professor Department of Orthopaedic Surgery Inselspital, University of Berne Berne, Switzerland Chapter 26: Pes Cavus

Jeffrey E. Johnson, MD Professor Department of Orthopaedic Surgery Chief, Foot and Ankle Service Barnes-Jewish Hospital at Washington University School of Medicine Saint Louis, Missouri Chapter 27: Diabetes

Douglas W. Kress, MD Division of Pediatric Dermatology Children’s Hospital of Pittsburgh Wexford, Pennsylvania Chapter 16: Dermatology of the Foot and Lower Extremity

Ari J. Kaz, MD Orthopaedic Surgeon Illinois Bone and Joint Institute, LLC Assistant Professor of Clinical Orthopaedics Department of Orthopaedic Surgery University of Illinois–Chicago Chicago, Illinois Chapter 8: Keratotic Disorders of the Plantar Skin Travis J. Kemp, MD Coughlin Foot and Ankle Clinic Saint Alphonsus Regional Medical Center Boise, Idaho Chapter 23: Ring External Fixation in the Foot and Ankle John P. Ketz, MD Assistant Professor Department of Orthopaedics University of Rochester Rochester, New York Chapter 36: Pilon Fractures Sandra E. Klein, MD Assistant Professor Department of Orthopaedic Surgery Barnes-Jewish Hospital at Washington University School of Medicine Saint Louis, Missouri Chapter 27: Diabetes

L. Scott Levin, MD, FACS Paul B. Magnuson Professor of Bone and Joint Surgery Chairman Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Professor of Surgery, Division of Plastic Surgery Department of Surgery University of Pennsylvania Health System Philadelphia, Pennsylvania Chapter 17: Soft Tissue Reconstruction for the Foot and Ankle James M. Linklater, MBBS, FRANZCR Castlereagh Sports Imaging St Leonards, New South Wales, Australia Chapter 3: Imaging of the Foot and Ankle Roger A. Mann, MD Private Practice Orthopaedic Surgery Oakland, California Director, Foot Fellowship Program Associate Clinical Professor of Orthopaedic Surgery University of California School of Medicine San Francisco, California Chapter 1: Biomechanics of the Foot and Ankle Chapter 8: Keratotic Disorders of the Plantar Skin Florian Nickisch, MD Assistant Professor Department of Orthopaedics University of Utah Salt Lake City, Utah Chapter 39: Fractures and Fracture-Dislocations of the Talus

Contributors

David I. Pedowitz, MS, MD Assistant Professor Department of Orthopedic Surgery Thomas Jefferson University Rothman Institute Philadelphia, Pennsylvania Chapter 14: Soft Tissue Disorders of the Foot Walter J. Pedowitz, MD Clinical Professor Department of Othopaedic Surgery Columbia University New York, New York Union County Orthopaedic Group Linden, New Jersey Chapter 14: Soft Tissue Disorders of the Foot Phinit Phisitkul, MD Clinical Assistant Professor Department of Orthopaedics and Rehabilitation University of Iowa Iowa City, Iowa Chapter 32: Arthroscopy of the Foot and Ankle Stefan Rammelt, MD, PhD Professor of Surgery Department of Trauma and Reconstructive Surgery University Hospital Carl Gustav Carus Technische Universität Dresden Dresden, Germany Chapter 38: Fractures of the Calcaneus R. Lor Randall, MD, FACS The L.B. & Olive S. Young Endowed Chair for Cancer Research Director, Sarcoma Services and Chief, SARC Lab Professor of Orthopaedics Huntsman Cancer Institute and Primary Children’s Medical Center University of Utah Salt Lake City, Utah Chapter 18: Soft Tissue and Bone Tumors John W. Read, MBBS, FRANZCR, DDU Radiologist Castlereagh Sports Imaging St Leonards, New South Wales, Australia Chapter 3: Imaging of the Foot and Ankle Mark A. Reed, MD Private Practice of Orthopedic Surgery Orthopaedic Specialists of Seattle Seattle, Washington Chapter 12: Disorders of the Nerves

Charles L. Saltzman, MD Chairman, Department of Orthopaedics Louis S. Peery MD Endowed Presidential Professor University of Utah University Orthopaedic Center Salt Lake City, Utah Chapter 21: Ankle Arthritis Chapter 22: Ankle Replacement Chapter 28: Amputations of the Foot and Ankle Roy W. Sanders, MD Chief, Department of Orthopaedic Surgery Tampa General Hospital Director, Orthopaedic Trauma Services Florida Orthopaedic Institute Tampa, Florida Chapter 35: Dislocations of the Foot Chapter 36: Pilon Fractures Chapter 37: Ankle Fractures Chapter 38: Fractures of the Calcaneus Lew C. Schon, MD Attending Orthopaedic Surgeon Department of Orthopaedic Surgery Chief, Foot and Ankle Fellowship and Orthobiologic Laboratory MedStar Union Memorial Hospital Assistant Professor Orthopaedics Johns Hopkins School of Medicine Assistant Professor Biomedical Engineering, Johns Hopkins University Baltimore, Maryland Associate Professor of Orthopaedics Georgetown School of Medicine Washington, DC Chapter 12: Disorders of the Nerves Chapter 24: Disorders of Tendons Faustin R. Stevens, MD Private Practice of Foot and Ankle Surgery Tri-City Orthopaedics Kennewick, Washington Chapter 19: Arthritis of the Foot and Ankle Jeffrey Swenson, MD Professor of Anesthesiology University of Utah Salt Lake City, Utah Chapter 5: Anesthesia Norman E. Waldrop, III, MD Director, Foot and Ankle Orthopaedic Surgery Andrews Sports Medicine American Sports Medicine Institute Birmingham, Alabama Chapter 30: Athletic Injuries to the Soft Tissues of the Foot and Ankle

Contributors

Art Walling, MD Foot and Ankle Surgery Musculoskeletal Oncology Florida Orthopaedic Institute Tampa, Florida Chapter 37: Ankle Fractures

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Keith L. Wapner, MD, FACS Clinical Professor of Orthopaedic Surgery Director, Foot and Ankle Division Director, Foot and Ankle Fellowship Program University of Pennsylvania Adjunct Professor of Orthopedic Surgery Drexel College of Medicine Philadelphia, Pennsylvania Chapter 4: Conservative Treatment of the Foot

Preface

In 1959, Henri L. DuVries, MD, published the first edition of Surgery of the Foot. This text summarized his 30-year personal experience in diagnosing and treating disorders, deformities, and injuries of the foot and ankle. His book became a classic, but it was also significant because it was written by a physician who originally had obtained his training as a podiatrist and then subsequently became a doctor of medicine. In 1965, Dr. DuVries expanded the book to include several other contributors, taking a form that is a model even for the current textbook. Included in this second edition were Verne T. Inman, MD, chairman of the Department of Orthopaedic Surgery at the University of California, San Francisco, and Roger A. Mann, MD, a senior resident in orthopaedic surgery. Eight years later, in 1973, Dr. Inman succeeded Dr. DuVries as the editor of the third edition of Surgery of the Foot. Again, with this text, an expanded objective included discussion of the ankle joint as well as an in-depth analysis of the biomechanics of the foot and ankle. Five years later, in 1978, Dr. Mann became the editor of the fourth edition. Dr. Mann, having been a resident under Dr. Inman and having served a fellowship under Dr. DuVries, was presented with a unique opportunity to blend the special interests of these two unique clinicians—Dr. Inman’s basic biomechanical research and Dr. DuVries’ wealth of clinical knowledge. In 1986, Dr. Mann edited a revised fifth edition. In 1978, as Dr. Mann’s first foot and ankle fellow, I had the opportunity to be exposed to both his philosophy of patient care and the creativity with which he addressed the evaluation and treatment of his patients. His meticulous surgical technique and comprehensive postoperative program were coupled with an introspective method of assessing the results of specific procedures to delineate the preferred treatment regimen. Dr. Mann’s 45 years in private practice, stimulated by more than 75 foot and ankle fellows, have complemented my interaction with him. In 1999, I initiated my own fellowship program and have learned a great deal from the 15 fellows who I have trained. I also have frequently reviewed the surgical procedures used in my everyday practice, with the common goal of defining the strengths of individual procedures as well as their weaknesses. From the 34 years that I have been in private practice in Boise, Idaho, I have come to

believe that the principles initially espoused by Drs. Inman and DuVries and expanded on by Dr. Mann have given me a unique perspective. In 1993, Dr. Mann and I collaborated on the sixth edition, which was expanded to a comprehensive twovolume text. In 1999, this was revised by us as the seventh edition and, in 2005, it was published as a colorized eighth edition, in which we were joined by, Dr. Charles L. Saltzman, as a co-editor. This is a living text and has continued to evolve from the initial work of Henri L. DuVries. Much of our orthopaedic careers have been devoted to working with this text; Dr. Mann has contributed to or edited all but one of the first eight editions, and I have contributed to or edited half of the editions. However, change and growth are important! As of this edition, Dr. Mann has become an editor emeritus but has continued to give us his input and valued advice. To recognize and honor his invaluable contributions to the textbook, we have named this ninth edition Mann’s Surgery of the Foot and Ankle. Most important, Robert B. Anderson, MD, a past fellow of John Gould, MD, joins Dr. Saltzman and me as an editor of this text. Dr. Anderson brings a wealth of clinical knowledge and a sports medicine background to this association. Just as Dr. DuVries complemented his text by adding Dr. Inman, and Dr. Inman introduced Dr. Mann, we feel strongly that Dr. Anderson’s addition will make this a stronger and more well-rounded work. The ninth edition is also enhanced by the work of many of our excellent fellows and colleagues from around the world who have made substantial sacrifices to contribute to this textbook. In this edition, 25 authors continue to contribute, but 42 new authors have been added. These contributing authors are at the forefront of their specific area of foot and ankle surgery. Each contributing author has covered a specific topic in a comprehensive fashion, which we believe will leave the reader with a clear, concise appreciation of the subject. Although this book is not meant to be encyclopedic in nature, our goal has always been to provide the reader with a method of evaluating and treating a particular problem. More than 40% of the ninth edition has been completely rewritten by both new and returning contributors, and the remaining chapters have been updated. xiii

Preface

In 1990, Dr. Mann and I published the Video Textbook of Foot and Ankle Surgery, the second volume of which appeared in 1995. This enabled foot and ankle surgeons to view a surgical procedure while simultaneously reading about the operative technique. Encouraged by the success of this endeavor, the eighth edition of Surgery of the Foot and Ankle incorporated, for the first time, 60 edited videos on two DVDs. This unique addition has now become an industry standard. To enhance the current edition, we have retained 45 classic videos narrated by Dr. Mann and added 75 new videos contributed by us as well as many other colleagues. Furthermore, advances in Internet and online learning have enhanced the electronic version of the ninth edition textbook and video compilation to allow viewing on smartphone and tablet devices before performing surgical procedures, affecting both learning and improving patient care. This new edition has been divided into 10 sections that have been subdivided into chapters. Specific surgical techniques within the chapters are described and illustrated in detail to afford the reader an understanding of the indications for each procedure and insight into the performance of the technique. Although many different treatment regimens are presented, our goal is to recommend a specific treatment plan for each pathologic entity. Furthermore, some topics are presented in more than one section, enabling the reader to appreciate the varying points of view presented by individual contributors. It is our goal to provide the reader with an accurate assessment of both the attributes and the deficiencies of specific orthopaedic foot and ankle procedures, new and old. In this edition, we present our most up-to-date thinking regarding the diagnosis, treatment, and specific surgical care of foot and ankle problems. In Part I, General Considerations, the biomechanics, examination, and conservative treatment of foot and ankle problems are addressed. In large part, the initial principles advocated by Dr. DuVries, Dr. Inman, and Dr. Mann, as presented in their early editions, are included in this portion of the text but have been updated. Anesthetic techniques have been completely rewritten and have been updated to include popliteal blocks and indwelling catheters. Discussions of imaging methods, an integral part of the evaluation process for foot and ankle disorders, have also been completely rewritten and include in-depth coverage of magnetic resonance imaging and computed tomography. In Part II, Forefoot, an extensive analysis of deformities of the great toe, along with complications associated with individual hallux valgus procedures, has been completely revised to make the reader aware of primary surgical techniques as well as salvage techniques used for postsurgical complications. Inclusion of newer, popular surgical techniques has been added. The chapter on lesser toes has been completely rewritten and updated because of the vast number of advances made in the area of

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plantar plate tears and treatment of this complex problem. The chapters on sesamoids, keratotic disorders, and toenail abnormalities have all been updated as well. Part III, Nerve Disorders, and Part IV, Miscellaneous, have been completely updated to cover both acquired and static neurologic disorders; the material about heel pain has been rewritten and updated by new authors. Part V, Soft Tissue Disorders of the Foot and Ankle, includes revised chapters on infection, dermatology, and soft tissue reconstruction and a completely new chapter on tumors of the foot and ankle. Part VI, Arthritis, Postural Disorders, and Tendon Disorders, has been completely revamped, updating our current knowledge and treatment of systemic inflammatory arthritis, traumatic arthritis, and osteoarthritis. The chapter on total ankle arthroplasty presents substantial changes because of the dramatic developments that have occurred over the past decade in ankle joint replacement. Revisions of the chapters on pes planus and pes cavus are included. The chapter on arthrodesis of the foot has been replaced by one on arthritis of the hindfoot and midfoot, containing both assessment and surgical treatment of conditions in this region. The chapter on tendon abnormalities has been extensively rewritten to reflect significant technical advances in this area. A separate section, Part VII, Diabetes, contains three completely updated chapters on diabetes, amputations, and prostheses of the foot and ankle. Part VIII, Sports Medicine, includes a comprehensive chapter on athletic soft tissue injuries as well as specific chapters regarding stress fractures and arthroscopy; all three chapters have been revised and updated to familiarize the reader with this exciting and evolving area of orthopaedic technology. Pediatrics is covered in Part IX with two chapters: a general pediatric chapter and a separate chapter on congenital and acquired neurologic disorders, where new authors have added significant new information. Finally, Part X, Trauma, includes six chapters. These chapters, which have been updated and revised, include discussion of fractures of the distal tibia; ankle; dislocations of the foot and ankle; and calcaneus talus, midfoot, and forefoot fractures, which are covered in a comprehensive fashion. As Roger Mann stated in the preface of the fifth edition, “As medicine continues to progress, the information of this textbook will again need to be upgraded. The principles presented, however, are basic in their approach and will not change significantly over the years.” We believe that the ninth edition of Mann’s Surgery of the Foot and Ankle will strongly enhance this dynamic and exciting field of orthopaedics and will complement the learning experience of the resident and fellow-in-training as well as the practicing surgeon. Michael J. Coughlin, MD

We acknowledge the previous editions of this text and the editors of each edition: SURGERY OF THE FOOT 1st Edition, 1959, editor: Henri L. DuVries, MD 2nd Edition, 1965, editor: Henri L. DuVries, MD 3rd Edition, 1973, editor: Verne T. Inman, MD 4th Edition, 1978, editor: Roger A. Mann, MD 5th Edition, 1986, editor: Roger A. Mann, MD SURGERY OF THE FOOT AND ANKLE 6th Edition, 1993, editors: Roger A. Mann, MD, and Michael J. Coughlin, MD

7th Edition, 1999, editors: Michael J. Coughlin, MD, and Roger A. Mann, MD 8th Edition, 2007, editors: Michael J. Coughlin, MD; Roger A. Mann, MD; and Charles L. Saltzman, MD MANN’S SURGERY OF THE FOOT AND ANKLE 9th Edition, 2014, editors: Michael J. Coughlin, MD; Charles L. Saltzman, MD; and Robert B. Anderson, MD

Acknowledgments We acknowledge those who have assisted us in the preparation of this text: Video productions: Boise, Idaho Travis J. Kemp, MD—surgical videography, video editing, and video production; Saint Alphonsus Hospital day surgery employees for their assistance in surgical videography; Eileen Brown, LPN, for assistance in surgical procedures and videography Artwork: Boise, Idaho Barbara Kirk of Graphic Source—color artwork

Executive and administrative support: Saint Alphonsus Health Care Systems, Boise, Idaho Sally Jeffcoat, President and CEO of Saint Alphonsus Health Systems; David F. Kirk, MHA, Director of Operations, Saint Alphonsus Medical Group; Annie T. Sutton, MBA, Clinic Manager, Coughlin Foot and Ankle Clinic at Saint Alphonsus Hospital Secretarial and technical support: Salt Lake City, Utah Rebecca Nielson

Clinical and literary assistance: Boise, Idaho Margaret C. Collins, RN, ONC—patient follow-up photography and patient verification; Sandra Hight—librarian, the Kissler Medical Family Library

Michael J. Coughlin, MD Charles L. Saltzman, MD Robert B. Anderson, MD

We are proud to dedicate the ninth edition of Surgery of the Foot and Ankle to Roger A. Mann, MD, and have changed the official name to Mann’s Surgery of the Foot and Ankle. Dr. Mann served as a mentor and teacher at a time when there were few foot and ankle fellowships or fellows. He guided the American Orthopaedic Foot and Ankle Society in its early years and promoted education of residents and surgeons in active practice through programs at the American Academy of Orthopedic Surgeons and the American Orthopaedic Foot and Ankle Society meetings. Prolific in his studies and publications, he has introduced more than 75 fellows to his methods of investigation and surgery, thus truly changing surgery in America during his time. He took the rather small primer entitled Surgery of the Foot and changed it to a two-volume color textbook—Surgery of the Foot and Ankle, with a video supplement—that has become the definitive textbook for foot and ankle surgery in the world. His vision and action are proof that one man can truly make a difference, and he has done that.

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List of Video Clips

AMPUTATIONS 1. Symes Amputation 2. Transmetatarsal Amputation 3. Trans-Phalangeal Amputation of the Great Toe ANESTHESIA 4. Toe Block 5. Ankle Block 6. Popliteal Block 7. Popliteal Block with Indwelling Catheter ANKLE 8. Brostrom Repair with Gould Modification 9. Brostrum—Clanton Technique 10. Lateral Ankle Ligament Reconstruction with Peroneus Brevis Tendon 11. Coughlin Lateral Ankle Reconstruction with Allograft 12. Lateral Ligament Repair with Semi-Tendinosis Allograft and Interference Screws 13. ATFL Ligament Repair with Brostrom–Evans (Partial Peroneus Brevis Transfer) 14. OATS Procedure 15. Os Trigonum Excision—Lateral Approach and Medial Approaches ANKLE ARTHROPLASTY 16. Total Ankle Arthroplasty-STAR© Technique 17. Total Ankle Arthroplasty-InBone© Technique 18. Total Ankle Arthroplasty-Salto© Technique 19. Total Ankle Arthroplasty-Zimmer Technique 20. Total Ankle Arthroplasty-Hintegra© Technique ARTHRODESIS 21. Ankle Arthrodesis with Screw Fixation 22. Ankle Arthrodesis Through Lateral Approach and Plate Fixation 23. Ankle Arthrodesis Through Anterior Approach 24. Tibiotalar Calcaneal Arthrodesis Through Lateral Approach with Lateral Plate 25. Tibiotalar Calcaneal Arthrodesis with I.M. Rod 26. Subtalar Joint Arthrodesis with Screw Fixation 27. Subtalar Joint Arthrodesis with Divergent Screw Technique 28. Calcaneocuboid Arthrodesis with Proximal Tibia Bone Graft 29. Double Arthrodesis (Calcaneocuboid and Talonavicular) 30. Triple Arthrodesis with Screw Fixation

ARTHRITIS OF THE FOREFOOT 31. Cheilectomy for Hallux Rigidus 32. Cheilectomy and Chondroplasty for Hallux Rigidus 33. First Metatarsophalangeal Joint Arthrodesis with Dorsal Plate Fixation 34. First Metatarsophalangeal Joint Arthrodesis with Iliac Crest Bone Graft and Revision Plate 35. First Metatarsophalangeal Arthrodesis with Steinmen Pins 36. Rheumatoid Forefoot Reconstruction ARTHROSCOPY 37. Arthroscopy of the Ankle 38. Arthroscopy of the Subtalar Joint 39. Microfracture of Talar Osteochondral Lesion 40. Posterior Ankle Arthrosopy with Debridement and Autograft of Intra-Osseous Talar Cysts 41. Arthroscopic Excision of a Haglund Deformity— Endoscopic Calcaneoplasty 42. Arthroscopic Debridement of Flexor Hallucis Longsus PVNS BUNIONETTE 43. Chevron Bunionette Repair 44. Weil Osteotomy for Bunionette Repair 45. Sponsel Osteotomy for Bunionette Repair 46. Coughlin Diaphyseal Oblique Osteotomy CAVUS FOOT 47. Plantar Facial Release 48. Dwyer Calcaneal Osteotomy 49. Transfer of Peroneus Longus to Brevis 50. Dorsiflexion Osteotomy of First Metatarsal 51. First Toe Jones Procedure GREAT TOE 52. Akin Osteotomy 53. Akin Procedure with Screw Fixation 54. Chevron + Akin Procedure 55. Distal Soft Tissue Repair 56. Proximal Crescentic Osteotomy with Distal Soft Tissue Repair 57. Lapidus Repair 58. Triple Osteotomy for Juvenile Hallux Valgus 59. Scarf Procedure 60. Keller Procedure 61. Hallux Varus Repair with Extensor Hallucis Longus Tendon Transfer

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List of Video Clips

62. Bi-Planar Chevron Ostetotomy 63. First Interphalangeal Joint Arthrodesis 64. Tibial Sesamoid Shaving 65. Medial Sesamoid Excision 66. Turf Toe—Acute Plantar Plate Repair Through Medial Approach 67. Turf Toe—Acute Plantar Plate Repair Through Lateral Approach 68. Turf Toe—Repair of Chronic Injury LESSER TOE DEFORMITIES 69. DuVries Condylectomy 70. Weil Osteotomy 71. Freibergs Infraction 72. Plantar Plate Repair of Lesser Metatarsophalangeal Joints 73. Crossover Fifth Toe Repair 74. Mallet Toe Repair 75. Hammer Toe with Kirschner Wires 76. Hammer Toe Repair with Intramedullary Implant 77. Flexor Tendon Transfer 78. Lateral Condylectomy 79. Repair of Hard Corn 80. Repair of Soft Corn MIDFOOT 81. Excision Exostosis Midfoot 82. Midfoot Arthrodesis with a Medial Plate 83. Midfoot Arthrodesis for Subacute Ligamentous Lisfranc Injury 84. Midfoot Arthrodesis with Uni-CP Clips 85. Tarsometatarsal Arthrodesis with Uni-CP Clips, Posterior Tibial Tendon Resection with Flexor Digitorum Longus Transfer NERVES 86. Excision of Interdigital Neuroma 87. Resection of Superficial and Deep Peroneal Nerve and Burying in Bone 88. Tarsal Tunnel Release PEDIATRICS 89. Excision of Calcaneonavicular Coalition 90. Excision of Talocalcaneal (Subtalar) Coalition Through a Medial Approach 91. Ponseti Method of Clubfoot Casting 92. Vertical Talus Corrected with Serial Casting TENDON DISORDERS—ACHILLIES 93. Reconstruction of Achilles Tendon for Tendinosis with FHL Transfer 94. Excision of Haglund Deformity 95. Percutaneous Repair of an Acutely Ruptured Achilles Tendon 96. Open Repair of an Acutely Ruptured Achilles Tendon 97. Open Repair of a Chronic Achilles Tendon Rupture 98. Debridement of Calcific Tendonitis with Ultrasound Guidance and Platelet Rich Plasma Injection 99. Repair of Haglund Deformity with Suture Bridge© and FHL Transfer

xxii

100. Repair of Haglund Deformity with Speed Bridge© and FHL Transfer 101. Strayer Procedure 102. Gastrocnemius Recession TENDON DISORDERS—PERONEAL TENDONS 103. Excision of Peroneal Tubercle 104. Peroneal Tendon Primary Repair 105. Peroneal Tendon Debridement and Tubularization 106. Peroneus Longus to Brevis Tenodesis for Ruptured Peroneus Longus 107. Peroneus Longus to Brevis Tenodesis for Degenerative Peroneus Longus 108. Excison of Os Vesalianum with Repair of Peroneus Brevis 109. Repair of Dislocating Peroneal Tendons with Rerouting Beneath the Calcaneofibular Ligament 110. Repair of Dislocating Peroneal Tendons with Indirect Groove Deepening Procedure 111. Repair of Dislocating Peroneal Tendons with Groove Deepening Procedure 112. Peroneal Tendon Reconstruction with FHL Autograft and Elmslie Ankle Reconstruction with Suture Anchors 113. Subtalar Joint Arthrodesis with Peroneal Tendon Excision and FHL Transfer TENDON DISORDERS—ANTERIOR AND POSTERIOR TIBIAL TENDONS, MISCELLANEOUS TENDONS 114. Extensor Hallucis Longus Repair with Allograft 115. Anterior Tibial Tendon Reconstruction 116. PTT Reconstruction with FDL Transfer 117. PTT Reconstruction with Medial Calcaneal Displacement Osteotomy 118. Calcaneal Osteotomy - Modified Malerba Type 119. Step Cut Osteotomy for Lateral Column Lengthening and Medial Displacement of the Calcaneus TRAUMA 120. ORIF Fifth Metatarsal Jones Fracture 121. Fixation of Lesser Metatarsal Fracture with Percutaneous Intramedullary Technique 122. ORIF Ligamentous Lisfranc Fracture 123. Syndesmosis Fixation with Endobutton Device Following Maisonneuve Fracture 124. Closed Reduction with Percutaneus Fixation Calcaneous Fracture 125. ORIF Calcaneus TOENAILS 126. Infected Toenail Decompression 127. Winograd Procedure 128. Heifitz Procedure 129. Zadic Procedure 130. Terminal Symes Amputation of the Great Toe Video Editing by Travis J. Kemp, MD Most voiceovers by Michael J. Coughlin, MD, and Roger A. Mann, MD

Chapter

Biomechanics of the Foot and Ankle Andrew Haskell, Roger A. Mann CHAPTER CONTENTS GAIT CYCLE Walking Cycle First Interval Second Interval Third Interval Running Cycle KINEMATICS OF HUMAN LOCOMOTION Vertical Body Displacements Lateral Body Displacements Horizontal Limb Rotation KINETICS OF HUMAN LOCOMOTION Measuring Whole Body Kinetics and Plantar Pressure Types of Studies Data Representations Measurement Variability Kinetics of Walking Whole Body Kinetics Plantar Pressure Kinetics Kinetics of Running BIOMECHANICS OF THE COMPONENT OF THE LOCOMOTOR SYSTEM Heel Strike to Foot Flat: Supple for Impact Absorption Ankle Joint Subtalar Joint Transverse Tarsal Joint Complex Foot Flat to Toe-Off: Progression to a Rigid Platform Ankle Joint Subtalar Joint Transverse Tarsal Articulation Plantar Aponeurosis Metatarsophalangeal Break Talonavicular Joint Swing Phase Component Mechanics of Running SURGICAL IMPLICATIONS OF BIOMECHANICS OF THE FOOT AND ANKLE Biomechanical Considerations in Ankle Arthrodesis

4 4 4 5 6 7 7 8 9 9 10 10 11 13 14 15 16 17 18 19 19 19 20 22 23 24 25 25 25 26 27 27 28 28 29

Hindfoot Alignment Midfoot Alignment Forefoot Principles Tendon Transfers Ligaments of the Ankle Joint

29 30 31 31 31

The human foot is an intricate mechanism that functions interdependently with other components of the locomo tor system. Failure of the functioning of a single part, whether by disease, external forces, or surgical manipula tion, will alter the functions of the remaining parts. To further complicate things, wide variations occur in the normal component parts of the foot and ankle, and these variations affect the degree of contribution of each part to the function of the entire foot. Depending on the contributions of an individual component, the loss or functional modification of that component by surgical intervention may result in minor or major alterations in the function of adjacent components. This variation helps to explain why the same procedure performed on the foot of one person produces a satisfactory result, whereas in another person the result is unsatisfactory. Yet the surgeon is called on constantly to change the anatomic and structural components of the foot. When so doing, awareness of the consequences of these changes is fundamental to achieving desired results. Put another way, an understanding of interrelationships between foot and ankle components and how they interact with the greater locomotor system is critical to achieving predictable outcomes when altering these components surgically. Understanding the biomechanics of the foot and ankle also contributes to sound surgical decision making and adds to the success of postoperative treatment. Appre ciating the mechanical behavior of the foot allows the physician to differentiate foot disabilities that may be successfully treated by nonsurgical procedures rather than approached surgically. Furthermore, some operative pro cedures that fail to completely achieve the desired result can be improved by minor alterations in the behavior of adjacent components through shoe modification or the use of orthotic inserts or braces. 3

Part I ■ General Considerations

With increased attention being given to athletics, the physician must have a basic knowledge of the mechanics that occur during running. Many of the same basic mech anisms that will be described for the biomechanics of the foot and ankle are not significantly altered during running. The same stabilization mechanism within the foot occurs during running as during walking. The major differences observed during running are that the gait cycle is altered considerably, the amount of force generated (as measured by force plate data) is markedly increased, the range of motion of the joints of the lower extremities is increased, and the phasic activity of the muscles of the lower extrem ities is altered. Differences between walking and running will be highlighted in the following sections. Starting this textbook with a chapter focused on foot and ankle biomechanics is meant to provide a foundation for the reader upon which the remaining chapters are built. It has been assumed that the orthopaedic surgeon possesses an accurate knowledge of the anatomy of the foot and ankle. If this knowledge is lacking, textbooks of anatomy are available that depict in detail the precise anatomic structures constituting this part of the human body.46,49 In this chapter, the gait cycle is reviewed, kine matic and kinetic aspects of gait are explored, and specific anatomic interrelationships of the foot and ankle are emphasized. Throughout this discussion, mechanics that differentiate running from walking are described. Finally, clinical examples are explored, and methods for func tional evaluation of the foot are presented as practical demonstrations of the concepts within. GAIT CYCLE

Walking Cycle Human gait is a rhythmic, cyclic forward progression involving motion of all body segments. A single cycle is often defined as the motion between the heel strike of one step and the heel strike of the same foot on the sub sequent step. Gait parameters, such as stride length, veloc ity, and cadence, are easy to measure based on this definition. A single cycle can be divided further. The walking cycle for one limb is broken into a stance phase and a swing phase. The stance phase typically constitutes 62% of the cycle and the swing phase 38%. The stance phase is further divided into a period of double limb support (from 0% to 12%), in which both feet are on the ground, followed by a period of single limb support (from 12% to 50%) and a second period of double limb support (from 50% to 62%), after which the swing phase begins (Fig. 1-1). The opposite leg also goes through a predictable sequence during a gait cycle. The position and activities of this contralateral leg can be seen at predictable times. For instance, contralateral toe-off is typically at 12% of the gait cycle, occurring after the ipsilateral foot has reached a foot-flat position. Ipsilateral heel rise begins at 4

Heel Strike

Foot Flat

Heel Rise

Opposite Toe-off

Heel Strike

Toe-off

Opposite Heel Strike

Stance phase Double Limb Support

Single Limb Support

0 7 12

Swing phase Double Limb Support

100

Percent of gait cycle Figure 1-1 Phases of the walking cycle. Stance phase constitutes approximately 62%, and swing phase 38% of cycle. During stance phase of walking, there are two periods of double limb support and one period of single limb support. Stance phase is further divided into three intervals: from heel strike to foot flat at approximately 7% of the gait cycle, foot flat to heel rise at approximately 34% of the gait cycle, and heel rise to toe-off at approximately 62% of the gait cycle.

34% as the contralateral leg swings through and passes the stance foot. Finally, contralateral heel strike occurs at 50% of the gait cycle. In a patient with spasticity, the initial heel strike may be toe contact, and foot flat may not occur by 7% of the cycle. Heel rise may be premature if spasticity or an equinus contracture is present or delayed in the case of weakness of the gastrocnemius–soleus muscle group. Weakness of anterior compartment leg musculature resulting in a footdrop may lead to accentuated hip and knee flexion during swing-through and alteration in attaining a foot-flat position. The walking cycle being one of continuous motion is difficult to appreciate in its entirety because so many events occur simultaneously. To help appreciate the dif ferent activities and functions of the components of the foot and ankle during gait, the stance phase can be divided into three intervals: the first interval, extending from initial heel strike to the foot laying flat on the floor; the second interval, occurring during the period of foot flat as the body passes over the foot; and the third inter val, extending from the beginning of ankle joint plantar flexion as the heel rises from the floor to when the toes lift from the floor. First Interval The first interval occurs during approximately the first 15% of the walking cycle and is defined from the moment of initial heel strike to when the foot becomes flat on the floor. Typically, the opposite heel has lifted from the floor, but weight remains on the forefoot. During the first inter val, the foot helps to absorb and dissipate the forces generated by the foot striking the ground.

Biomechanics of the Foot and Ankle ■ Chapter 1

First interval

Body weight

125% Percentage 100% of 50% body weight

˚ ˚

Dorsiflexion

Plantar flexion

Ankle rotation Neutral standing position

˚ ˚

EMG activity

Intrinsic muscles of foot Posterior tibial muscles

Anterior tibial muscles

˚ ˚

Supination

Pronation

Neutral standing position

˚ ˚ 20 ˚ 10 ˚ 20

Internal rotation

Subtalar rotation

appears to play a role in restricting this motion at initial ground contact. The subtalar joint links rotation of the hindfoot to rotation of the leg. During the first interval, eversion of the calcaneus is translated by the subtalar joint into inward rotation that is transmitted proximally across the ankle joint into the lower extremity (Fig. 1-2E). Distally, this hindfoot eversion unlocks the transverse tarsal joint (Fig. 1-2D), allowing the midfoot joints to become supple. This allows the flattening of the longitudinal arch that contributes to energy dissipation during this phase. At heel strike, the center of gravity of the body is decel erated by ground contact, then immediately accelerated upward to carry it over the extending lower extremity. The heel’s impact and body’s center of gravity shift accounts for a vertical floor reaction that exceeds body weight by 15% to 25% (Fig. 1-2A). Eccentric contraction of the anterior compartment leg muscles slows the rapid ankle plantar flexion during this phase from heel strike until a foot-flat position is reached. The posterior calf muscles all are electrically quiet, as are the intrinsic muscles in the sole of the foot (Fig. 1-2C). There is no muscular response in those muscles usually considered important in supporting the longitudinal arch of the foot. Weakness of the anterior compartment muscles leads to a loss of this deceleration and a charac teristic slap foot gait.

External rotation

˚ 20 ˚ 10

Horizontal rotation of tibia Neutral standing position 0%

15% Percentage of walking cycle

Figure 1-2 Composite of events of first interval of walking, or period that extends from heel strike to foot flat. EMG, electromyograph.

The ankle joint undergoes rapid plantar flexion from heel strike until foot flat is achieved. At approximately 7% of the walking cycle, dorsiflexion begins (Fig. 1-2B). As the foot is loaded with the weight of the body during the first interval, the calcaneus rapidly everts and the longitudinal arch flattens. This flattening of the arch originates in the subtalar joint and reaches a maximum during this interval (Fig. 1-2D). The hindfoot is often mildly supinated at initial ground contact associated with ankle dorsiflexion during swing-through. The hindfoot moving from supination to pronation during the first interval is a passive mechanism, and the amount of motion appears to depend entirely on the configuration of the articulating surfaces, their capsular attachments, and ligamentous support. No significant muscle function

Second Interval The second interval extends from 15% to 40% of the walking cycle. During this interval, the body’s center of gravity passes from behind to in front of the weightbearing leg. It reaches a maximum height as it passes over the leg at about 35% of the cycle, after which it com mences to fall. During this interval, the foot transitions from a flexible, energy-absorbing structure to a more rigid one, capable of bearing the body’s weight. The ankle joint undergoes progressive dorsiflexion during the second interval, reaching its peak at 40% of the walking cycle. This is when the force across the ankle joint has reached a maximum of 4.5 times body weight. Heel rise begins at 34% of the cycle as the contralateral leg passes by the stance foot and precedes the onset of plantar flexion, which begins at 40% (Fig. 1-3B). During the second interval, the subtalar joint progres sively inverts. This starts at about 30% of the cycle in a normal foot and at about 15% of the cycle in a flatfoot (Fig. 1-3D). Multiple factors contribute to this inversion, but precisely which plays the greatest role is unclear. Above the subtalar joint, the swinging contralateral limb externally rotates the stance limb. This external rotation torque is translated by the subtalar joint into hindfoot inversion. The oblique nature of the ankle joint axis, the oblique setting of the metatarsal break, and the function of the plantar aponeurosis also contribute to hindfoot inversion. Inversion of the subtalar joint is passed distally into the midfoot, increasing the stability of the transverse 5

Part I ■ General Considerations

Second interval Third interval Percentage of body weight

A Dorsiflexion

Plantar flexion

125% 100% 50%

˚ ˚

Ankle rotation

˚ ˚

Neutral standing position

20 10 10 20

Intrinsic muscles of foot Posterior tibial muscles Anterior tibial muscles C 20 10 Supination

˚ ˚

Pronation

D Internal rotation

External rotation

Body weight

˚ 20 ˚ 20 ˚ 10 ˚ 10

˚ 20 ˚15% 10

˚ ˚

EMG activity

Dorsiflexion

Plantar flexion

˚ 20 ˚

Ankle rotation

Neutral standing position

EMG activity

Intrinsic muscles of foot Posterior tibial muscles

Subtalar rotation

Anterior tibial muscles

Neutral standing position Horizontal rotation of tibia

Neutral standing position 30% Percentage of walking cycle

˚ ˚

40%

Figure 1-3 Composite of events of second interval of walking, or period of foot flat. EMG, electromyograph.

tarsal articulation and transforming the flexible midfoot into a rigid structure. During this interval, full body weight is not borne on the foot, smoothing the transition to single limb support. Force plate recordings show that the load on the foot may be as low as 70% to 80% of actual body weight (Fig. 1-3A). During the second interval, important functional changes occur in both the foot and leg, which are the result of muscular action. The posterior and lateral com partment leg muscles (triceps surae, peroneals, tibialis posterior, long toe flexors) and intrinsic muscles in the sole of the foot demonstrate electrical activity (Fig. 1-3C). Intrinsic muscle activity of the normal foot begins at 30% of the cycle, whereas in flatfoot, activity begins at 15% of the cycle. The posterior calf musculature slows the forward movement of the tibia over the fixed foot, which permits the contralateral limb to increase its step length. Weak ness of the posterior compartment muscles may lead to premature contralateral heel strike and shortened stride length. 6

Body weight

125% Percentage 100% of 50% body weight

Supination

Pronation

Internal rotation

External rotation

˚ 20 ˚ 20 ˚ 10 ˚ ˚ ˚

Subtalar rotation

Neutral standing position

Horizontal rotation of tibia Neutral standing position

10 20

40%

65% Percentage of walking cycle

Figure 1-4 Composite of all events of third interval of walking, or period extending from foot flat to toe-off. EMG, electromyograph.

Third Interval The third interval constitutes the last of the stance phase and extends from 40% to 62% of the walking cycle. The ankle joint demonstrates rapid plantar flexion during this interval as the foot essentially extends the stance, effective length. The subtalar joint continues to invert during this interval, reaching its maximum at toe-off (Fig. 1-4D). This completes the conversion of the forefoot from the flexible structure observed in the first interval at the time of weight acceptance to a rigid struc ture at the end of the third interval in preparation for toe-off. The inversion is a continuation of the processes that began in the second interval. These include external rotation of limb above the foot passing across the ankle

Biomechanics of the Foot and Ankle ■ Chapter 1

and subtalar joints as well as mechanisms in the foot such as the obliquity of the ankle joint, the function of the plantar aponeurosis, and obliquity of the metatarsal break. Distally, the transverse tarsal joint is converted from a flexible structure into a rigid one by the progressive inversion of the calcaneus. The talonavicular joint also is stabilized during this period by the pressure placed across the joint by both body weight and the intrinsic force created by the plantar aponeurosis. At the beginning of the third interval, force plate recordings demonstrate an increase in the percentage of body weight borne by the foot resulting from the center of gravity falling. The load on the foot exceeds body weight by approximately 20%. Later in the interval, the vertical floor reaction force falls to zero as the body’s weight is transferred to the opposite foot (Fig. 1-4A). Ankle plantar flexion during the third interval is caused primarily by the concentric contraction of the posterior calf musculature, in particular the triceps surae (Fig. 1-4B). The plantar flexion leads to relative elongation of the extremity. Although full plantar flexion at the ankle joint occurs during this interval, electrical activity is observed only until 50% of the cycle, after which there is no longer electrical activity in the extrinsic muscles (Fig. 1-4C). The remainder of ankle joint plantar flexion occurs because of the transfer of weight from the stance leg to the contralateral limb. The intrinsic muscles of the foot are active until toe-off. Although the intrinsic muscles help to stabilize the longitudinal arch, the main stabilizer is the plantar aponeurosis, which is functioning maxi mally during this period as the toes are brought into dorsiflexion and the plantar aponeurosis is wrapped around the metatarsal heads, forcing them into plantar flexion and elevating the longitudinal arch. The anterior compartment muscles become active in the last 5% of this interval, probably to initiate dorsiflexion of the ankle joint immediately after toe-off. Running Cycle The changes that occur in the gait cycle during running relative to walking are illustrated in Figure 1-5. During walking, one foot is always in contact with the ground; as the speed of gait increases, a transition occurs wherein a float phase is incorporated, during which time both feet are off the ground. Rather than a period of double limb support as occurs during walking, there is a period of no limb support. As the speed of gait continues to increase, the time the foot spends on the ground, both in real time and in percentage of cycle, decreases considerably. The speed at which one transitions from walking to running is greater than the speed at which one transitions back from running to walking. KINEMATICS OF HUMAN LOCOMOTION

Humans use a unique and characteristic orthograde bipedal mode of locomotion. But walking is more than

CYCLE TIME

Stance

Float

Swing

Float Run 0.6

Jog 0.7 Walk

0.2

0.4

0.6

0.8

1.0

Sec Figure 1-5 Variations in gait cycle for running, jogging, and walking. Note that as the speed of gait increases, stance phase decreases. In this illustration, subject is walking at 3.75 miles per hour, jogging at about 1 mile per 9 minutes, and running about 1 mile per 5 minutes.

merely placing one foot in front the other. During walking, all major segments of the body are in motion. Displace ments of the body segments occur in a well-preserved fashion and can be accurately described. Kinematics is the study of the motion of these body segments. Human locomotion is a learned process; it does not develop as the result of an inborn reflex.59 The first few steps of an infant holding onto his or her parent’s hand exemplify the learning process necessary to achieve ortho grade progression. The result of this learning process is the integration of the neuromusculoskeletal mechanisms, with their gross similarities and individual variations, into an adequately functioning system of locomotion. Once a person has learned to walk, the mechanisms of ambulation are adaptable and work whether the person is an amputee learning to use a prosthesis, a long-distance runner, or a high-heeled shoe wearer. A smoothly performing locomotor system results from the harmonious integration of many components. Because human locomotion involves all major segments of the body, certain suprapedal movements demand spe cific functions from the foot, and the manner in which the foot functions or fails to function may be reflected in patterns of movement in the other segments of the body. Similarly, alterations in movements above, such as a stiff knee or hip from arthritis or knee hyperextension from postpolio quadriceps weakness, may be reflected below by changes in the behavior of the foot. Although bipedal locomotion imposes gross similari ties in the manner in which all of us walk, each of us exhibits minor individual differences that allow us to be recognized by a friend or acquaintance, even from a dis tance. The causes of these individual characteristics of 7

Part I ■ General Considerations

Figure 1-6 Displacement of center of gravity of body in smooth sinusoidal path. (From Saunders JB, Inman VT, Eberhart HD: The major determinants in normal and pathological gait. J Bone Joint Surg Am 35A:543-558, 1953.)

locomotion are many. Each of us differs somewhat in the length and distribution of mass of the various segments of the body, segments that must be moved by muscles of varying fiber length. Furthermore, individual differences occur in the position of axes of movement of the joints, with concomitant variations in effective lever arms. These and many more such factors combine to establish in each of us a final idiosyncratic manner of locomotion. Just as no two people walk exactly alike, gait kinemat ics will not always be identical even within the same individual. The contribution of a single component varies under different circ*mstances. Type of shoe, amount of fatigue, weight of load carried, and other such variables can cause diminished functioning of some components, with compensatory increased functioning of others. An enormous number of variations in the behavior of indi vidual components are possible; however, the diversely functioning components, when integrated, are comple mentary and will produce smooth forward progression. Average values of single anthropometric observations of gait kinematic parameters are alone of little value. The surgeon should be alert to the anthropometric variations that occur within the population, but it is more important to understand the functional interrelationships among the various components. This is particularly true in the case of the foot, where anatomic variations are extensive. If average values are the only bases of comparison, it becomes difficult to explain why some feet function adequately and asymptomatically, although their mea surements deviate from the average, whereas others function symptomatically, even though their measure ments approximate the average. Therefore, in this chapter, emphasis is placed on functional interrelationships and not on lists of kinematic measurements. Vertical Body Displacements The rhythmic upward and downward displacement of the body during walking is familiar to everyone, and is 8

particularly noticeable when someone is out of step in a parade. These displacements in the vertical plane are a necessary concomitant of bipedal locomotion. When the legs are separated, as during transmission of the body weight from one leg to the other (double weight bearing), the distance between the trunk and the floor must be less than when it passes over a relatively extended leg, as during midstance. Smoothing and minimizing vertical oscillations of the body’s center of gravity minimizes energy expenditure. Physics principles tell us that much more energy is needed to lift the body against gravity and slow its descent (verti cal displacement) than to move perpendicular to gravity’s pull (fore–aft or lateral displacement). Because the nature of bipedal locomotion demands such vertical oscillations of the body, they should occur in a smooth manner. The center of gravity of the body does displace in a smooth sinusoidal path; the amplitude of displacement is approx imately 4 to 5 cm (Fig. 1-6).65,66 The body’s center of gravity reaches its maximum elevation immediately after passage over the weight-bearing leg and then begins to fall. This fall is stopped at the termination of the swing phase of the opposite leg as the heel strikes the ground. Much of the coordination of motion between the dif ferent segments of the lower limbs results in minimizing the vertical displacement of the body’s center of gravity. Although movements of the pelvis and hip modify the amplitude of the sinusoidal pathway, the knee, ankle, and foot are particularly involved in converting what would be a series of intersecting arcs into a smooth, sinusoidal curve.66 This conversion requires both simultaneous and precise sequential motions in the knee, ankle, and foot. In a well-functioning system, the body’s falling center of gravity is smoothly decelerated, because relative short ening of the leg occurs at the time of impact against a gradually increasing resistance. The knee flexes against a graded contraction of the quadriceps muscle; the ankle plantar flexes against the resisting anterior tibial muscle. After the foot-flat position is reached, further shortening

Biomechanics of the Foot and Ankle ■ Chapter 1

is achieved by pronation of the foot to a degree permitted by the ligamentous structures within. So, to reemphasize, hindfoot pronation constitutes an important additional factor to that of knee flexion and ankle plantar flexion needed to smoothly decelerate and finally to stop the downward path of the body. If one were forced to walk stiff-kneed or without a mobile foot and ankle, the downward deceleration of the center of gravity at heel strike would be instantaneous. The body would be subjected to a severe jarring force, and the locomotor system would lose kinetic energy. After reaching its nadir, the center of gravity moves upward to propel it over the stance leg. The leg function ally elongates by transitory extension of the knee, further plantar flexion of the ankle as the heel elevates, and supi nation of the foot. Elevation of the heel is the major component contributing to upward acceleration of the center of gravity at this time.

approximately over the weight-bearing foot. Watching someone walk from behind highlights this subtle side-toside shift of their center of gravity toward the stance limb. When walking side by side with a companion, if one gets out of step with the other, their bodies may bump from this side-to-side sway. The body is shifted slightly over the weight-bearing leg, with each step creating a sinusoidal lateral displacement of the center of gravity of approximately 4 to 5 cm with each complete stride. This lateral displacement can be increased by walking with the feet more widely separated and decreased by keeping the feet close to the plan of progression (Fig. 1-7). Normally, the slight valgus of the tibiofemoral angle (physiologic genu valgum) permits the tibia to remain essentially vertical and the feet close together while the femurs diverge to articulate with the pelvis, minimizing the lateral displacement. Horizontal Limb Rotation

Lateral Body Displacements When a person is walking, the body does not remain precisely in the plane of progression but oscillates slightly from side to side to keep the center of gravity

In addition to vertical and lateral displacements of the body, a series of axial rotatory movements occur that can be measured in the horizontal (transverse) plane. Rota tions of the pelvis and the shoulder girdle are easy to see

Figure 1-7 A, Slight lateral displacement of body occurring during walking with feet close together. B, Increased lateral displacement of body occurring during walking with feet wide apart. (From Saunders JB, Inman VT, Eberhart HD: The major determinants in normal and pathological gait. J Bone Joint Surg Am 35A:543-558, 1953.)

Part I ■ General Considerations

when watching someone walk. Similar horizontal rota tions occur in the femoral and tibial segments of the extremities. The tibias rotate about their long axes, inter nally during swing phase and into the first interval of stance phase and externally during the latter phases of stance. The degree of these rotations is subject to marked individual variations. In a series of 12 male subjects, the recorded average horizontal rotation of the tibia was 19 degrees during a gait cycle but varied between 13 and 25 degrees.48 At heel strike, progressive inward rotation occurs in the lower extremity, which consists of the pelvis, femur, and tibia, and this inward rotation reaches a maximum at the time of foot flat. The internal rotation at heel strike is initiated by the collapse of the subtalar joint into valgus, and its magnitude is determined by the flexibility of the foot and its ligamentous support. After contralateral toeoff, at about 12% of the cycle, progressive outward rota tion occurs, which reaches a maximum at the time of toe-off, when inward rotation resumes (Fig. 1-8). Once the foot is on the ground, progressive external rotation is probably initiated by the contralateral swinging limb, which rotates the pelvis forward, imparting a certain degree of external rotation to the stance limb. This exter nal rotation subsequently is passed from the pelvis dis tally to the femur and tibia, across the ankle joint, and is translated by the subtalar joint into inversion, which reaches its maximum at toe-off. The external rotation is enhanced by the external rotation of the ankle joint axis, the oblique metatarsal break, and the plantar aponeurosis after heel rise begins.

Heel strike

Degrees

10 in 0 out 10

PELVIC ROTATION Toe-off

Heel strike

TIBIAL ROTATION

10 in 0 out 10

90 100

Percent of walk cycle Figure 1-8 Transverse rotation occurring in the lower extremity during walking. Internal rotation occurs until approximately 15% of cycle, at which time progressive external rotation occurs until toe-off, when internal rotation begins again.

To begin a review of gait kinetics, one must recognize that the ambulating human is both a physical machine and a biologic organism subject to physical laws and beholden to muscular action. Gait kinematics and lower-extremity anatomic interrelationships strive to achieve a system that takes us from one spot to another with the least expendi ture of energy.60 Said another way, human locomotion is a blending of physical and biologic forces that combine to achieve maximum efficiency at minimum cost. Kinetics is the study of these energy expenditures. All characteristics of muscular behavior are exploited in locomotion. Muscle groups may accelerate or deceler ate body segments at different points in the gait cycle. They may contract concentrically (as they shorten) or eccentrically (as they lengthen). Part of energy conserva tion during the gait cycle involves having muscles work near their peak efficiency, which tends to be at or longer than their resting length.14,17,65 When motion in the skel etal segments is decelerated or when external forces work on the body, activated muscles become efficient. Activated muscles, in fact, are approximately six times as efficient when resisting elongation (eccentric contraction) as when shortening to perform external work.1,5,6 In addition, non contractile elements in muscles and specific connective tissue structures assist muscular action by providing an elastic component that stores and later releases kinetic energy. Assessment of the forces and torques imparted by the ground on the lower extremity has illuminated the bio mechanical processes at work during gait. Investigation of the pressures experienced by the various regions of the plantar foot has provided insight into the pathogenesis and treatment of many foot and ankle disorders. A number of tools have evolved to study gait kinetics. These are described in detail in the next section, followed by an analysis of kinetics during gait. Measuring Whole Body Kinetics and Plantar Pressure

FEMORAL ROTATION

10 in 0 out 10

KINETICS OF HUMAN LOCOMOTION

Studying the foot’s interaction with the ground has a long history, ranging from examining footprints in soil to realtime mapping of plantar pressure under natural condi tions. Plantar pressure and ground reaction force measurements are well established in the research realm and have been instrumental in refining our understand ing of foot and ankle biomechanics. In conjunction with other technology, including high-speed cameras, video motion-sensing equipment, electrogoniometers, and electromyograph (EMG) devices, the study of the ground– foot interaction has aided the understanding of gait kinet ics and kinematics. Despite improvements in available measurement methods, however, practical collection of clinically novel information remains difficult. The wide variability of normal measures makes clinical comparisons difficult.

Biomechanics of the Foot and Ankle ■ Chapter 1

The large number of measurement systems and equally large number of data analysis techniques make it difficult to generalize results. Although confirmation of areas of excess pressure and monitoring the effects of treatment may prove useful, there is little specificity between plantar pressure patterns and clinical syndromes. Types of Studies A variety of measurement techniques have been used to study the interaction of the foot with the ground. Indirect techniques rely on correlating other measurable gait parameters to plantar characteristics and offer the advan tage of not relying on expensive and often bulky equip ment. For example, an estimation of ground reaction force can be made based on a simple-to-measure tempo ral variable, foot–ground contact time.13 Direct measurement techniques rely on physical prop erties or electronic transducers to translate the interaction between the foot and the ground into a measurable quantity. Multiple direct measurement systems are avail able that use a variety of strategies to record plantar pressure or ground reaction force. Unfortunately, results obtained with different systems under similar conditions are not always similar, and even qualitative comparisons may not be appropriate.38 Spatial resolution and sample rate affect the ability of a system to record true peak

plantar pressures and to isolate particular areas under the foot. The earliest direct measurement methods relied on physical properties of a material to capture the interac tion of the foot with the ground. Casts of the foot in clay, plaster, or soil were used with the assumption that areas of deeper penetration represented areas of highest pressure.10,21 Rubber mats incorporating longitu dinal ridges,54 pyramidal projections,21 or a multilevel grid (such as the Harris-Beath mat),67,78 use the elastic property of rubber which, when stood or walked on, distorts in proportion to the pressure applied (Fig. 1-9). Although fast, inexpensive, and portable, these methods have low measurement resolution and lack temporal discrimination.67 Optically based systems rely on visualizing the plantar aspect of the foot during stance or gait. The simplest allows observation or photographic recording of the plantar foot through a clear platform (Fig. 1-10). This provides an accurate, dynamic, qualitative representation of foot morphology. Addition of a physical transduction device between the foot and glass plate allows quantifica tion of regionalized plantar pressures and adds the tem poral component missed using a physical transduction system alone.21 The pedobarograph places a thin plastic sheet over the clear plate.4 The sheet is illuminated at the edges, and pressure on the plastic distorts the light in

Figure 1-9 Pressure distribution on plantar aspect of foot as demonstrated by use of barograph. As dots get larger and denser, pressure distribution is greater. (From Elftman H: A cinematic study of the distribution of pressure in the human foot. Anat Rec 59:481-491, 1934.)

Part I ■ General Considerations

B2 A2 Figure 1-10 Feet and legs of person standing on barograph. A, Weight bearing with muscles relaxed. B, Rising on toes.

VERTICAL FORCE

FORE–AFT SHEAR

Percent of walk cycle

100

140

100

Fwd. Percent of body weight

Percent of body weight

proportion to the pressure applied. The images can be recorded and calibrated to provide a spatial resolution and temporal responsiveness not found with the HarrisBeath mat. However, slow responsiveness at high forces may bias results.36 A force plate measures the ground reaction force, that is, the force exerted by the ground on the foot, in three degrees of freedom (vertical force, forward shear, side shear), and allows calculation of the torques around the foot and ankle (axial torque, sagittal torque, coronal torque). Force transducers are configured in orthogonal planes at the corners of a section of floor. The resulting data provide a representation of the average forces expe rienced by the foot over the gait cycle (Fig. 1-11). One advantage of this type of system is that shear forces and torques can be measured in addition to vertical force. The limitations include the lack of ability to map specific regions of plantar pressure. This limitation can be circum vented with the addition of an optical diffraction system, as described above, or with a series of smaller force plates placed in tandem.71

100 60 20

20 0 20

Aft Heel strike

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100

Newton-meters

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Heel strike

TORQUE

MEDIAL–LATERAL SHEAR 0

Toe-off

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Toe-off

Heel strike

Toe-off

Heel strike

Figure 1-11 Ground reaction to walking. A, Vertical force. B, Fore–aft shear. C, Medial–lateral shear. D, Torque. Ext., External; Fwd., forward; Int., internal; Lat., lateral; Med., medial.

Biomechanics of the Foot and Ankle ■ Chapter 1

32 ms

128 ms

224 ms

320 ms

416 ms

512 ms

576 ms Figure 1-12 Pressure distribution under bare foot during walking. Height of display above ground is proportional to pressure. (From Clarke TE: The pressure distribution under the foot during barefoot walking [doctoral dissertation], University Park, Pa, 1980, Pennsylvania State University.)

The ability to place pressure transducers on discrete parts of the foot has become possible, as their size has shrunk. They can be placed on strategic points of the foot, or an array can be created to map the pressures exerted by the foot during stance or gait. These data provide a spatial and temporal map of plantar pressure over the gait cycle54,62 (Fig. 1-12). Many of these systems use a floor mat or platform built into the floor with a grid of pressuresensitive transducers. An alternative is to place a thin film containing a pressure transduction array into a shoe (Fig. 1-13). In this way, the plantar pressures experienced by the foot can be measured in a wider variety of settings and under multiple impacts as well as account for the effect of shoe wear.42,77 For example, feet experience 10% to 50% higher plantar pressures in a flat, flexible shoe compared with a soft shoe with a firm rubber sole.63 The floor mat and in-shoe methods correlate well when the shoe used has a firm sole or when barefoot.7 A number of system-specific and analysis-dependent factors affect the results of pressure transducer array mea surements, including pressure transducer density, respon siveness, linearity, resolution, and range of the transducers. Methods of analyzing the data also differ, including

Figure 1-13 Peak plantar pressure map using an in-shoe thin-film pressure transducer. Red represents areas of relatively high pressure, and violet, areas of low pressure. (Courtesy Ken Hunt, MD.)

reporting results as force versus pressure, peak values versus sum of values over time, and strategies of regional izing the foot’s plantar surface. Increasing pressure trans ducer density provides better spatial representation of plantar pressure, whereas systems with relatively lower transducer density may underestimate measurements, such as peak pressure, because the true peak may be missed. Some transducers may have a nonlinear response at the extremes of their measurable range or have a lowlevel cutoff. The maximum sample rate affects contact time measurements, and low sample rates may underes timate peak pressure measurements because the true peak pressure may be missed. Data Representations Output from the different measurement systems reflects the nature of their measurement mechanisms. The Harris mat reports pedal pressure but does not vary with time. The force plate reports a true ground reaction force but in not spatially discriminative. The optical systems and the transduction arrays each report pedal pressure that varies with time. The data measured by these systems is subject to sensor density, resolution, and sample rate limitations discussed above. To simplify the information and allow comparisons between subjects or after treat ments, a variety of derivative parameters have been 13

416 Adults (n = 111) Children (n = 15)

380

314 216 141 99

312

277

95 59

119

Figure 1-14 Peak pressure values under selected foot regions demonstrate impact in heel region, minimal weight bearing in midfoot, buildup of pressure beneath metatarsal heads, and transfer of weight to great toe region. (From Hennig EM, Rosenbaum D: Pressure distribution patterns under the feet of children in comparison with adults. Foot Ankle 11:306-311, 1991.)

defined based on these raw data. Not all systems or measurement methods are able to derive all of these measurements. The ground reaction force is a vector quantity varying temporally and spatially over the gait cycle that represents the average reciprocal force exerted by the floor in response to the foot. It has a magnitude and direction, and the starting point may be projected onto a representation of the plantar foot at the point of average maximum vertical force (Fig. 1-14). The ground reaction force can be decon structed into vertical force, anterior–posterior shear, and medial–lateral shear. The vertical ground reaction force represents the force of the ground pushing upward on the foot, and can be calculated from systems that measure plantar pressure for the whole foot or for defined regions of the foot.76 Typically, it has two peaks; the first peak occurs as the body weight is transferred from dual- to single-leg stance and the second as the body weight moves forward over the metatarsal heads. Studies of ground reac tion forces may focus on the magnitude of one or the other vertical peak or the timing of the peaks and valleys. Torque (moment) and power around a joint also can be calculated from the ground reaction force, joint geometry, timing parameters, and kinematics. Another frequently reported measurement is the maximum pressure recorded, or peak pressure. It is usually reported over a spatially subdivided map of the plantar foot. Peak pressure for areas such as the heel, individual or grouped metatarsal heads, and toes are common. Alternatively, peak pressure can be reported as a temporally varying measure by displaying its location 14

Ankle power (watts/kg)

Part I ■ General Considerations

0.6

Postoperative

0.4

Preoperative

0.2 0 -0.2 10

100

Percent of gait cycle Figure 1-15 Joint power generated (positive) or absorbed (negative) during the gait cycle before and after total ankle replacement. (Modified from Brodsky JW, Polo FE, Coleman SC, Bruck N: Changes in gait following the Scandinavian Total Ankle Replacement. J Bone Joint Surg Am 93:1890-1896, 2011.)

and magnitude on a diagram of the foot. Peak force can be calculated from peak pressure because the size of the pressure transducers is known. Calculated joint moments represent the torque applied by muscles to counteract the measured ground reaction force, and joint power is cal culated from the joint moment and angular velocity (Fig. 1-15). Timing measurements can also be made. The time intervals from heel strike to metatarsal strike, toe strike, heel-off, metatarsal-off, and toe-off can be calculated. The pressure·time integral, or impulse, for the whole foot or defined regions can be calculated. This may be standard ized for each region as a percentage of the total impulse for a given foot. The impulse may characterize plantar loading better than peak pressure by taking both pressure and time into consideration. Finally, the pattern of plantar loading can be catego rized based on the pressure measurements. Patients may tend to load the medial ray, the medial and central rays, the central rays, or the central and lateral rays.35 Put another way, there is an inverse relationship between peak pressure under the first metatarsal head and toe rela tive to the lesser metatarsal heads.25 As walking speed increases, a medialization of forefoot pressure occurs such that peak pressure under the first metatarsal head increases and that under the lesser metatarsal heads decreases.64 Measurement Variability Many sources of variability affect the results of these measurements. Separating important clinical or research findings from differences based on testing apparatus, measurement methodology, patient demographic factors, or analysis methodology requires an understanding of how these factors affect the measured results. Differ ences between the different testing apparatus have been described above. Other sources of variability can be divided into methodology, analysis, and patient-specific factors. Walking speed affects the magnitude of plantar pres sures during gait. Velocity is linearly related to peak verti cal and fore–aft ground reaction forces,3,57 and inversely

Biomechanics of the Foot and Ankle ■ Chapter 1 related to the pressure·time integral.81 As velocity increases, peak pressures on the heel, medial metatarsal heads, and the first toe increase while peak pressure in the fifth metatarsal head decreases.35,64 This medialization may be related to increased magnitude and velocity of hindfoot eversion and medial shear force at heel strike. Timing measurements also change with increasing speed. The normalized time to peak pressure is decreased on the heel but unchanged in the midfoot and forefoot, suggest ing the rollover process is mainly accelerated by reducing the time from heel strike to foot flat.64 To minimize vari ability introduced because of walking speed, subjects may walk at a fixed rate or at their natural pace.81 Deviations from a normal gait pattern can occur if the subject has to take a long or short stride in an effort to place the foot on the appropriate measurement area of floor-based systems. To minimize this effect, the measure ment platform is placed flush with the floor and hidden from the subject with a thin, uniform floor covering. The traditional midgait method uses a short lead-up walk before the foot strikes the measurement platform. A three-step or two-step lead-up is as reproducible, but a one-step lead-up is not adequate.15,56 Variability of the measurements is also dependent on the type of gait. For example, plantar pressures measured when standing differ from pressures measured during gait.10 Variations in walking patterns, such as a shufflingtype gait, alter the peak forces on the foot.82 Gait pattern alteration can be seen in certain conditions, such as after ankle fracture fixation or with concurrent knee pathology.3,8 Drift and calibration of the measurement systems affect the variability of measurements. Plantar pressure measurement systems need to be calibrated to allow comparisons between systems. Transducer output varies between different transducers, with temperature, when an in-shoe system is removed and reinserted, and with the number of trials performed. Pressure can vary by as much as 20% with repeated measurements on the same insert.63 There may be an offset that drifts with time.56 The mea surements may be adequate for relative ranking purposes but need repeated calibration with a fixed system if accu rate values are needed. Variability is also introduced in the methods by which the acquired data are analyzed. For example, peak pres sure can be reported for the whole surface of the foot during a gait cycle, but the clinical utility of this is limited because different regions of the foot experience different plantar pressures during the gait cycle. Subdividing the regions of the plantar foot and recording peak pressures in each of these areas over the gait cycle provides more meaningful data. The heel is often represented as a single region but may be subdivided into medial, central, and lateral.64 Midfoot peak pressures may be useful in patho logic conditions, such as rocker-bottom deformity, and can classify foot morphology into planus, normal, and cavus categories.64 The base of the fifth metatarsal can be included as part of the midfoot or can be identified as a

separate pressure zone. Improvements in sensor technol ogy have allowed measurement of individual metatarsal heads and toe forefoot pressures.25,37 Definition of these regions (masks) is still a manual process and is repeated for each trial. Having a single person define the regions may decrease variability.37 Subject-specific characteristics also introduce variabil ity. Children’s feet have a dramatically different loading pattern and lower peak pressure because of high relative foot area27 (see Fig. 1-14). Differences in joint mobility and forefoot pressure based on a subject’s ethnicity have been shown in neuropathic diabetics.73 The patient’s dominant side may experience greater static and dynamic vertical force,42 although others have found no side domi nance.29 Foot morphology also affects plantar pressure; cavus feet have different midfoot loading characteristics and rate and degree of hindfoot eversion than flatfeet.64 During running, fatigued subjects tend to have decreased step time, decreased peak and integral force and pressure under heel, and medialization of forces.77 After a hindfoot fusion, greater contact force at heel strike has been observed.45,69 This could be due to the inability of the calcaneus to move into a valgus position after heel strike.2 The effect of body weight on plantar pressure is less direct than might be expected. Although some have cor related maximum vertical force during gait and body weight,42 many other studies found little correlation.26,27,39 In children, the correlation of body weight to peak plantar pressures is clear and plays a greater role in determining peak pressure than in adults.27,35 The area of peak pressure most highly correlated with body weight in children is the fourth metatarsal head,35 and in adults may be the fourth metatarsal head or the midfoot.27,35 Individuals load the foot with different spatial patterns as well. After heel strike, the forefoot may be loaded more medially or laterally across the metatarsal heads and may load the metatarsals and toes simultaneously or in turn. A variety of classification systems have been proposed to group these types of loading, and biomechanical theories have been proposed to explain the different loading pat terns.35,37,76 Finally, there is an inherent variability in an individual’s gait from step to step that ranges from less than 1% for vertical ground reaction force to much higher for timing-dependent variables and values calculated as a product of measures.29 Measured values may vary by more than 10% under identical testing conditions. Averaging data from as few as three trials improves the reliability of the measurement.39 Kinetics of Walking Force plates measure the force felt by the floor produced by displacement of the body’s center of gravity. By New ton’s law of equal and opposite forces, this is the same force experienced by the foot and represents the effect of gravitational forces on the whole body while walking.19 The principle of the force plate is seen when one stands on a bathroom scale and flexes and extends the knees to 15

Part I ■ General Considerations

raise and lower the body. The indicator on the dial moves abruptly as vertical floor reaction is registered. Whole Body Kinetics The only forces that can produce motion in the human body are those created by gravity, by muscular activity, and, in a few instances, by the elasticity of specific con nective tissue structures. A force plate instantaneously records the forces imposed by the body through the foot onto the floor. These measurements include vertical floor reactions, fore and aft shears, medial and lateral shears, and horizontal torques. During the stance phase of walking, the floor reactions in all four categories are con tinuously changing. Figure 1-11 demonstrates the force plate data obtained during normal walking. The slower an individual walks, the less the center of gravity moves, and the resultant forces are less. Conversely, the faster the gait, the greater the movement of the center of gravity, and hence a larger force is experienced. When shoes are donned, these forces are transmitted through the interface between the sole of the shoe and the walking surface. This can attenuate rapid spikes, such as the heel striking the ground, and distribute the force over a larger area of the foot, diminishing peak plantar pressures. The vertical element of ground reaction force is the largest of the component vectors and represents the force required to oppose the pull of gravity. It demonstrates an initial spike and rapid decline as the heel contacts the ground. Shoe material can alter the magnitude of the spike: a softer heel will result in a smaller initial spike, and a harder heel in a larger spike. The vertical ground reaction force curve then has two peaks during the stance phase. The first whole body vertical force peak is 10% to 15% greater than body weight and is caused by the upward acceleration of the body’s center of gravity. This is followed by a dip to approximately 20% less than body weight as the center of gravity reaches the top of its trajec tory and begins to fall. A second peak of 10% to 15% greater than body weight results from resisting the falling of the center of gravity as the body moves over the stance leg. After this, the force rapidly declines to zero at toe-off as weight transfers to the opposite limb (see Fig. 1-11A). We see from the lack of a vertical ground reaction peak at the end of stance phase that the toes do not push off but rather are lifted from the floor as the weight transfers to the other side. Forward shear occurs at initial heel strike representing the braking of the body as it resists forward momentum. After the center of gravity has passed in front of the weight-bearing foot, an aft shear occurs. The aft shear reaches a maximum as the opposite limb strikes the ground at 50% of the walking cycle. The aft shear approaches zero at the time of toe off, once again showing the lack of push off during normal walking gait. The magnitude of the fore–aft shear, however, is only about 10% to 15% of body weight (see Fig. 1-11B). Medial shear is the force exerted toward the midline at the time of heel strike, after which there is a persistent 16

lateral shear until opposite heel strike at 50% of the cycle. A medial shear is not seen in persons with an above-knee amputation in whom a lateral shear mode is always present because of lack of abductor control of the pros thesis. The magnitude of the medial–lateral shear is about 5% of body weight (see Fig. 1-11C). Lower extremity rotation during the stance phase causes a torque of the foot against the ground. After heel strike, there is an internal torque that reaches maximum at the time of foot flat, after which there is a progressive external torque that reaches a maximum just before toeoff. This torque corresponds to the inward and outward rotation of the lower extremity (see Fig. 1-11D). The majority of this rotation occurs with the foot firmly placed on the floor. The rotations, therefore, generate an internal torque of 7 to 8 newton-meters, which is of con siderable magnitude.19 The ankle and subtalar joints facil itate the transmission of rotatory forces between the foot and lower limb. The movement of the ground reaction force vector along the bottom of a normal foot follows a consistent pattern41 (Fig. 1-16). After heel strike, it moves rapidly forward until it reaches the metatarsal area, where it dwells for about half of the stance phase, then passes distally to the great toe. In a patient with a rheumatoid arthritis–related hallux valgus deformity and significant metatarsalgia, the center of pressure remains in the pos terior aspect of the foot, avoiding the painful metatarsal area, then rapidly passes over the metatarsal heads along the middle of the foot (Fig. 1-17).24 In patients with amputation of the great toe, the center of pressure passes in a more lateral direction (Fig. 1-18).51

60 55 50 45 40 35 30 25

20 15 10 5 2

Figure 1-16 Peak plantar pressure map with superimposed path of instantaneous center of ground reaction force (black line). The red dots and corresponding labels represent the location of the ground reaction force at a given percentage of the gait cycle.

Biomechanics of the Foot and Ankle ■ Chapter 1

Force (lb)

200 +

•

+ +

50 0

++ ++ ++ +

•

• •• ••• • • 10

100

150

• • • • 15 20 X cm

•

Y cm

+ ++++++ +

A + + + + + + ++ + ++ +

100

+ +

50 0 5

•• • •• • • • ••• 10 • • • 15 20 X cm

Force (lb)

150

•

Figure 1-18 Movement of center of pressure after amputation of great toe. A, Normal progression of center of pressure. B, Abnormal movement of center of pressure after amputation of great toe. Note that pressure tends to dwell more laterally in the metatarsal area, then passes out toward the third toe rather than the great toe. (From Mann RA, Poppen NK, O’Konski M: Amputation of the great toe. a clinical and biomechanical study. Clin Orthop 226:192-205, 1988.)

Y cm

+ + + ++++ + + + ++ + + + +

Vertical ground reaction force Anterior–posterior shear force

Figure 1-17 Progression of center of pressure in normal and abnormal foot, beginning at the right and progressing to the left. Blue line is the vertical component of ground reaction force, and tan line is anterior–posterior shear component of ground reaction force. Marks along the path represent 125 -second intervals. A, Note progression of center of pressure from heel toward toes during normal walking cycle. The center of pressure moves rapidly from the heel, dwells in metatarsal head region, then passes rapidly to the great toe at toe-off. B, Progression of center of pressure in a patient with rheumatoid arthritis with severe hallux valgus deformity and significant metatarsalgia. Note that the center of pressure remains toward the heel, then rapidly progress across the metatarsal head area with little or no pressure borne by the great toe. Patients with rheumatoid arthritis or significant metatarsalgia keep their weight in the posterior aspect of foot to avoid pressure over the painful portion of foot, which may lead to a shuffling gait. (From Grundy M, Tosh PA, McLeish RD, Smidt L: An investigation of the centres of pressure under the foot while walking. J Bone Joint Surg Br 57:98-103, 1975.)

Plantar Pressure Kinetics Research on plantar pressure during gait has proved useful in a number of clinically relevant areas, including forefoot pressure involving a number of clinical syn dromes. Increased forefoot pressures may lead to meta tarsalgia or neuropathic ulceration and is mitigated by simple insole modifications. Diabetic and neuropathic foot ulceration correlate with areas of increased vertical and shear forces.58 The weight-bearing pattern in these patients tends to shift from the medial to the lateral border of the forefoot, and the load taken by the toes is reduced.18 The rheumatoid foot demonstrates similar findings.2 A soft pad placed proximal to the metatarsal heads decreases metatarsal head pressure from 12 to 60%.34 Placement of a 1 2 -inch lateral heel wedge decreased pressure under the third through fifth meta tarsal heads by 24% and increased pressure under first and second metatarsal heads by 21%.63 A 1 2 -inch medial heel wedge decreased the pressure under the first and second metatarsal heads by 28% and under the first toe by 31%. Patients with hallux valgus may develop transfer meta tarsalgia as plantar pressure increases under the lesser metatarsal heads and decreases under the first toe in rela tion to the size of the deformity.11,40 Those patients with hallux valgus and lesser toe metatarsalgia have greater peak pressure and peak pressure·time integral under the second through fifth metatarsal heads than those without metatarsalgia.74 Measurement of plantar pressure may be predictive because no patients with less than 20 N·cm−2 17

Part I ■ General Considerations

peak pressure had metatarsalgia, and all patients with more than 70 N·cm−2 peak pressure had metatarsalgia. Hallux valgus correction with proximal first metatarsal osteotomy and distal soft tissue procedure decreases peak pressure under the second and third metatarsal heads.80 After a distal chevron osteotomy for mild-to-moderate hallux valgus, the degree of plantar displacement of the distal first metatarsal osteotomy correlates with increased pressure under the first metatarsal head and to a decrease in clinical metatarsalgia.75 Procedures that destabilize the first metatarsophalangeal joint, such as Keller resec tion arthroplasty and silicone (Silastic) implant arthro plasty, increase pressure on the lesser metatarsal heads (Fig. 1-19).20,28,40,70 The Achilles tendon and plantar fascia also influence plantar pressure and gait biomechanics.33 The Achilles tendon contributes to heel rise, leading to a reduction in the vertical displacement of the center of gravity and minimizing energy expenditure.47 During the stance phase, energy is stored in the gastrocnemius–soleus complex as the ankle dorsiflexes, and the tendon is elasti cally stretched and is returned after heel rise as the ankle plantar flexes. This elastic recoil facilitates shortening of the gastrocnemius–soleus complex at rates well above those possible by maximal muscle contraction and allows

Preoperative

47.3 78.6

Postoperative

36.5 129.6

the muscles to act at a rate and length of maximum effi ciency over the gait cycle.31,32 Gastrocnemius–soleus work increases with step length, effectively lengthening the limb by plantar flexing the ankle.32 A chronically elon gated or ruptured tendon leads to a paradoxically rigid ankle by recruiting other ankle stabilizers.12 The time to initial peak vertical force is shortened, highlighting a loss of shock absorption, but the second peak vertical force, representing metatarsal head pressure, is not dimin ished.72 In diabetic patients with plantar ulceration, adding Achilles tendon lengthening to total contact casting leads to increased rate of healing and decreased recurrence of neuropathic ulcers.55 Ankle dorsiflexion is increased, and both plantar-flexion torque and peak plantar pressure are reduced after Achilles tendon length ening initially, but plantar-flexor torque and peak pres sure return by 7 months even though accentuated dorsiflexion remains.55 This suggests that the decrease in peak plantar pressure may be related to a weakening of ankle plantar flexors rather than to an increase in ankle dorsiflexion. Kinetics of Running The forces involved during running are considerable, reaching 2.5 to 3 times body weight (Fig. 1-20). The larger forces generated are related to increased displacement of the center of gravity as the speed of gait increases. At initial ground contact, increasing the range of motion at the ankle, knee, and hip joints helps absorb these larger forces. As the speed of gait further increases, the degree of motion in these joints also increases to help absorb the added impact. Muscles are active over a greater percentage of the gait cycle during running. The gastrocnemius– soleus contribution to forward propulsion is minimal during normal walking but plays a larger role as walking speed increases.23

52.3

70.5

Figure 1-19 Peak forces (in newtons) measured in four areas of foot before and after silicone arthroplasty of first metatarsophalangeal joint. Preoperatively, there is significant weight bearing by first metatarsal and great toe relative to lateral metatarsals. Postoperatively, there is decreased weight bearing by first metatarsal and great toe and increased weight bearing beneath lesser metatarsal head region. This demonstrates effect of loss of windlass mechanism, by which pressure is transferred to great toe, which, in turn, depresses first metatarsal head. (From Beverly MC, Horan FT, Hutton WC: Load cell analysis following silastic arthroplasty of the hallux. Int Orthop 9:101-104, 1985.)

Body weight (%)

250

Walking Running

200 150 100 50

100

Time (% stance phase) Figure 1-20 Comparison of vertical ground reaction for walking (blue line) and jogging (red line). The horizontal axis is scaled as a percentage of total time in stance phase for walking (0.6 sec) and running (0.24 sec). The vertical axis is shown as a percentage of body weight. (From DeLee JC, Drez D, Miller MD, editors: DeLee & Drez’s orthopaedic sports medicine, 3rd ed, New York, 2009, Elsevier.)

Biomechanics of the Foot and Ankle ■ Chapter 1

BIOMECHANICS OF THE COMPONENT OF THE LOCOMOTOR SYSTEM

The human foot too often is viewed as a semirigid base whose principal function is to provide a stable support for the superincumbent body. Instead, it has evolved as a dynamic mechanism functioning as an integral part of the locomotor system. From the moment of heel strike to the instant of toe-off, floor reactions, joint motions, and mus cular activity are changing constantly. Floor reactions and pedal pressure measurements demonstrate the forces transmitted through the foot, continuous geometric mea surements record joint motion, and electromyographic studies show the phasic activity of the intrinsic and extrin sic muscles during gait. To make it easier to understand the various events that occur during a step, a discussion of the biomechanics of the various articulations and muscles that control their function is presented. The dis cussion divides the gait cycle into two separate themes. The first discusses mechanisms by which the foot and ankle contribute to energy absorption during the early phases of stance, followed by a section discussing mecha nisms by which the foot converts from a supple to a rigid platform allowing heel rise and toe-off. Swing phase is discussed, and finally, distinctions between walking and running gait are highlighted. Heel Strike to Foot Flat: Supple for Impact Absorption Ankle Joint At heel strike, the ankle is initially dorsiflexed from swingthrough and rapidly plantar flexes, reaching a maximum of 10 degrees at 7% of the cycle once foot flat has occurred

(see Fig 1-2). After heel strike, the anterior compartment leg muscles function as a group to slow the rapid ankle plantar flexion rotation. This activity continues until plantar flexion is complete. During this time, the muscle undergoes an eccentric (lengthening) contraction that helps absorb the energy of heel strike and transfer of weight from the opposite leg. Clinically, if the anterior tibial muscle group is not functioning, a foot slap is noted after heel strike, resulting from lack of control of initial ankle plantar flexion. The direction of the ankle axis in the transverse plane of the leg dictates the vertical plane in which the foot will flex and extend. In the clinical literature, this plane of ankle motion in relation to the sagittal plane of the leg is referred to as the degree of tibial torsion. Rotation of the ankle axis in the horizontal plane can affect only the amount of toeing-out or toeing-in of the foot. Although it is common knowledge that the ankle axis is directed laterally as projected on the transverse plane of the leg, it is not widely appreciated that the ankle axis is also directed laterally and downward, as seen in the coronal plane. Inman, in anthropometric studies, found that, in the coronal plane, the axis of the ankle may deviate 88 to 100 degrees from the vertical axis of the leg (Fig. 1-21A).43 The axis of the ankle passes just distal to the tip of each malleolus, allowing the examiner to obtain a reasonably accurate estimate of the position of the empiric axis by placing the tips of the index fingers at the most distal bony tips of the malleoli (Figs. 1-21B and 1-22). Because the ankle joint axis is obliquely oriented, an apparent rotation of the foot relative to the horizontal plane of the leg occurs with movements of the ankle. With the foot free and the leg fixed, the oblique ankle joint axis causes the foot to deviate outward on dorsiflexion and

_ x = 82 ° _ x = 93°

Range 88 ° SD = ± 2.7 °

SD = ±

3.6 °

94 °

100 °

74 °

Figure 1-21 A, Variations in angle between midline of tibia and plafond of mortise. B, Variations in angle between midline of tibia and empiric axis of ankle. SD, Standard deviation; x , arithmetic mean. (From Inman VT: The joints of the ankle, Baltimore, 1976, Williams & Wilkins.)

Part I ■ General Considerations

inward on plantar flexion, as seen by the projection of the foot onto the transverse plane (Fig. 1-23). The amount of this rotation will vary with the obliquity of the ankle axis and the amount of dorsiflexion and plantar flexion. Con versely, with the foot fixed to the floor, the oblique ankle axis causes the tibia to rotate internally with dorsiflexion and externally with plantar flexion. Rotations of the leg and movements of the foot caused by an oblique ankle axis, when observed independently, are qualitatively and temporarily in agreement. However, when the magnitudes of the various displacements are studied, it becomes clear that rotation of the leg attribut able to ankle axis obliquity is much smaller than the degree of horizontal rotation of the leg that actually occurs. In normal locomotion, ankle motion ranges from 20 to 36 degrees, with an average of 24 degrees.9,65 The obliquity of the ankle axis ranges from 88 to 100 degrees,

with an average of 93 degrees from the vertical.43 Even in the most oblique axis and movement of the ankle through the maximum range of 36 degrees, only 11 degrees of rotation of the leg around a vertical axis will occur. Subtalar Joint The subtalar joint works in cooperation with the ankle to account for the additional leg rotation not explained by the obliquity of the ankle joint axis. The subtalar joint is a sliding single-axis joint that acts like a mitered hinge connecting the talus and the calcaneus. The axis of the subtalar joint passes from medial to lateral at an angle of approximately 16 degrees and from the horizontal plane approximately 42 degrees17,53 (Fig. 1-24). Individual vari ations are extensive and impart variability to the behavior of this joint during locomotion. Furthermore, the subta lar joint appears to be a determinative joint of the foot, Light

Light

Fixed in space

Horizontal plane

Figure 1-22 Estimation of obliquity of empirical ankle axis by palpating tips of malleoli.

Figure 1-23 Effect of obliquely placed ankle axis on rotation of foot in horizontal plane during plantar flexion and dorsiflexion, with foot free. Displacement is reflected in shadows of foot.

Subtalar axis

Figure 1-24 Variations in subtalar joint axes. A, In transverse plane, subtalar axis deviates approximately 23 degrees medial to long axis of foot, with range of 4 to 47 degrees. B, In horizontal plane, axis approximates 41 degrees, with range of 21 to 69 degrees. x , arithmetic mean. (Modified from Isman RE, Inman VT: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10:97, 1969.)

_ x = 23°

Axis of subtalar joint

47° 21°

_ x = 41 °

Horizontal plane

A 20

69 °

Biomechanics of the Foot and Ankle ■ Chapter 1

complexity of the movement, subsequent studies have confirmed qualitatively the direction of movement, namely, eversion after heel strike until foot flat, then inversion until toe-off (Fig. 1-26). Eversion of the hind foot at heel strike occurs passively, dictated by the lateral

influencing the performance of the more distal articula tions and modifying the forces imposed on the skeletal and soft tissues. Based on its inclined axis, the subtalar joint functions essentially like a hinge connecting the talus and the cal caneus. The functional relationships that result from such a mechanical arrangement are illustrated in Figure 1-25A, which shows two boards jointed by a hinge. The vertical board represents the tibia and the horizontal board the foot. If the axis of the hinge is at 45 degrees, a simple torque converter has been created. Rotation of the vertical member causes equal rotation of the horizontal member. Changing the angle of the hinge alters this one-to-one relationship such that a more horizontally placed hinge causes a greater rotation of the horizontal member for each degree of rotation of the vertical member; the reverse holds true if the hinge is placed more vertically. The model can be refined further (Fig. 1-25B) by divid ing the horizontal “foot” segment into a short proximal and a long distal segment, with a pivot between the two segments. This pivot represents the transverse tarsal joint complex, which consists of the talonavicular and calca neocuboid joints. The longer distal segment remains fixed to the floor in this model, and rotation at the transverse tarsal joint complex accommodates hindfoot inversion and eversion during stance phase. Thus the distal segment remains stationary, and only the short segment adjacent to the hinge rotates. The specific mechanics of this joint complex are discussed in the following section. The interrelated rotation described by these models helps to demonstrate motion of the subtalar joint during walking.79 At the time of heel strike, the subtalar joint is slightly inverted and rapidly everts, reaching a maximum at foot flat, after which progressive inversion occurs until the time of toe-off. In the normal foot, approximately 6 degrees of rotation occurs. Although quantification of subtalar joint motion remains elusive because of the

B Figure 1-25 Simple mechanism demonstrating functional relationships. A, Action of mitered hinge. B, Addition of pivot between two segments of mechanism.

SUBTALAR ROTATION Heel strike

Toe-off

Heel strike

10 Normal foot

0 Inversion 10 Eversion

Flatfoot

10 0

100

Percent of walk cycle Figure 1-26 Subtalar joint motion in normal foot and flatfoot. Shaded areas indicate period of activity of intrinsic muscles in normal foot and flatfoot.

Part I ■ General Considerations

Figure 1-27 Hindfoot alignment radiographs demonstrating placement of the calcaneus relative to the weight-bearing axis of the tibia. A, A hindfoot with physiologic valgus shows the weight-bearing axis of the lower extremity passing through the medial aspect of the calcaneus. B, A flatfoot with calcaneus valgus shows the weight-bearing axis passing medial to the calcaneus. C, A cavus foot with calcaneus varus shows the weight-bearing axis passing through the lateral aspect of the calcaneus.

placement of the subtalar axis relative to the weightbearing axis through the tibia (Fig. 1-27). Energy is pas sively absorbed by the stretch of the surrounding ligaments that control subtalar eversion. At heel strike, there is also progressive inward rotation in the lower extremity, reaching a maximum at the time of foot flat. The internal rotation at heel strike is initiated by the collapse of the subtalar joint into eversion through the obliquity of the subtalar joint axis. The flexibility of the foot and its surrounding ligamentous support deter mine the magnitude of this rotation. The recording of torques imposed on a force plate substantiates these rotations. Magnitudes vary but range from 7 to 8 newtonmeters.19 Because the foot does not typically rotate on the floor, this torque is absorbed by the joint complexes and surrounding ligaments, further contributing to energy absorption during this part of stance phase. Of interest, in persons with flatfeet, the axis of the subtalar joint is more horizontal than in persons with “normal” feet; therefore the same amount of rotation of the leg imposes greater supinatory and pronatory effects on the foot. Furthermore, people with asymptomatic flat feet usually show a greater range of subtalar motion than do persons with more neutrally aligned hindfeet. In the neutral foot, approximately 6 degrees of rotation occurs, and in flatfoot, about 12 degrees (see Fig. 1-26). The reverse holds true for people with pes cavus, in whom the generalized rigidity of the foot, more vertical subtalar axis, and limited motion in the subtalar joint often are observed. 22

Transverse Tarsal Joint Complex The calcaneocuboid and talonavicular articulations together often are considered to make up the transverse tarsal joint complex. Each possesses some independent motion and has been subjected to intensive study.22 However, from a functional standpoint, they perform together. Elftman22 demonstrated that the axes of these two joints are parallel when the calcaneus is in an everted position and are nonparallel when the calcaneus is in an inverted position. The importance of this is that, when the axes are parallel, there is flexibility within the trans verse tarsal joint, whereas when the axes are nonparallel, there is rigidity at the transverse tarsal joint (Fig. 1-28). Imagine a door where the hinges all line up and will open and close easily, whereas if the hinges of a door diverge, the door will be stuck in one position. The transverse tarsal joint transmits the motion that occurs in the hindfoot distally into the forefoot, which is fixed to the ground. To approach the true anatomic situ ation of the human foot even more closely, the wooden foot model described above is modified to split the distal portion of the horizontal member into two structures (Fig. 1-29A and B). The medial one represents the three medial rays of the foot that articulate through the navicu lar and cuneiform bones to the talus; the lateral one represents the two lateral rays that articulate through the cuboid to the calcaneus. In Figure 1-29C and D, the entire mechanism has been placed into the leg and foot to demonstrate the mechanical linkages resulting in specific

Biomechanics of the Foot and Ankle ■ Chapter 1

EVERSION

INVERSION

Figure 1-28 Function of transverse tarsal joint, (as described by Elftman H: The transverse tarsal joint and its control, Clin Orthop Relat Res 16:41-46, 1960.) demonstrates that when the calcaneus is in eversion, the resultant axes of talonavicular (TN) and calcaneocuboid (CC) joints are parallel. When the subtalar joint is in an inverted position, the axes are nonparallel, giving increased stability to the midfoot.

Figure 1-29 Distal portion of horizontal member replaced by two structures. A and B, Mechanical analog of principal components of foot. C and D, Mechanical components inserted into foot and leg.

movements in the leg and foot. External rotation of the leg causes inversion of the heel, elevation of the medial side of the foot, and depression of the lateral side. Inter nal rotation of the leg produces the opposite effect on the foot.

Figure 1-30 Anatomic specimen with the foot removed at the transverse tarsal joint complex, demonstrating the relationship between talus and calcaneus during hindfoot motion. The talar head (T) and calcaneal side of the calcaneocuboid joint (C) are shown. The vertical line highlights motion of the calcaneus relative to the talus. K-wires mark the axes of the respective joints. When the calcaneus is in the everted position, the talonavicular and calcaneocuboid joint axes are parallel, and the transverse tarsal joint complex is mobile. When the calcaneus is in an inverted position, following the direction of the arrow, the talonavicular and calcaneocuboid joint axes diverge, and the transverse tarsal joint complex is locked.

At the time of heel strike, as the calcaneus moves into eversion, the joints of the transverse tarsal joint complex become parallel, and the midfoot becomes flexible. Although quantification of motion in this joint has not been achieved, Figure 1-30 visually demonstrates the degree of motion that occurs in the transverse tarsal joint when the hindfoot is everted, contrasted to when it is inverted. The suppleness of the midfoot and stretch of surrounding ligaments further contributes to energy absorption during the period from heel strike to foot flat. From a clinical standpoint, the importance of this joint is observed if a subtalar arthrodesis is placed into too much inversion, resulting in stiffness of the midfoot region and causing excessive weight on the lateral border of the foot and a tendency to vault over the rigid midfoot. Foot Flat to Toe-Off: Progression to a Rigid Platform All of the essential mechanisms discussed in this section are pictorially summarized in Figure 1-10. The two lower photographs, taken with the subject standing on a baro graph, reveal the distribution of pressure between the foot and the weight-bearing surface. (A barograph records reflected light through a transparent plastic platform; the intensity of the light is roughly proportionate to the pres sure the foot imposes on the plate.) In Figure 1-10A, the subject was asked to stand with muscles relaxed. Note 23

Part I ■ General Considerations

Ankle Joint With the foot fixed on the ground during midstance, the body passing over the foot produces dorsiflexion of the ankle (see Fig. 1-3). The ankle undergoes progressive dor siflexion until approximately 40% of the gait cycle, at which time plantar flexion once again begins, reaching a maximum at the time of toe-off (see Fig 1-4). The oblique ankle axis initially imposes an internal rotation on the leg, the degree of which depends on the amount of dor siflexion and the obliquity of the ankle axis (Fig. 1-31).48 During midstance, as the ankle dorsiflexes, a resulting internal rotational torque to the leg occurs. As the heel rises in preparation for lift-off, the ankle is plantar flexed.

This, in turn, reverses the horizontal rotation, causing the leg to rotate externally. The posterior calf muscles basically function as a group, although the tibialis posterior and peroneus longus muscles usually begin functioning by about 10% of the stance phase, whereas the other posterior calf muscles tend to become functional at about 20% of the stance phase. As the ankle joint undergoes progressive dorsiflexion from foot flat until heel rise at 40% of the cycle, these muscles contract eccentrically. After heel rise, as ankle plantar flexion begins, they continue to contract, but now via a concentric contraction. It is interesting to note, however, that by 50% of the cycle, the electrical activity in these muscles ceases, and the remainder of the plantar flexion of the ankle joint is a passive event. Highspeed motion pictures have demonstrated that during steady-state walking, at the time of toe-off, the foot is lifted from the ground, and the toes do not actively push off. The function of the posterior calf group during stance phase is to control the forward movement of the tibia on the fixed foot.68,72 Control of the forward movement of the stance leg tibia is critical to normal gait because it permits the contralateral leg to take a longer step, increas ing stride length and improving walking efficiency. In pathologic states in which the calf muscle is weak, the stride length shortens, and dorsiflexion occurs at the ankle joint after heel strike because it is a position of stability. Paradoxically, the ankle is held more rigidly by secondary stabilizers to make up for the inability to control ankle dorsiflexion.12 Forces across the ankle joint reach a peak at approxi mately 40% of the cycle, which is when the transition from dorsiflexion to plantar flexion occurs (Fig. 1-32). The force across the ankle joint reaches approximately 4.5

Force in percent body weight

that the leg is moderately rotated internally and the heel is slightly everted (in valgus position). The body weight is placed on the heel, the outer side of the foot, and the metatarsal heads. In Figure 1-10B, the subject was asked to rise on his toes. Note that the leg is now externally rotated, the heel is inverted (in varus position), and the longitudinal arch is elevated. The weight is concentrated on the metatarsal heads and is shared equally by the metatarsal heads and the toes. Contraction of the intrinsic and extrinsic muscles contributes to stability of the foot and ankle as the body weight is transferred to the forefoot and the heel is raised. Dorsiflexion of the toes tightens the plantar aponeurosis and assists in inversion of the heel. The supinatory twist activates the “locking” mechanism in the transverse tarsal articulation and talo navicular joint, thus converting a flexible foot into a rigid lever. The following sections describe these changes in detail.

500 400 300 200 100 0 10

100

Percent stance phase

Figure 1-31 Foot fixed to floor. Plantar flexion and dorsiflexion of ankle produce horizontal rotation of leg because of obliquity of ankle axis.

Figure 1-32 Compressive forces across ankle joint during stance phase of walking. Note that for normal subjects, force across ankle joint is approximately 4.5 times body weight at 60% to 70% of stance phase. This corresponds to 40% of walking cycle when ankle plantar flexion is beginning. (From Stauffer RN, Chao EY, Brewster RC: Force and motion analysis of the normal, diseased, and prosthetic ankle joint. Clin Orthop 127:189-196, 1977.)

Biomechanics of the Foot and Ankle ■ Chapter 1

Figure 1-33 Rearrangement of skeletal components of foot. A, Supination of forefoot and eversion of heel permitting maximal motion in all components of foot. B, Pronation of forefoot and inversion of heel resulting in locking of all components of foot and producing rigid structure.

times body weight. This much force confined to a small surface area probably is one reason the components of total ankle joints may loosen and why malreduced ankle fractures rapidly progress to arthritis. Subtalar Joint After the hindfoot reaches maximal eversion during the initial phase of stance, it progressively inverts from the foot-flat phase through toe-off for a total arc of 6 degrees in a normal foot (see Fig. 1-26). Both passive and active mechanisms lead to this progressive inversion of the hindfoot. Hindfoot inversion stabilizes the midfoot during the later stages of stance phase by producing a rigid transverse tarsal articulation. Muscle activity in the deep posterior compartment contributes to hindfoot inversion (see Fig. 1-3). As the posterior tibial muscle–tendon complex contracts, the hindfoot is pulled into inversion. Activity of the intrinsic muscles of the foot also contributes to midfoot stability and correlates fairly closely with the degree of subtalar joint rotation. In the normal foot, the intrinsic muscles become active at about 30% of the walking cycle, whereas in flatfoot, they become active during the first 15% of the walking cycle (see Fig. 1-26).50 Passive mechanisms contributing to hindfoot inver sion and midfoot stabilization include the plantar apo neurosis and metatarsophalangeal break, which will be described below. Linkage of leg rotation to hindfoot motion also contributes to hindfoot inversion during the later stages of stance. The pelvis, thigh, and leg rotate externally during the last two thirds of stance. This exter nal rotation is converted to hindfoot inversion through the oblique axis subtalar joint.19 Transverse Tarsal Articulation The importance of the transverse tarsal articulation lies not in its axes of motion while non–weight bearing but in how it functions during the stance phase when the foot is required to support the body’s weight. The amount of

motion achievable by the transverse tarsal articulation with the forefoot fixed depends on the position of the heel. This phenomenon can be seen when examining the foot. If the examiner holds the hindfoot in an everted position, it seems the midfoot becomes “unlocked” and that maximum motion is possible in the transverse tarsal articulation. However, if the hindfoot is inverted and held firmly in one hand, the transverse tarsal articulation appears to become “locked.” The previously elicited motions all become suppressed, and the midfoot becomes rigid (Fig. 1-33). The phenomenon is explained by con vergence and divergence of the transverse tarsal joint axes (see Fig. 1-30). The same relationship between hindfoot position and midfoot suppleness holds during the stance phase of gait. At the time of heel strike, as the calcaneus moves into eversion, there is flexibility in the transverse tarsal joint, and at the time of toe-off, the calcaneus is in an inverted position, resulting in stability of the transverse tarsal joint and hence the longitudinal arch of the foot. This relation ship contributes to longitudinal arch stability as the heel rises from the floor, allowing the foot to act as an exten sion of the leg and improving stride length. Plantar Aponeurosis The plantar aponeurosis is a band of fibrous tissue arising from the tubercle of the calcaneus and passing distally to insert into the base of the proximal phalanx. As the plantar aponeurosis passes the plantar aspect of the meta tarsophalangeal joints, it combines with the joint capsule to form the plantar plate. The function of the plantar aponeurosis has been likened to a windlass mechanism (Fig. 1-34).30 The plantar aponeurosis is the most significant stabi lizer of the longitudinal arch between heel rise and toeoff. As the body moves over the fixed foot and the heel begins to rise, the proximal phalanges dorsiflex, pulling the plantar aponeurosis over the metatarsal heads. This tightens the plantar fascia, resulting in a depression of the 25

Part I ■ General Considerations

Plantar pads Flexor tendon

Capsule

Plantar pad

Plantar aponeurosis

Figure 1-34 Plantar aponeurosis. A, Division of plantar aponeurosis around flexor tendons. B, Components of plantar pad and its insertion into base of proximal phalanx. C, Extension of toes draws plantar pad over metatarsal head, pushing it into plantar flexion.

metatarsal heads and an elevation of the longitudinal arch (Fig. 1-35). This mechanism is passive in that no muscle function per se brings about this stabilization. The plantar aponeurosis is most functional on the medial side of the foot and becomes less functional as one moves laterally toward the fifth metatarsophalangeal articulation. Based on its medial attachment to the calca neus, plantar fascia tightening also contributes to hind foot inversion, tibial external rotation, and transverse tarsal joint stabilization.16 These changes stabilize the midfoot and allow the foot to act as a rigid lever during the toe-off phase of gait. The mechanics of the windlass mechanism can be demonstrated clinically by having an individual stand and forcing the great toe into dorsiflexion. As this occurs, one observes elevation of the longitudinal arch by the depression of the first metatarsal by the proximal phalanx, and, at the same time, inversion of the calcaneus. Careful observation of the tibia demonstrates that it externally rotates in response to this calcaneal inversion. Metatarsophalangeal Break The metatarsophalangeal break refers to the axis formed by the unequal forward extension of the metatarsals. The head of the second metatarsal is the most distal head; that of the fifth metatarsal is the most proximal. Although the first metatarsal usually is shorter than the second (because the first metatarsal head is slightly elevated and is 26

C Figure 1-35 Dynamic function of plantar aponeurosis. A, Foot at rest. B, Dorsiflexion of metatarsophalangeal joints, which activates windlass mechanisms, brings about elevation of longitudinal arch, plantar flexion of metatarsal heads, and inversion of heel. C, Superimposed tracing of lateral radiographs of the foot at rest (outline) and with first ray dorsiflexion (gray figure). Notice that dorsiflexion of the first toe tightens the plantar aponeurosis, which results in depression of the metatarsal heads, elevation and shortening of the longitudinal arch, inversion of the calcaneus, and elevation of the calcaneal pitch. (From DeLee JC, Drez D, Miller MD, editors: DeLee & Drez’s orthopaedic sports medicine, 3rd ed, New York, 2009, Elsevier.)

supported by the two sesamoid bones), it often function ally approximates the length of the second. When the heel is elevated during standing or at the time of toe lift-off, all the metatarsal heads normally share the weight of the body. To achieve this fair division, the foot must supinate slightly and deviate laterally. After

Biomechanics of the Foot and Ankle ■ Chapter 1

_ x = 62 o

ta bre tarsa ak l

53.5 o

72.5 o

Figure 1-37 Supination and lateral deviation of foot during raising of heel caused by oblique metatarsophalangeal break. A, Wooden mechanism without articulation. If no articulation is present, leg deviates laterally. B, Wooden mechanism with articulation. Leg remains vertical; hence some type of articulation must exist between foot and leg. C, Articulation similar to that of subtalar joint. In addition to its other complex functions, subtalar joint also functions to permit leg to remain vertical. Figure 1-36 Variations in metatarsal break in relation to longitudinal axis of foot. (From Isman RE, Inman VT: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10:97, 1969.)

wearing a new pair of shoes for a while, one notices the appearance of an oblique crease in the area overlying the metatarsophalangeal articulation (Fig. 1-36). This oblique crease demonstrates the metatarsophalangeal break. The angle between the metatarsophalangeal break and the long axis of the foot may vary from 50 to 70 degrees.44 The more oblique the metatarsophalangeal break, the more the foot must supinate and deviate laterally after heel rise. If the leg and foot acted as a single rigid member without ankle, subtalar, or transverse tarsal articulations, the metatarsophalangeal break would cause lateral incli nation and external rotation of the leg (Fig. 1-37A). However, the subtalar joint accommodates this supina tion and permits the leg to remain in a vertical plane during walking (Fig. 1-37B and C). Talonavicular Joint The talonavicular joint morphology adds additional sta bility to the longitudinal arch when force is applied across it during the last half of the stance phase. The joint surface has different curvature of radius in the anteroposterior and lateral projections (Fig. 1-38). When force is applied across a joint of this shape, stability is enhanced. This occurs at toe-off, when the plantar aponeurosis has stabilized the longitudinal arch and most of the body weight is being borne by the forefoot and medial longi tudinal arch.

Navicular

Talus

Figure 1-38 Talonavicular joint. Left, Anterior view. Right, Lateral view. Relationship of head of talus to navicular bone shows differing diameters of head of talus. (From Mann RA: Intractable Plantar Keratoses. In Nicholas JA, Hershman EB, editors: The lower extremity and spine in sports medicine, ed 2, St Louis, 1995, Mosby.)

Swing Phase During swing phase, dorsiflexion occurs at the ankle joint. Beginning at about 55% of the cycle and throughout swing phase, the anterior compartment muscles contract concentrically to dorsiflex the ankle. The medial insertion of the tibialis anterior tendon pulls the hindfoot into slight inversion during swing phase such that the calca neus is slightly inverted at initial heel strike. This is why most people will wear down the outer edge of the heel in their shoes asymmetrically. Anterior compartment mus culature weakness results in a footdrop gait, characterized 27

Part I ■ General Considerations

by accentuated hip flexion or circumduction of the hip during swing phase to avoid the toes of the dropped foot hitting the floor during swing-through. Component Mechanics of Running During running, the stance phase is diminished from approximately 0.6 second while walking to 0.2 second while sprinting (Fig. 1-39). During this brief period of stance phase, the forces involved in the vertical plane are increased to 2.5 to 3 times body weight. The range of

30 20 Dorsiflexion 10

PLANTAR FLEXION–DORSIFLEXION to

Heel strike

Run

0 10 Plantar flexion 20 30

Gastroc-soleus Anterior tibialis

Degrees

20 Dorsiflexion 10

Jog Heel strike

0 10 Plantar flexion 20 30

Gastroc-soleus Anterior tibialis

30 to

20 Dorsiflexion 10

Walk Heel strike

0 10 Plantar flexion 20 30

Gastroc-soleus Anterior tibialis

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 Seconds Figure 1-39 Ankle joint dorsiflexion–plantar flexion during running, jogging, and walking. Note that time of walking cycle decreases from 1 second for walking to approximately 0.6 second for running. Stance-phase time decreases significantly, as well. Muscle function is characterized by gastrocnemius–soleus muscle group and anterior tibial muscle. Note that gastrocnemius–soleus muscle group becomes active in late swing phase for jogging and running, compared with stance-phase muscle for walking. (From Mann RA: Intractable Plantar Keratoses. In Nicholas JA, Hershmann EB, editors: The lower extremity and spine in sports medicine, ed 2, St Louis, 1995, Mosby.)

motion of the joints is increased approximately 50%, and the muscles in the lower extremity must control these motions over a short time when measured in real time but over a considerable period when expressed as percent age of the gait cycle. It is probably because of the increased forces and muscle action required over a shorter period of time, and the repetitive nature of sport, that overuse injuries occur during running. Considerable alterations occur around the ankle joint when comparing jogging or running with walking. The gait cycle time progressively decreases from 1 second to 0.6 second. The ankle’s total arc of motion increases from 30 degrees during walking to 45 degrees during running. This motion occurs during 0.6 second for walking and 0.2 second for running. The direction of motion also changes: during walking, plantar flexion occurs at heel strike, whereas during jogging and running, there is pro gressive dorsiflexion. Rapid plantar flexion occurs at toe-off during all speeds of gait. Along with this increase in the range of motion and in the forces generated during running, the muscle function in the lower extremity also is altered. In real time, the phasic activity of most muscles decreases; however, when considered as a percentage of the gait cycle, the period of activity of these muscles increases considerably. Generally speaking, at initial ground contact, the majority of the muscles about the hip, knee, and ankle joints are active, and their period of activity, which begins during the late float phase, increases as the speed of gait increases. This is probably related to the rapid motion required by these joints in preparation for the impact of ground contact. During walking, there is adequate time for most of the preparation for ground contact to be carried out rather passively, but with the markedly increased range and speed of motion of these joints during running, muscle function plays a more active role. As the speed of gait increases, the muscle function in the posterior calf group changes significantly. During walking, the posterior calf group functions in stance phase, and during jogging and running, it performs in late swing phase; its activity is ongoing from the time of initial ground contact through most of the stance phase. The muscle group controls the ankle dorsiflexion that occurs after initial ground contact, the forward movement of the tibia, and brings about plantar flexion of the ankle joint. Similar changes in both the magnitude of motion and muscle function occur about the hip and knee joints as well. During running and changing direction, as well as acceleration and decel eration, the toes play an active role in push-off, whereas push-off is minimal during steady-state walking. SURGICAL IMPLICATIONS OF BIOMECHANICS OF THE FOOT AND ANKLE

The purpose of this section is to correlate the biomechani cal principles discussed thus far with some of the surgical procedures carried out about the foot and ankle. The deci sions made by the orthopaedic surgeon when planning

Biomechanics of the Foot and Ankle ■ Chapter 1

and undertaking a surgical procedure depend on a thor ough understanding of biomechanical principles. Biomechanical Considerations in Ankle Arthrodesis Because the subtalar and ankle joints work together during gait, it is important that certain anatomic facts be kept in mind when carrying out an ankle arthrodesis. An arthrodesis of the ankle joint places increased stress on the subtalar joint below and the knee joint above. The degree of internal or external tibial torsion, genu varum or genu valgum, proximal muscle weakness, and configu ration of the longitudinal arch should be considered. When an ankle arthrodesis is carried out, the degree of transverse rotation placed in the ankle mortise must be carefully considered so that increased stress is not caused within the foot. If the ankle is placed into excessive inter nal rotation, the patient experiences difficulty when the center of gravity passes over the foot. The position of internal rotation places increased stress on the subtalar and midtarsal joint region, which may become painful as a result of increased stress. Knee pain, and possibly hip pain, also may develop secondarily as a result of attempts to externally rotate the lower limb to help compensate for the abnormal position of the foot. If the ankle is placed into too much external rotation, the patient tends to roll over the medial border of the foot. This position permits the patient to easily roll over the foot, but in turn, it places increased stress on the medial side of the first metatarso phalangeal joint, which can lead to a hallux valgus defor mity. It may also cause increased stress along the medial side of the knee joint. The degree of varus or valgus tilt of the ankle joint must be carefully considered and should be related to the degree of subtalar joint motion and the overall alignment of the knee and tibia. If the subtalar joint is stiff and unable to compensate for any malalignment, it is impera tive to place the ankle joint into sufficient valgus position to obtain a plantigrade foot. If the ankle joint is placed into varus position, the patient will walk on the lateral

border of the foot. This not only causes the patient dis comfort because of localized weight bearing in a relatively small area, but the persistent varus position of the subta lar joint keeps the transverse tarsal joint in a semirigid state, resulting in a rather immobile forefoot that is dif ficult for the body to pass over during the stance phase. The degree of dorsiflexion and plantar flexion of the ankle joint must also be carefully considered when carry ing out an ankle arthrodesis. If there is a short lower extremity or an unstable knee joint as a result of weakness or loss of quadriceps function, the ankle joint should be placed into plantar flexion (10 to 15 degrees) to help give stability to the knee joint. If the pathologic process involves only the ankle joint, a neutral position is con sidered the position of choice. If the ankle joint is placed into excessive plantar flexion, the involved limb is length ened, which, in turn, causes a back-knee thrust on the knee joint, uneven gait pattern, and stress across the midfoot. If the ankle is placed into too much dorsiflexion, the impact of ground contact is concentrated in one small area of the heel, which may result in chronic pain. After an ankle arthrodesis, patients usually develop increased motion in the sagittal plane, which helps to compensate for loss of ankle motion. In our study of 81 ankle fusions, the sagittal arc of motion of the talar first metatarsal aver aged 24 degrees (9 to 43 degrees), at the talonavicular joint 14 ± 5 degrees, and at the talocalcaneal joint 8 ± 6 degrees (Fig. 1-40).52 Hindfoot Alignment Rotation occurs in the transverse plane during normal walking. This transverse rotation increases as we proceed from the pelvis to the ankle. Internal rotation occurs at initial ground contact, followed by external rotation until toe-off, when internal rotation begins again (see Fig. 1-8). This transverse rotation passes across the ankle joint and is translated by the subtalar joint to the calcaneus and foot. The loss of subtalar joint motion may result from trauma, arthritis, surgery, or congenital abnormality. This loss of rotation causes increased stress to be placed on the

Figure 1-40 Increased motion in transverse tarsal and subtalar joints to compensate for ankle arthrodesis. A, Dorsiflexion. B, Plantar flexion.

Part I ■ General Considerations

Figure 1-41 Etiology of a ball-and-socket ankle joint in adults. A, As a result of a congenital abnormality of the subtalar joint that eliminated subtalar motion, the ankle joint absorbed transverse rotation that normally occurs in subtalar joint. B, A congenital talonavicular fusion, which results in loss of subtalar joint motion, causes the ankle to absorb transverse rotation, resulting in a ball-and-socket ankle joint.

Figure 1-42 Talar beaking after increased stress as result of subtalar coalition.

along the lateral aspect of the foot. This position also holds the forefoot in a semirigid position, so the patient must either vault over it or place the foot in external rota tion to roll over the medial aspect. The position of choice is a valgus tilt of about 5 degrees in the subtalar joint because this permits satisfactory sta bility of the ankle joint, and the weight-bearing line of the body will pass medial to the calcaneus; therefore no stress will be placed on the lateral collateral ligament structure. This position results in slight pronation of the forefoot, which permits even distribution of weight on the plantar aspect of the foot. The slight valgus position also allows the forefoot to remain flexible so that the body can more easily pass over it. Midfoot Alignment

joint above (ankle) and below (transverse tarsal) the immobile joint. These changes brought on by lack of subtalar joint function may lead to chronic pain. The increased stress may cause secondary changes to occur in some individuals, which may take the form of a ball-andsocket ankle joint (Fig. 1-41). At other times, beaking may occur in the talonavicular joint in a patient with a subtalar coalition (Fig. 1-42). When a subtalar joint is fused, the transverse rotation that occurs in the lower extremity is partially absorbed in the ankle joint because it no longer can pass through the subtalar joint into the foot. The varus or valgus alignment of the subtalar joint will affect the position of the fore foot, so accurate alignment is essential. If the subtalar joint is placed into too much varus, the forefoot is rotated into supination, and the weight-bearing line of the extremity then passes laterally to the calcaneus and fifth metatarsal. This results in increased stress on the lateral collateral ligament structure and abnormal weight bearing 30

When surgical stabilization of the talonavicular or trans verse tarsal joint is carried out, motion in the subtalar joint is largely eliminated. For motion to occur in the subtalar joint, rotation of the navicular over the head of the talus must occur. If it cannot, there is essentially no subtalar joint motion. An isolated fusion of the calcaneo cuboid joint results in about a 30% loss of subtalar joint motion. Motion of the subtalar joint directly affects the stability of the foot through its control of the transverse tarsal joint. When the subtalar joint is in valgus position, the transverse tarsal joint is unlocked and the forefoot is flexible. Conversely, when the subtalar joint is inverted, the transverse tarsal joint is locked and the forefoot is fairly rigid. Because of the role the transverse tarsal joint plays in controlling the forefoot, it is essential that the foot be placed in a plantigrade position when the joints are stabilized. If the foot is placed into too much supina tion, the medial border of the foot is elevated, and undue stress is placed on the lateral aspect of the foot. It also

Biomechanics of the Foot and Ankle ■ Chapter 1

creates a rigid forefoot. The position of choice is neutral rotation or slight pronation, which ensures a flexible plantigrade foot. When a triple arthrodesis is carried out, the position of choice is 5 degrees of valgus for the subtalar joint and neutral rotation of the transverse tarsal joint. It should be emphasized, however, that it is better to err on the side of too much valgus and pronation to keep the weightbearing line medial to the calcaneus because that pro duces a more flexible plantigrade foot. When carrying out a pantalar arthrodesis, the same basic principles apply. Surgical stabilization of the intertarsal and medial three tarsometatarsal joints can be carried out with minimum loss of function or increased stress on the other joints in the foot. The intertarsal joints, which are distal to the transverse tarsal joint and proximal to the metatar sophalangeal joints, have little or no motion between them. The lateral two tarsometatarsal joints are more flex ible, and surgically, strategies that maintain flexibility are favored to fusion.

metatarsophalangeal joint, but it is unusual to see any form of degenerative change. An isolated arthrodesis of the interphalangeal joint of the great toe does not seem to have any significant effect on the biomechanics of gait, nor does an arthrodesis of the proximal and distal interphalangeal joints of the lesser toes. Resection of a single sesamoid bone because of a pathologic condition, such as a fracture, avascular necro sis, or intractable plantar keratosis, may be done with relative impunity. If, however, one sesamoid already has been removed, the second sesamoid probably should not be removed because of risk of a co*ck-up deformity of the metatarsophalangeal joint. This occurs because the intrin sic muscle insertion into the proximal phalanx of the great toe encompasses the sesamoids, and when the sesa moid is removed, this insertion is impaired to a varying degree. If adequate intrinsic function is not present, flexion of the proximal phalanx cannot be brought about, and a co*ck-up deformity results.

Forefoot Principles

Tendon Transfers

Removal of the base of the proximal phalanx of the great toe causes instability of the medial longitudinal arch as a result of disruption of the plantar aponeurosis and the windlass mechanism. This leads to decreased weight bearing of the first metatarsal head, which results in weight being transferred to the lesser metatarsal heads. Surgical techniques that remove the proximal phalanx base but preserve the plantar plate may lessen this effect. If the base of the proximal phalanx of one of the lesser toes is removed, a similar problem of instability occurs, but to a much lesser degree, particularly moving laterally across the foot. Conversely, resection of the meta tarsal head, except in severe disease states such as rheu matoid arthritis or diabetes, results in a similar problem because the windlass mechanism is destroyed as a result of the relative shortening of the ray. This also causes increased stress and callus formation beneath the adja cent metatarsal head, which is subjected to increased weight bearing. When carrying out an arthrodesis of the first metatar sophalangeal joint for such conditions as hallux rigidus, recurrent hallux valgus, or degenerative arthritis, the alignment of the arthrodesis site is critical. The metatar sophalangeal joint should be placed into approximately 10 to 15 degrees of valgus and 15 to 25 degrees of dorsi flexion in relation to the first metatarsal shaft. The degree of dorsiflexion depends to a certain extent on the heel height of the shoe that the patient desires to wear. An arthrodesis of the first metatarsophalangeal joint has a minimum effect on gait. The arthrodesis places increased stress on the interphalangeal joint of the hallux. This increased stress may result in degenerative changes over time, but these rarely become symptomatic. From a theoretic standpoint, increased stress is placed on the first metatarsocuneiform joint after arthrodesis of the

When evaluating muscle weakness or loss about the foot and ankle, the diagram in Figure 1-43 can be useful. It demonstrates the motion that occurs around each joint axis and the location of the muscles in relation to the axes. By considering the muscles in relation to the axes, it is possible to carefully note which muscles are function ing and thereby determine which muscles might be trans ferred to rebalance the foot and ankle. Generally speaking, if inadequate strength is present to balance the foot ade quately, it is important to establish adequate plantar flexion function over that of dorsiflexion; an equinus gait is not as disabling as a calcaneal-type gait. Also keep in mind that it is much more difficult to retrain a muscle that has been a stance-phase muscle to become a swingphase muscle than to retrain a swing-phase muscle to become a stance-phase muscle. Therefore, if possible, an in-phase muscle transfer will produce a more satisfactory result because no phase conversion is necessary. Ligaments of the Ankle Joint The configuration and alignment of the ligamentous structures of the ankle are such that they permit free movement of the ankle and subtalar joints to occur simul taneously. Because the configuration of the trochlear surface of the talus is curved to produce a cone-shaped articulation whose apex is directed medially, the single fan-shaped deltoid ligament is adequate to provide stabil ity to the medial side of the ankle joint (Fig. 1-44). On the lateral aspect of the ankle joint, however, where there is a larger area to be covered by a ligamentous structure, the ligament is divided into three bands: the anterior and posterior talofibular ligaments and the calcaneofibular ligament. The relationship of these ligaments to each other and to the axes of the subtalar and ankle joints must 31

Part I ■ General Considerations

Dorsiflexors

rsion

Inve

Invertors

Evertors

la bta Su xis

Tib. ant.

Plantar flexi

Ext. hal. longus Ext. dig. longus

Dorsiflexi

Tib. post. n rsio Eve

Plantar flexors

F. dig. longus F. hal. longus

Ankle a

xis

Peroneus long. Peroneus brevis

T. calcaneus

Figure 1-43 Left, Diagram demonstrates rotation that occurs about subtalar and ankle axes. Right, Diagram demonstrates relationship of various muscles about subtalar and ankle axes. (From Haskell A, Mann RA. Chapter 23: Biomechanics of the Foot. In American Academy of Orthopaedic Surgeons: Atlas of Orthoses and Assistive Devices, ed 4, Philadelphia, 2008, Mosby.)

Talus

Apical angle

Mortise

Apical angle Figure 1-44 Curvature of trochlear surface of talus creates cone whose apex is based medially. From this configuration, one can observe that the deltoid ligament is well suited to function along the medial side of ankle joint, whereas laterally, where more rotation occurs, three separate ligaments are necessary. (From Inman VT: The joints of the ankle, Baltimore, 1976, Williams & Wilkins.)

always be considered carefully when these joints are examined or ligamentous surgery is contemplated. Figure 1-45 demonstrates the anterior talofibular and calcaneofibular ligaments in relation to the subtalar joint axis. The calcaneofibular ligament is parallel to the sub talar joint axis in the sagittal plane. As the ankle joint is dorsiflexed and plantar flexed, this relationship between the calcaneofibular ligament and the subtalar joint axis 32

does not change. Furthermore, the calcaneofibular liga ment crosses both the ankle and the subtalar joint. This ligament is constructed to permit motion to occur in both of these joints simultaneously. It is important to appreci ate that, when the ankle joint is in neutral position, the calcaneofibular ligament is angulated posteriorly, but as the ankle joint is brought into more dorsiflexion, the calcaneofibular ligament is brought into line with the fibula, thereby becoming a true collateral ligament. Con versely, as the ankle joint is brought into plantar flexion, the calcaneofibular ligament becomes horizontal to the ground. In this position, it provides little or no stability for resisting inversion stress. The anterior talofibular liga ment, on the other hand, is brought into line with the fibula when the ankle joint is plantar flexed, thereby acting as a collateral ligament. When the ankle joint is brought up into dorsiflexion, the anterior talofibular liga ment becomes sufficiently horizontal so that it does not function as a collateral ligament. It can thus be appreci ated that, depending on the position of the ankle joint, either the calcaneofibular or the anterior talofibular liga ment will be a true collateral ligament with regard to providing stability to the lateral side of the ankle joint. The relationship between these two ligaments has been quantified and is presented in Figure 1-46. This demonstrates the relationship of the angle produced by the calcaneofibular and the anterior talofibular ligaments to one another. The average angle in the sagittal plane is approximately 105 degrees, although there is consider able variation, from 70 to 140 degrees. This is important because, from a clinical standpoint, it partially explains why some persons have lax collateral ligaments. If we assume that when the ankle is in full dorsiflexion the calcaneofibular ligament provides most of the stability

Biomechanics of the Foot and Ankle ■ Chapter 1

Calcaneofibular ligament

Anterior talofibular ligament

No. of specimens measured

0 Degrees

100

120

140

Figure 1-46 Average angle between calcaneofibular and talofibular ligaments in sagittal plane. Although the average angle is 105 degrees, there is considerable variation, from 70 to 140 degrees. (From Inman VT: The joints of the ankle, Baltimore, 1976, Williams & Wilkins.)

C Figure 1-45 Calcaneal fibular ligament and anterior talofibular ligament. A, In neutral position of ankle joint, both anterior talofibular and calcaneofibular ligaments provide support to joint. B, In plantar flexion, anterior talofibular ligament is in line with fibula and provides most of support to lateral aspect of ankle joint. C, In dorsiflexion, calcaneofibular ligament is in line with the fibula and provides support to the lateral aspect of ankle joint. (From Inman VT: The joints of the ankle, Baltimore, 1976, Williams & Wilkins.)

and that in full plantar flexion the anterior talofibular ligament provides stability, then as we pass from dorsi flexion to plantar flexion and back there will be a certain period in which neither ligament is functioning as a true collateral ligament. If we assume there is an average angle of approximately 105 degrees between these ligaments, then generally speaking, an area in which an insufficient lateral collateral ligament is present is unusual; however, if we have angulation of 130 to 140 degrees between these two ligaments, there is a significant interval while the ankle is passing from dorsiflexion to plantar flexion and back in which neither ligament is functioning as a col lateral ligament. This may explain why some persons are susceptible to chronic ankle sprains. Some patients who are thought to have ligamentous laxity may, in reality, possess this anatomic configuration of lateral collateral ligaments. The other factor that needs to be considered is the relationship of the calcaneofibular ligament to subtalar joint motion. The primary stabilizers of the subtalar joint are the interosseus talocalcaneal ligaments that reside within the sinus tarsi, not the calcaneofibular ligament.61 Because motion in the subtalar joint occurs about an axis that deviates from dorsal-medial to plantar-lateral (see Fig. 1-24), and the calcaneal attachment of the calcaneo fibular ligament lies on the subtalar joint axis, motion of the subtalar joint around this axis occurs with minimal change in calcaneofibular length. Instead, as the subtalar joint moves, the calcaneofibular ligament moves along a path approximating the surface of a cone whose apex is the intersection of the ligament and the subtalar joint axis.43 This relationship of the calcaneofibular ligament to the ankle and subtalar joint axes is critical when con templating ligamentous reconstruction because any liga ment reconstruction that fails to take this normal 33

Part I ■ General Considerations

Figure 1-47 A, Stress radiographs of ankle in dorsiflexion (DF) demonstrate no instability in calcaneofibular ligament. Same ankle stressed in plantar flexion (PF) demonstrates loss of stability caused by disruption of anterior talofibular ligament. Note anterior subluxation present when this ligament (L) is torn (anterior drawer sign). B, Stress radiograph of ankle in plantar flexion demonstrates no ligamentous instability. Same ankle stressed in dorsiflexion demonstrates laxity of calcaneofibular ligament. C, Stress radiograph of ankle joint in dorsiflexion, plantar flexion, and anteriorly all demonstrate evidence of ligamentous disruption. This indicates complete tear of lateral collateral ligament structure.

anatomic configuration into consideration results in a situation in which motion in one or both of these joints is restricted. From a clinical standpoint, when one is evaluating the stability of the lateral collateral ligament structure, the ankle joint should be tested in dorsiflexion to 34

demonstrate the competency of the calcaneofibular liga ment and in plantar flexion to test the competency of the anterior talofibular ligament. If both ligaments are com pletely disrupted, there will be no stability in either posi tion. Furthermore, to test for stability of the anterior talofibular ligament, the anterior drawer sign should be

Biomechanics of the Foot and Ankle ■ Chapter 1

elicited, with the ankle joint in neutral position, when the anterior talofibular ligament is in a position to resist anterior displacement of the talus from the ankle mortise (Fig. 1-47). REFERENCES 1. Abbott BC, Bigland B, Ritchie JM: The physiological cost of nega tive work. J Physiol 117:380–390, 1952. 2. Alexander IJ, Chao EY, Johnson KA: The assessment of dynamic foot-to-ground contact forces and plantar pressure distribution: a review of the evolution of current techniques and clinical applications. Foot Ankle 11:152–167, 1990. 3. Andriacchi TP, Ogle JA, Galante JO: Walking speed as a basis for normal and abnormal gait measurements. J Biomech 10:261– 268, 1977. 4. Arcan M, Brull MA: A fundamental characteristic of the human body and foot, the foot-ground pressure pattern. J Biomech 9:453–457, 1976. 5. Asmussen E: Positive and negative muscular work. Acta Physiol Scand 28:364–382, 1953. 6. Banister E, Brown S: The relative energy requirements of physical activity. In Falls H, editor: Exercise physiology, New York, 1968, Academic Press. 7. Barnett S, Cunningham JL, West S: A comparison of vertical force and temporal parameters produced by an in-shoe pressure mea suring system and a force platform. Clin Biomech (Bristol, Avon) 15:781–785, 2000. 8. Becker HP, Rosenbaum D, Kriese T, et al: Gait asymmetry fol lowing successful surgical treatment of ankle fractures in young adults. Clin Orthop 311:262–269, 1995. 9. Berry FJ: Angle variation patterns of normal hip, knee and ankle in different operations. Univ Calif Prosthet Devices Res Proj Rep Ser 11, February 1952. 10. Betts RP, Franks CI, Duckworth T, et al: Static and dynamic footpressure measurements in clinical orthopaedics. Med Biol Eng Comput 18:674–684, 1980. 11. Blomgren M, Turan I, Agadir M: Gait analysis in hallux valgus. J Foot Surg 30:70–71, 1991. 12. Boyden EM, Kitaoka HB, Cahalan TD, et al: Late versus early repair of Achilles tendon rupture. Clinical and biomechanical evaluation. Clin Orthop 317:150–158, 1995. 13. Breit GA, Whalen RT: Prediction of human gait parameters from temporal measures of foot-ground contact. Med Sci Sports Exerc 29:540–547, 1997. 14. Bresler B, Berry F: Energy and power in the leg during normal level walking. Univ Calif Prosthet Devices Res Proj Rep Ser 11, May 1951. 15. Bryant A, Singer K, Tinley P: Comparison of the reliability of plantar pressure measurements using the two-step and midgait methods of data collection. Foot Ankle Int 20:646–650, 1999. 16. Carlson RE, Fleming LL, Hutton WC: The biomechanical rela tionship between the tendoachilles, plantar fascia and metatar sophalangeal joint dorsiflexion angle. Foot Ankle Int 21:18–25, 2000. 17. Close J, Inman V: The action of the subtalar joint. Univ Calif Prosthet Devices Res Proj Rep Ser 11, May 1953. 18. Ctercteko GC, Dhanendran M, Hutton WC, et al: Vertical forces acting on the feet of diabetic patients with neuropathic ulcer ation. Br J Surg 68:608–614, 1981. 19. Cunningham D: Components of floor reaction during walking. Univ Calif Prosthet Devices Res Proj Rep Ser 11, November 1950. 20. Duckworth T, Betts RP, Franks CI, et al: The measurement of pressures under the foot. Foot Ankle 3:130–141, 1982. 21. Elftman H: A cinematic study of the distribution of pressure in the human foot. Anat Rec 59:481–491, 1934.

22. Elftman H: The transverse tarsal joint and its control. Clin Orthop Relat Res 16:41–46, 1960. 23. Fujita M, Matsusaka N, Norimatsu T, et al: The role of the ankle plantar flexors in level walking. In Winter DA, editor: Biomechanics IX-A, Champaign, Ill, 1985, Human Kinetics Publishers, pp 484–488. 24. Grundy M, Tosh PA, McLeish RD, et al: An investigation of the centres of pressure under the foot while walking. J Bone Joint Surg Br 57:98–103, 1975. 25. Hayafune N, Hayafune Y, Jacob AC: Pressure and force distribu tion characteristics under the normal foot during push-off phase in gait. Foot 9:88–92, 1999. 26. Hennig EM, Rosenbaum D: Pressure distribution patterns under the feet of children in comparison with adults. Foot Ankle 11:306–311, 1991. 27. Hennig EM, Staats A, Rosenbaum D: Plantar pressure distribu tion patterns of young school children in comparison to adults. Foot Ankle Int 15:35–40, 1994. 28. Henry AP, Waugh W, Wood H: The use of footprints in assessing the results of operations for hallux valgus. A comparison of Keller’s operation and arthrodesis. J Bone Joint Surg Br 57:478– 481, 1975. 29. Herzog W, Nigg BM, Read LJ, et al: Asymmetries in ground reac tion force patterns in normal human gait. Med Sci Sports Exerc 21:110–114, 1989. 30. Hicks JH: The mechanics of the foot. II. The plantar aponeurosis and the arch. J Anat 88:25–30, 1954. 31. Hof AL: In vivo measurement of the series elasticity release curve of human triceps surae muscle. J Biomech 31:793–800, 1998. 32. Hof AL, Geelen BA, Van den Berg J: Calf muscle moment, work and efficiency in level walking; role of series elasticity. J Biomech 16:523–537, 1983. 33. Hof AL, Van Zandwijk JP, Bobbert MF: Mechanics of human triceps surae muscle in walking, running and jumping. Acta Physiol Scand 174:17–30, 2002. 34. Holmes GB Jr, Timmerman L: A quantitative assessment of the effect of metatarsal pads on plantar pressures. Foot Ankle 11:141– 145, 1990. 35. Hughes J, Clark P, Jagoe JR, et al: The pattern of pressure distribu tion under the weightbearing forefoot. Foot 1:117–124, 1991. 36. Hughes J, Clark P, Klenerman L: The importance of the toes in walking. J Bone Joint Surg Br 72:245–251, 1990. 37. Hughes J, Clark P, Linge K, et al: A comparison of two studies of the pressure distribution under the feet of normal subjects using different equipment. Foot Ankle 14:514–519, 1993. 38. Hughes J, Kriss S, Klenerman L: A clinician’s view of foot pres sure: a comparison of three different methods of measurement. Foot Ankle 7:277–284, 1987. 39. Hughes J, Pratt L, Linge K, et al: Reliability of pressure measure ments: the EMED F system. Clin Biomech 6:14–18, 1991. 40. Hutton WC, Dhanendran M: The mechanics of normal and hallux valgus feet—a quantitative study. Clin Orthop 157:7–13, 1981. 41. Hutton WC, Stott JRR, Stokes JAF: The mechanics of the foot. In Klenerman L, editor: The foot and its allied disorders, Oxford, 1982, Blackwell Scientific Publications, p 42. 42. Imamura M, Imamura ST, Salomao O, et al: Pedobarometric evaluation of the normal adult male foot. Foot Ankle Int 23:804– 810, 2002. 43. Inman V: The joints of the ankle, Baltimore, 1976, Williams & Wilkins. 44. Isman R, Inman V: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10-11:97, 1969. 45. Katoh Y, Chao EY, Laughman RK, et al: Biomechanical analysis of foot function during gait and clinical applications. Clin Orthop Relat Res 177:23–33, 1983.

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46. Kelikian AS, Sarrafian SK: Anatomy of the foot and ankle, ed 3, Philadelphia, 2011, JB Lippincott. 47. Kerrigan DC, Della Croce U, Marciello M, et al: A refined view of the determinants of gait: significance of heel rise. Arch Phys Med Rehabil 81:1077–1080, 2000. 48. Levens A, Inman V, Blosser J: Transverse rotation of the segments of the lower extremity in locomotion. J Bone Joint Surg Am 30A:859–872, 1948. 49. Logan BM, Hutchings RT: McMinn’s color atlas of foot and ankle anatomy, ed 4, St Louis, 2012, Elsevier. 50. Mann R, Inman VT: Phasic activity of intrinsic muscles of the foot. J Bone Joint Surg Am 46:469–481, 1964. 51. Mann RA, Poppen NK, O’Konski M: Amputation of the great toe. A clinical and biomechanical study. Clin Orthop Relat Res 226:192–205, 1988. 52. Mann RA, Rongstad KM: Arthrodesis of the ankle: a critical analysis. Foot Ankle Int 19:3–9, 1998. 53. Manter J: Movements of the subtalar and transverse tarsal joints. Anat Rec 80:397–410, 1941. 54. Morton DJ: Structural factors in static disorders of the foot. Am J Surg 9:315–328, 1930. 55. Mueller MJ, Sinacore DR, Hastings MK, et al: Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A random ized clinical trial. J Bone Joint Surg Am 85-A:1436–1445, 2003. 56. Mueller MJ, Strube MJ: Generalizability of in-shoe peak pressure measures using the F-scan system. Clin Biomech (Bristol, Avon) 11:159–164, 1996. 57. Nilsson J, Thorstensson A: Ground reaction forces at different speeds of human walking and running. Acta Physiol Scand 136:217–227, 1989. 58. Pollard JP, Le Quesne LP, Tappin JW: Forces under the foot. J Biomed Eng 5:37–40, 1983. 59. Popova T: Quoted in Issledovaniia po biodinamike lokomotsii. In Bernstein N, editor: Biodinamika khod’by normal’nogo vzroslogo muzhchiny, Moscow, 1935, Idat Vsesoiuz Instit Eksper Med. 60. Ralston HJ: Energy-speed relation and optimal speed during level walking. Int Z Angew Physiol 17:277–283, 1958. 61. Ringleb SI, Dhakal A, Anderson CD, et al: Effects of lateral liga ment sectioning on the stability of the ankle and subtalar joint. J Orthop Res 29:1459–1464, 2011. 62. Rodgers MM, Cavanagh PR: Pressure distribution in Morton’s foot structure. Med Sci Sports Exerc 21:23–28, 1989. 63. Rose NE, Feiwell LA, Cracchiolo A 3rd: A method for measuring foot pressures using a high resolution, computerized insole sensor: the effect of heel wedges on plantar pressure distribution and center of force. Foot Ankle 13:263–270, 1992. 64. Rosenbaum D, Hautmann S, Gold M, et al: Effects of walking speed on plantar pressure patterns and hindfoot angular motion. Gait Posture 2:191–197, 1994.

65. Ryker NJ: Glass walkway studies of normal subjects during normal walking. Univ Calif Prosthet Devices Res Proj Rep Ser 11, January 1952. 66. Saunders JB, Inman VT, Eberhart HD: The major determinants in normal and pathological gait. J Bone Joint Surg Am 35-A:543– 558, 1953. 67. Silvino N, Evanski PM, Waugh TR: The Harris and Beath foot printing mat: diagnostic validity and clinical use. Clin Orthop 151:265–269, 1980. 68. Simon SR, Mann RA, Hagy JL, et al: Role of the posterior calf muscles in normal gait. J Bone Joint Surg Am 60:465–472, 1978. 69. Stein H, Simkin A, Joseph K: The foot-ground pressure distribu tion following triple arthrodesis. Arch Orthop Trauma Surg 98:263–269, 1981. 70. Stokes IA, Hutton WC, Stott JR, et al: Forces under the hallux valgus foot before and after surgery. Clin Orthop Relat Res 142:64–72, 1979. 71. Stott JR, Hutton WC, Stokes IA: Forces under the foot. J Bone Joint Surg Br 55:335–344, 1973. 72. Sutherland DH, Cooper L, Daniel D: The role of the ankle plantar flexors in normal walking. J Bone Joint Surg Am 62:354– 363, 1980. 73. Veves A, Sarnow MR, Giurini JM, et al: Differences in joint mobility and foot pressures between black and white diabetic patients. Diabet Med 12:585–589, 1995. 74. Waldecker U: Metatarsalgia in hallux valgus deformity: a pedo graphic analysis. J Foot Ankle Surg 41:300–308, 2002. 75. Wanivenhaus A, Brettschneider W: Influence of metatarsal head displacement on metatarsal pressure distribution after hallux valgus surgery. Foot Ankle 14:85–89, 1993. 76. Wearing SC, Urry SR, Smeathers JE: Ground reaction forces at discrete sites of the foot derived from pressure plate measure ments. Foot Ankle Int 22:653–661, 2001. 77. Willson JD, Kernozek TW: Plantar loading and cadence altera tions with fatigue. Med Sci Sports Exerc 31:1828–1833, 1999. 78. Winson IG, Rawlinson J, Broughton NS: Treatment of metatar salgia by sliding distal metatarsal osteotomy. Foot Ankle 9:2–6, 1988. 79. Wright DG, Desai SM, Henderson WH: Action of the subtalar and ankle-joint complex during the stance phase of walking. J Bone Joint Surg Am 46:361–382, 1964. 80. Yamamoto H, Muneta T, Asahina S, et al: Forefoot pressures during walking in feet afficted with hallux valgus. Clin Orthop 323:247–253, 1996. 81. Zhu H, Wertsch JJ, Harris GF, et al: Walking cadence effect on plantar pressures. Arch Phys Med Rehabil 76:1000–1005, 1995. 82. Zhu HS, Wertsch JJ, Harris GF, et al: Foot pressure distribution during walking and shuffling. Arch Phys Med Rehabil 72:390– 397, 1991.

Chapter

Principles of the Physical Examination of the Foot and Ankle Todd A. Irwin, Robert B. Anderson, W. Hodges Davis

CHAPTER CONTENTS OVERVIEW SEQUENCE OF EXAMINATION TOPOGRAPHIC ANATOMY Ankle and Hindfoot Lateral Ankle Medial Ankle Posterior Ankle Anterior Ankle Plantar Hindfoot Midfoot Forefoot Hallux Complex Lesser Metatarsals and Toes EXAMINATION IN SEQUENCE Standing Examination Sitting Examination General Visual Overview General Skeletal Overview Neurovascular Examination Range of Motion of the Joints Relationship of Forefoot to Hindfoot Direct Palpation Muscle Function Specific Examination Components for Individual Consideration Supine Examination Prone Examination Gait Shoe Examination

37 38 38 38 38 39 40 41 41 43 46 46 46 47 47 50 50 50 51 52 55 56 57 58 58 58 59 60

You may not see it, but it sees you. Jack Hughston, MD, discussing the physical examination The foot, ankle, and leg are parts of the body that are readily accessible to careful physical examination. In the vast majority of cases, a definitive diagnosis can be reached by obtaining a careful history, conducting a proper physical examination, and using the indicated

ancillary diagnostic procedures. Effective examination of the lower extremity can be dependent on the patient’s age and receptiveness to examination. In this chapter, the focus is on examination of the mature foot and ankle. The reader will receive a framework for a systematic approach to the normal examination. This will give a background for understanding the pathology described in subsequent chapters. In addition, a detailed description of the topographic anatomy of the foot and ankle is provided. It is with this knowledge that the practitioner can best evaluate the abnormalities in this easily palpable body part. It must be stressed that one sees only what one is looking for, or, in the words of a wise Southern gentleman physician “you may not see it [foot pathology], but it sees you.” Keep your eyes wide open. OVERVIEW

To prevent overlooking pertinent findings, the examiner should follow a rigorous routine. The particular routine adopted will vary depending on personal preference and arrangement of office facilities. The suggestion is to consciously formulate this routine and school oneself to deviate rarely from it. This will best ensure nothing is missed. However, no matter what procedure is used, the examiner must consider the foot and ankle from three different points of view. First, the foot and ankle should be seen systemically or as part of the greater body. In the detailed examination, the effects of systemic problems cannot be underestimated. The foot examination can reveal the presence of systemic disease as well as give evidence of circulatory, neuropathic, metabolic, and cutaneous abnormalities. The examiner should not be so focused on the foot as to miss a much more illustrative and often treatable global disease. Second, the foot and ankle should be considered an important component of the locomotor system. They play reciprocal roles with the suprapedal segments, and abnormal function of any part of the locomotor 37

Part I ■ General Considerations

apparatus is reflected in adaptive changes in the normal parts. Therefore it is helpful for the examiner to observe the patient walking over an appreciable distance. Third, the human foot and ankle should be viewed as relatively recent evolutionary acquisitions; thus they are subject to considerable individual anatomic and functional variation. It is regrettable that in most of the anatomic and orthopaedic literature, only average values for the positions of axes of the major articulations and for ranges of motion about these axes are given (see Chapter 1). It so happens that an average person is difficult to find, particularly among patients seeking help in our offices. The examiner should be aware of these variations and should also be cognizant of their functional implications. In most patients, the luxury of a “normal” contralateral extremity allows the examiner the most definitive pertinent comparison. Only with such knowledge and insight can the examiner determine the proper therapeutic course and realistically evaluate the chances of success or failure of that choice.

Figure 2-1 Lateral ankle and hindfoot topography, anterior lateral view. A, Distal fibula; B, fibular shaft; C, lateral gutter of the ankle; D, distal syndesmosis; E, lateral wall of the calcaneus; F, the peroneal tubercle; G, sinus tarsi; H, lateral talar process; I, peroneal tendons; J, insertion point of the superior peroneal retinaculum; K, calcaneofibular ligament; L, anterior talofibular ligament; M, extensor digitorum brevis muscle; N, sural nerve.

SEQUENCE OF EXAMINATION

When examining the foot and ankle, the examiner should follow as closely as possible the procedural sequence taught in courses in introductory physical diagnosis. After taking an adequate history, the examiner first inspects, then palpates, and finally (in an orthopaedic examination) manipulates. This sequence must be modified and repeated several times as the patient performs tasks in various positions and under various stresses. The following outline for the examination of the foot and ankle has proved useful. In subsequent sections, the authors detail specific portions of the particular examination that should be stressed. It is helpful for the patients to be in shorts, skirts, or loose-fitting trousers to allow easy observation of the legs and knees. In general, all socks or hose are removed. The examination area should allow gait and stance observation from front and rear. The usual sequence of examination begins with the examiner first observing the patient walking because this often can be done even before taking the history. Second is the standing examination, which is done from front and rear, and must include visualization of the knee and its alignment. Third, the bulk of the examination is done with the patient sitting on a table slightly above the examiner. This allows for easy inspection, palpation, and manipulation of both extremities. Examination with the patient prone or supine is optional and is done as the first three portions of the examination dictate. The amount of time spent on each portion of this examination sequence depends on the patient’s presentation. TOPOGRAPHIC ANATOMY

The importance of topographic anatomy to the examination of the foot and ankle cannot be overstated. The 38

experienced examiner can palpate the vast majority of the pathologic structures and use radiographic tests for confirmation only. The authors divide this discussion into anatomic regions, with the palpable bones, joints, nerves and vascular structures, and ligaments and tendons highlighted. Ankle and Hindfoot Lateral Ankle The examination of the osteology of the lateral ankle begins with the easily palpable tip of the fibula (Fig. 2-1). From the tip, the distal fibula (A) and the shaft (B) can be felt in its entirety by running the examiner’s fingers proximally. The lateral gutter of the ankle joint (C) can be found by running the thumb medially over the anterior and medial edge of the fibula. The lateral shoulder of the talus can be felt at the joint line by dorsiflexing and plantar flexing the ankle. The distal syndesmosis (D) is felt by following the medial edge of the fibula superior to the joint line. The lateral wall of the calcaneus (E) can be palpated with little difficulty inferior and posterior to the tip of the fibula. If this lateral wall is palpated distal and inferior to the tip of the fibula, the peroneal tubercle (F) can be felt as the calcaneal neck nears the calcaneocuboid joint. The sinus tarsi (G) (the space in front of the posterior facet of the subtalar joint) is a palpable soft spot approximately 1 cm distal and 1 cm inferior to the tip of the fibula. The anterior portion of the posterior facet of the subtalar joint can be located with deep thumb palpation into the sinus tarsi. The lateral talar process (H) is palpated on the posterior wall of the sinus tarsi. The anterior process of the calcaneus is the anterior wall of the sinus tarsi.

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

The palpable tendons, muscles, and ligaments in the lateral ankle and hindfoot can best be referenced from the tip of the fibula. Superior and posterior to the tip of the fibula are the peroneal tendons (I). The peroneus brevis is deep to the peroneus longus. The tendons can be felt in the groove, and the anterior edge of the fibular groove is sharp and is the insertion point of the superior peroneal retinaculum (J). Inferior and extending posterior and inferior is the calcaneofibular ligament (K). It passes deep to the peroneal tendons as the tendons clear the fibula. From the tip of the fibula, if the examiner runs a finger 1 to 1.5 cm along the anterior edge, the anterior talofibular ligament (L) can be felt. In the uninjured patient, it can be felt as a soft tissue thickening that can be rolled against the anterior lateral talar shoulder. If the examiner continues to run a finger superior on the anterior fibula up to the junction with the distal tibiofibular connection, the most inferior fibers of the syndesmotic ligament (D) can be felt (anterior distal tibiofibular ligament). The remainder of the anterior syndesmotic ligament can be felt by palpating directly superior to the tibia and fibula junction. To truly assess this portion of the syndesmosis requires deep palpation. The extensor digitorum brevis muscle (M) can be located by palpating the sinus tarsi (G) because this muscle covers this space. The peroneal tendons can be felt on the lateral calcaneal wall, extending from the distal end of the fibular groove, which runs inferior then distal. The brevis is dorsal as the tendons turn distal. The peroneus brevis is also dorsal at the peroneal tubercle, and the peroneus longus is plantar. In this area, the tendons can be felt in their separate sheaths created by the inferior peroneal retinaculum and the tubercle. The nervous topography in this region is fairly straightforward. The sural nerve can be felt in the fatty soft spot directly posterior to the peroneal tendons running in the fibular groove (Fig. 2-2). In a thin patient, this nerve can be rolled under a finger, just posterior to the course of the peroneal tendons as the tendons enter the lateral midfoot. The superficial peroneal nerve can first be palpated as a number of branches just superior to the distal ankle

Figure 2-2 Sural nerve, surface anatomy.

syndesmosis. Again, it is best seen and palpated by rolling the branch under a finger as the ankle is plantar flexed. Medial Ankle The topography of the medial ankle and hindfoot (Fig. 2-3) is as accessible as the lateral. The reference point here is the tip of the medial malleolus (A), which also allows a reference for medial ankle osteology. The tip of the malleolus is the most distal bony prominence palpated on the medial tibia. From this point, the anterior medial tibiotalar joint line (B) can be located by sliding a thumb 2 cm superior and then lateral until the thumb feels a soft spot. This is the medial gutter, the articular space between the medial malleolus and the medial talar body. Following the gutter proximally allows palpation of the anterior distal tibial plafond. This can be followed laterally across the joint. Following the malleolus posteriorly and proximally allows palpation of the entire posterior medial edge of the malleolus and tibia. From the tip of the medial malleolus, with the ankle at neutral, a line drawn distal and slightly plantar will run through the navicular bone (C). The navicular is best felt with the hindfoot slightly supinated. With the hindfoot pronated and the midfoot abducted, the talar head (D) can be felt on the medial foot just proximal to the navicular. The medial talonavicular joint can be delineated by adducting and abducting the transverse tarsal joint. If the line between the navicular and the medial malleolus is divided in half and drops plantarward 1 to 1.5 cm, the sustentaculum tali (E)—a medial ossicle of the calcaneus— can be palpated. The palpable tendons and ligaments of the medial hindfoot can also be referenced from the tip of the medial malleolus. The superficial deltoid ligament (F) fans out from the malleolus but can best be palpated anterior and distal to it. The anterior fascicles of the deltoid can be felt by following the anterior edge of the malleolus only

Figure 2-3 Medial ankle and hindfoot topography, direct medial view. A, Tip of the medial malleolus; B, anterior medial tibiotalar joint line; C, navicular bone; D, the talar head; E, sustentaculum tali; F, superficial deltoid ligament; G, posterior tibial tendon; H, flexor digitorum longus; I, flexor hallucis longus; J, pulse of the posterior tibial artery.

Part I ■ General Considerations

Figure 2-4 Examination of the posterior tibial tendon. A, The foot is plantar flexed and abducted to neutralize the pull of the anterior tibial tendon. B, The posterior tibial tendon is palpated. C, The patient attempts to adduct the foot, and the strength of the posterior tibial tendon is assessed.

1 cm. If the examiner feels the medial gutter, the origin of the superficial deltoid has been passed. The most anterior fascicles of the superficial deltoid (anterior tibionavicular and anterior tibioligamentous) can be palpated because they originate from the anterior ridge of the malleolus. The portion of the superficial deltoid originating from the tip of the malleolus can be located as it courses deep to the tendons of the medial ankle. The individual fasicles of the deep deltoid ligament cannot be isolated by palpation. The more posterior aspects of the superficial deltoid cannot be palpated directly. The posterior tibial tendon (G) can be appreciated along its entire course. It begins at the musculotendinous junction, 5 to 7 cm from the tip of the medial malleolus, just off the posterior bony margin of the distal tibia, and travels distally, almost adherent to the posterior aspect of the medial malleolus. The tendon curves around the medial malleolus and then extends distally to the plantar medial insertion on the navicular. The flexor digitorum longus (FDL) (H) is easily palpated posterior and medial to the posterior tibialis tendon at a level 1 to 2 cm from the tip of the malleolus. It can be felt again in the midfoot as it crosses deep to the flexor hallucis longus (FHL) tendon. The FHL tendon (I) is best palpated in the ankle slightly posterior and deep to the posterior tibial artery and nerve at the level 1 to 2 cm proximal to the medial malleolus. The FHL also can be felt as it passes plantar to the sustentaculum tali. The superomedial aspect of the spring ligament (superomedial calcaneonavicular ligament) is palpated plantar and deep to the posterior tibial tendon, just proximal to the tendon’s insertion on the plantar-medial navicular (Fig. 2-4). It is import to locate the neurovascular structures of the medial ankle. The pulse of the posterior tibial artery 40

Figure 2-5 The posterior tibial artery pulse is best felt 2 cm from the malleolar tip.

(see J in Fig. 2-3) can be felt 1 to 2 cm posterior and medial to the medial edge of the medial malleolus. The pulse is strongest approximately 2 cm posterior to the malleolar tip (Fig. 2-5). The posterior tibial nerve runs with the artery in the tarsal tunnel. The nerve bifurcates into the medial and lateral plantar nerves at the level of the tip of the malleolus. The medial branch courses distally and plantarly and can be palpated as it runs under the abductor hallucis muscle at the level of the medial gutter of the ankle joint (Fig. 2-6). The lateral plantar nerve travels straight inferior from the tarsal tunnel and can be palpated as it runs deep to the abductor hallucis. The saphenous nerve can sometimes be palpated on the medial malleolus by rolling it gently under the fingers. Posterior Ankle The Achilles tendon (Fig. 2-7A) defines the posterior ankle and hindfoot. This large tendon can best be examined with the patient prone. The tendon transects the

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

laterally, and posteriorly. The retrocalcaneal space (C), which is deep to the Achilles at its insertion, can be easily pinched by pressure from either medial or lateral. The space or its bursa (or both) is an area that is easily delineated from the Achilles proper. The posterior lateral ankle is another access point for the peroneal tendons (D) as they pass posterior to the fibula and can be an easier way to feel both tendons in the fibular groove. The same can be said for the FHL tendon (E), which is a posteromedial ankle tendon at this point (Fig. 2-8).

B Figure 2-6 A, Anatomic specimen demonstrating the posterior tibial nerve. B, The posterior tibial nerve may be palpated just inferior to the medial malleolus.

Figure 2-7 Posterior ankle and hindfoot. A, Achilles tendon; B, the Achilles insertional ridge of the calcaneus; C, retrocalcaneal space; D, the peroneal tendons; E, flexor hallucis longus tendon.

posterior ankle and can be easily palpated because of the tendon’s subcutaneous course. The tendon inserts into the calcaneus broadly, and the Achilles insertional ridge of the calcaneus (B) is palpated at the distal insertion of the tendon. The posterior calcaneus is palpated medially,

Anterior Ankle The anterior ankle (Fig. 2-9) is defined by the readily palpable anterior tibialis tendon (A). The tendon is found by asking the patient to actively dorsiflex the ankle. The anterior tibialis, first felt at or near the midanterior ankle just proximal to the malleoli, is the largest tendon structure that passes more medially as it travels distally. Its insertion on the plantar medial cuneiform and plantar first metatarsal is defined with the same dorsiflexion maneuver (Fig. 2-10). On either side of the anterior tibialis tendon, the anterior ankle joint (B) can be felt by deep palpation. The distinction between the tibia and the talus is more easily felt with gentle dorsiflexion and plantar flexion of the ankle joint. The transition from anterior tibia to anterior fibula is quite superficial and can help guide the estimation of the location of the less superficial midanterior tibia and talus. The branches of the superficial peroneal nerve (C) are palpated by gently rolling the fingers over the superficial portions of the anterior ankle (Fig. 2-11). All of these branches are found lateral to the anterior tibialis. The pulse of the dorsalis pedis artery is usually felt not at the ankle but in the dorsal midfoot. The remaining tendons of the anterior ankle (see Fig. 2-9) are all found lateral to the anterior tibialis. From medial to lateral, these easily palpable tendons are the extensor hallucis longus (EHL) (D), the extensor digitorum longus (EDL) (E), and the peroneus tertius (F) (found in most people). The examination of these tendons can be made easier by active dorsiflexion or passive plantar flexion of the toes and ankle. Medial to the anterior tibialis, no tendons are normally present. Plantar Hindfoot Examination of the plantar-lateral aspect of the hindfoot is all about defining the anatomy of the lateral calcaneal area (Fig. 2-12). If the examiner begins at the posteriormost aspect of the calcaneus and runs a finger distal to it, the lateral edge of the calcaneus can be felt as separate from the lateral aspect of the plantar fat pad (Fig. 2-13). The fat pad begins to be prominent as the skin texture changes from thin to thick as the weight-bearing surface of the heel becomes apparent. On the plantar surface (see Fig. 2-12), the lateral band of the plantar fascia and the abductor digiti minimi (A) are most often indistinguishable as a pinchable band originating from the palpable lateral calcaneus and extending distal to the fifth 41

Part I ■ General Considerations

Figure 2-8 Achilles tendon. A, The normal tendon is examined from behind. B, Tendinosis is seen in the Achilles tendon on the left. C, Excursion of the ankle joint is noted. A defect in the Achilles tendon after a rupture is observed (D) and palpated (E) on examination.

Figure 2-9 Anterior ankle. A, Anterior tibialis tendon; B, anterior ankle joint; C, branches of the superficial peroneal nerve; D, extensor hallucis longus; E, extensor digitorum longus; F, peroneus tertius.

metatarsal head. The sural nerve can be felt as a cord just plantar to the peroneal tendons as they run along the calcaneal wall. The plantar-medial hindfoot is best located from the posterior calcaneus by running a finger along the plantarmedial border of the bone. Soon, the bone becomes less subcuticular as the soft tissues of the arch are more prominent. The abductor hallucis muscle (B) can be palpated as it originates from the plantar-medial calcaneus and extends distally to insert on the plantar-medial first metatarsophalangeal (MTP) joint. The medial cord of the plantar fascia (C) is palpated just plantar and lateral to the abductor hallucis. It is felt most readily by passively dorsiflexing the toes. The origin of the medial cord of the plantar fascia is best felt by passively dorsiflexing the toes and then running a thumb posterior until it is felt on the proximal plantar calcaneus. Deep palpation is required, as the examiner feels posteriorly, because the thick plantar fat pad (D) covers this area by covering the posterior-plantar calcaneus. The heel pad is thinner as the plantar hindfoot transitions to the non–weight-bearing arch. There are no palpable neural or vascular structures in the plantar hindfoot, but the medial and lateral plantar nerves are just deep to the abductor hallucis muscle as they cross into the plantar hindfoot. Deep palpation can elicit tenderness in the respective distributions of these nerves.

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

C Figure 2-10 A, Normal anterior tibial tendon. B, Rupture of anterior tibial tendon noted on left (right foot). C, Rupture and contraction leaves a mass on the anterior ankle. (B and C, Courtesy L. Schoen, MD.)

Figure 2-11 Superficial peroneal nerves. A, Superficial anatomy. B, Anatomic dissection demonstrating superficial peroneal nerve branches.

Midfoot The structures of the dorsal midfoot, in most cases, can be appreciated with a careful examination (Fig. 2-14A and B). The bones of the midfoot can all be palpated most readily on the dorsum. The osteology of the dorsal

midfoot is best felt by starting proximal at the talonavicular joint (A). The detail of the bony edges can be defined by the palpable joints. The talonavicular joint can be felt as the most mobile joint on the medial side. By moving the foot into abduction and supination, the mobility of 43

Part I ■ General Considerations

Figure 2-12 Plantar hindfoot. A, Lateral band of the plantar fascia and the abductor digiti minimi; B, abductor hallucis muscle; C, medial cord of the plantar fascia; D, plantar fat pad.

B Figure 2-13 Plantar fascia. A, Clinical examination of plantar fascia. B, Anatomic dissection demonstrating the plantar fascia.

the joint can be felt. Whereas some motion is present in the more distal joints, in the normal foot, the talonavicular joint is most mobile. Once the talonavicular joint is found medially, the dorsal joint can be felt by running a finger along the navicular. Palpating distally while staying dorsal, the examiner will feel a subtle ridge or thickening at the navicular cuneiform joint and the first tarsometatarsal joint (B). The edges of the joints can be followed to define the bony architecture of the corresponding bones. The bases of the lesser tarsometatarsal joints are best isolated by following the lesser metatarsal shafts from distal to proximal. The second base is proximal to the first base, inset between the first and the third (C). The lateral aspect of the midfoot is more mobile than the medial and is best referenced from the prominent base of the fifth metatarsal (D). This is the most lateral bony area on the lateral midfoot. It is both prominent and mobile. The calcaneocuboid joint (E) is isolated by holding the hindfoot stable and then dorsiflexing and plantar flexing the midfoot. The calcaneocuboid joint is the mobile segment just proximal to the base of the fifth metatarsal as the examiner feels along the lateral calcaneal wall. The anterior process of the calcaneus (F) is found by running a finger dorsally on the calcaneocuboid joint. The most dorsal palpable bony structure on this line is the anterior process of the calcaneus. The fourth and fifth tarsometatarsal joint can be located by the same dorsiflexion and plantar flexion used for the calcaneocuboid joint, but the fifth joint is at the base of the fifth metatarsal, and the fourth joint is slightly medial and dorsal to the fifth metatarsal. The midfoot represents the insertion area of many of the ankle tendons. The medial midfoot is the insertion area for the posterior tibialis, the anterior tibialis, and the peroneus longus tendons. The insertion of the posterior tibialis (G) is best felt at the navicular. When a patient actively supinates and inverts the foot, the tendon can be isolated proximally at the medial malleolus and followed to its insertion. The same can be done for the anterior tibialis (H) as it inserts on the plantar-medial aspect of the cuneiform and plantar proximal first metatarsal. The insertion of the peroneus longus cannot be palpated specifically except in very thin patients, but its insertion on the plantar base of the first metatarsal is an area that can be mobile with peroneus longus activity. Asking the patient to actively plantar flex the first metatarsal can isolate the peroneus longus tendon (see Fig. 2-14C and D). The medial midfoot is an area where the examiner can palpate extrinsic tendons that insert distal in the forefoot. Directly plantar to the medial cuneiform (Fig. 2-15), the point where the FHL and FDL cross (see Fig. 2-14), the master knot of Henry (I) can be located by deep palpation. This is made easier by active plantar flexion of the five toes. The medial cord of the plantar fascia covers the knot, but the moving tendons can be felt deep and medial to the medial cord of the static fascia. The EHL and EDL

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

C Figure 2-14 Midfoot. A, Dorsal view. A, Talonavicular joint; B, first tarsometatarsal joint; C, second metatarsal base; D, base of the fifth metatarsal; E, calcaneocuboid joint; F, anterior process of the calcaneus; G, insertion of the posterior tibialis; H, insertion of the anterior tibialis; J, peroneus brevis insertion. B, Plantar view. D, base of the fifth metatarsal; G, insertion of the posterior tibialis; I, master knot of Henry; J, peroneus brevis insertion; K, cuboid tunnel. C, Anatomic specimen demonstrating peroneus longus and brevis. D, Plantar view of peroneus longus insertion.

Figure 2-15 Anatomic specimen demonstrating the knot of Henry.

cross the dorsal medial midfoot and also are best palpated after active dorsiflexion of the toes. On the lateral side, the peroneus brevis insertion (J) on the base of the fifth metatarsal is best appreciated with active eversion. The peroneus longus can be palpated as it exits the inferior peroneal retinaculum plantar to the peroneus brevis. As the peroneus longus crosses superficial to the calcaneocuboid joint, it is felt as it dives plantar to head into the cuboid tunnel (K) and then across the bottom of the foot to the base of the first metatarsal. The cuboid tunnel and the peroneus longus in it can be palpated by deep pressure at the plantar-lateral cuboid. The plantar fascia (PF) can be appreciated on the plantar foot with passive dorsiflexion of the toes (the Windlass mechanism). At the midfoot, the PF is wider than and not as thick as it is in the hindfoot. At this point, the examiner also can see the PF inserting to the five toes. The intrinsic foot muscles can be palpated as a group, but, 45

Part I ■ General Considerations

D I

G E Figure 2-16 Hallux complex. A, Dorsal view. A, Head of the first metatarsal; D, dorsal medial hallucal nerve; F, dorsal lateral hallucal nerve; G, extensor hallucis longus. B, Plantar view. B, Tibial (medial) sesamoid; C, fibular (lateral) sesamoid; E, plantar medial hallucal nerve; I, flexor hallucis longus. C, Medial view. A, Head of the first metatarsal; B, tibial (medial) sesamoid; D, dorsal medial hallucal nerve; E, plantar medial hallucal nerve; H, abductor hallucis tendon.

A B

other than the abductor hallucis (medial) and abductor digiti minimi (lateral), the specific muscles cannot be isolated. Forefoot Hallux Complex The forefoot examination often begins with the hallux and its surrounding complex (Fig. 2-16). The first metatarsal can be palpated along its entire course. Beginning with the base of the proximal metatarsal, the first metatarsal can be followed distally to the head of the metatarsal (A). At the first metatarsal’s distal plantar extent, the tibial (medial) (B) and fibular (lateral) sesamoids (C) can be appreciated. They can best be felt by passive dorsiflexion of the hallux MTP joint and deep palpation of the fat pad plantar to the joint. The proximal phalanx is very superficial and can be felt almost circumferentially. The hallux interphalangeal joint and the distal phalanx of the hallux can also be palpated circumferentially. The sensory nerves of the hallux are very superficial and can be palpated in a thin patient. The clinically significant nerves are the dorsal hallucal nerve and the plantar medial hallucal nerve. The dorsal hallucal nerve (D) is felt as a rounded cord on the dorsomedial edge of the medial eminence of the first metatarsal. The plantarmedial hallucal nerve (E) is found on the plantar-medial 46

first metatarsal, just medial and dorsal to the tibial sesamoid bone and the dorsal lateral hallucal nerve (F) on the lateral aspect of the hallux. The dorsalis pedis artery pulse is appreciated proximal to the bases of the first and second metatarsals as the artery goes to the plantar foot. The tendons of the hallux are palpated circumferentially. Dorsally, the EHL (G) (larger) and EHB (smaller and lateral) can best be seen with active dorsiflexion of the hallux (Fig. 2-17). The abductor hallucis tendon (see Fig. 2-16) (H) is appreciated dorsal to the tibial sesamoid at the joint line of the hallux MTP joint. The FHL (I) is appreciated between the sesamoids plantarly. It can be found lying on the proximal phalanx by rolling a finger across the plantar proximal phalanx all the way to the FHL insertion on the plantar base of the distal phalanx. The flexor hallucis brevis cannot be felt directly, but its location can be estimated by allowing a finger to slide proximally and distally on the sesamoids. Lesser Metatarsals and Toes The lesser metatarsals and the corresponding toes can be discussed as a group (Fig. 2-18A and B). As in the hallux, the bony anatomy is quite superficial. The metatarsal shafts can be palpated their entire length dorsally. The shafts are best located at the midmetatarsal and can be palpated distally or proximally as indicated. The plantar metatarsals cannot be directly palpated until the distal

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

B Figure 2-17 A, Normal appearance of the extensor hallucis longus (EHL). B, After a cerebrovascular accident, an overactive EHL causes excess dorsiflexion of the hallux.

C end or head. The metatarsal heads are always felt, but the detail is variable depending on the thickness of the plantar fat pad. The dorsal toe bones are easier to palpate than the plantar bones. Regardless, the MTP joints can be appreciated by passive plantar and dorsiflexion of the toes. The proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints can be appreciated by passive or active plantar flexion of the joints (Fig. 2-18C and D). As the toes get smaller, the joints become less active and more passive. The fifth toe has little active control. The tendons of the lesser toes move as a unit and are best examined together. The EDL can be seen best with active dorsiflexion of the toes. The EDB can usually be seen with the same maneuver in the second and third toes, but it is less accessible in the fourth. The FDL can be best palpated plantar at the base of the toes with a finger sweep in the transverse direction. Active flexion of the toes can help with this. The plantar plate of the MTP joint is in the space between the plantar metatarsal head and the base of the proximal phalanges. EXAMINATION IN SEQUENCE

As mentioned earlier, the systematic sequence of the foot and ankle examination allows the examiner to be thorough and complete. Observation is the key first

Figure 2-18 Forefoot. Dorsal (A) and plantar (B) views of the lesser metatarsals and toes. C, Extension of lesser toes. D, Flexion of lesser toes.

component to the physical examination. The standing examination is performed, followed by a thorough seated examination. Supine and prone examinations are helpful for specific situations. Finally, if necessary, observation of the patient’s gait and evaluation of footwear can add important information. Standing Examination The standing examination can provide the examiner with a tremendous amount of information. Asymmetry is best addressed on standing examination by using a direct visual comparison with the opposite extremity. First, the patient is asked to stand facing the examiner, either on the floor or on a raised stool, with feet shoulder width apart (Fig. 2-19). This allows visualization of the anterior pelvis, the patellae, and the tibial tubercle. Using these anatomic landmarks, the rotation of the foot in relation to the tibia, hip, and pelvis can be established. To estimate pelvic tilt from the front, the examiner places an index finger on either the anterior superior iliac spines or the iliac crests. An anatomic or functional shortening 47

Part I ■ General Considerations

Figure 2-19 Standing examination. A, Patient facing the examiner. B, Patient facing away from the examiner.

D Figure 2-20 Examples of pes planus. A, Severe pes planus. B to D, Varying degrees of pes planus.

of one leg can be seen readily if the shortening is greater than ¼ inch. Inspection of the popliteal creases reveals whether major shortening is in the thigh or in the lower leg. Gross abnormalities of the lower extremity, including circumference difference of the thighs and calves and excessive deviation in skeletal alignment in all planes (varus, valgus, flexion, extension, and rotation), are best appreciated during the standing examination. 48

Once overall leg alignment is established, inspection of the foot and ankle begins with the medial longitudinal arch. The presence of pes planus or pes cavus can be determined. There are least two general categories of pes planus for the purposes of the physical examination. In one category, the longitudinal arch is depressed, with a relatively normal valgus hindfoot position and straight midfoot and forefoot (Fig. 2-20A and B). In addition, the

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

Achilles tendon remains relatively in line with the hindfoot. In the second category, the foot appears to have fallen inward, like the tilting of a half-hemisphere (Fig. 2-20C and D). The heel is in excessive valgus, the outer border of the foot shows angulation at the midfoot, and the forefoot is abducted, creating a more complex deformity. In contrast to the first category, the Achilles tendon deviates laterally when the patient bears weight on the relaxed foot. The pathologic implications of these two types of flatfoot are different. The pes cavus or high arch foot also has two main types, although the two are often combined. In the first, the heel is in neutral to slight valgus, but the forefoot flexibility allows good ground accommodation through forefoot pronation or a plantar-flexed first ray (Fig. 2-21A). In the second, the heel is fixed in varus and the midfoot and forefoot have compensated by forefoot adduction, which results in lateral column overload (Fig. 2-21B). The presence of heel varus during the front-facing examination is indicated by the ability to visualize the medial border of the heel. Again, the pathologic process associated with the two types is different. The Coleman block test is an excellent way to determine whether the cavus foot position is being driven by the forefoot or the hindfoot (see Chapter 6). Both flatfoot and cavus foot consist of a spectrum of deformities that involve both bony and soft tissue components, the majority of which are normal physiologic variations. However, a consistent definition of “normal,” when speaking of flatfoot and cavus foot, is unclear. Finally, the front-facing standing examination gives a good view of the toes and how they contact the ground. The valgus or varus position of the hallux is highlighted with weight bearing. The pronation of the hallux in relation to the rest of the foot is seen best in this posture. The lesser toes can also be appreciated in this way. Crossover deformities, co*ck-up deformities, joint contractures, floating toes, and dynamic location of callus (terminal or dorsal) are most efficiently examined with the patient standing on a stool. The examiner also should note whether the toes touch the ground (Figs. 2-22A and B).

At this point, the patient should be observed while facing away from the seated examiner (see Fig. 2-19B). Again, the feet should be shoulder width apart to ascertain the true hindfoot alignment. The pelvis, femur, thigh, knee, tibia, and calf symmetry is reexamined from this view. In particular, the relationship of the heel axis to the ankle joint and the rest of the foot are appreciated. Excessive heel valgus or varus should be noted. The lateral metatarsal and toes are seen normally from this view, although the ability to visualize more toes on one side compared with the other may indicate a pathologic flatfoot deformity. Asymmetry in this examination goes a long way in illustrating the cause and solution in hindfoot, midfoot, and ankle disorder. While the patient is facing away from the examiner, it is helpful to have the patient elevate to balance on the toes. If the foot is functioning normally, the heel promptly inverts, the longitudinal arch rises, and the leg rotates externally (Fig. 2-23). Failure of these movements to occur can indicate a weak foot or a specific pathologic process. The patient should also be asked to single-limb toe raise on each foot (Fig. 2-24). This can demonstrate early weakness, especially when the patient is asked to do it multiple times, or marked weakness if the patient is unable to single-limb toe raise at all. In patients who are able to perform the task, it is importation to ask if it elicits pain and where the pain occurs. Do not place too much stock in the single-limb toe raise in elderly patients, because many elderly patients are unable to accomplish this maneuver even when all joints and tendons are normal. Inversion of the heel is achieved through proper performance of the subtalar and transverse tarsal articulations and the tendons that act across these joints. Failure of the heel to invert or eliciting pain during the maneuver should immediately focus the examiner’s attention on possible malfunction of these structures. Some conditions that can limit activity in these joints are muscle weakness, dysfunction of the tibialis posterior, arthritic changes in the hindfoot, and such skeletal abnormalities as vertical talus and tarsal coalition.

Figure 2-21 A, View of the lower extremity from behind, highlighting cavus foot with neutral hindfoot alignment. B, Cavovarus foot posture with lateral column overload.

Part I ■ General Considerations

Figure 2-22 A, The neutral or unpronated hallux, which is considered normal. B, Significant pronation (malrotation) of the hallux in association with valgus malalignment.

B Figure 2-23 Dynamic arch creation. A, Flatfoot at stance. B, Arch creation at toe-off.

Sitting Examination The patient is asked to sit on the edge of the table with the legs dangling over the edge (Fig. 2-25). The examiner should sit lower on a stool. This allows for easy inspection, palpation, and manipulation of both extremities. It is at this point that the lessons learned in the topographic anatomy section are best used. General Visual Overview Any visible abnormalities should be noted at this time. Varicosities, areas of telangiectasia, erythema, and ecchymosis, and generalized edema should be noted. The skin is examined for local areas of swelling, and the structures in these areas are palpated. The skin over joints normally is cooler than the skin over muscular areas of the extremity. The examiner should observe the various muscle 50

groups, looking for atrophy in the anterior, lateral, and posterior calf region, as well as the medial side of the foot. The distribution of hair on the foot should be carefully noted. Loss of distal foot or toe hair can suggest a systemic disorder, such as peripheral vascular disease or lupus. The skin on the plantar aspect of the foot and about the toes is inspected carefully for callus formation, which often indicates abnormal pressure on the foot. All scars, wounds, and ulcerations should be noted, surgical or otherwise, because this can give the examiner insight into the history of that particular foot. General Skeletal Overview Gross skeletal deformities are readily discernible and can hardly be overlooked even by the most inexperienced examiner. Deviation in the hallux MTP joints, lesser toe

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

D Figure 2-24 Single-limb toe-raise examination. A, Anterior view. B, Posterior view before examination (patient’s left foot has a ruptured posterior tibial tendon). C, Patient is able to stand on tip toe on the right foot without difficulty. D, On the left foot, the arch sags; the patient is not able to perform a repetitive toe raise.

deformities, and asymmetric midfoot deformity can be observed grossly at this point. The bony prominences about the foot are carefully noted. A prominence over the region of the tarsometatarsal joints may be the first sign of arthrosis of these joints, and a prominence over the fifth metatarsal head can indicate a bunionette deformity. Difficulties in making a diagnosis are more likely to arise in patients whose feet, on casual inspection, appear relatively normal.

Figure 2-25 Sitting examination. Note the position of the examiner.

Neurovascular Examination Evaluating the neurovascular status should be performed after inspection as it can offer clues to systemic or focal issues present. The posterior tibial and dorsalis pedis pulses should be palpated and their strength noted. When the pulses are difficult to palpate, testing capillary refill time by compressing the distal nail bed and measuring time to reperfusion is a helpful way to gauge overall perfusion. Normal capillary refill time is considered to be less than 2 seconds. Weak or absent pulses may indicate problems such as peripheral vascular disease, systemic autoimmune disorders, or diabetes, which are important considerations, especially in surgical candidates. 51

Part I ■ General Considerations

The detailed peripheral nerve evaluation is best directed by the history. When the patient complains of a burning type of pain, often accompanied by a feeling of numbness, a careful sensory examination should be conducted because this is most often nerve pain. Such complaints often indicate peripheral nerve disorders and may be early symptoms of a generalized neuritis or neuropathy. Systemic disorders, such as diabetes and sensory axonal neuropathy, are commonly first suspected after a careful foot examination. Simple office tools, such as the SemmesWeinstein monofilament test (Fig. 2-26), can be used to assess the degree of sensory deficit in the patient. The examiner should check not only for deficits in cutaneous sensation and reflexes but also for diminished positional and vibratory sensation. There are several areas in the foot in which the peripheral nerve may be locally entrapped and irritated. The most common site is the tibial nerve as it passes through the tarsal tunnel, which is located behind the medial malleolus. Percussion along the course of the nerve as it passes through the tunnel to elicit tingling can indicate compression or irritation of the nerve. The deep peroneal nerve can be entrapped beneath the extensor retinaculum of the dorsum of the foot and ankle; this is known as anterior tarsal tunnel syndrome. When the diagnosis is suspected, the examiner should carefully percuss over the inferior extensor retinaculum and along the course of the deep peroneal nerve to look for evidence of tingling, which indicates irritability of the nerve. Besides being compressed at the level of the extensor retinaculum, the irritation of the nerve may occur as it passes over a dorsal exostosis at the talonavicular joint or more distally at the tarsometatarsal articulation. Burning pain that radiates to the web space between the third and fourth toes should raise suspicion of interdigital neuroma. Firm palpation in the plantar web space usually reproduces the neuritic symptoms. Palpation of the plantar metatarsal heads should be performed at the same time because metatarsalgia is another common cause of plantar foot pain, in particular when the complaints are centered around the first and second web

Figure 2-26 Semmes-Weinstein monofilament.

space. Mediolateral compression of the foot, particularly when examining the third web space, can result in a click and pain radiating toward the toes. Finally, direct palpation in the distal aspect of the web space while dorsiflexing the toes is a sensitive test for interdigital neuroma, because this maneuver pulls the interdigital nerve against the offending intermetatarsal ligament. On rare occasions, a tight band of transverse crural fascia entraps the superficial peroneal nerves. This is detected by carefully percussing along the inferior margin of the crural fascia when examining a patient who complains of discomfort over the dorsum of the foot. Nerve entrapment also can occur around a surgical scar or in an area that has been crushed, and these areas should be carefully noted. The sural nerve is particularly at risk for surgical scar entrapment or injury after lateral hindfoot procedures, such as the extensile lateral approach for calcaneus fractures. Range of Motion of the Joints While the patient remains on the table, the joints of the foot and ankle should be assessed for motion. The passive and active range of motion of all major articulations of the foot should be checked for limitation of motion, painful movement, and crepitus. These findings can occur separately or in any combination or sequence. ANKLE JOINT The ankle joint should be moved through its full range of motion (Fig. 2-27). Normal ankle range of motion is approximately 10 to 15 degrees of dorsiflexion to 45 to 50 degrees of plantar flexion. Although the ankle is essentially a single-axis joint, its axis travels along a line that is reasonably estimated by placing the tips of the index fingers just below the most distal projections of the two malleoli (Fig. 2-28). Therefore the axis travels posteriorly and inferiorly from a medial to lateral direction. In

Figure 2-27 Ankle range of motion documented on the lateral aspect with a goniometer.

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

addition, based on the conical nature of the talus, with the radius of curvature being longer laterally than medially, rotation of the ankle joint results in medial deviation of the foot in plantar flexion and lateral deviation of the foot in dorsiflexion. Because an oblique axis of the ankle assists in absorbing the horizontal rotation of the leg, its range of motion on gross examination is related to the range of motion in the subtalar joint. The ankle joint should also be checked for instability in the sagittal, coronal, and rotational planes. The anterior drawer examination and the inversion stress test examine the stability of the lateral ankle ligaments (in particular the anterior talofibular ligament [ATFL] and calcaneofibular ligament [CFL], respectively) (Fig. 2-29A and B). Adding an external rotation moment to the anterior drawer examination can check the stability of the deltoid ligament, although this can be a very subtle finding. Normally, there is no lateral shift of the talus in the mortise even when the foot is in full plantar flexion. Any lateral or medial displacement of the talus within the

Figure 2-28 Estimating the location of the ankle axis.

mortise that is seen on examination indicates an abnormality of the mortise. The stability of the syndesmosis is checked by both the calf compression test and the external rotation test (Fig. 2-30A and B). Actual laxity is often difficult to appreciate, although, if either of these tests creates pain along the syndesmosis, an injury to these ligaments should be suspected. When checking stability, it is extremely important and helpful to use the opposite extremity for comparison. SUBTALAR JOINT The amount of motion in the subtalar joint varies. Isman and Inman1 found a minimum of 20 degrees and a maximum of 60 degrees of motion in a series of feet in cadaver specimens. Motion in the subtalar joint is intimately involved with motion in the talonavicular joint and calcaneocuboid joint. If one of these joints is stiff or arthritic, it can significantly affect the motion seen in the other joints. A gross method of determining the degree of subtalar motion is to apply rotatory force on the calcaneus in the coronal plane while permitting the rest of the foot to move passively. When this is combined with a rotatory force applied to the forefoot, the foot proceeds through large displacements in motion through the talonavicular and calcaneocuboid joints that are additive to subtalar motion. This method allows gross analysis of the flexibility or rigidity of the hindfoot, which can be important in certain clinical situations, such as adult-acquired flatfoot (see Chapter 25). The most accurate, but not practical, method of determining the degree of subtalar motion is to place the patient prone and flex the knee to approximately 135 degrees. The axis of the subtalar joint now lies close to the horizontal plane. The examiner then passively inverts and everts the heel while measuring the extent of motion with a gravity goniometer or level (Fig. 2-31). This method is used primarily for research purposes. A more practical method of determining the degree of subtalar motion is accomplished while the patient is sitting on the examining table. The calcaneus is placed in

Figure 2-29 A, The anterior drawer examination. The foot is pulled anteriorly, with the ankle in slight plantar flexion and counterpressure applied to the anterior tibia. B, Inversion or talar tilt stress test. The heel is inverted while maintaining the ankle in a neutral dorsiflexed position. A finger placed on the lateral talar process during inversion will assist in determining that the instability is arising from the ankle and not subtalar joint.

Part I ■ General Considerations

Figure 2-30 A, The calf compression or “squeeze” test. Pain elicited with this maneuver is suggestive of a syndesmotic injury. B, External rotation stress test may identify a syndesmotic injury with production of pain or instability. With the knee flexed, rotate the foot externally while maintaining the leg in a fixed position.

reproducible measurement for this joint. Lack of subtalar motion should alert the examiner to the possibility of arthrosis of the subtalar joint, peroneal spastic flatfoot, or an anatomic abnormality such as tarsal coalition.

Goniometer Subtalar joint axis

Figure 2-31 Spheric goniometer attached to the calcaneus to measure the degree of subtalar motion.

line with the long axis of the tibia. With the calcaneus held in one hand and the forefoot (including the transverse tarsal joint) in the other, the subtalar joint is brought into inversion and eversion. It is helpful to place a fingertip on the lateral process of the talus to determine if any of the inversion is occurring through the ankle joint. While carrying out this motion, it is important to note not only the total range of motion but also the amount of inversion and eversion. There usually is twice as much inversion as eversion. Occasionally, in a patient with flatfoot, although there is full total range of motion, the plane of motion is such that little or no inversion occurs. It also is important to observe any asymmetry of subtalar motion in a percentage fashion. This is often the most 54

TRANSVERSE TARSAL JOINT The motion of the transverse tarsal joint (talonavicular and calcaneocubiod joints) is observed by holding the calcaneus in line with the long axis of the tibia (the subtalar neutral position) and the forefoot parallel to the floor. Adduction and abduction of this joint can be isolated (Fig. 2-32). Although these measurements are somewhat variable, a general rule is that there is twice as much adduction as abduction at the transverse tarsal joint. As with the subtalar joint, it is imperative that the total range of motion is noted as well as the degree of adduction and abduction. In some pathologic states, such as posterior tibial tendon dysfunction or arthrosis of the midtarsal joints, the foot is maintained in a chronically abducted position, and a neutral position cannot be achieved. This fixed abduction should be noted to highlight the joints with the primary disorder. TARSOMETATARSAL JOINTS The first metatarsocuneiform joint has variable range of motion in both the sagittal and coronal plane. To test this motion in the sagittal plane, the four lesser metatarsal heads should be held in one hand while the first metatarsal head should be translated dorsally and plantarly. This test determines first-ray mobility, which is important in hallux valgus pathology. Hypermobility of this joint is

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

Figure 2-32 Evaluation of the transverse tarsal joint. The hindfoot is stabilized and the forefoot is abducted (A) and adducted (B).

Figure 2-33 Range of motion of the first metatarsophalangeal joint. A, Normal resting position. B, Passive dorsiflexion.

not well defined and is examiner dependent, although getting a sense of the normal range of mobility comes with experience. The second and third metatarsocuneiform joints have minimal motion in the normal setting. The fourth and fifth tarsometatarsal joints are extremely flexible in the sagittal plane and can also be isolated by holding the medial three metatarsal heads while translating the fourth and fifth dorsally and plantarly. Axial rotation of the forefoot while holding the subtalar neutral position can elicit midfoot pain in the setting of tarsometatarsal arthrosis. METATARSOPHALANGEAL JOINTS Motion at the MTP joints is measured by placing the ankle at a right angle and having the patient actively dorsiflex and plantar flex the MTP joints and the interphalangeal joints. Then passive motion can be

determined at the same time. Again, there is a great deal of individual variability, with dorsiflexion ranging from 45 to 90 degrees and plantar flexion from 10 to 40 degrees, depending on the mobility of the individual joints. Dorsal translation of the lesser MTP joints can be tested by holding the metatarsal head in one hand and the base of the proximal phalanx in the other hand and directing a dorsal force with the thumb. This examination tests the integrity of the plantar plate and is especially important in the second and third MTP joint. The critical factor is, again, to compare the sides for asymmetry. The motion of the interphalangeal joints is likewise observed (Fig. 2-33). Relationship of Forefoot to Hindfoot After the range of motion of the foot has been determined, the relationship of the hindfoot to the forefoot 55

Part I ■ General Considerations

should be ascertained. This relationship is important because it can be the underlying cause of the patient’s clinical problem. Determination of this relationship is best carried out with the patient sitting on the examining table with the knees flexed at 90 degrees. The hindfoot is grasped and placed into its neutral position (the calcaneus in line with the long axis of the leg or the Achilles). When examining the right foot, the heel is grasped with the examiner’s right hand, and the area of the fifth metatarsal head is grasped with the left hand. The examiner’s right thumb is placed over the talonavicular joint, and this joint is manipulated until the examiner feels that the head of the talus is covered by the navicular. This movement is brought about by the examiner’s left hand moving the forefoot in relation to the hindfoot. Once the neutral hindfoot position has been achieved, the relationship of the forefoot, as projected by a plane parallel to the metatarsals, is related to a plane perpendicular to the long axis of the calcaneus. Based on this measurement, the forefoot will be in one of three positions in relation to the hindfoot: Neutral: The plane of the metatarsals and the plane of the calcaneus are perpendicular to each other. ■ Forefoot varus: The lateral aspect of the foot is more plantar flexed than the medial aspect, placing the forefoot in a supinated position (Fig. 2-34). ■ Forefoot valgus: The medial border of the foot is more plantar flexed in relation to the lateral border of the foot, placing the foot in a pronated position.

surgery to create a plantigrade foot. A fixed varus or valgus forefoot deformity does not permit the foot to become plantigrade once the hindfoot is placed into neutral position, and thus the extent of the fusion mass needs to include the transverse tarsal joint in order to realign the forefoot. Conversely, when the forefoot is supple or neutral, realignment of the hindfoot alone permits the forefoot to be plantigrade. Direct Palpation The importance of direct palpation cannot be emphasized enough in the examination of the foot and ankle. The ready access to the bony, tendinous, and ligamentous

Heel = Neutral Forefoot = Neutral

■

This measurement should be carried out two or three times to be sure an error is not made (Fig. 2-35). The importance of this measurement is that by relating the position of the forefoot to the hindfoot, various types of clinical problems can be identified. In the normal foot, the forefoot and hindfoot planes are almost perpendicular to each other, although a moderate degree of variability in the measurement is of no clinical significance. The relation of the forefoot to the hindfoot may be supple or rigid. This determination is important when considering

Heel = Neutral Forefoot = Varus (supinated)

Heel = Neutral Forefoot = Valgus

Heel = Valgus (compensated) Forefoot = Varus

Heel = Compensated varus Forefoot = Neutral

Figure 2-34 Forefoot varus.

Figure 2-35 Relationship of hindfoot to forefoot. A, Normal alignment; forefoot perpendicular to calcaneus. B, Forefoot varus (uncompensated); lateral aspect of the forefoot is plantar flexed in relation to the medial aspect. C, Forefoot varus (compensated); with the forefoot flat on the floor, the heel assumes a valgus position, which can result in impingement of the calcaneus against the fibula. D, Forefoot valgus (uncompensated); the medial aspect of the forefoot is plantar flexed in relation to the lateral aspect. E, Forefoot valgus (compensated); with the forefoot flat on the floor, the heel assumes a varus position.

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

structures, in combination with a focused history, is essential to finally determining the exact structure that is pathologic. The distance between the tender area in two medial tendons, FHL and posterior tibialis, is only a few millimeters but makes a world of difference in treatment and prognosis. Careful study of the topographic anatomy (see earlier) allows a mastery of this portion of the seated examination. The systematic palpation must be done carefully and directly. The tools used most often are the tip of the examiner’s dominant index finger or, for deeper structures, the tip of the thumb. It is not unusual to arrive at a diagnosis after a careful history and a single palpation with a question: Does it hurt here? One important structure to palpate is the plantar aponeurosis or plantar fascia, which should be palpated along its entire surface. Dorsiflexion of the toes makes the fascia more prominent and facilitates palpation (Fig. 2-36). In the case of a suspected plantar fascial rupture, palpating the proximal portion of both plantar fascias while dorsiflexing the toes will demonstrate a fullness and loss of discrete medial fascial border on the affected side.

Figure 2-36 Palpation of the plantar aponeurosis facilitated by dorsiflexion of the toes.

Muscle Function Muscle function about the foot and ankle should be carefully tested. Most of the testing is done while the patient is seated. It is important to observe the strength of each muscle, particularly in a patient who has demonstrated some evidence of muscle weakness. It is also helpful to palpate each tendon to be sure that compensation by another muscle is not masking loss of function. It is imperative that the examiner considers all the information gleaned during each component of the physical examination. For example, a patient who is unable to actively dorsiflex his or her ankle may have a ruptured tibialis anterior tendon, a peroneal nerve palsy, or a significant Achilles contracture. The adept examiner will be able to combine the findings, correlate with the history, and arrive at a presumptive diagnosis. Sometimes, specific muscle groups lead to confusion. The function of the tibialis posterior is important to assess because it is the principal invertor of the foot. However, the tibialis anterior acts as a secondary invertor as well. To isolate tibialis posterior function from tibialis anterior function, it is important to keep the foot plantar flexed while having the patient actively invert the foot against resistance and palpating the tibialis posterior tendon. In addition, the foot should be placed into an everted position, and then the patient is asked to invert against some resistance. In some patients, this can be done easiest with the patient’s legs crossed (Fig. 2-37). Another helpful technique is to ask the patient to point each foot down and in toward the other foot. Asymmetry in the amount of foot inversion is an indication of posterior tibial tendon pathology. The extrinsic muscles of the lateral foot can lead to similar difficulties. The peroneus brevis muscle functions mainly to evert the foot, and the peroneus longus functions mainly to plantar flex the medial column of the foot. To get a sense of peroneal strength, the patient should be asked to externally rotate the foot against resistance both from an externally rotated and internally rotated position. The eversion function of the peroneus

Figure 2-37 Isolation of posterior tibialis muscle function. A, The muscle is tested with the patient’s foot dependent to gravity with the legs crossed. B, The strength is tested from full eversion to full inversion.

Part I ■ General Considerations

Figure 2-38 Demonstration of the Silverskiold test for determining origin of an Achilles contracture. Dorsiflex the ankle with subtalar neutral and knee extended (A), and then flex the knee (B). If ankle dorsiflexion improves with knee flexion, as in this case, then the gastrocnemius portion of the gastrocnemius–soleus complex is considered to be the primary origin.

brevis is tested by simply asking the patient to evert against the resistance. The eversion function of the peroneus longus is quite weak. To isolate the peroneus longus, the patient should be asked to plantar flex the medial side of the foot while the examiner resists beneath the first metatarsal head. This is also an opportune time to examine the stability of the peroneal tendons in the retrofibular groove. The patient is asked to dorsiflex and evert the foot against resistance while the examiner gently palpates the lateral ridge of the distal fibula. An insufficient superior peroneal retinaculum will lead to subluxation of the tendons over the fibular ridge. Circumduction of the foot can also help assess for tendon stability, as well as elicit tendon snapping or intrasheath subluxation.2 Not only should the strength of each muscle group be tested, but it is also important to determine whether a contracture is present. In the hindfoot, the most common contracture is the calf muscle complex. To check the gastrocnemius–soleus complex for contracture, with the knee flexed, the hindfoot is first placed into neutral position, and the navicular is centered over the head of the talus. With the foot in neutral position, passive dorsiflexion of the ankle to approximately 10 to 15 degrees should be possible. If not, there is an element of contracture of the muscle group. The knee is then fully extended and the same maneuver carried out. If dorsiflexion past neutral cannot be achieved, then the gastrocnemius portion of the gastrocnemius–soleus complex is contracted. If the subtalar joint is permitted to pass into valgus while the examiner is attempting to measure dorsiflexion at the ankle joint, the presence of a contracture can easily be masked (Fig. 2-38A and B). Specific Examination Components for Individual Consideration Supine Examination The supine examination is mentioned for completeness. The most common use of the supine examination is for a detailed inspection of the plantar foot. In particular, in an obese patient, body habitus prevents adequate inspection of the bottom of the foot while sitting. Rotational and length discrepancies of the lower extremity can also 58

Figure 2-39 Prone examination.

be confirmed or further evaluated during the supine examination. Prone Examination The prone examination is a specialty examination that can make certain areas of the foot and ankle more readily accessible (Fig. 2-39). In particular, the posterior calcaneus, Achilles tendon, and calf are best examined prone. The tendon can be palpated along its entirety under direct vision. This allows access to defects and masses. Resting tension of the Achilles is best evaluated prone by asking the patients to flex both knees and visualizing the position of the foot from the end of the bed. Normal resting tension of the Achilles should result in about 10 to 15 degrees of plantar flexion; an asymmetric drop of one foot indicates insufficiency or tear of the Achilles. A Thompson test should also be performed in this position, which consists of squeezing the gastrocnemius–soleus muscle mass and visualizing whether the foot plantar flexes. Lack of plantar flexion in this test indicates discontinuity of the Achilles tendon, most commonly a rupture. The skin over the tendon can also be manipulated in this position to differentiate between a number of Achilles pathologies. The posterior calcaneus can best be viewed and palpated from this approach, in particular at the insertional ridge where the Achilles attaches.

Principles of the Physical Examination of the Foot and Ankle ■ Chapter 2

Gait Evaluation of a patient’s gait is an important component of the physical examination in certain clinical scenarios. Because many diagnoses and treatment plans can be made without observing gait, it is helpful to reserve this component of the examination toward the end, when it is clinically relevant. It is important to observe the patient walking at various speeds and with shoes on and off. The hands should be empty and arms hanging freely at the sides. The following observations should be made: 1. Detect obvious abnormalities of locomotion. This is best observed, for examination purposes, by trying to examine each leg through a number of strides individually. This allows the examiner to separate out sidedness on loss of stride length and gait phase of a limp. 2. Perceive asymmetric behavior of the two sides of the body. This asymmetry can be in torso rotation, upper extremity swing, or lower extremity unilateral gait disturbances. As a rule, the shoulders rotate 180 degrees out of phase with the pelvis; this is a passive response to pelvic rotation. If there are no abnormalities in the spine or upper extremities, rotation of the shoulders is reflected in equal and symmetric arm swing. If the arm swing is asymmetric, horizontal rotation of the pelvis also is asymmetric. Because such asymmetric pelvic rotation can be the result of abnormality in any of the components of the lower extremity, it is mandatory that the practitioner take extra care in examining not only the foot and ankle but also the knees and hips. 3. Observe the position of the patella and tibial tubercle in standing and walking. They are indicators of the degree of horizontal rotation of the leg in the axial plane and can guide the examiner to look more proximal for the primary pathologic process.

4. Observe the degree of toeing in or out (Fig. 2-40). The phase of gait when this deformity occurs is the key to understanding the cause. At toe-off, the leg has achieved its maximal external rotation, and the foot toes out slightly. During swing phase, the entire leg and foot rotate internally. The average amount of rotation is about 15 degrees, but this varies greatly from person to person. It may be almost imperceptible (3 degrees) or considerable (30 degrees).3 At the time of heel strike, the long axis of the foot has approached, to a varying degree, the plane of progression. The degree of parallelism between the long axis of the foot and the plane of progression at this point is subject to considerable individual variation. However, the transition from heel strike to foot flat, which occurs rapidly, should be carefully observed. Some persons show an increase in toe-in during the very short period of plantar flexion of the ankle, indicating a greater degree of obliquity of the ankle axis (see Chapter 1). 5. Observe the longitudinal arch during the first half of stance phase walking (see Fig. 2-23). Look for dynamic pronation or supination at the stance phase to assess midstance stability. Normally, the foot pronates as it is loaded with the body weight during the first half of stance phase. The amount of pronation is subject to extreme individual variation. The important factor, however, is whether the foot remains pronated during the period of heel rise and lift-off. In the normally functioning foot, as the heel rises, there is almost instantaneous inversion of the heel. If the heel fails to invert at this time, the examiner should check the strength of the intrinsic and extrinsic muscles of the foot and the range of motion in the articulations of the hindfoot and midfoot. 6. Note the amount of heel inversion and supination of the foot during lift-off and the presence or absence of rotatory slippage of the forefoot on the floor. Except on

Figure 2-40 Examination of patella and tibial tubercle position. A, Intoeing in a child. B, External rotation of lower extremities.

B 59

Part I ■ General Considerations

Figure 2-41 Position of heel in stance phase. A, Excess heel valgus (right foot). B, Excess heel varus (right foot).

slippery surfaces, the shoe does not visibly rotate externally or slip on the floor at the time of lift-off. Failure of the ankle and subtalar joints to permit adequate external rotation of the leg during this phase of walking can result in direct transmission of the rotatory forces to the interface between the sole of the shoe and the walking surface, with resultant rotatory slippage of the shoe on the floor. On noting slippage, the examiner should look for possible muscle imbalance and should check the obliquity of the ankle axis and the range of motion in the subtalar joint (Fig. 2-41). 7. Observe the position of the foot in relation to the floor at the time of heel strike. Normally, the heel strikes the ground first, followed by rapid plantar flexion. If this sequence does not occur, further investigation is indicated. In pathologic conditions, the patient might contact the ground with the foot flat or possibly on the toes. The time of heel rise also should be carefully noted; it occurs normally at 34% of the walking cycle just after the swinging leg has passed the stance foot. Early heel rise can indicate tightness of the gastrocnemius–soleus muscle complex. A delay in heel rise can indicate weakness in the same muscle group. If the implications of the preceding statements are not readily apparent, it is suggested that the reader review Chapter 1. Shoe Examination Because the type of shoe and the heel height affect the way a person walks, they must be noted in the history and in the examination sequence. When wearing high heels, for example, women show less ankle-joint motion than when wearing flat heels, and in tennis shoes they show little difference from men in gait. It is most convenient for the examiner to inspect the shoes during the history taking, although the information

gleaned from this inspection should be correlated with the gait analysis. The examination should include 1. Path of wear from heel to toe: Early lateral hindshoe and midshoe wear indicates a supination deformity. Loss of the medial sole and counter indicates a pronation deformity. 2. Presence of supportive devices or corrections in the shoes: Arch supports, heel pads, heel wedges, leather manipulation to accommodate deformity, or forefoot pads indicate previous difficulties. 3. Obliquity of the angle of the crease in the toe of the shoe: The angle varies from person to person; the greater the obliquity of the crease in the shoe to its long axis, the greater the amount of subtalar motion required to distribute the body weight evenly over the metatarsal heads. 4. Impression the forefoot has made on the insole of the shoe: This can often give important information about the patient’s force distribution on the plantar foot. 5. Presence or absence of circular wear on the sole of the shoe: Such wear indicates rotatory slippage of the foot on the floor during lift-off, from lack of subtalar motion. 6. The shape of the shoe compared with the shape of the foot: This gives the examiner clues as to the proper sizing of the patient’s shoes. The shape of the shoe (e.g., narrow pointed shoe or broad toe box), and the overall shape of the foot when the patient is weight bearing should be carefully observed. REFERENCES 1. Isman RE, Inman VT: Anthropometric studies of the human foot and ankle, Bull Prosthet Res 10–11:97–129, 1969. 2. Raikin SM, Elias I, Nazarian LN: Intrasheath subluxation of the peroneal tendons, J Bone Joint Surg Am 90:992–999, 2008. 3. Levens AS, Inman VT, Blosser JA: Transverse rotation of the segments of the lower extremity in locomotion, J Bone Joint Surg Am 30:859–872, 1948.

Chapter

Imaging of the Foot and Ankle James M. Linklater, John W. Read, Catherine L. Hayter

CHAPTER CONTENTS ROLE OF IMAGING Effective Use of Imaging Choice of Test Radiation Safety RADIOGRAPHS ULTRASOUND Basic Science Use of Ultrasound NUCLEAR MEDICINE Basic Science Technetium-99m–Methylene Diphosphonate Bone Scanning Single Photon Emission Computed Tomography Gallium Scanning and White Cell Scanning Use of Nuclear Scanning COMPUTED TOMOGRAPHY Basic Science Use of Computed Tomography Scanning MAGNETIC RESONANCE IMAGING Basic Science Magnetic Resonance Imaging Clinical Sequences T1-Weighted Fast Spin-Echo Sequences T2-Weighted Fast Spin-Echo Sequences Proton-Density–Weighted Fast Spin-Echo Sequences Short Tau Inversion Recovery or “Fat-Sat” Sequences Gradient-Recalled Echo Sequences Magnetic Resonance Arthrogaphy New Magnetic Resonance Imaging Technique: Biochemical Imaging T2 Mapping Delayed Gadolinium-Enhanced Magnetic Resonance Imaging of Cartilage T1 Rho (ρ) Mapping Contraindications to Magnetic Resonance Imaging Pitfalls and Artifacts in Magnetic Resonance Imaging Magic Angle Phenomenon Bone Marrow “Edema” Use of Magnetic Resonance Imaging

61 62 62 62 63 66 66 69 76 76 82 84 84 85 86 86 87 88 88 90 90 91

IMAGING OF FOOT AND ANKLE PATHOLOGY Imaging Ligament Injury Ankle and Transverse Tarsal Joint Ligament Complex Injury Midfoot Ligamentous Injury Forefoot Ligament Injury Imaging Chondral and Osteochondral Lesions Imaging Articular Cartilage Repair Imaging Impingement Syndromes Imaging Tendon Pathology Tendinosis Stenosing Tenosynovitis Tendon Tears Imaging Inflammatory Arthropathies Imaging Nerve Pathology in the Foot and Ankle Imaging Tumors in the Foot and Ankle Imaging Infections in the Foot and Ankle Miscellaneous Conditions in the Foot and Ankle Complex Regional Pain Syndrome Arthrofibrosis Posttraumatic Fat Necrosis Foreign Bodies Avascular Necrosis of Bone in the Foot and Ankle INTERVENTIONAL RADIOLOGY IN THE FOOT AND ANKLE

93 93 95 96 97 97 98 100 101 101 105 105 105 109 110 112 113 113 113 114 114 115 116

91 91 91 91 92 92 92 92 92 92 92 93 93

Imaging is an essential component in the diagnostic workup of many conditions of the foot and ankle. This chapter reviews the basic principles of imaging, with the aim of providing a solid foundation for routine clinical practice. In the limited space available, the authors’ approach will be clinically pragmatic and focused on general concepts, rather than individual conditions. ROLE OF IMAGING

For the foot and ankle surgeon, imaging is often central to diagnosis, management, and treatment planning. It offers a noninvasive window into the nature of anatomic derangements about which surgical decisions must be made. Imaging can assist with accurate early diagnosis, assessment of lesion grade and extent, assessment 61

Part I ■ General Considerations

of treatment response, objective documentation of pathology in medicolegal settings, exclusion of sinister or systemic processes, and preoperative planning. With the advent of minimally invasive surgical techniques, the need to assess lesion suitability for arthroscopic treatment has further increased the importance of imaging. Various percutaneous needle interventions are also now possible using various imaging modalities for accurate guidance. Effective Use of Imaging Although valuable as a diagnostic tool, imaging should only be requested if the result will be used to guide management and is most effective when used to confirm or exclude a specific clinical hypothesis or to narrow a clinical differential. In this setting, the test has a specific purpose, and the result has direct clinical meaning. The importance of a thorough clinical assessment therefore cannot be overemphasized, because it is only on the basis of specific questions that arise from the history and physical examination that the most appropriate imaging test(s) can be chosen. A valid clinical role for imaging can include the detection or exclusion of sinister or systemic disease when clinical “red flags” are present (Table 3-1). It is important that the request form should, apart from describing the general symptomatic context (e.g., forefoot pain), further state the actual question(s) to be answered (e.g., “stress fracture second metatarsal?”). This allows the supervising radiologist to both optimize the imaging protocol and provide a clinically relevant report. Incidental imaging findings are common and can include normal variants, age-related degenerative changes, old posttraumatic changes and old surgical changes. Such findings can be problematic, particularly when imaging is used in place of a proper physical examination. Choice of Test Any imaging workup should generally commence with plain radiographs. This low-cost approach carries an acceptable low radiation dose and provides basic diagnostic information that cannot be readily obtained by any other means (e.g., bone alignment in the weight-bearing foot). When combined with a careful clinical assessment,

Table 3-1 Clinical Red fa*gs Age > 50 years Constitutional symptoms Atypical symptoms Risk factors (e.g., diabetes, immune deficiency) Nonmechanical pain (e.g., night pain at rest) Complex past history Previous malignancy Family history of arthritis Other clues (e.g., progressive neurologic deficit, urinary symptoms) Poor response to therapy

plain films alone are often sufficient for both diagnosis and management. When negative, they are still useful in ruling out common differential considerations and demonstrating features that sophisticated tests alone, such as magnetic resonance imaging (MRI) and ultrasound, may otherwise entirely miss or misinterpret (e.g., soft tissue calcifications, foreign bodies, bone spurs and loose bodies, accessory centers of ossification, deformities and malalignments, old injuries, anatomic predispositions, bone tumor characterization). Particularly in the current era of MRI, the fundamental and enduring importance of plain radiographs should never be forgotten. When further imaging is required, the choice of exactly which test to order can sometimes be challenging because a wide range of imaging tests and variations in imaging technology are available. In general, the specialist foot and ankle surgeon who is expected to resolve a difficult clinical problem should select the locally available test that is most reliable for the diagnosis under consideration. This may vary in any given locale for reasons such as equipment availability and radiologist expertise. Other factors that may influence the choice of imaging test can include (1) patient concerns, such as cost, convenience, discomfort; (2) safety risks, including patient age, radiation dose, and contrast sensitivity; and (3) costs to third parties, such as sporting clubs, insurers, or the taxpayer. Radiation Safety Plain radiographs, computed tomography (CT) scans and isotope bone scans all expose patients to ionizing radiation that carries a risk of both cancer induction and genetic damage. This risk is well established at high doses (e.g., Hiroshima victims) but remains uncertain at low doses, such as those used in medical imaging. Because all populations are exposed to the natural background radiation of cosmic rays (Table 3-2) and also have an incidence of cancers arising from causes other than radiation, it is statistically difficult to evaluate the cancer risk associated with medical radiations at doses of 100 mSv or less.25 A cautious “linear no-threshold model” has therefore been adopted that assumes that even the smallest radiation dose carries a level of risk and that this risk increases linearly with cumulative lifetime exposure. It is also well recognized that, depending on age, children can be up to 10 times more sensitive to ionizing radiation than adults, and an actual effect equivalent to one excess case of leukemia and one excess case of brain tumor per 10,000

Table 3-2 Typical Effective Radiation Dose3,42,44 Average U.S. background radiation/yr Single trans-Atlantic flight Radiograph: chest (PA) Radiograph: foot (single exposure) Computed tomography: ankle Isotope (Tc-99m–MDP) bone scan MDP, methylene diphosphonate; PA, posteroanterior.

3.0 mSv 0.04 mSv 0.02 mSv 0.001 mSv 0.07 mSv 6.3 mSv

Imaging of the Foot and Ankle ■ Chapter 3

been correctly positioned. Poor radiographic technique may contribute to diagnostic error by invalidating established radiographic signs, measurements, and alignment criteria. Whenever the relevant anatomy of clinical interest has not been clearly demonstrated, the examination is technically inadequate and should be repeated.2 Film interpretation requires knowledge of (1) normal bone development in the pediatric patient65 (Fig. 3-1) and (2) normal anatomic variants at all ages. Secondary centers of ossification and sesamoids of the foot can both be mistaken for fractures65 (Fig. 3-2). A full discussion of normal variants is beyond the scope of this chapter, but appropriate references should be consulted when in doubt.30,66 The routine ankle series consists of an anteroposterior (AP) view, mortise view, and lateral view (Fig. 3-3). The routine foot series consists of an AP view (Fig. 3-4), oblique view (Fig. 3-5) and a lateral view (Fig. 3-6). The optimal assessment of alignment and joint space at the foot and ankle requires weight-bearing views whenever possible (Figs. 3-7 to 3-10). The diagnostic impact of weight-bearing views can be substantial (Fig. 3-11). Depending upon clinical context, a limited number of additional views may be warranted.

head CT scans has recently been shown for the first time in children younger than 10 years who underwent multiple CT head scans with a cumulative dose of 50 to 60 mGy.57 These risks should be kept in perspective. The radiation dose associated with a basic three-view foot radiograph is at least 10 times lower than the exposure associated with a single trans-Atlantic air flight (Table 3-2), and it is generally accepted that medical imaging tests are justified if there is a reasonable likelihood they will provide a health benefit or inform patient management.6 Nevertheless, medical exposures should always be kept “As Low As Reasonably Achievable” (ALARA principle), and alternative tests, such as ultrasound and MRI, which avoid ionizing radiations altogether are preferable to CT or isotope studies whenever they offer equivalent or superior diagnostic efficacy, particularly in children and especially for follow-up imaging. In clinical practice, radiologists normally exercise caution and specify imaging protocols that minimize the ionizing radiation dose. The surgeon should also feel comfortable that the doses involved in foot and ankle imaging are mostly extremely low (see Table 3-2). Last, the American Association of Physicists in Medicine has recently issued a reassuring policy statement that asserts that “the risks of medical imaging at effective doses below 50 mSv for single procedures or 100 mSv for multiple procedures over short time periods are too low to be detectable and may be nonexistent.”1

1. Ankle impingement: Lateral dorsiflexion or plantarflexion views (Fig. 3-12); “lazy” lateral view (Fig. 3-13) 2. Talocalcaneal coalition: Harris-Beath view (Fig. 3-14), oblique views (Fig. 3-15), Brodén views (Fig. 3-16) 3. Trauma: AP view of proximal fibula if Maisonneuve fracture suspected (Fig. 3-17); reverse oblique view of ankle if medial malleolus fracture suspected (Fig. 3-18)

RADIOGRAPHS

An effective radiographic examination provides fine anatomic detail and comprises appropriate views that have

yrs 3–4 yrs 4–5

yrs 12–17 yrs 15–20

1°—A wks 8–9 (fetal)

wks 36 (fetal) A to 2 mths

yrs 12–14 F yrs 8–12 A yrs 9–14

1°

yrs 13–17 yrs 15–19

Birth

6 mths

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2 yrs

3 yrs

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mths 9–22 A

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10 yrs

yrs 14–16 yrs 15–18

A mths 3–10 12 yrs FIBULA

TIBIA

14 yrs

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FOOT

Figure 3-1 Stages of normal osseous development of the foot and ankle. 1°, primary center of ossification: stippled areas and regions shaded black indicate secondary centers of ossification; A, age at first appearance; F, age at fusion. (From Scheuer L, Black S: Developmental juvenile osteology, Oxford, England, 2000, Elsevier Academic Press.)

Part I ■ General Considerations

Figure 3-2 Secondary centers of ossification and sesamoids of the foot. Sesamoid bones are shaded black. Secondary centers of ossification are 1, os tibiale externum; 2, processus uncinatus; 3, os intercuneiforme; 4, pars peronea metatarsalia; 5, cuboides secundarium; 6, os peroneum; 7, os vesalianum; 8, os intermetatarseum; 9, os supratalare; 10, talus accessories; 11, os sustentaculum; 12, os trigonum; 13, calcaneus secundarium; 14, os subcalcis; 15, os supranaviculare; 16, os talotibiale. (From Keats TE: Atlas of normal roentgen variants that may simulate disease, ed 4, Chicago, 1988, Year Book Medical Publishers, pp xv, 1085.)

4 8

8 2

1 9

7 5

10 12

Anteroposterior (AP) view

Mortise view

Lateral view

Figure 3-3 Non–weight-bearing views of the ankle. A, The anteroposterior (AP) view is obtained with the toes pointing directly upward and a vertical primary beam centered on the ankle joint. In this position, the talus is slightly externally rotated, the lateral gutter of ankle joint is partially obscured by the lateral malleolus, and the anterior tubercle of the tibia overlaps the distal fibula. B, The mortise view is obtained by internally rotating the foot 15 to 20 degrees to bring the talus into its true AP position and the malleoli equidistant from the cassette. In this position, the entire profile of the talar dome is well seen, and both the medial and lateral clear spaces of ankle joint are well displayed and may be compared. The primary beam must be centered on the joint space, and the foot should be dorsiflexed to avoid the tip of the lateral malleolus being overlapped by the calcaneus. C, The lateral view requires a straight tube centered on the ankle joint and superimposition of the medial and lateral malleoli, but it is often poorly taken. An ankle joint effusion can be readily appreciated as water density distending the anterior joint recess on a correctly positioned and exposed lateral view. Note the fractured base of fifth metatarsal in the example shown here. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill and Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-4 Non–weight-bearing anteroposterior (AP) view of the foot. The AP view is obtained with the primary beam centered on the base of third metatarsal and angled 15 degrees cephalad. Note the prominent os tibiale externum in the example shown here with the related synchondrosis showing overlying soft tissue swelling of active stress reaction. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

15°

Anteroposterior (AP) view

Oblique view

Figure 3-5 Non–weight-bearing oblique view of the foot. This view is obtained by elevating the lateral border of foot 30 degrees and directing the primary beam at the base of fifth metatarsal. It is used to assess the toes, metatarsals, and tarsal bones anterior to the ankle joint. The oblique view is particularly helpful in assessing calcaneonavicular coalitions and the lateral tarsometatarsal articulations. Note prominent os tibiale externum in the example shown here. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Part I ■ General Considerations

Lateral view Figure 3-6 Non–weight-bearing lateral view of foot. This view provides a critical overview of foot anatomy and is also used to assess the plantar soft tissues in clinical settings such as foreign body and plantar fasciitis. Lateral radiographs are obtained with the primary beam directed perpendicular to a point just above the base of fifth metatarsal. Note that non–weight-bearing lateral views are inferred when the tibia is not vertical to the talus. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill and Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Figure 3-7 Weight-bearing anteroposterior view of ankles. A, The patient is positioned on a 5-cm block, with the film cassette behind the heels and a horizontal beam centered between the ankle joints at joint level. B, Radiograph illustrates essentially symmetric joints with slight tilt of talar articular surface. The angle of the talar articular surface can normally be a few degrees off horizontal in either a medial or lateral direction. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

4. Ankle instability: Stress views of ankle joint (Figs. 3-19 and 3-20); stress view of distal tibiofibular syndesmosis (Fig. 3-21) 5. Heel: Lateral and axial views of calcaneus (Fig. 3-22) 6. Navicular: Navicular view (Fig. 3-23) 7. Talus: Talar neck view (Fig. 3-24). 8. Tarsometatarsal joints or base of second metatarsal: Plantar-dorsal projection of midfoot (Fig. 3-25) 9. Toes: Lateral and lateral-oblique phalangeal views (Fig. 3-26) 10. Sesamoids: Axial, medial-oblique, lateromedial, and stress views of sesamoids (Figs. 3-27 to 3-30). Common radiographic measurements used to assess foot deformities are shown in Figures 3-31 to 3-37. However, the significance of any apparent radiographic abnormality should always be weighed in the overall 66

clinical context because radiographic measurements are subject to a wide range of normal variation and are also susceptible to error through poor radiographic technique. ULTRASOUND

Basic Science Ultrasound (US) uses the SONAR (SOund NAvigation and Ranging) principle to build up cross-sectional images of soft tissue anatomy. Sound waves above the pitch of human hearing (typically in the 5- to 18-MHz range for musculoskeletal imaging) are generated by a handheld transducer applied to the skin. These propagate through the tissues and are reflected by various acoustic tissue interfaces as returning echoes of differing intensity and

Imaging of the Foot and Ankle ■ Chapter 3

10-15°

Figure 3-8 Weight-bearing anteroposterior (AP) view of feet. Weight-bearing views of the feet provide functional information and are recommended for all evaluations unless clinically contraindicated. There are significant measurement differences between weight-bearing and non–weightbearing views when assessing alignment abnormalities. Lisfranc diastasis injuries are often missed if no weightbearing view has been obtained. A, Diagrams show patient positioning for simultaneous AP views with the primary beam centered between the feet at the first metatarsophalangeal joint and with a 10- to 15-degree cephalad tube tilt. B, Weight-bearing AP radiograph shows a Lisfranc fracture-dislocation on the right, with widened proximal 1–2 metastarsal interspace, malalignment at the second tarsometatarsal joint (TMTJ2), and a small avulsion fracture fragment (arrow). (Diagrams from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier. Radiographs from Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-9 Weight-bearing lateral view of foot. Lateral weight-bearing views must be taken individually. A, Diagrams show patient positioning. B, Normal weightbearing lateral radiograph. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

B 67

Part I ■ General Considerations

Figure 3-10 Infant weight-bearing views of foot. Special techniques are required to obtain adequate foot views in young children and infants. These involve active immobilization and compression by a gloved assistant or a static immobilization system. Radiographs of the contralateral foot may be helpful for comparison. A, Positioning for anteroposterior (AP) and lateral views with immobilization technique. B, AP radiograph. C, Lateral radiograph. (From Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Figure 3-11 Effect of weight bearing. Non–weight-bearing (A) and weight-bearing (B) lateral views of the ankle show the value of functional loading. Marked joint space narrowing is revealed on the weight-bearing view in this example of ankle arthrosis. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-12 Ankle impingement views. These views are used to assess any bony contribution to ankle impingement. The anterior impingement or “lunge” view (A) is a weight-bearing lateral view obtained in maximum ankle dorsiflexion, with the example shown here demonstrating direct bony abutment between an anterior tibial bone spur and new bone formation at the dorsal neck of talus. The posterior impingement view (B) is a weight-bearing lateral view obtained in extreme plantar flexion, with the example shown here demonstrating direct bony abutment between a posterior tibial bone spur and a prominent posterior process of talus. This case also shows loose ossific bodies posteriorly, and osteophyte at the anterior margin of ankle joint that would predispose to concomitant anterior impingement symptoms. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-13 Lazy lateral view of ankle. This view profiles the lateral tubercle of the posterior process of talus (posterolateral process talus) and is used to identify a small os trigonum that may be contributing to posterior ankle impingement yet remains invisible on the standard lateral view of ankle. It is obtained as a lateral projection with the foot in 10 to 15 degrees of external rotation to profile the lateral rather than medial tubercle (posterolateral process). In the example shown here, the true lateral view of ankle (A) appears normal, but the lazy lateral view (B) reveals an os trigonum (arrowhead). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

time-of-flight that are then assembled line by line to form a “gray-scale” image. The whole process occurs rapidly enough to allow real-time imaging. Use of Ultrasound The advantages of US include low cost, patient comfort, an absence of hazardous ionizing radiation, the clinically

interactive nature of the test (Fig. 3-38), the ability to assess tissue dynamics such as tendon glide and stability (Fig. 3-39), the ability of Doppler techniques to detect soft tissue hyperemia and neovascularity (Fig. 3-40), and the ability to guide diagnostic and/or therapeutic injections accurately (Fig. 3-41). The clinical aspect of directly probing the visualized anatomy with an US transducer allows the operator to accurately correlate any site(s) of 69

Figure 3-14 Harris-Beath view. This view profiles the posterior and middle subtalar joints. The patient is seated on the x-ray table with the leg extended and heel resting on the film cassette. The ankle is then placed in dorsiflexion and held in this position by the patient using a strap to apply traction to the forefoot. The x-ray tube is angled 45 degrees cephalad, with the primary beam entering the sole of the foot at the level of the base of fifth metatarsal. Slight internal rotation of the foot will improve the view by bringing the sustentaculum tali into profile. A, A normal hindfoot is shown with the arrow indicating the posterior subtalar joint and arrowhead indicating the middle subtalar joint. B, Osseous coalition of the middle subtalar joint (asterisk). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-15 Oblique views of subtalar joint. A, Internal oblique view is similar to mortise view but with more plantar flexion and 45 degrees of internal rotation. B, External oblique view is obtained with a straight tube and 45 degrees of external rotation. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier. Radiograph from Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Imaging of the Foot and Ankle ■ Chapter 3

30°

10°

40°

X-ray

10°

20°

30°

40°

Figure 3-16 Brodén view. This technique profiles the posterior subtalar facet for the evaluation of subtalar coalitions and intraarticular fractures of the calcaneus. Brodén views are obtained with the ankle in neutral dorsiflexion, the leg internally rotated 30 degrees, and the x-ray beam centered over the lateral malleolus, with cephalad tube tilt varying between 10 and 40 degrees to tangent-differing segments of the curved posterior subtalar facet. The radiograph shown here demonstrates an intraarticular fracture of the calcaneus. (Diagrams from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier, and Burdeaux BD Jr: The medial approach for calcaneal fractures. Clin Orthop Rel Res 290:96–107, 1993. Radiograph from Lee KB, Park CH, Seon JK, Kim MS: Arthroscopic subtalar arthrodesis using a posterior 2-portal approach in the prone position. Arthroscopy 26:230–238, 2010.)

Figure 3-17 Anteroposterior (AP) view of proximal fibula. Maisonneuve fractures can easily be overlooked if the symptoms and signs at the ankle level dominate. An AP view of fibula should therefore be obtained whenever standard ankle views raise suspicion on the basis of either lateral talar displacement or tibiofibular widening without distal fibular fracture, or if there is a seemingly isolated fracture of posterior malleolus. In the example shown here, the AP view of the ankle (A) shows widening of the medial ankle gutter and tibiofibular syndesmosis in keeping with tibiofibular diastasis injury. An AP view of fibula (B) subsequently confirmed a Maisonneuve fracture. Radiograph B from Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Part I ■ General Considerations

45°

Figure 3-18 Reverse oblique view of ankle. This view is used to assess fractures of the medial malleolus. A, A straight beam is centered on the joint space with the ankle positioned in 45-degree external rotation. B, A reverse oblique view shows a fracture of medial malleolus. (Radiograph from Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

>4mm

Figure 3-19 Anterior drawer stress view of ankle. This technique detects anterior talofibular ligament insufficiency. Cross-table lateral views of the ankle both at rest (A) and with vertical stress applied (B) are taken with the heel elevated on a support. A positive examination shows greater than 4 mm anterior displacement (arrow) of the talus when vertical stress is applied, illustrated in images C and D. (From Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

pain and/or tenderness with the imaging appearance. This has been described as “sonopalpation” and can be very helpful in confirming a symptomatic structure or clinically relevant finding. Similarly, the demonstration of locally increased tissue vascularity using Doppler techniques serves to increase the likelihood of a gray-scale finding being relevant to symptoms.62 72

The limitations of US include an inability to see through bone/gas/metal, image quality degraded by obesity and marked subcutaneous edema, reduced resolution and sensitivity at tissue depths greater than 3 cm, the local availability of a reliable and well-trained operator, the “keyhole” nature of images that may be difficult for the surgeon to orient and understand, and image

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-20 Varus and valgus stress views of the ankle. Positioning for varus (A) and valgus (B) stress views of the ankle is illustrated. Varus stress in ankle plantar flexion tests for anterior talofibular and calcaneofibular ligament insufficiency. Valgus stress tests for deltoid ligament insufficiency. The use of stress radiography remains controversial because reliability may be compromised by the large range of normal variation in joint laxity. In the acute trauma setting, local analgesia probably increases accuracy. An abnormal varus or valgus stress examination is regarded as demonstrating either (a) talar tilt greater than or equal to 10 degrees more than the normal side, or (b) greater than or equal to 3 mm discrepancy in lateral ankle joint opening distance between the injured and normal side, as measured from the most lateral aspect of the talar dome to the adjacent tibial articular surface. In the example here, an abnormal varus stress radiograph (D) is shown relative to the normal side (C). (From Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Figure 3-21 Stress view of distal tibiofibular syndesmosis. This view can be helpful when distal tibiofbular disastasis is suspected but the initial radiographs are negative. An anteroposterior view is obtained with maximum external rotation stress applied to the foot against a firmly held tibia. An abnormal syndesmosis will widen with applied stress. In the example shown here, the medial clear space of ankle joint and distal tibiofibular syndesmosis are both questionably widened on the nonstressed view (A) but clearly open on the stress view (B). This indicates injury of both the syndesmosis and deltoid ligament. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Part I ■ General Considerations

45°

30°–45°

Prone

Weight bearing

40°

Supine

Figure 3-22 Axial view of calcaneus. Diagrams show various methods of obtaining an axial view of the calcaneus. The supine or prone positions may be used in trauma. The actual radiograph shown here demonstrates a subtle fracture of the medial calcaneal tuberosity (arrowhead). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGrawHill; Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

15°

Figure 3-23 Navicular view. This view facilitates the detection of subtle navicular stress fractures. A, The forefoot is elevated on a 15-degree wedge to optimally profile the proximal and distal articular surfaces of the navicular. Detail resolution is improved by coning to the region of interest. B, This example shows a chronic complete stress fracture disrupting the middle third of the navicular (arrowheads). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Imaging of the Foot and Ankle ■ Chapter 3

B Figure 3-24 Talar neck view. This view is used to evaluate fractures. A, The ankle is placed in maximum equinus with the foot pronated 15 degrees, the x-ray beam angled 15 degrees cephalad and centered on the talar neck. B, The talar neck is viewed in the frontal plane. (From Myerson M, editor: Foot and ankle disorders, Philadelphia, 1999, WB Saunders.)

Part I ■ General Considerations

Figure 3-25 Planto-dorsal view of midfoot. This view optimally profiles the tarsometatarsal joint spaces and is extremely valuable when evaluating for tarsometatarsal joint injury or stress fractures at the base of second metatarsal. A, The patient is placed in prone position with the dorsal surface of foot flat against the film cassette and a straight tube centered on the base of second metatarsal. B, An example showing a stress fracture of second metatarsal (arrowheads). C, An example showing a sagittal diastasis injury involving the 1–2 intermetatarsal, medial intercuneiform, and naviculomedial cuneiform joints.

artifacts that can limit visualization of some tendon segments or be a diagnostic pitfall for the inexperienced (Fig. 3-42). US is well suited to the assessment of many superficial tendons and ligaments (Figs. 3-43 and 3-44), foreign bodies, ganglion cysts (Fig. 3-45), and other superficial masses (Fig. 3-46; see Fig. 3-38). In addition, because metal does not distort the sonographic image, US is a good alternative to MRI for the assessment of soft tissue structures adjacent to orthopedic hardware (Fig. 3-47).

NUCLEAR MEDICINE

The major role of nuclear medicine imaging around the ankle is to identify bone injuries and other processes that are occult on plain radiographs or CT scanning. In this regard, nuclear imaging offers an alternative to MRI. Radiographically occult fractures are common around the ankle because of complex anatomy and curved surfaces. Nuclear medicine bone scans are also valuable for demonstrating marrow changes that may be associated with bone contusion, overuse injury, reflex sympathetic dystrophy, tumors, or pain of unknown origin. Basic Science Nuclear medicine imaging is based on the injection, into a patient, of radiopharmaceutical agents, which emit radiation that can then be detected and used to form a 76

diagnostic image. A large number of radiopharmaceutical agents have been developed to address a variety of medical conditions. Nuclear medicine imaging therefore has the advantage of providing both anatomic and physiologic information.26 After administration of the radiopharmaceutical agent, a gamma camera is used to record the pattern of radiopharmaceutical distribution in the patient. The radioactivity emitted passes through a lead collimator and interacts with scintillator crystals in the camera. A resultant reaction gives off photons of light, which are coupled to photomultiplier tubes. These, in turn, release an amplified number of electrons, proportional to the intensity of the incident light. The electrons produce an image, which can be recorded on film or by a computer for further processing. The collimator is a major factor determining image resolution, and the type of collimator used can be adjusted depending on imaging needs. For example, pinhole collimators have high spatial resolution and are useful for imaging small body parts (such as the ankle), although they suffer from lower sensitivity. The radiopharmaceutical agents most commonly used for evaluation of the musculoskeletal system include technetium-99m (Tc-99m) diphosphonates (bone scan), gallium-67 (Ga-67) citrate (gallium scan), and indium111 (In-111)– or Tc-99m–labeled leukocytes (white blood cell/leukocyte scan). The specific agent used will depend on the clinical question to be answered. Text continued on p. 82

Figure 3-26 Additional phalangeal views. When detailed evaluation of the phalanges is required, the standard views of the foot may be supplemented with lateral and/or lateral-oblique views of the toes. A, For a lateral phalangeal view, the foot is laterally positioned with the uninvolved toes flexed and, if possible, the involved toe extended by padding. B, An illustrative lateral radiograph of the great toe shows a fracture. C, For a lateral-oblique phalangeal view, the plantar surface of the foot is obliquely oriented as shown in the diagram, with the primary beam centered on the first metatarsophalangeal joint. D, A lateral-oblique radiograph illustrates improved visualization of phalanges, particularly the great toe. (Drawings and images from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier; source, in turn, borrowed image D from Clarke KC: Positioning in radiography, ed 9, London, 1973, Ilford.)

10°

Figure 3-27 Axial sesamoid view. The axial (or ”skyline”) sesamoid view profiles the sesamoid bones, metatarsosesamoid articulations, and median articular ridge of the first metatarsal. A, Supine patient positioning using a straight beam, with the toes dorsiflexed and the plantar surface of the foot at a 75-degree angle to the cassette. B, Preferred prone patient positioning with 10-degree cephalad tube angulation and the toes held in dorsiflexion by pressure against the cassette. C, Radiograph shows a case of chronic lateral sesamoid bone stress with sclerosis, cystic change, and probable fracture. (Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier. Radiograph from Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Part I ■ General Considerations

Dorsiflexion Figure 3-30 Sesamoid stress view. A lateral radiograph with the first metatarsophalangeal joint (MTPJ1) in dorsiflexion demonstrates disruption of the synchondrosis of the medial sesamoid, which was not clearly evident on standard radiographs of the foot.

Figure 3-28 Medial oblique sesamoid view. The medial sesamoid may be further assessed in oblique projection by raising the medial side of the foot and centering on the first metatarsal head. The example here shows a fracture of the medial sesamoid with cystic change at the fracture margins. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

40°

Figure 3-29 Lateromedial sesamoid view. This oblique projection can provide good anatomic detail of the medial and lateral sesamoids with minimized bony overlap. A, The patient is positioned with the medial side of the foot against the cassette to give a lateral projection of the first metatarsophalangeal joint and the x-ray beam angled 40 degrees toward the heel. B, Radiograph illustrates separation of sesamoids and improved anatomic detail. (From Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier.)

Imaging of the Foot and Ankle ■ Chapter 3

sADTA = 80° LDTA = 89° (86-92°)

Figure 3-31 Talotibial angles. A, On the anteroposterior projection of ankle, the average lateral distal tibial angle (LDTA) between the central diaphyseal axis of tibia and the talar dome is 89 degrees, and the axis of the tibia lies slightly medial to the center of talus. B, On the lateral weight-bearing view of ankle, the central axis of the tibia normally passes through the lateral process of talus, and the anterior-to-posterior distal tibial angle (sADTA) measures 80 degrees. (A, Modified from Paley D: Principles of deformity correction, New York, 2002, Springer-Verlag. Diagram from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier; source, in turn, redrawn from Paley D: Principles of deformity correction, New York, 2002, Springer-Verlag.)

20°

A B Figure 3-32 Hindfoot alignment view. A, The hindfoot alignment view is obtained with the patient standing on an elevated platform with the x-ray beam posterior to the heel, angled 20 degrees caudal from the horizontal. The cassette is placed in front of the patient, perpendicular to the beam, angled 20 degrees off the vertical. It is critical that the long axis of second metatarsal is oriented rectangular to the film cassette because rotation of the foot will alter the measurement of hindfoot alignment angle. B, The midline of the calcaneal tuberosity (arrow) normally lies slightly lateral to the middiaphyseal axis of the tibia, giving a normal hindfoot angle of 0 to 5 degrees valgus. (Drawing A modified from Jones CP, Younger ASE: Imaging of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Mosby Elsevier; Image B modified from Buck FM, Hoffmann A, Mamisch-Saupe N, Espinosa N, et al: Hindfoot alignment measurements: rotation-stability of measurement techniques on hindfoot alignment view and long axial view radiographs, AJR Am J Roentgenol 197:578–582, 2011.)

A = Calcaneal pitch angle (normal 10°– 30°) B = Bohler’s angle (normal 22°– 48°) C = 5th metatarsal base height (normal 2.3 – 3.8 cm)

Figure 3-33 Lateral weight-bearing foot measurements. Commonly used measurements and their normal values are illustrated. The talar–first metatarsal angle (Meary angle) assesses the longitudinal arch of the medial column of foot and is measured between (A) the long axis of talus drawn from the midheight of talar body through the middiameter of talonavicular joint, and (B) the long axis of the first metatarsal is obtained by finding the diaphyseal centers at both proximal and distal shaft levels. The fifth metatarsal base height is a measure of the longitudinal arch of the lateral column of foot. (From Meary R: On the measurement of the angle between the talus and the first metatarsal, Rev Chir Orthop 53:389, 1967.)

Kite angle normal 15°–30°

Figure 3-34 Anteroposterior (AP) talocalcaneal angle. The AP talocalcaneal angle (Kite angle) is formed between the long axis of the talus and a line drawn along the lateral surface of the calcaneus, but it can be difficult to measure because of poor penetration of the hindfoot on many weight-bearing AP projections. In the adult foot, angles greater than 30 degrees indicate hindfoot valgus, and angles less than 15 degrees indicate hindfoot varus. Note that the long axis of talus normally extends along the first metatarsal, and the central long axis of calcaneus normally extends along the fourth metatarsal.

C A

Talar–first metatarsal angle (normal – 4°– +4°)

Talonavicular coverage angle normal = 1.8° –19.3° male 6.7°–21.7° female Figure 3-35 Talonavicular coverage angle. An anteroposterior (AP) weight-bearing view is used to assess “coverage” of the talar head by the navicular. With pes planus, there is lateral peritalar subluxation of the navicular and abduction of the forefoot. With pes cavus, there is medial peritalar subluxation of the navicular and supination of the forefoot. The talonavicular coverage angle is measured between lines drawn across the respective articular corners of talus and navicular. The normal values shown here have been taken from a recent study by Murley et al. (From Murley GS, Menz HB, Landorf KB: A protocol for classifying normal- and flat-arched foot posture for research studies using clinical and radiographic measurements, J Foot Ankle Res 2:22, 2009.)

Hallux valgus interphalangeal angle (normal < 10°) Hallux valgus angle (normal < 15°)

DMAA Normal < 10° (average 7°)

1– 2 intermetatarsal angle (normal < 9°)

Figure 3-36 Hallux valgus assessment. An anteroposterior weight-bearing view is required to assess great toe malalignment when planning a surgical correction of hallux valgus deformity. The long axes of the metatarsals and phalanges are determined by finding the diaphyseal midpoints at metadiaphyseal level (“x” calipers). Normal hallux alignment values are shown.

Figure 3-37 Distal metatarsal articular angle (DMAA) assessment. Although radiographic assessment of the DMAA is limited by poor interobserver reliability, this measurement is relevant when a distal medial closing-wedge osteotomy is being considered for the surgical treatment of hallux valgus deformity. The DMAA is the lateral slope of the articular surface of first metatarsal head relative to the long axis of first ray, normally measuring less than 10 degrees. The significance of an increased DMAA is determined by joint congruity. A congruent joint exists when lines drawn across the articular corners of both the proximal phalanx (dotted line) and first metatarsal head (DMAA line) are parallel. Hallux valgus is usually associated with an incongruent or subluxed joint that will benefit from surgical correction to restore alignment (as in the example shown here). However, some cases of hallux valgus with increased DMAA retain normal joint congruence. In these instances, a conventional surgical correction may result in a stiff joint or recurrent deformity, and an extraarticular approach to osteotomy is instead required to avoid causing an incongruent joint.

MT head

MT shaft

Figure 3-38 Value of sonopalpation. Long-axis ultrasound images obtained over the plantar aspect of the 2–3 metatarsal (MT) interspace in a patient with recurrent metatarsalgia after a Morton neurectomy showed a bulbous hypoechoic swelling of “stump” neuroma (arrows), in continuity with the common plantar digital nerve (arrowheads). Palpation directly over this point reproduced the clinical complaint and confirmed the relevance of the imaging observation.

Part I ■ General Considerations

CIRCUMDUCTION PRE-SNAP

POST-SNAP

B B

LT PERONEAL TENDONS TRANS Figure 3-39 Value of dynamic ultrasound. Preclick and postclick cine-loop frames from a real-time ultrasound examination obtained during active ankle circumduction in a patient with painful retrofibular clicking demonstrate intrasheath subluxation of the peroneus brevis tendon. Transverse images showed the click to correspond with sudden displacement of the peroneus brevis (B) tendon from beneath peroneus longus (L) tendon, although both remained within the retromalleolar space (F). Note the intact overlying superior peroneal retinaculum (arrowheads) and also the predisposing convexity of the peroneal groove. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

T T Figure 3-40 Value of Doppler ultrasound. A case of chronic medial ankle pain and tenderness persisting more than 10 months after ankle inversion injury was thought clinically to be due to tibialis posterior tendonopathy. However, transverse and long-axis power Doppler ultrasound images instead showed features of deltoid desmitis with a thickened hypoechoic deltoid ligament demonstrating convex bulge of the outer surface (arrowheads) and accompanying interstitial hyperemia (colored pixels). Note overlying normal tibialis posterior tendon (asterisk). M, medial malleolus; T, talus. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Technetium-99m–Methylene Diphosphonate Bone Scanning Technetium-99m (Tc-99m)–methylene diphosphonate (MDP) bone scanning provides a map of osteoblastic activity and is one of the staples of nuclear medicine scanning. Vigorous osteoblastic activity occurs in the growth plates of the juvenile skeleton, healing fractures, and pathologic conditions stimulating skeletal blood flow and bone repair. Bone scanning takes advantage of the fact that there is normally a continuous balance between 82

bone breakdown and new bone formation in the skeleton. Focal increased or decreased uptake of the Tc-99m– MDP can be recognized as abnormal and highlight sites of pathology. Although bone scanning is sensitive, it is not specific because increased metabolic activity is a final common pathway for many diseases that alter osteoblast activity. Tc-99m–MDP is administered intravenously and is delivered to the skeletal system based on vascular distribution. Within minutes, osteoblasts begin to assemble

Imaging of the Foot and Ankle ■ Chapter 3

FIB v Retromalleolar groove

TAL

LT anterolateral ankle injection Figure 3-41 Accurate needle guidance. By directing a needle within the imaging plane of the ultrasound transducer, an advancing needle tip can be visualized in real time and accurately guided into specific anatomic spaces. In a case of anterolateral ankle impingement because of hypertrophic posttraumatic scarring of the anterior talofibular ligament (arrow), a needle (arrowheads) was directed into the anterolateral recess of ankle joint at the deep margin of the pathologically thickened ligament for the purpose of corticosteroid injection. FIB, fibula; LT, left; TAL, talus.

RT ankle medial trans Figure 3-43 Tibialis posterior tendon dislocation. Transverse ultrasound image over the medial malleolus shows avulsion of the flexor retinaculum (arrowheads) and anteromedial dislocation of both the tibialis posterior (T) and flexor digitorum longus (D) tendons. Posterior tibial artery (a) and veins (v) are indicated. RT, right; trans, transverse.

CALC

RT Achilles tendon long

FHL tendon long Figure 3-42 Anisotropy. Ultrasound image artifacts can be a diagnostic pitfall for the inexperienced. One of the most important of these is the result of tissue reflectivity varying according to the angle of beam incidence (anisotropy). Structures with highly organized and regular fiber orientation, such as tendons and ligaments, are affected by anisotropy, as shown in this example of normal flexor hallucis longus (FHL) tendon, where the segment that is perpendicular to the insonating beam is accurately represented with echogenic fibers (arrows), but the segment that is oblique to the beam appeared falsely hypoechoic (arrowheads).

the labeled diphosphonates into the hydration shell of hyroxyapatite crystals as they are formed and modified. Three-phase and four-phase bone scans are used to determine the vascular nature of the lesion and to separate soft tissue injury or infection from focal osseous disease. Phase 1 (“blood flow”) is a dynamically acquired arterial phase. Phase 2 (“blood pool”) is a set of static images, representing the blood pool and soft tissue phase. Phase 3 (“delayed”) is acquired 3 to 4 hours later and represents delayed skeletal uptake. Phase 4 can be acquired the

Figure 3-44 Achilles tendon partial-thickness tear. Long-axis ultrasound image shows chronic noninsertional Achilles tendonosis (fusiform hypoechoic thickening indicated by arrowheads) with small transverse anechoic defect in fiber continuity because of complicating partial-thickness tear (arrow). CALC, calcaneus, RT, right.

CUN MT3

RT foot dorsum long Figure 3-45 Midfoot ganglion. Although no mass was clinically palpable, the site of pain indicated by the patient corresponded with a small, rounded, anechoic spaceoccupying lesion located directly over the tarsometatarsal joint line with no perceptible wall thickness (arrow). These features are consistent with a tarsometatarsal joint ganglion. CUN, lateral cuneiform; MT3, third metatarsal; RT, right.

Part I ■ General Considerations

following morning if better skeletal detail is required, usually when the patient has poor renal function (e.g., diabetic foot infection).

Figure 3-46 Morton neuroma. Long-axis proton-density– weighted magnetic resonance image and corresponding long-axis ultrasound image have been obtained over the distal metatarsal interspace at metatarsophalangeal joint level and show the typical position and appearance of a Morton neuroma. The neuroma (m) is appreciated on ultrasound as an ovoid hypoechoic thickening that shows smoothly tapering continuity with the more proximal segment of common plantar digital nerve (arrowheads). Fluid is seen within the adjacent intermetatarsal bursa (arrows).

Single-Photon Emission Computed Tomography Single photon emission computed tomography (SPECT) is an imaging alternative to routine planar scanning, providing images with improved contrast and spatial resolution. A series of planar images are obtained by means of a gamma camera, which travels in an arc around the patient. Information from these acquisitions is postprocessed to produce axial images, which can be reformatted in sagittal and coronal planes. SPECT is a new diagnostic tool that combines a multihead gamma camera and CT scanner mounted together with a common imaging table. This allows the morphologic information of CT to be fused with the biologic information of bone scanning, allowing precise localization of pathology.8,27 SPECT has been shown to be useful in evaluating midfoot arthritis, where the number and configuration of joints are complex,55 and assessing the precise location of pathology in patients presenting with obscure foot and ankle pain.76 SPECT may be useful in the management of osteochondral lesions of the talus by demonstrating the degree of activity of the lesion and the precise location of the active segment in multiple lesions.33,43 Gallium Scanning and White Cell Scanning Gallium-67 is an agent that accumulates in infections, areas of inflammation, and in some tumors.56 It is also a weak bone scanning agent. After administration of Ga-67, imaging is performed at 24, 48, and 72 hours. Wholebody imaging is usually performed, but scanning can be

FHL Trans

FHL Long

Figure 3-47 Imaging adjacent to metal. Ultrasound is useful in assessing the soft tissues adjacent to metallic surgical hardware (when magnetic resonance imaging may be nondiagnostic). This is illustrated in a case of flexor hallucis longus (FHL) tendinosis and peritendonitis secondary to impingement by surgical screws after internal fixation of a calcaneal fracture. The FHL tendon at the level of sustentaculum tali is shown on a sagittal proton-density–weighted magnetic resonance image (left), a transverse gray-scale ultrasound image (middle), and a long-axis power Doppler ultrasound image (right). Surgical screws (short arrows) directly impinge upon a distorted segment of FHL tendon (arrowheads). A markedly thickened and hyperemic peritendon (long arrows) is best appreciated on ultrasound.

Imaging of the Foot and Ankle ■ Chapter 3

limited to the area of interest. Ga-67 is limited by its poor photon yield per disintegration; therefore it is a suboptimal imaging agent. Ga-67 scanning has been replaced by leukocyte scanning for evaluation of osteomyelitis in most regions of the skeleton, but it remains the procedure of choice for diagnosing spinal osteomyelitis. Leukocyte scanning is an alternative technique used to detection of infection or inflammation. Radionuclides available for leukocyte scanning include In-111 and Tc-99m. Whole blood is drawn from the patient and is centrifuged to extract the leukocytes. The leukocytes are then incubated with the radionuclide and reinjected into the patient.38 Imaging is performed at 4 hours and at 24 hours. Because the majority of leukocytes labeled are neutrophils, the procedure is most useful for identifying neutrophil-mediated inflammatory processes, such as bacterial infections.

injury, even in patients with osteoporosis.41 Bone scanning will be positive in patients with midfoot sprain and normal radiographs54; however, uptake on bone scan is nonspecific and can also occur with chronic instability or osteoarthritis. Reflex sympathetic dystrophy, or complex regional pain syndrome, can also be diagnosed with bone scans.12 Because of the inappropriately increased vascular

Use of Nuclear Scanning Nuclear medicine scanning is increasingly being replaced by MRI in the field of musculoskeletal imaging. Bone scanning, however, remains the primary means of evaluating the entire skeleton for a potentially polyostotic process, such as metastatic disease, bone dysplasias, or diffuse arthritis. Evaluation of foot and ankle pain of unknown cause also is another common indication for bone scanning. Bone scanning can detect bone stress, occult fractures, osteochondral injuries, osteoid osteomas, and arthritis (Figs. 3-48 to 3-50).26 Radionuclide uptake in occult fractures occurs within 72 hours of

Figure 3-48 Painful os peroneum syndrome. Delayed-phase bone scan image demonstrating increased radiotracer uptake in an os peroneum that was tender to palpation, consistent with painful os peroneum syndrome (POPS).

Blood pool

RT Anterior LT Trans

RT LAT/LT MED Cor

RT Anterior LT Sag

Figure 3-49 Fibular stress fracture. A single-photon emission computed tomography (SPECT) study demonstrates a stress fracture of the distal fibula that was not evident on plain radiographs. Blood pool image (top left) and delayed planar images (top middle and right) demonstrate increased radiotracer uptake at the distal fibula. Cor, coronal; LAT, lateral; LT, left; MED, medial; RT, right; Sag, sagittal; Trans, transverse. (Image courtesy Dr. Hans Van Der Wall.)

Part I ■ General Considerations

Figure 3-51 Physiologic technetium-99m–methylene diphosphonate uptake in an athlete. Multiple sites of increased isotope uptake are present in the foot and ankle of this young athlete.

COMPUTED TOMOGRAPHY

B Figure 3-50 Depiction of occult fractures. Bone scanning demonstrates a vertical fracture of the distal fibula (A) and a fracture of the body of the talus, adjacent to the subtalar joint (B). Neither fracture was evident on the prior radiographs.

response, one extremity will demonstrate diffuse increased tracer uptake on blood flow, blood pool, and delayedphase scans. In the highly trained athlete, areas of increased isotope uptake in the foot and ankle are incredibly common and may therefore be considered almost “normal.” This is particularly so in the adolescent athlete.10 Consequently, the clinical history and presentation must be carefully considered before interpreting the significance of an area of increased isotope uptake (Fig. 3-51). Infection is another indication for radionuclide scanning. In-111–labeled leukocyte scanning, combined with bone scanning, is the most common method used to diagnose osteomyelitis. Nuclear medicine scanning is particularly useful in imaging for occult infection because whole body images can be obtained. When infection is clearly localized to a particular area, MRI is more accurate in assessing the extent of osseous and soft tissue involvement and detecting complications such as bone abscess and soft tissue collections.46,77 86

Computed tomography provides excellent bony anatomic detail and is particularly useful in evaluation of the complex anatomy of the foot and ankle. Multidetector CT (MDCT) technology produces high-resolution thin-slice images that can be obtained in any plane, aiding in the visualization of fractures and assisting preoperative planning. CT is also useful to define loose bodies and avulsed fragments and to assess the tibiofibular syndesmosis for disruption. Basic Science A CT scanner consists of a scanning gantry, an x-ray generator, a computerized data processing system, and a movable patient table. A narrow, collimated beam of x-rays is generated on one side of the patient. After passing through the patient, the attenuated x-ray beam is detected by a fixed ring of detectors within the scanning gantry. Attenuation or absorption of the x-ray beam reflects the density of the imaged tissue. The x-ray tube rotates 360 degrees around the patient, and these measurements of x-ray transmission are repeated many times from different directions. A computer is used to mathematically reconstruct a cross-sectional image of the body from measurements of x-ray transmission through thin slices of patient tissue. The computer analyzes the average attenuation in a three-dimensional (3D) volume, or voxel, of tissue. The number is converted into a gray-scale value and is

Imaging of the Foot and Ankle ■ Chapter 3

displayed on the screen as a pixel. CT pixel numbers are proportional to the difference between average x-ray attenuation of the tissues within the voxel and that of water. The Hounsfield unit (HU) scale is used, whereby water is assigned a value of 0 HU. Hounsfield units are therefore not absolute values but are relative values that vary from one CT system to another. In general, bone is +400 to + 1000 HU, soft tissue is +40 to +80 HU, fat is −60 to −100 HU, and air is −1000 HU. The range and center of gray-scale value can be manipulated by altering the window width and window level, respectively. Narrow window widths and low window levels result in “soft tissue windows.” Wider window widths and higher window levels result in “bone windows.” The computer algorithm chosen for image reconstruction and the thickness of the scanned slice determines the voxel dimensions. In general, imaging the foot and ankle requires high-resolution scanning, with a slice thickness of 0.5 to 1 mm. Scanning is performed in the axial plane; images may be reformatted in sagittal, coronal, or oblique planes or as three-dimensional reconstructions. CT scanners have evolved from conventional scanners, which obtained a single slice at each indexed table interval with a short pause between images, to helical or spiral CT scanners. Multidetector helical CT (MDCT) is the current technology used by most scanners. It uses the principles of helical CT, whereby the patient table is moved at a constant speed through the CT gantry while the x-ray tube rotates continuously around the patient, but the instrument incorporates multiple rows of detector rings. This allows the acquisition of multiple slices per tube rotation, therefore increasing the area of the patient that can be scanned in a given time by the x-ray beam. Available systems have moved from 2 slices to 320 slices,

which covers 40 mm of patient length for each rotation of the x-ray tube. The advantage of MDCT includes faster imaging times and the ability to obtain thin (0.625 mm) slices, allowing the creation of isotropic voxels that can be reconstructed into any imaging plane without loss of resolution. The limitations of CT scanning include radiation dose (see Table 3-2), cost, and the limited ability of CT to assess soft tissues. Dual source CT (DSCT) is a new technology, originally developed for cardiac imaging, which can decrease radiation dose by more than half. A DSCT scanner is equipped with two x-ray tubes and two corresponding detectors that are oriented in the gantry at an angular offset of 90 degrees. This allows an increase in temporal resolution, increase in speed of acquisition, and decrease in radiation dose to the patient. By using x-ray beams at two different energy levels, DSCT can also allow the differentiation of different materials, based on their energy attenuation profiles. In the foot and ankle, this has been shown to be useful in distinguishing monosodium urate crystals from calcium hydroxyapatite crystals in the prospective diagnosis of gout.22 DSCT can also facilitate a reduction in artifact in the setting of in situ metal hardware. Use of Computed Tomography Scanning CT scanning provides high-resolution images of bony anatomy, which can be reconstructed in any plane. This is useful in the imaging of complex fractures of the foot and ankle, which may be radiographically occult or difficult to evaluate on plain radiographs. CT scanning is particularly helpful in the assessment of traumatic injuries to the midfoot (Fig. 3-52).24 CT of calcaneal fractures

Figure 3-52 Assessment of midfoot fractures using three-dimensional (3D) multidetector computed tomography (MDCT). Radiographs (A) demonstrate fracture-dislocations of the tarsometatarsal joints, fracture of the neck of the second metatarsal, and dislocations of the third and first metatarsophalangeal joints. Axial CT (B) is difficult to interpret, but 3D MDCT (C) helps in preoperative assessment of the complex injury and allows better understanding of the deformities. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Part I ■ General Considerations

can identify involvement of the posterior subtalar joint, sustentaculum tali, and calcaneocuboid joint (Fig. 3-53).18 Impingement by fracture fragments on adjacent soft tissue structures, such as the peroneal tendons, can also be identified.20,64 CT provides useful information in the evaluation of triplane, Tillaux, pilon, and trimalleolar fractures, aiding preoperative planning (Fig. 3-54).45 Three-dimensional reconstructions are particularly helpful for preoperative planning in these complex injuries. CT scanning can be useful in the assessment of tarsal coalitions (Fig. 3-55), neoplasms (Fig. 3-56), foreign bodies, osteochondral injuries, and subtalar joint arthritis. In the postoperative patient, CT scanning can evaluate for osseous fusion at a site of arthrodesis or at sites of internal fixation of fractures or osteotomies (Fig. 3-57). If a patient is unable to undergo MRI (e.g., because of a cardiac pacemaker), CT arthrography offers an alternative imaging modality to assess osteochondral injuries of the ankle joint.

MAGNETIC RESONANCE IMAGING

MRI is an increasingly valuable tool in foot and ankle imaging because of its superior soft tissue contrast and ability to assess articular cartilage and detect subtle bone marrow edema and occult fractures. MRI is particularly useful in the detection and characterization of ligament injuries, bone contusion, chondral and osteochondral lesions, and impingement syndromes. Basic Science MRI is a technique that produces tomographic images by means of magnetic fields and radio waves. Although CT evaluates only a single tissue parameter—attenuation of the x-ray beam—MRI can analyze multiple tissue characteristics, including proton (hydrogen) density, T1 and T2 relaxation times of tissue, and blood flow. Although a detailed description of MRI physics is beyond the scope of this chapter, it is helpful to have a basic understanding

Figure 3-53 Assessment of calcaneal fractures using multidetector computed tomography (MDCT). The morphology of comminuted calcaneal fractures and involvement of the subtalar joints is well displayed by MDCT images through the medial (A) and lateral (B) aspects of the posterior subtalar joint. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-54 Multidetector computed tomography of ankle fractures. Coronal CT (A) demonstrates an oblique fracture through the distal tibia, involving the growth plate and distal tibial eipiphysis. Three-dimensional reconstruction (B) clearly shows the injury to be a triplane fracture. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

A 88

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-55 Computed tomography (CT) assessment of coalition. A, CT demonstrates narrowing and irregularity of the left middle subtalar joint (white arrow) resulting from a cartilaginous coalition. B, In another patient, there are bilateral osseous coalitions of the middle subtalar joints (arrows). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-56 Computed tomography (CT) for assessment of tumors. A 26-year-old ballerina presented with persistent pain and symptoms of anterior ankle impingement. On magnetic resonance imaging (A), there is questionable shallow cortical erosion of the dorsal talar neck (arrow) with subcortical bone marrow edema and adjacent soft tissue edema. On CT (B), there is an intracortical nidus (arrow), consistent with an osteoid osteoma. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-57 Computed tomography (CT) for assessment of arthrodesis. Dual-energy CT demonstrating solid first tarsometatarsal joint arthrodesis (A) and nonunion of an attempted second tarsometatarsal joint arthrodesis (A and B).

B 89

Part I ■ General Considerations

of the method, terminology, and image characteristics involved. The following discussion has been adapted from Anderson and Read.2 Routine MRI utilizes the magnetic properties of unpaired hydrogen protons, and the chemical and magnetic environments in which they are found, to produce images of biologic tissues. The spin of the positively charged hydrogen proton makes it behave like a tiny bar magnet. When placed in a strong external magnetic field, these protons align themselves with the external magnetic field. Electromagnetic energy is then pulsed at the natural or “resonant” frequency of the proton (a radiofrequency, or RF, pulse), temporarily exciting the protons to a higher energy state. When this external RF pulse is switched off, the protons “relax” back into alignment with the external magnetic field (a lower energy state). This emits a corresponding amount of RF energy that can be detected and used to form an image. After the RF pulse is turned off, the protons return to their prior orientation in the field and gradually return to a random precession. This emits a radiowave signal, known as a T1 and T2. The signal characteristics and subsequent image formation depend on the ratio of the T1 and T2 information plus proton density (PD). Each tissue’s composition has a unique T1 and T2 character. The rate and nature of hydrogen proton relaxation are determined by the local chemical, structural, and magnetic environments in which these protons are found (e.g., lipids, free water, proteins). Different tissues therefore exhibit significant differences in their resonant behavior, which is the source of the superb image contrast provided by MRI. Most tissues can be differentiated by differences in their characteristic T1 and T2 relaxation times. T1 (spin-lattice [longitudinal] relaxation time) is a measure of a protons ability to exchange energy with its surrounding chemical matrix and represents a measure of how quickly a tissue can become magnetized. T2 (spinspin [transverse] relaxation time) conveys how quickly a given tissue loses its magnetization. External RF energy is introduced in a series of pulses (known as a pulse sequence), the timing of which determines which type of proton relaxation is emphasized in the resultant image, that is, whether an image is T1 weighted or T2 weighted. The two most important pulse parameters are time to repetition (TR) and time to echo (TE). TR is the amount of time between consecutive groups of RF pulses, and TE is the time between the initial RF pulse and subsequent signal detection. Using a short TR (≤500 msec) and short TE (≤20 msec) will produce a T1-weighted image, while using a long TR (≥2000 msec) and long TE (≥70 msec) will produce a T2-weighted image. Using a long TR (≥2000 msec) and intermediate TE (25-30 msec) will minimize the effects of T1 and T2 weighting and will instead produce an image reflecting hydrogen density: a proton-density– weighted image. The coils or antennae that detect and measure the RF signal returning from the patient are critical determinants 90

of image quality. These receiver coils were initially incorporated into the wall of the magnet (body coils). The role of MRI in characterizing the musculoskeletal system did not expand until the introduction of specialized extremity coils (surface coils) in the late 1980s. Surface coils are positioned close to the structures of interest, thereby improving signal-to-noise ratio and allowing the acquisition of high-resolution images. More recently, there have been even further improvements in image quality by combining multiple coils into a phased-array configuration. Magnetic resonance scanners can be classified as low field, midfield, and high field, depending on the strength of the external magnet, which is measured in tesla (T) units. The most common magnetic resonance scanners in current use are midfield 1.5 T and high-field 3 T scanners. Ultrahigh-field 7 T scanners are currently being used in research applications.29 High-field scanners offer improved resolution for small body parts and decreased imaging times. Magnetic Resonance Imaging Clinical Sequences The early years of clinical MRI were dominated by conventional spin-echo pulse sequences. These were prolonged acquisitions that were susceptible to patient movement, usually taking between 10 and 15 minutes each. The development of faster techniques has allowed high-resolution sequences to be performed in reasonable time frames of 2 and 5 minutes each. Fast spin-echo (FSE) sequences have now become the general workhorse of musculoskeletal imaging. These sequences are usually used in combination with supplementary sequences, such as short tau inversion recovery (STIR) or gradientrecalled echo (GRE). FSE techniques have also incorporated strategies to suppress the bright signal emanating from fat, which can obscure the high signal of pathology (fat suppression). T1-Weighted Fast Spin-Echo Sequences T1-weighted FSE sequences utilize short imaging parameters (TR ≤ 500 msec, TE ≤ 20 msec at 1.5 T) and reflect the T1 characteristics of tissue within the image. Fat, proteinaceous fluid, subacute hemorrhage, and gadolinium contrast will appear high signal (bright). Fluid (i.e., water) will appear low signal (dark). T1-weighted images have a high signal-to-noise ratio and therefore have the advantage of providing good anatomic detail. However, T1-weighted images result in poor delineation between the intermediate signal intensity cartilage and the low signal intensity joint fluid. T1-weighted images are insensitive to edema (fluid), and fat will appear high signal, which can mask adjacent pathology. The “magic angle” phenomenon (discussed below) is most conspicuous on T1 images. These factors can all cloud the delineation of anatomy or pathology and therefore limit the clinical value of T1-weighted images in musculoskeletal

Imaging of the Foot and Ankle ■ Chapter 3

imaging. T1-weighted sequences, however, remain useful for the demonstration of fractures and tumor tissue characterization. T2-Weighted Fast Spin-Echo Sequences T2-weighted FSE sequences utilize long imaging parameters (TR ≥ 2000 msec, TE ≥ 70 msec at 1.5 T) and reflect the T2 characteristics of tissue within the image. T2 images emphasize fluid and edema, which will appear high signal. On T2-weighted FSE sequences, fat is moderately high signal intensity, and muscle appears as intermediate signal. Tendons and ligaments appear low signal. The magic angle phenomenon is minimized because of the long TE; therefore T2-weighted sequences can be helpful whenever the magic angle phenomenon may confound image interpretation. T2-weighted sequences are often combined with fat-suppression techniques to highlight edema and are useful in assessing tissue characteristics of tumors. Proton-Density–Weighted Fast Spin-Echo Sequences Proton-density–weighted FSE sequences utilize intermediate imaging parameters (TR ≥ 2000 msec, TE = 25-40 msec at 1.5 T) and reflect the concentration of hydrogen protons, rather than the T1 or T2 characteristics of tissue within the image. PD-weighted sequences have become the general workhorse of musculoskeletal MRI because they provide high contrast resolution and high spatial resolution images with relatively high signal-tonoise ratio (i.e., good anatomic resolution), allowing for reasonably fast scan times. PD-weighted FSE sequences are particularly useful for assessment of articular cartilage. At 1.5 T, optimal image contrast between articular cartilage and joint fluid is obtained using TE values of 25 to 35 msec. This produces good contrast between the intermediate signal intensity articular cartilage, the low signal intensity fibrocartilage and subchondral bone and the high signal intensity synovial fluid. On PD-weighted FSE images, articular cartilage demonstrates a normal gray-scale stratification, which corresponds to the cartilage zonal anatomy. Partial thickness chondral lesions and chondral flaps are also well depicted with thin slice PD-weighted FSE sequences. The disadvantage of PD-weighted images is that the magic angle artifact remains moderately conspicuous and should not be misinterpreted as pathology. Short Tau Inversion Recovery or “Fat-Sat” Sequences The application of fat suppression to FSE images overcomes the problem of high signal fat obscuring edema and increases the contrast differences between cartilage, fluid, and synovium. The two most common imaging techniques used to achieve fat suppression in musculo skeletal imaging are frequency-selective fat-suppression techniques and STIR sequences. These produce images with low signal intensity fat and bone marrow but high signal intensity fluid and tissue edema.

Frequency-selective fat-saturation (“fat-sat”) techniques achieve fat suppression by applying an initial RF pulse that sets the magnetization of fat to zero (“nulling”) before the imaging pulses. This results in images with good spatial resolution and faster acquisition times when compared with STIR images. The images are, however, highly sensitive to magnetic field inhom*ogeneity and are therefore vulnerable to uneven fat suppression when imaging off-center in the magnet or when imaging curved body parts, such as the foot and ankle. They are also ineffective in the setting of metal. In these settings, inversion recovery techniques provide more robust fat suppression. STIR images achieve fat suppression by acquiring signal at a particular time in an inversion recovery pulse sequence (inversion time or TI ≈140 msec at 1.5 T), when the signal from fat is almost nulled, while maintaining water and soft tissue signal. STIR sequences provide robust fat suppression, even in the presence of metal, but carry a penalty of longer acquisition times and, consequently, reduced spatial resolution. Gradient-Recalled Echo Sequences GRE sequences are another distinct technique that utilizes an additional parameter known as “flip angle.” At large flip angles (45-90 degrees), the sequences give T1-weighted images, and at low flip angles (5-20 degrees), they give a unique type of image described as having “T2-star” (T2*) weighting. GRE sequences provide high signal-to-noise ratio (i.e., high spatial resolution images) and can also be obtained as volumetric (3D) acquisitions, allowing reconstructions in any imaging plane. Fat-suppressed T1 gradient-recalled echo sequences are more sensitive than conventional proton-density or fat-suppressed T2 sequences in demonstrating Achilles tendinosis. The disadvantages of GRE sequences include relatively long scan times and marked accentuation of magnetic susceptibility artifacts in the setting of metal (for example, residual micorometallic debris after surgery) or gas. Tissues with an increased concentration of paramagnetic compounds, such as methemoglobin, melanin, iron, and manganese have a “blooming” effect on GRE images, making the affected areas appear larger than on corresponding FSE sequences. In practice, this property of GRE sequences can be exploited when imaging hemosiderin (e.g., pigmented villonodular synovitis (PVNS), hemachromatosis), calcification, or loose bodies. Magnetic Resonance Arthrogaphy Routine MRI of the foot and ankle is usually performed using a nonarthrographic technique. MR arthrography has, however, been suggested to be helpful in the evaluation of osteochondral lesions and ankle soft tissue impingement.31,63 Under ultrasound or fluoroscopic guidance, dilute gadolinium is injected into the joint before MRI. The injected contrast separates the articular capsule from other structures and, because of the T1 shortening 91

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effect of gadolinium, outlines intraarticular structures on T1-weighted images.69 Although MR arthrography is still used in some centers, with the advent of high-resolution imaging and high-field (3 T) scanners, the authors consider the indications for MR arthrography in the foot and ankle to be extremely limited. New Magnetic Resonance Imaging Technique: Biochemical Imaging The integrity of articular cartilage and cartilage repair has traditionally been assessed using conventional PD-weighted FSE techniques or fat-suppressed 3D GRE images. Quantitative MR imaging techniques that allow a more sophisticated assessment of cartilage degeneration and cartilage repair are now being developed. These techniques detect changes in the ultrastructure of cartilage and provide an assessment of cartilage biochemistry. They therefore have the potential to detect changes in cartilage biochemistry that may precede discernible cartilage thinning found with traditional MR techniques. Quantitative MR imaging techniques are classified into those that detect alterations in collagen fiber orientation (T2 mapping) and those that detect alterations in the proteolgycan content (delayed gadolinium-enhanced magnetic resonance imaging of cartilage [dGEMRIC], T1 rho mapping). T2 Mapping T2 mapping is performed by acquiring several images at different echo times at the same slice location. The T2 calculation is performed on a pixel-by-pixel basis, by fitting the signal intensity from each echo image and the corresponding echo time, to an exponential decay equation. The T2 map of articular cartilage reflects the collagen fiber orientation and the mobile water content47 and is displayed using a color-coded map. Prolongation of T2 relaxation times is associated with osteoarthritis and breakdown in cartilage structure.48 Quantitative T2 measurements demonstrate excellent interobserver and intraobserver reliability,21,49 thereby offering a tool for reproducible assessment of cartilage status over time. Delayed Gadolinium-Enhanced Magnetic Resonance Imaging of Cartilage dGEMRIC exploits the fixed charge property of articular cartilage through the use of an injection of (negatively charged) gadolinium contrast. The fixed charge density in cartilage is largely the result of the concentration and distribution of the negatively charged glycosaminoglycan chains within the proteolgycan macromolecules. Gadolinium is administered intravenously; the patient performs 10 minutes of exercise; and, after a 90-minute delay, T1-weighted maps are obtained, usually through the use of a specialized inversion recovery pulse sequence.4 The gadolinium penetrates the articular cartilage; the amount of penetration is inversely proportional 92

to the glycosaminoglycan content. The gadolinium acts to shorten T1 relaxation times, allowing for the generation of T1 maps. In areas with depleted glycosaminoglycan content, there will be an increased distribution of gadolinium and therefore a higher T1 signal, which is reflected by a diminished “relative glycosaminoglycan index.” T1 Rho (ρ) Mapping T1 rho (ρ) is a technique used to assess the low-frequency interactions between hydrogen in macromolecules and free water.74 Similar to T2 mapping, T1 rho is calculated on a pixel-by-pixel basis by fitting the signal intensity from each spin-lock image and the corresponding spinlock length to an exponential decay equation. T1 rho has been shown to reflect proteolgycan content in articular cartilage. Subjects with osteoarthritis have longer T1 rho values than asymptomatic controls, and T1 rho may be even more sensitive to early cartilage degeneration than T2 mapping alone.34 Although clinically feasible at 1.5 T, T1 rho is largely applied at 3 T and is a promising technique to detect changes in proteolgycan content in early cartilage degeneration. Contraindications to Magnetic Resonance Imaging Contraindications to MRI include cardiac pacemakers (except in limited circ*mstances), ferromagnetic foreign bodies (particularly those near vital structures, such as intraocular foreign bodies), and certain metallic and electronic implants, including ferromagnetic cerebral aneurysm clips. MRI units screen patients for the presence of these implants with extensive prescan questionnaires and interviews. Pitfalls and Artifacts in Magnetic Resonance Imaging Magic Angle Phenomenon The signal intensity of ordered tissues, such as cartilage and tendons, depends on the orientation of the collagen fibers relative to the external magnetic field, which in a conventional MR scanner, runs parallel to the long axis of the patient’s body. When highly structured tissues are imaged at 55 degrees to the external magnetic field, using a short TE (i.e., T1, PD, and GRE sequences), there is a normal prolongation of T2 values, a phenomenon known as the magic angle effect.16 The magic angle phenomenon is observed within tendons, articular cartilage, or menisci and results in a spurious high signal, which can mimic pathology. A common example in foot and ankle imaging is seen in the peroneal tendons at the submalleolar level when the ankle is scanned in neutral flexion. T2-weighted sequences can be helpful whenever magic angle phenomenon may cloud image interpretation because true pathology is usually brighter on T2 than on T1- or PD-weighted images.

Imaging of the Foot and Ankle ■ Chapter 3 Bone Marrow “Edema” A marrow edema-like signal is defined as focal areas of T2 hyperintensity and T1 hypointensity. This is a nonspecific finding that can be due to a number of causes, including hematopoietic marrow, infection, trauma, and tumor. The bone marrow edema pattern is relatively common in foot and ankle MRI and may not always indicate true pathology. Foci of high T2 signal can be seen in the tarsal bones of asymptomatic patients, particularly those younger than 15 years. These foci are thought to be due to perivascular foci of red marrow, physiologic stress, or increased bone turnover resulting from weight-bearing or normal skeletal growth.32,68 High T2 signal, rounded foci are often also seen in the anterior calcaneus at the angle of Gissane and should not be misinterpreted as pathologic.78 These foci are thought to represent nutrient channels or intraosseous ganglion cysts. A similar appearance may be seen in the dorsal talar neck and along the plantar surface of the sinus tarsi, which are also though to relate to vascular channels.23 Finally, a bone marrow edema pattern has been described in the foot and ankle within the first 12 weeks after immobilization. This pattern was not found to correlate with pain or the clinical syndrome of reflex symphathetic dystrophy and tended to resolve by 18 weeks postimmoblization.14 Presumably this relates to disuse osteopenia. Use of Magnetic Resonance Imaging Indications for MRI include the assessment of acute or chronic trauma, instability, impingement, osteochondral pathology, occult fractures or stress reactions, osteonecrosis, soft tissue and osseous tumors, nerve entrapment syndromes, arthropathies, tendon pathology, and infection.

These conditions and the role of MRI are discussed in more detail in the following section of this chapter. IMAGING OF FOOT AND ANKLE PATHOLOGY

Imaging Ligament Injury Ligaments in the foot and ankle are in general uniformly hypointense (dark) on commonly utilized MR imaging sequences. Although some ligaments may be visualized completely on a single MR image, it is not uncommon for the ligaments to lie in a plane that is slightly oblique to the MR image plane such that ligament assessment requires review of multiple contiguous images. If the ligament is superficially situated and amenable to ultrasound assessment, it usually demonstrates a mildly fibrillar sonographic architecture, provided the ultrasound beam is perpendicular to the ligament fibers. CT lacks sufficient contrast resolution to provide direct assessment of ligament injury. The spectrum of acute ligament injury demonstrable on imaging ranges from minor strain injury to complete tear. On MRI, minor strain injury manifests as subtle intraligament signal hyperintensity, often with mild ligament thickening and periligamentous edema. On ultrasound, ligamentous strain injury manifests as hypoechoic ligament thickening, often with associated reactive hyperemia on color Doppler assessment. Acute complete ligament tears usually demonstrate clear-cut ligament fiber discontinuity on MRI and ultrasound, with fluid evident at the point of tear (Figs. 3-58 to 3-60). In the subacute stage of ligament injury, the injured ligament usually appears thickened and edematous, and the point of ligament fiber discontinuity will often be obscured by early scar response (Fig. 3-61). The potential for scar

Figure 3-58 Acute lateral ligament tear. Sagittal (A), coronal (B), and axial (C) proton-density fast spin-echo magnetic resonance images demonstrate an acute complete tear of the distal anterior talofibular ligament (arrow in A and C) and an avulsion of the calcaneofibular ligament from the fibula (arrow in B).

Part I ■ General Considerations

Figure 3-59 Triligamentous syndesmotic ligament complex injury. Sagittal proton-density (PD) fat-saturated (A), axial PD (B), and coronal PD fast spin-echo (C and D) magnetic resonance images demonstrate a complete tear of the anterior-inferior talofibular ligament (AITFL) from the fibula (white arrow in images B and D), moderate-grade partial tear of the inferior interossous ligament (open arrow in C), and high-grade partial tear of the posterior-inferior talofibular ligament (PITFL) from the tibia (black arrow in images A and B).

T T

RT AITFL

LT AITFL

Figure 3-60 Ultrasound of syndesmotic injury. On the symptomatic right side (A), there is an acute complete midsubtance tear of the anterior-inferior talofibular ligament (AITFL) with a transversely oriented hypoechoic defect and fiber discontinuity (arrow). This contrasts with the normal left side (B), where the AITFL (open arrow) is intact. F, fibula; T, tibia.

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-61 Ligament remodeling on magnetic resonance imaging. Axial proton-density (A and B) images 6 weeks postinversion injury demonstrate early remodeling of the anterior talofibular ligament, which remains hyperintense and thickened (white arrow). At 20 weeks postinjury (C and D), there is mature scar remodeling of the ligament (black arrow), which now appears uniformly hypointense and only marginally thickened.

remodeling of injured ligaments in the foot and ankle is substantial, particularly the anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL), such that a previously injured ligament may appear near normal on imaging once it has undergone mature scar remodeling, a process that may continue to evolve over 12 to 18 months. Although imaging is helpful in assessing ligament injury and scar healing, it does not provide direct assessment of ligament laxity. Ankle and Transverse Tarsal Joint Ligament Complex Injury Because most acute ankle sprains settle without significant complication, the role of imaging in the acute trauma setting is mainly to exclude ancillary pathology that might require early intervention. To this end, the Ottawa Ankle Rules can be used to decide whether a plain radiograph is initially warranted.70 These guidelines state that an examiner is unlikely to miss a clinically significant fracture if there is no bony tenderness and the patient is able to bear weight for at least four steps. Failing this, or

if symptoms/signs persist more than 4 weeks after injury, a plain radiograph examination should be performed. Although plain radiography will detect gross diastasis of the distal tibiofibular joint, a significant proportion of syndesmotic injuries will remain occult to plain radiographic assessment. Although more sophisticated imaging tests are generally not indicated in the assessment of acute ankle injuries in the general population, early MRI of the sprained ankle in the elite or professional athlete is now commonly performed to distinguish between injury to the lateral ankle ligament complex (Fig. 3-62), syndesmotic ligament complex,15 and transverse tarsal joint complex (Fig. 3-63), and to clarify extent of injury and prognosis. A targeted ultrasound examination is a valid alternative to MRI for the differentiation of lateral ankle ligament injury from syndesmosis injury (see Fig. 3-60). The scar healing potential of injuries to the lateral ankle ligament complex, syndesmotic and transverse tarsal joint complex, with appropriate treatment, is very good. At 6 to 12 weeks postinjury, complete ATFL tears 95

Part I ■ General Considerations

Figure 3-62 Partial-tear superomedial fibers of the spring ligament. Axial (A) and coronal (B) proton-density imaging of a moderate-grade partial tear of the superomedial fibers of the spring ligament.

Figure 3-63 Transverse tarsal joint sprain. Sagittal proton-density (PD) fat-saturated (A and B) and PD fast spin-echo (C) magnetic resonance images demonstrate a subacute sprain of the dorsal talonavicular joint capsule, with thickened edematous immaturely scarred dorsal capsule (white arrows in A and C) and subacute sprain of the lateral limb of the bifurcate ligament and dorsal capsule of the calcaneocuboid joint (black arrow in B).

commonly show ill-defined bridging scar tissue of intermediate signal on MRI and no evidence of residual laxity on physical examination.11 Eventually, most injured ligaments remodel with mature scar and appear as welldefined structures of hom*ogeneously low signal (see Fig. 3-61). Isolated spring ligament tears are an uncommon but important cause of posttraumatic planovalgus deformity that is readily demonstrated on MRI (see Fig. 3-62) and may be suspected on ultrasound. 96

Midfoot Ligamentous Injury Significantly displaced midfoot injuries are generally imaged with radiographs and CT. There is some variation in the approach to the imaging assessment and management of subtle Lisfranc ligament complex injuries in which there is no or minimal displacement on weightbearing radiographs. Some surgeons find stress radiography under anesthesia useful in determining whether to internally fix the midfoot.60 Others advocate the use of MRI in determining the extent of capsuloligamentous

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Figure 3-64 Acute Lisfranc ligament complex disruption on computed tomography (CT) and magnetic resonance imaging (MRI). Long-axis CT images demonstrate flake avulsion fracture fragment (arrow, A) related to medial cuneiform avulsion of the plantar oblique C1–M3 ligament flake avulsion fracture fragment (arrow, B) related to metatarsal avulsion of the interosseous Lisfranc ligament and CT widening of the C1–M2 interval dorsally (arrowheads, C). Corresponding MR images demonstrate the C1–M3 ligament stump (arrows, D), the interosseous Lisfranc ligament stump (arrow, E), and the widening of the C1–M2 interval (arrows, F). The flake avulsion fragments are difficult to appreciate on MRI.

injury and using this to determine whether to proceed to examination under anesthesia58 (Fig. 3-64). Some surgeons use the increased sensitivity of CT in detecting subtle displacement and cortical flake avulsion fragments not evident on plain radiographs59 (see Fig. 3-64). Forefoot Ligament Injury Injuries to the first metatarsophalangeal (MTP) joint capsuloligamentous complex are relatively common and may involve the collateral ligaments and plantar or dorsal capsule. In the setting of plantar plate (sesamophalangeal ligament) disruption, the diagnosis may be inferred by demonstrating proximal sesamoid migration on weightbearing radiographs (Fig. 3-65). MRI provides direct assessment of the capsuloligamentous disruption (see Fig. 3-65).37

Degeneration and tear of the lateral plantar plate of the second MTP joint is a common cause of metatarsalgia. Although the presence of a lateral plantar plate tear can be inferred by the presence of varus drift of the second toe on clinical assessment or weight-bearing radiographs, ultrasound and MRI can readily demonstrate the nature of the plantar plate pathology, allowing differentiation between attritional attenuation-elongation and frank tear, aiding preoperative assessment (Fig. 3-66).37 Imaging Chondral and Osteochondral Lesions Isolated chondral lesions in the ankle and foot generally remain occult to plain radiographic assessment. If there is an associated acute traumatic fracture of the subchondral plate and cancellous subchondral bone, the fracture 97

Part I ■ General Considerations

Figure 3-65 Turf toe. Weight-bearing radiograph (A) demonstrates retraction of the medial sesamoid (black arrow) and lateral sesamoid (open black arrow) of the right first metatarsophalangeal joint. Long-axis fat-saturated proton-density (PD) (B) and sagittal PD (C and D) magnetic resonance images demonstrate avulsion of the medial plantar plate off the medial sesamoid. with an associated flake fracture fragment (white arrow). There is avulsion of the lateral plantar plate off the base of the proximal phalanx (open white arrow).

line may be demonstrable on plain radiographs (Fig. 3-67). With chronicity, central osteophyte formation, subchondral cystic change, or sclerosis may develop locally at the site of the chondral lesion. There may also be osteophyte formation at the joint margins. CT is more sensitive in demonstrating and characterizing undisplaced fracture, subchondral cystic change, sclerosis, and central osteophyte formation. However, it does not provide direct assessment of articular cartilage and will not demonstrate subchondral bone marrow edema. High-resolution MRI provides direct assessment of articular cartilage and will demonstrate bone marrow edema that anecdotally correlates with activity of the osteochondral lesion. In addition to demonstrating chondral pathology in the ankle, high-resolution MRI has the ability to demonstrate chondral pathology in the subtalar joint, midfoot, and forefoot (Figs. 3-68 and 3-69). 98

Imaging Articular Cartilage Repair Talar dome chondral injuries may spontaneously heal or repair may be surgically assisted using either arthroscopic techniques (e.g., debridement, curettage, and drilling) or chondral or osteochondral grafts. Spontaneous repair and marrow stimulation techniques both attempt to fill a chondral or osteochondral defect with reparative fibrocartilage, which lacks the resilience and durability of normal hyaline cartilage. The bony component of an osteochondral defect will often fail to spontaneously fill with new bone. Autologous osteochondral grafting (e.g., mosaicplasty) and autologous chondrocyte implantation (ACI) are alternative surgical techniques that attempt to deliver a more physiologic, stable, and durable reconstruction of the joint surface. MRI provides the best assessment of progress after these surgical procedures (Figs. 3-70 and

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-66 Tear of the lateral plantar plate second metatarsophalangeal (MTP) joint. On the radiograph (A), there is slight varus drift of the second toe and a relatively short first metatarsal, with resultant second metatarsal head protrusion, predisposing to overload of the second ray. Short-axis PD (B), sagittal proton-density (PD) fat-saturated (C), and sagittal PD (D) magnetic resonance images demonstrate degeneration and high-grade partial-thickness tear of the lateral plantar plate of the second MTP joint (arrows).

Figure 3-67 Talar dome osteochondral lesion. Plain radiographs demonstrate undisplaced arrows, (A) and a displaced double arrow, (B) osteochondral fractures of the lateral talar dome and a chronic medial talar dome osteochondral lesion with subchondral cystic change and sclerosis (arrow, C). (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Part I ■ General Considerations

Figure 3-68 Talar dome chondral flap. Sagittal proton-density (PD) fat-saturated (A) and coronal PD (B) magnetic resonance images demonstrate an arthroscopically confirmed in situ full-thickness chondral flap at the lateral talar dome, with breach of the chondral surface at the superior margin of the lateral gutter articular facet (open arrow) and basal delamination at the weight-bearing aspect. There is minor subchondral sclerosis without an adjacent bone marrow pattern.

Figure 3-69 Chondral flap second metatatarsal head. Long-axis fat-saturated proton-density (PD) (A) and sagittal PD (B) magnetic resonance images demonstrate an in situ full-thickness chondral flap at the mid-to-dorsal aspect of the second metatarsal head (white arrows), with breach of the chondral surface at the dorsal and medial margins (open arrows). There is no subchondral bone marrow edema. C, Arthroscopic image in the same patient demonstrates the chondral flap.

3-71), although the signal characteristics of a graft do not allow reparative fibrocartilage to be reliably differentiated from hyaline-like articular cartilage.72 Quantitative MR techniques, such as dGEMRIC, T1 rho, and T2 mapping, show some promise in this regard.72 100

Imaging Impingement Syndromes Impingement is a clinical syndrome of end-range joint pain and/or motion restriction resulting from the direct mechanical abutment of bone and/or soft tissues. Impingement syndromes at the ankle may occur after

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-70 A, Sagittal fat-suppressed proton-density (PD) magnetic resonance (MR) image demonstrating a chronic medial talar dome osteochondral lesion with in situ unstable osteochondral fragment (white arrow) and cystic change and extensive bone marrow edema at the margins of the potential osteochondral crater (black arrow). B, Postarthroscopic excision of the osteochondral fragment, deroofing of the cystic change, and osteoplasty. On sagittal fat-suppressed PD MR sequencing, there is 100% fill of the crater, with reparative fibrocartilage that demonstrates a smooth surface. There has been substantial reduction in the extent of bone marrow edema. No residual cystic change is evident. On sagittal fat-suppressed PD (B) and coronal PD (C) sequencing, signal hyperintensity at the basal layer of the reparative fibrocartilage indicates immature basal integration (open arrows).

either acute macrotrauma or repetitive microtrauma. Various underlying pathologies and anatomic variations may predispose to impingement. Modern imaging modalities can usefully demonstrate these changes and assist with patient management.36 Implicit in the definition of impingement as a clinical syndrome is that the diagnosis remains “clinical” because imaging changes alone do not reliably predict symptoms or clinical relevance. Impingement syndromes in the ankle may be classified according to location and by the type of underlying pathology—soft tissue or bony. Posttraumatic synovitis, intraarticular fibrous bands–scar tissue, capsular scarring, or developmental and acquired bony spurs or prominences are the most common causes of ankle impingement. Sites of impingement at the ankle include anterolateral, anterior, anteromedial, posteromedial, and posterior.36 Bony impingment lesions at the ankle may be confirmed on plain radiographs, often supplemented by specific views, for instance, oblique radiographs of the foot for anteromedial impingement spurs and a lazy lateral view to show an os trigonum. MRI may demonstrate bone marrow edema at the site of an active impingement lesion and adjacent synovitis, capsular thickening, and pericapsular edema (Fig. 3-72 to 3-74).36 Soft tissue impingement lesions around the ankle are usually best demonstrated on MRI. MR arthrography and the use of intravenous contrast have been advocated as means of increasing the sensitivity of MRI for detecting impingement lesions. In routine clinical practice, a high-resolution nonarthrographic approach is usually adequate. Ultrasound can be helpful in the diagnosis of soft tissue impingement lesions and can be used to guide corticosteroid injections.

Imaging Tendon Pathology Tendons connect muscles and bones, transmitting forces generated by muscle contraction on to bone, allowing movement of joints. The basic constituents of tendon are collagen bundles, tenocytes, and ground substance, which is rich in proteoglycans. Collagen bundles provide tensile strength, while ground substance provides structural support for the collagen fibers and regulates the maturation of collagen. Tenocytes synthesize ground substance and collagen. Tendinosis is characterized by degeneration of tendon cells and collagen fibers and an increase in noncollagenous matrix. Intratendon inflammation is not a feature of tendinosis. However, peritendon inflammation is commonly seen in association with tendinosis or in isolation, being described as a tenosynovitis, if there is a tendon sheath, or paratenonitis, if there is a paratenon, such as in the Achilles tendon. Tendinosis Tendinosis may be demonstrated on ultrasound or MRI. On ultrasound, tendinosis manifests as a hypoechoic echotextural change, with alteration of the normal fibrillar architecture of the tendon (Fig. 3-75). If the ultrasound beam is not perpendicular to the tendon, then it may appear artifactually hypoechoic because of anisotropy, which, if unrecognized, can lead to a false-positive diagnosis of tendinosis. Ultrasound has the advantage of providing assessment of tendon and peritendon blood flow by using color Doppler. Tendon and peritendon hyperemia is commonly seen in tendinosis and peritendinitis and may be a marker of activity of the pathology (Fig. 3-76). On MRI, tendinosis usually first manifests on fatsuppressed T1 GRE sequencing as a subtle increase in 101

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Figure 3-71 Autologous chondrocyte implantation (ACI) of a lateral talar dome osteochondral lesion. Despite multiple prior arthroscopic debridements, the lateral talar dome lesion remained symptomatic. Pre-ACI sagittal (A) and coronal (B) fatsuppressed proton-density (PD) magnetic resonance (MR) images demonstrate multilocular subchondral cystic change and surrounding bone marrow edema (arrowhead) and incomplete basal delamination of reparative fibrocartilage anteriorly (white arrow). One year post-ACI, sagittal (C) and coronal (D) fat-suppressed PD MR images demonstrate there has been resolution of the subchondral cystic change and bone marrow edema, 100% fill of the graft with smooth graft surface, and evidence of mature basal and peripheral integration (double arrows).

signal intensity (Fig. 3-77). If the tendon fibers are at 55 degrees to the longitudinal axis of the magnetic field in the MR unit, then the magic angle phenomenon can result in tendon signal hyperintensity in normal tendons, mimicking tendinosis. This is commonly seen in the peroneal tendons at the submalleolar level and may be seen in the posterior tibial tendon at the submalleolar level. The magic angle phenomenon is largely absent on a heavily T2-weighted sequence. Peritendon inflammation may be seen on ultrasound as a thickened peritendon space, tendon sheath effusion, and tenosynovial thickening with associated hyperemia on color Doppler. An inert-appearing tendon sheath effusion is not diagnostic of a peritendonitis. On MRI, thickening of 102

the peritendon space and tenosynovial thickening may be more subtle when compared with ultrasound. There may edema in the fat plane adjacent to the tendon sheath/paratenon. Use of intravenous contrast may help distinguish an inert tendon sheath effusion from a tenosynovitis. Insertional Achilles tendinosis differs from noninsertional tendinosis seen in the Achilles tendon and other tendons. Impingement may play a role in the pathogenesis of insertional Achilles tendinosis resulting from bony overgrowth of the posterosuperior process of the calcaneus, usually with an associated retrocalcaneal bursitis. However, a subgroup of insertional Achiless tendinosis does not involve impingement and is often

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-72 Posterior ankle impingement. Sagittal proton-density (PD) fat-saturated (A) and PD (B) magnetic resonance images demonstrate a moderate-sized os trigonum (white arrow) with a bone marrow edema pattern across the synchondrosis (white arrows), synovitis in the posterior recess of the ankle and subtalar joint, and adjacent pericapsular edema (open arrow). The findings are suggestive of active posterior impingement.

Figure 3-73 Anteromedial ankle impingement. Sagittal proton-density (PD) fat-saturated (A) and sagittal PD (B) magnetic resonance images demonstrate a prominent dorsomedial talar neck spur (black arrow) and moderate anteromedial plafond spur (open black arrow), respectively. There is capsulosynovial thickening in the anteromedial gutter, with adjacent pericapsular edema (white arrow). The findings would predispose to anteromedial impingement symptoms.

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Figure 3-74 Anterolateral impingement and meniscoid lesion and posteromedial impingement (POMI) lesion. Sagittal proton-density (PD) fat-saturated (A), sagittal PD (B), and axial PD (C) magnetic resonance images in a patient 3 months postinversion injury, with ongoing pain. There is a dense traumatic synovitis in the anterolateral gutter, with an immature meniscoid lesion (white arrow). There is hypertrophic scarring of the deep fibers of the deltoid ligament, with protrusion into the medial gutter posteriorly (black arrow), predisposing to POMI.

Figure 3-75 Acute tibialis anterior tendinosis and peritendinitis. Longitudinal ultrasound images from a cyclist who presented with acute right anterior lower leg pain. On the symptomatic right side, there is subcutaneous edema (open arrow), thickening of the tibialis anterior tendon, mild decrease in echogenicity (arrow pointing superiorly), and thickening of the peritendon space (oblique arrow pointing inferiorly), when compared with the asymptomatic left side.

LT Long

Figure 3-76 Stenosing peroneus longus tenosynovitis. A, Transverse ultrasound image of the peroneal tendons at the level of a prominent peroneal tubercle demonstrating thickening of the inferior peroneal retinaculum toward the insertion on the peroneal tubercle (white arrow), manifesting as a hypoechoic thickened septum between the peroneus longus and brevis tendons, with adjacent thickening of the peroneus longus tendon and peritendon space. B, Longitudinal power Doppler image demonstrates moderate hyperemia within the thickened peritendon space (open arrow), indicating a peritendinitis. TNS, tendons.

Tibialis anterior

LT Per TNS trans mid

LT Per TNS long mid

MID

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Figure 3-77 Active Achilles tendinosis. Sagittal (A) and axial (C) fat-suppressed T2 magnetic resonance (MR) images demonstrate fusiform thickening of the midfibers of the Achilles tendon, with an instrasubtance longitudinal fissure (arrows) and moderately active surrounding tendinosis, only appreciable on sagittal (B) and axial (D) fat-suppressed T1 gradient-recalled echo MR images as an area of ill-defined signal hyperintensity (open arrow).

characterized by dystrophic intratendon ossification and enthesial bony spurring (Fig. 3-78). Stenosing Tenosynovitis A stenosing tenosynovitis may involve the peroneal tendons, typically at the level of the peroneal tubercle. The imaging findings in this setting are often very subtle and are not totally specific, consisting of thickening of the inferior peroneal retinaculum, usually with prominence of the peroneal tubercle. A stenosing tenosynovitis may also affect the flexor hallucis longus tendon at the level of the fibroosseous tunnel. Tendon Tears Acute tendon tears in the foot and ankle may range from complete tears, most commonly seen in the mid-Achilles tendon, to small intrasubstance transversely oriented tears. Although, clinically, most acute complete tendon tears are obvious to the foot and ankle surgeon and do not necessarily require imaging, the patient will often have already undergone imaging of the injured tendon before their index presentation to the foot and ankle surgeon. Not uncommonly, ultrasound examinations of a complete tear of the Achilles tendon may be misinterpreted by the inexperienced sonologist as indicating a partial tear. In this setting, MRI may be required to document the complete tear. Imaging can also provide information on the quality of the tendon edge, the distance between the two tendon edges, and the degree, if any, of muscle atrophy (Figs. 3-79 and 3-80).

Attritional longitudinal tears are commonly seen in the peroneus brevis tendon and posterior tibial tendon and may also be seen in the peroneus longus tendon, Achilles tendon, and distal fibers of the tibialis anterior tendon (Fig. 3-81). When using ultrasound and MRI, it sometimes can be a struggle to characterize peroneal tendon split tears at the retromalleolar sulcus level, that is, caused by close apposition of the peroneus longus and brevis tendons to the lateral malleolus as the tendons curve around the malleolus. Imaging Inflammatory Arthropathies The role of imaging in the evaluation of the patient with an inflammatory arthropathy in the foot and ankle may range from initial diagnosis (Fig. 3-82), evaluating extent of disease, assessing for active inflammation, and differentiating active inflammation from a secondary degenerative arthropathy or a complication of treatment such as avascular necrosis. Occasionally, imaging may play a role in the diagnosis of psoriatic arthritis in a patient presenting with a dactylitis, helping rule out infection and other differential diagnoses (Fig. 3-83). Occasionally, a patient’s index presentation of an inflammatory arthropathy may consist of a rheumatoid nodule in the foot and ankle or an MTP joint synovitis or intermetatarsal bursitis. Initial imaging assessment of the patient with a suspected inflammatory arthropathy should commence with plain radiography, which in the early stages will be 105

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RT Achilles long distal

Figure 3-78 Insertional Achilles tendinosis with dystrophic tendon calcification-ossification. Sagittal (A) and axial (B) fatsuppressed T1 gradient-recalled echo magnetic resonance images demonstrating focal insertional Achilles tendon thickening and signal hyperintensity toward the superficial margin (arrow), with overlying low-grade adventitial bursopathy, and small bony spur at the superficial margin. No intratendon calcification-ossification is evident. C, Longitudinal ultrasound image of the corresponding area demonstrates echogenic foci consistent with dystrophic calcification-ossification (open arrow). D, On power Doppler, there is corresponding tendon and peritendon hyperemia.

negative. MRI and ultrasound are more sensitive in detecting and characterizing the extent of an inflammatory arthropathy. Use of intravenous contrast may provide further insight into the extent and severity of an inflammatory arthropathy and may help differentiate between an inert joint effusion and an active synovitis. Intravenous contrast administration can be combined with an MR angiographic sequence, providing further information on the degree of hyperemia associated with an inflammatory arthropathy. MR angiography can also be helpful in assessing a peripheral vasculitis. Ultrasound, with the use of color Doppler, provides a noninvasive assessment for hyperemic synovitis and can also assess periarticular erosions. In the setting of an advanced inflammatory arthropathy with secondary degenerative change, plain radiography often provides sufficient imaging assessment, sometimes supplemented with CT or MRI. Some 106

seronegative inflammatory arthropathies may present with an isolated enthesitis, which can be a more challenging diagnosis. MRI may demonstrate enthesial bone marrow edema and contrast enhancement, although, in more advanced cases, bony erosion and proliferative bony reaction may be evident (Fig. 3-84). These latter changes may be evident on plain radiographs. Nuclear medicine bone scan provides a nonspecific but reasonably sensitive means of assessing for an inflammatory arthropathy. Gout, when presenting in typical fashion in the first MTP joint, rarely needs cross-sectional imaging. In acute gout in the early stages of the disease, plain radiographs will often only demonstrate soft tissue swelling. With chronicity, punched out periarticular erosions may be seen. Less commonly, gout may present with involvement of other sites, including tendons around the foot and ankle and the joints of the hindfoot. In such cases, there

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-79 Complete midsegment Achilles tendon rupture. A sagittal proton-density–weighted magnetic resonance image shows a complete tear appreciated as a gap in tendon continuity produced by retraction of the proximal stump and filled largely by fat (arrow). There are changes of underlying tendonosis at the separated proximal and distal tendon stumps (asterisks).

Figure 3-80 Complex partial tear of triceps surae complex in a 51-year-old recreational soccer player with acute-onset calf pain. Coronal proton-density (PD) (right) and fatsuppressed sagittal PD (left) magnetic resonance images show a mildly retracted tear of the medial head gastrocnemius tendon component of the triceps surae complex (arrows), a largely intact soleal component (arrowhead), and background changes of proximal Achilles tendonosis (asterisk). The patient was successfully managed conservatively.

Figure 3-81 Longitudinal split-tear peroneus brevis tendon and peroneal peritendonitis. Axial fat-suppressed axial T2-weighted (A) and axial proton-density–weighted (B and C) magnetic resonance images show the peroneus brevis tendon (white arrows) separated into two halves by a line of high signal. The adjacent peroneus longus tendon (black arrows) is thickened and demonstrates intrasubstance tendonosis signal. The peroneal tendon sheath is distended by effusion (white arrowhead) and shows contained stranding indicative of synovitis. There is fluid within the flexor hallucis longus tendon sheath (F).

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Figure 3-82 Inflammatory synovitis with periarticular erosion. A, Sagittal fat-suppressed proton-density (PD) magnetic resonance (MR) image demonstrating talonavicular middle subtalar joint synovitis, with thickened edematous dorsal capsule (white arrow) and periarticular bone marrow edema at the capsular insertions. B, Coronal PD MR image demonstrating a periarticular erosion at the dorsomedial aspect of the talar head (white arrow), with moderate adjacent synovial thickening.

Figure 3-83 Psoriatic arthropathy related dactylitis mimics infection. Long-axis (A) and sagittal fat-suppressed proton-density (B) magnetic resonance images demonstrate a dactylitis involving the second and third toes, with subcutaneous edema, metatarsophalangeal and interphalangeal joint effusions, and flexor tendon sheath effusions.

Figure 3-84 Seronegative inflammatory arthropathy presenting with enthesitis, synovitis, and tenosynovitis. A, Sagittal fatsuppressed proton-density (PD) magnetic resonance (MR) image demonstrating extensive bone marrow edema at the calcaneal origin of the plantar fascia, with mild adjacent fascial signal hyperintensity (white arrow), compatible with an enthesitis. B, Sagittal fat-suppressed PD MR image demonstrating bone marrow edema at the margins of the cuboid tunnel for the peroneus longus tendon (white arrow) and a small calcaneocuboid joint effusion and mild synovitis (open arrow). C, Axial fat-suppressed PD MR image demonstrating a thickened edematous long plantar ligament (white arrow) with periligamentous soft tissue edema and enthesial bone marrow edema at the cuboid insertion. Note also the changes of peroneus longus peritendinitis at cuboid tunnel level (open arrow).

Imaging of the Foot and Ankle ■ Chapter 3

may be a role for cross-sectional imaging in establishing a diagnosis and assessing disease severity. The recent development of dual energy CT allows differentiation of gout crystals from calcium hydroxyapatite. Imaging Nerve Pathology in the Foot and Ankle Advances in MRI and ultrasound technology now allow direct high-resolution visualization of peripheral nerves in the foot and ankle. The most frequent application of this technology is in the assessment of Morton neuroma. High-resolution techniques can accurately assess for neural thickening, infiltration of the perineural fat plane, and intermetatarsal bursopathy (Figs. 3-85 to 3-87). Some studies have cast doubt on the accuracy of imaging in assessing for Morton neuroma. This in part reflects that some Morton neuromas may be asymptomatic and that some patients may have a painful common plantar digital nerve without a Morton neuroma being present. Of note, however, both ultrasound and MRI of the central forefoot can be technically demanding and have a significant learning curve. Imaging plays a role in assessing the patient with suspected tarsal tunnel syndrome by way of identifying compressive neural lesions, such as ganglia or accessory flexor muscles, and identifying focal neural pathology, such as benign peripheral nerve sheath tumor, posttraumatic neuroma, and perineural fibrosis (Figs. 3-88 to 3-90). Both ultrasound and MRI are efficacious in this regard, with the exception that perineural fibrosis may be more conspicuous on MRI and that ultrasound assessment of

the distal tarsal tunnel is technically more demanding than MRI. Both ultrasound and MRI can be helpful in the assessment of superficial peroneal nerve and sural nerve pathology (see Fig. 3-89) In addition to providing direct assessment of peripheral nerves in the foot and ankle, MRI, and to a lesser extent, ultrasound can demonstrate a denervation effect in the intrinsic muscles of the foot in the distribution of

n b

Figure 3-85 Ultrasound of Morton neuroma. A long-axis view has been obtained over the plantar aspect of the 3–4 web space at metatarsophalangeal joint level. An ovoid hypoechoic thickening (n) of the common digital nerve consistent with a Morton neuroma is demonstrated. Arrowheads indicate the normal segment of common digital nerve proximal to the neuroma. Fluid is seen within the adjacent intermetatarsal bursa (b).

Figure 3-86 Magnetic resonance (MR) imaging of Morton neuroma. Coronal (short axis) T1 (A) and T2 (B) MR images demonstrating a moderate-sized 2–3 web-space Morton neuroma (white arrows). Note the normal neurovascular bundle in the 3–4 web space (open arrow). C, In sagittal cross section, the fusiform morphology of the Morton neuroma is readily appreciated (white arrows). D, In contrast, note the normal neurovascular bundle in sagittal cross section (open arrow).

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B A

Figure 3-88 Tarsal tunnel ganglion with lateral plantar nerve (LPN) denervation effect. A, Axial proton-density (PD) magnetic resonance (MR) image demonstrating a tarsal tunnel ganglion cyst (white arrow) displacing and compressing the LPN (open arrow). B, Sagittal PD MR image demonstrating the tarsal tunnel ganglion cyst (white arrow) arising from a fibrous extraarticular talocalcaneal coalition (open arrow). C, Short-axis MR image through the forefoot demonstrating subacute denervation effect in the interossei and adductor hallucis muscles (open arrows). Note normal signal intensity of the two heads of flexor hallucis brevis and abductor hallucis.

B Figure 3-87 Magnetic resonance (MR) imaging of intermetatarsal effusion. A, Coronal T2-weighted MR image demonstrating 2–3 and 3–4 intermetatarsal effusions (white arrows), seen as confluent high (fluid) signal at the mid-to-dorsal aspect of the web spaces. Note the normal neurovascular bundles at the plantar aspects of the web spaces (open arrows). B, Long-axis fat-suppressed protondensity MR image again demonstrates the intermetatarsal bursal effusions (white arrows), rendered more conspicuous by the use of fat suppression.

the affected nerve, providing a secondary sign of peripheral nerve pathology (see Fig. 3-88). In the case of denervation effect involving the abductor digiti minimi muscle, imaging often fails to demonstrate the site of the nerve abnormality. In the postoperative setting, MRI and ultrasound are both well suited to demonstrating posttraumatic neuroma formation. Ultrasound because of its unlimited multiplanar capability is often better able to demonstrate neural abnormalities in longitudinal cross section when compared with MRI. Ultrasound is also superior to MRI in demonstrating surgical sutures traversing a nerve. Imaging Tumors in the Foot and Ankle Approximately 7% of bone and soft tissue tumors occur in the foot and ankle, and most are benign or 110

nonneoplastic soft tissue tumors. Benign soft tissue tumors include lipoma, angioleiomyoma, vascular malformation, schwannoma, and superficial acral fibromyxoma. Nonneoplastic soft tissue lesions occurring in the foot and ankle include giant cell tumor of tendon sheath, pigmented villonodular synovitis, fibroma of tendon sheath, plantar fibroma, Morton neuroma, reactive pseudotumor (reactive periostitis, bizarre parosteal osteochondromatous proliferation [BPOP]) subungual exostosis, and turret exostosis, ganglia, and adventitial bursae. Bone tumors are also more commonly benign than malignant. Common benign bone tumors include enchondroma, periosteal chondroma, osteochondroma, chondromyxoid fibroma, chondroblastoma, osteoid osteoma, osteoblastoma, and nonneoplastic lesions, such as aneurysmal bone cyst and simple bone cyst. Notwithstanding that they are uncommon, sarcomas do occur in the foot and ankle, and, as a consequence, all masses in the foot and ankle require detailed and rigorous imaging assessment. In general, benign soft tissue tumors are superficial in location and less than 5 cm in size. Soft tissue sarcomas are more commonly located in the deeper tissue layers and are often relatively large at presentation. Synovial sarcoma is the commonest sarcoma in the foot and ankle and is usually seen in young adults (Fig. 3-91). It deserves special mention because of the relatively high frequency of delay in diagnosis resulting from misinterpretation on imaging as a ganglion or plantar fibroma.

Imaging of the Foot and Ankle ■ Chapter 3

Hernia

RT SPN trans Standing

LT SPN long

Figure 3-89 Posttraumatic neuroma superficial peroneal nerve (SPN) and adjacent muscle hernia. A, Transverse ultrasound image performed with the patient standing demonstrates thickening of the left SPN in the lower leg and bulging in contour of the investing fascia of the anterior compartment consistent with a muscle hernia. Note normal right SPN and investing fascia. B, Long-axis ultrasound image demonstrating transition in caliber of the SPN as it emerges from the deep fascia (arrows). C, D and E, Descending transverse proton-density (PD) magnetic resonance images demonstrate the muscle hernia (open arrow) and thickening of the SPN (white arrows). F, Long-axis PD MR image demonstrates thickening of the SPN as it emerges from the deep fascia (white arrow).

Figure 3-90 Perineural scar after prior tarsal tunnel release. A, Axial proton-density (PD) magnetic resonance image demonstrating perineural scar encasem*nt of the medial plantar nerve and neural thickening and edema (white arrow), with similar findings on a coronal PD image (B).

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A B

Figure 3-91 Synovial sarcoma. A, Sagittal ultrasound image demonstrates a nonspecific bilobular hypoechoic lesion in the region of the 1–2 intermetatarsal bursa (white arrow). B, Long-axis fat-suppressed proton-density (PD), C, sagittal PD, and D, fat-suppressed PD and E, short-axis T2 magnetic resonance images demonstrate a solid T2 hyperintense lesion, which, on excision biopsy, was a synovial sarcoma (white arrows).

Malignant bone tumors in the foot and ankle, when they occur, are most commonly chondrosarcomas, osteogenic sarcoma, or Ewing tumors (Fig. 3-92). Radiographs and MRI are the main initial imaging investigations in the workup of a tumor in the foot and ankle. In suspected malignant tumors, positron emission tomography (PET) and chest CT are indicated to assess for metastatic disease. A radiograph is helpful in demonstrating calcifications in soft tissue tumors and in characterizing the matrix of bone tumors. A radiograph is also useful in demonstrating periosteal reaction, bone destruction and expansion, and pressure erosion. Ultrasound can be helpful in the diagnosis of Morton neuroma and ganglia. It is critical to adhere to strict sonographic criteria for a diagnosis of a ganglion to avoid misdiagnosis of solid tumors as ganglia. MRI is superior to ultrasound with respect to providing an overview of the region of interest and in its ability to characterize the tumor and its extent. Intravenous contrast administration is generally indicated when characterizing a tumor, providing further insight into lesion vascularity and extent. If there is uncertainty regarding a potential diagnosis of a bone or soft tissue tumor in the foot and ankle, or if the lesion is thought to be malignant, then a diagnostic biopsy should be performed, preferably at a center where there is a multidisciplinary team that includes a radiologist, oncologic surgeon, and a pathologist. A core biopsy 112

may be performed percutaneously under imaging guidance by a radiologist, or an open surgical biopsy may be performed. In general, fine needle biopsy, as opposed to core biopsy, does not provide sufficient material for accurate diagnosis. Imaging Infections in the Foot and Ankle Although diagnostic imaging can demonstrate imaging features compatible with infection, the diagnosis of infection must take into account the clinical picture, the results of serum markers of inflammation, and appropriate aspirates or biopsy of suspected infected tissue. The commonest clinical scenarios of infection in the foot and ankle are hematogenous spread of osteomyelitis in the skeletally immature, the infected diabetic foot, and postoperative infection. Imaging assessment of suspected infection should commence with plain radiographs. In the setting of osteomyelitis, plain radiographic findings may range from being normal to demonstrating localized osteolysis, periosteal reaction, and possibly a sequestrum. CT scanning may demonstrate subtle areas of osteolysis, periosteal reaction, and sequestrum formation that are not readily appreciated with plain radiography. Ultrasound can be helpful in confirming the presence of a soft tissue collection, joint or tendon sheath effusion, and can provide

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-92 Ewing sarcoma in distal tibia. A, Lateral radiograph of the ankle demonstrates a lytic lesion in the distal tibia posteriorly, with adjacent soft tissue mass. B, Computed tomography scan demonstrates aggressive pattern of permeative osteolysis. Axial proton-density (C) and postintravenous contrast sagittal fat-suppressed T1 (D) magnetic resonance images demonstrate the extensive associated soft tissue mass.

guidance for aspiration and microbiologic assessment. Contrast-enhanced MRI, with its greater contrast resolution, is the modality of choice for the evaluation of most suspected soft tissue and osseous infections in the foot and ankle (Fig. 3-93). The typical MR finding in infection consists of edema, manifesting as high signal on fatsuppressed PD or T2 sequencing and low signal on T1 sequencing, with a corresponding thick rind of contrast enhancement. For osseous infections, bone scans (high sensitivity, low specificity), radiolabeled leukocyte scans (higher specificity than bone scan), and F-18–fluorodeoxyglucose positron emission tomography (18F-FDG PET) (high sensitivity, intermediate specificity) can be used to detect and localize sites of infection in the ankle and foot. Note that in the diabetic foot false-negative nuclear medicine scans may occur because of ischemia and resultant insufficient accumulation of radiotracer in the focus of osteomyelitis. Miscellaneous Conditions in the Foot and Ankle Complex Regional Pain Syndrome Complex regional pain syndrome (CRPS) is a complex and poorly understood condition of severe pain that follows trauma or surgery and exhibits features such as local vasomotor disturbances, trophic changes (e.g., hair loss, thin skin, increased sweating, a sensation of cold), and restricted or painful movement.67 CRPS can easily be overlooked, and mild forms of this condition often go unrecognized, but physical examination is the mainstay of diagnosis. Plain radiographs are usually normal in

early-stage CRPS (0-3 months) and show only nonspecific osteopenia in 60% of cases (Fig. 3-94) during the later stages (3-12 months)75 but must be performed to rule out associated disorders. Joint effusions may be variably associated with the early stages of CRPS. Power Doppler US may show soft tissue hyperemia in the affected lower limb.52 MRI (Fig. 3-95) is unreliable and does not have an established role in the diagnosis of CRPS.75 Isotope bone scan remains the only sensitive, specific, and generally accepted diagnostic imaging modality in the lower extremity.39 Arthrofibrosis Arthrofibrosis is an exaggerated fibrosis of joint capsule after trauma or surgery that results in joint stiffness, pain, and impingement symptoms.35 Any joint may be affected, but the knee, elbow, shoulder, wrist, hand, and ankle are most frequent. Relative postsurgical or posttraumatic immobility is a known risk factor15 and rationale for postoperative range of motion exercises. The likelihood of arthrofibrosis is also related to the severity of the initiating injury, with an increased incidence when multiple ligaments have been injured or multiple procedures have been performed.53 Fibrosis and associated capsular contracture can result in abnormal joint surface contact pressures and predispose to osteoarthrosis. Although the diagnosis is usually clinical, MRI can be helpful in atypical or unsuspected cases, or if concomitant pathology exists that may confuse the clinical picture. The MRI findings in cases of established ankle arthrofibrosis are those of a thickened joint capsule (usually >3 mm) with low signal intensity (Fig. 3-96). 113

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Figure 3-93 Chronic osteomyelitis calcaneus with cloaca. Lateral radiograph (A) of the heel demonstrates ill-defined sclerosis (white arrow) in the calcaneus adjacent to the calcaneal apophysis. Coronal proton-density (PD) (B), sagittal PD (C), and axial fat-suppressed T2 sequencing (D) demonstrates a lytic lesion in the posterior tubercle of the calcaneus adjacent to the apophysis, with a cloaca at the lateral border (white arrows) and infiltration of the overlying subcutaneous fat.

Figure 3-94 Clinical photograph (left) of cutaneous vasomotor disturbance and radiograph (right) of nonspecific osteopenia in complex regional pain syndrome.

Posttraumatic Fat Necrosis Posttraumatic fat necrosis is a painful condition involving subcutaneous fat that follows direct contusion, crush, or shear injury and is characterized by organizing hemorrhage, fat necrosis, and fibrosis.73 There is often a delay of weeks before a tender palpable lump is appreciated, and 114

a majority of patients do not recall any inciting injury. In the early stages, there may be a visible ecchymosis and corresponding high signal on MRI. This resolves and, in the later stages, MRI may show only low signal and a loss of subcutaneous fat volume. On ultrasound, there is a thickened, tender, and indurated subcutaneous fat space containing poorly-marginated areas of increased echogenicity with variable hyperemia. Of importance, imaging does not show any discrete mass apart from an occasional oil cyst (Fig. 3-97). Fat necrosis may occur at any age, is more common in women, and is most frequent at sites prone to direct trauma (e.g., breast, thigh, shin). The tender lump may take months to subside. Fat necrosis can cause skin contour deformity resulting from fibrosis, oil cysts, and radiographic calcifications. Foreign Bodies Foreign body localization and removal can be challenging. Appropriate imaging is often a key to surgical success. Plain radiographs should always be obtained, with any additional advanced imaging choices based on those results and the character of the injury. Ultrasound can generally be used to identify, mark the overlying skin, provide a depth to target, and assess the pertinent anatomic relationships of radiolucent foreign bodies.

Imaging of the Foot and Ankle ■ Chapter 3

Figure 3-95 Magnetic resonance imaging appearance in a case of warm-phase reflex sympathetic dystrophy (RSD). Sagittal T1 (A) and sagittal STIR (B) images show a coarse blotchy pattern of diffuse marrow edema involving multiple bones. There is also an area of soft tissue edema over the dorsum of midfoot. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Figure 3-96 Arthrofibrosis. Sagittal proton-density–weighted magnetic resonance images show focal thickening of the anterior ankle capsule (asterisk) consistent with arthrofibrotic change after arthroscopy. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

Preoperative hookwire localization under CT guidance has also been described.5 Avascular Necrosis of Bone in the Foot and Ankle Avascular necrosis (AVN) is an uncommon pathology in the foot and ankle, usually seen in the talus as a complication of a talar neck fracture but also described in virtually all bones in the foot and ankle. Imaging diagnosis of established AVN relies on the demonstration of demarcated sclerosis resulting from laying down of new bone over necrotic trabeculae, with revascularization and resorption at the edge of the osteonecrotic segment, accounting for the demarcated margins (Fig. 3-98). The reparative interface between necrotic tissue and viable granulation tissue may be seen as the “double-line sign” on MRI, a low signal intensity rim in which the inner

aspect becomes high signal on T2-weighted images. Although this sign is characteristic of AVN of the femoral head, it is less frequently seen in the ankle and foot.7 Early diagnosis of avascular necrosis can be difficult. In the talus, the absence of subchondral osteopenia in the talar dome at 4 to 8 weeks posttalar neck fracture (Hawkin sign) has been reported to have an association with avascular necrosis of the talus; however, it lacks specificity.61 Bone marrow edema on MRI is also a nonspecific imaging finding, particularly in the setting of recent fracture.7,51 Dynamic contrast-enhanced (DCE) MRI has been used to attempt to characterize the perfusion status in the setting of suspected early avascular necrosis.51 At this stage, there are no validated criteria for DCE MRI diagnosis of avascular necrosis, and there has been no demonstrated superiority of DCE MRI over conventional MRI in the diagnosis 115

Part I ■ General Considerations

RT MID foot Dorsomedial trans

T1-weighted

RT MID foot Dorsomedial long

Fat-suppressed PD-weighted

Figure 3-97 Fat necrosis. This example of fat necrosis was imaged 3 weeks after crush injury of the foot. Ultrasound (top) shows thickened echogenic subcutaneous space and small oil cyst (arrows). Arrowheads indicate a cutaneous laceration that had been sutured. Magnetic resonance image (bottom) confirms the oily nature of the cyst seen on ultrasound because the lesion shows high T1 signal that completely suppresses with fat saturation (arrows). Also note extensive marrow edema resulting from bone bruising.

of AVN.13,71 In the early stage of avascular necrosis, relatively increased enhancement may be seen because of venous stasis, with reduced time to peak enhancement,9 which is paradoxic to the expected decreased perfusion in an avascular necrotic segment and creates difficulties in the interpretation of such studies. INTERVENTIONAL RADIOLOGY IN THE FOOT AND ANKLE

Imaging guidance can facilitate accurate delivery of an injectate in the foot and ankle. Corticosteroid formulations are most commonly injected. There is increasing use of platelet-rich plasma (PRP) injections for the treatment of tendinopathy and plantar fasciosis. Other newer injection therapies include the use of cultured autologous tenocytes for treatment of tendinopathy and adipocytederived stem cells for the treatment of osteoarthritis. Other interventional procedures that may be done under imaging guidance include RF ablation of nerves or neural lesions such as a Morton neuroma. The choice of imaging modality for image guidance will vary with local expertise and availability. There has been a substantial increase in the proportion of 116

ultrasound-guided procedures over the last 10 years. These include ganglion aspiration, Morton neuroma injection, joint injection, tendon sheath injection, Achilles paratenon brisem*nt, plantar fascia injection (with steroid or PRP), and dry needling. One limitation of ultrasound-guided joint injection is that there is only limited ability to demonstrate on static images the distribution of the injectate. Fluoroscopic-guided joint injections have the advantage of showing the distribution of contrast within the joint after injection. Computed tomography has a limited role in imaging-guided procedures in the foot and ankle. Its principal role lies in guiding radiofrequency ablation of osteoid osteoma. Minimally invasive imaging-guided percutaneous intervention has grown enormously in recent years. Although clinical guidance is adequate for some injections, others may benefit from a more precise and controlled procedure under direct imaging control. The radiologist is uniquely placed to perform these more demanding interventions by using a variety of imaging tools (e.g., fluoroscopy, CT, ultrasound). Such procedures may include joint injections (Fig. 3-99), tendon sheath injections, bursal injections, platelet-rich plasma injections, perineural injections (Fig. 3-100),40 aspirations of

Imaging of the Foot and Ankle ■ Chapter 3

Wt. bearing

Lat RT Med LT Fe

Figure 3-98 Spontaneous avascular necrosis of the talar dome in a 50-year-old male with a remote background history of ankle trauma. A, Anteroposterior radiograph demonstrates sclerosis, fragmentation, and partial collapse of the talar dome, and old posttraumatic changes at the medial and lateral malleoli. B and C, Sagittal and axial proton-density magnetic resonance (MR) images demonstrate geographically marginated, mildly heterogeneous, low signal consistent with sclerosis. A linear high-signal fracture line is also evident. Note the sparing of the medial portion of the talar dome. D, Coronal fat-suppressed MR image demonstrates edema-like signal in a mildly heterogeneous distribution within the osteonecrotic segment. E, Corresponding increased radiotracer uptake is evident on bone scan. Fe, feet; Lat, lateral; LT, left; Med, medial; RT, right; Wt., weight.

Figure 3-99 Fluoroscopic guidance has allowed accurate needle placement within the fourth tarsometatarsal joint, further confirmed with the injection of a small amount of radiopaque contrast material. Procedures of this type can document unequivocally the site injected, providing the surgeon with a high level of confidence and sometimes detecting unexpected communications with other joints, tendon sleeves or periarticular cysts. (From Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill.)

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LT 3 – 4 Webspace injection Figure 3-100 An ultrasound-guided technique of corticosteroid injection for a Morton neuroma is illustrated. The transducer is placed over the dorsum of the foot and oriented in the long axis of the relevant web space. The needle is then advanced from a distal interdigital approach to allow direct visualization (arrowheads) as the tip is placed within the zone of neural/ perineural thickening (arrow), and corticosteroid is then instilled. Note some spillage of injectate into the adjacent intermetatarsal bursa (asterisk).

T C TAL RT. Post-lat ankle long

RT. Post-lat ankle ASP

Figure 3-101 A posterior ankle ganglion is shown on the preaspiration image (arrow). After needle placement (arrowheads) and aspiration, the cyst was completely emptied. C, calcaneus; lat, lateral; RT, right; T, tibia; TAL, talus.

ganglion cysts (Fig. 3-101) and other fluid collections, alcohol17,28,50 or radiofrequency19 ablations of Morton neuromas. REFERENCES 1. AAPM position statement on radiation risks from medical imaging procedures. December 13, 2011. Policy Number PP 25-A. [database on the Internet]. American Association of Physicists in Medicine. Available at http://www.aapm.org/ org/policies/details.asp?id=318andtype=PPandcurrent=true. Accessed August 12, 2012. 2. Anderson IF, Read JW: Atlas of imaging in sports medicine, ed 2, Sydney, 2008, McGraw-Hill. 3. Bagshaw M: Cosmic radiation in commercial aviation, 2009. Available at http://www.iaasm.org/documents/Cosmic_ Radiation.pdf. Accessed July 21, 2012. 4. Bashir A, Gray ML, Burstein D: Gd-DTPA2- as a measure of cartilage degeneration, Magn Reson Med 36:665–673, 1996. 5. Bissonnette RT, Connell DG, Fitzpatrick DG: Preoperative localization of low-density foreign bodies under CT guidance, Can Assoc Radiol J 39:286–287, 1988.

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6. Brady Z, Cain TM, Johnston PN: Justifying referrals for paediatric CT, Med J Aust 197:95–98, 2012. 7. Buchan CA, Pearce DH, Lau J, White LM: Imaging of postoperative avascular necrosis of the ankle and foot, Semin Musculoskelet Radiol 16:192–204, 2012. 8. Bunyaviroch T, Aggarwa A, Oates ME: Optimized scintigraphic evaluation of infection and inflammation: role of single-photon emission computed tomography/computed tomography fusion imaging, Semin Nucl Med 36:295–311, 2006. 9. Chan WP, Liu YJ, Huang GS, et al: Relationship of idiopathic osteonecrosis of the femoral head to perfusion changes in the proximal femur by dynamic contrast-enhanced MRI, Am J Roentgenol 196:637–643, 2011. 10. Cooper R, Allwright S, Anderson J: Atlas of nuclear imaging in sports medicine, Sydney, 2003, McGraw-Hill. 11. De Simoni C, Wetz HH, Zanetti M, et al: Clinical examination and magnetic resonance imaging in the assessment of ankle sprains treated with an orthosis, Foot Ankle Int 17:177–182, 1996. 12. Demangeat JL, Constantinesco A, Brunot B, et al: Three-phase bone scanning in reflex sympathetic dystrophy of the hand, J Nucl Med 29:26–32, 1988.

Imaging of the Foot and Ankle ■ Chapter 3

13. Donati OF, Zanetti M, Nagy L, et al: Is dynamic gadolinium enhancement needed in MR imaging for the preoperative assessment of scaphoidal viability in patients with scaphoid nonunion? Radiology 260:808–816, 2011. 14. Elias I, Zoga AC, Schweitzer ME, et al: A specific bone marrow edema around the foot and ankle following trauma and immobilization therapy: pattern description and potential clinical relevance, Foot Ankle Int 28:463–471, 2007. 15. Enneking WF, Horowitz M: The intra-articular effects of immobilization on the human knee, J Bone Joint Surg Am 54:973–985, 1972. 16. Erickson SJ, Prost RW, Timins ME: The “magic angle” effect: background physics and clinical relevance, Radiology 188:23–25, 1993. 17. Fanucci E, Masala S, Fabiano S, et al: Treatment of intermetatarsal Morton’s neuroma with alcohol injection under US guide: 10-month follow-up, Eur Radiol 14:514–518, 2004. 18. Forrester DM, Kerr R: Trauma to the foot, Radiol Clin North Am 28:422–433, 1990. 19. Genon MP, Chin TY, Bedi HS, Blackney MC: Radio-frequency ablation for the treatment of Morton’s neuroma, ANZ J Surg 80:583–585, 2010. 20. Giachino AA, Uhthoff HK: Intra-articular fractures of the calcaneus, J Bone Joint Surg Am 71:794–797, 1989. 21. Glaser C, Mendlik T, Dinges J et al: Global and regional reproducibility of T2 relaxation time measurements in human patellar cartilage, Magn Reson Med 56:527–534, 2006. 22. Glazenbrook KN, Guimaraes L, Murthy NS, et al: Identification of intraarticular and periarticular uric acid crystals with dualenergy CT: initial evaluation, Radiology 261:516–524, 2011. 23. Gyftopoulos S, Bencardino JT: Normal variants and pitfalls in MRI imaging of the ankle and foot, Magn Res Clin North Am 18:691–705, 2010. 24. Hapamaki V, Kiuru M, Koskinen S: Lisfranc fracture-dislocation in patients with multiple trauma: diagnosis with multidetector computed tomography, Foot Ankle Int 25:614–619, 2004. 25. Health risks from exposure to low levels of ionizing radiation: BEIR VII Phase 2, Washington, DC, 2006, National Academies Press. Available at http://www.nap.edu/openbook.php?record_ id=11340. Accessed August 12, 2012. 26. Holder LE: Clinical radionuclide bone imaging, Radiology 176:607–614, 1990. 27. Horger M, Bares R: The role of single-photon emission computed tomography/computed tomography in benign and malignant bone disease, Semin Nucl Med 36:286–294, 2006. 28. Hughes RJ, Ali K, Jones H, et al: Treatment of Morton’s neuroma with alcohol injection under sonographic guidance: follow-up of 101 cases, AJR Am J Roentgenol 188:1535–1539, 2007. 29. Juras V, Welsch G, Bar P, et al: Comparison of 3T and 7T MRI clinical sequences for ankle imaging, Eur J Radiol 81:1846–1850, 2012. 30. Keats TE, Anderson MW: Atlas of normal roentgen variants that may simulate disease, ed 8, Philadelphia, 2007, Mosby Elsevier, pp xxii, 1321. 31. Kramer J, Stiglbauer R, Engel A, et al: MR contrast arthrography (MRA) in osteochondritis dissecans, J Comput Assist Tomogr 16:254–260, 1992. 32. Laor T, Jaramillo D: MR insights into skeletal maturation: what is normal? Radiology 250:28–38, 2009. 33. Leumann A, Valderrabano V, Plaass C, et al: A novel imaging method for osteochondral lesions of the talus—comparison of SPECT-CT with MRI, Am J Sports Med 39:1095–1101, 2011. 34. Li X, Han ET, Ma CB, et al: In vivo 3T spiral imaging based multi-slice T(1rho) mapping of knee articular cartilage in osteoarthritis, Magn Reson Med 54:929–936, 2005. 35. Lindenfeld TN, Wojtys EM, Husain A: Surgical treatment of arthrofibrosis of the knee, Instr Course Lect 49:211–221, 2000.

36. Linklater J: MR imaging of ankle impingement lesions [review], Magn Reson Imaging Clin N Am 17:775–800, vii-viii, 2009. 37. Linklater JM: Imaging of sports injuries in the foot, AJR Am J Roentgenol 199:500–508, 2012. 38. Love C, Palestro CL: Radionclude imaging of infection, J Nucl Med Technol 32:47–57, 2004. 39. Mackinnon SE, Holder LE: The use of three-phase radionuclide bone scanning in the diagnosis of reflex sympathetic dystrophy, J Hand Surg Am 9:556–563, 1984. 40. Markovic M, Crichton K, Read JW, et al: Effectiveness of ultrasound-guided corticosteroid injection in the treatment of Morton’s neuroma, Foot Ankle Int 29:483–487, 2008. 41. Matin P: The appearance of bone scans following fractures, including immediate and long-term studies, J Nucl Med 20:1227–1231, 1979. 42. National Council on Radiation Protection and Measurements: Ionizing radiation exposure of the population of the United States. Report No. 93, Bethesda, Md, 1987, NCRP Publishers. 43. Meftah M, Katchis SD, Scharf SC, et al: SPECT/CT in the management of osteochondral lesions of the talus, Foot Ankle Int 32:233–238, 2011. 44. Mettler FA Jr, Huda W, Yoshizumi TT, Mahesh M: Effective doses in radiology and diagnostic nuclear medicine: a catalog, Radiology 248:254–263, 2008. 45. Mitchell MJ, Ho C, Howard BA, et al: Diagnostic imaging of trauma to the ankle and foot; IV: fractures of the calcaneus, J Foot Surg 28:479–484, 1989. 46. Morrison WB, Schweitzer ME, Wapner KL, et al: Osteomyelitis in feet of diabetics: clinical accuracy, surgical utility and costeffectiveness of MR imaging, Radiology 196:557–564, 1995. 47. Mosher TJ, Dardzinski BL: Cartilage MRI T2 relaxation time mapping: overview and applications, Semin Musculoskelet Radiol 8:355–368, 2004. 48. Mosher TJ, Dardzinski BL, Smith MB: Human articular cartilage: influence of aging and early symptomatic degeneration on the spatial variation of T2—preliminary findings at 3T, Radiology 214:259–266, 2000. 49. Mosher TJ, Zhang Z, Reddy R, et al: Knee articular cartilage damage in osteoarthritis; analysis of MRI image biomarker reproducibility in ACRIN-PA 4001 multicenter trial, Radiology 258:832–842, 2011. 50. Musson RE, Sawhney JS, Lamb L, et al: Ultrasound guided alcohol ablation of Morton’s neuroma, Foot Ankle Int 33:196– 201, 2012. 51. Myerson M, Christensen JC, Steck JK, Schuberth JM: Avascular necrosis of the foot and ankle, Foot Ankle Spec 5:128–136, 2012. 52. Nazarian LN, Schweitzer ME, Mandel S, et al: Increased softtissue blood flow in patients with reflex sympathetic dystrophy of the lower extremity revealed by power Doppler sonography, AJR Am J Roentgenol 171:1245–1250, 1998. 53. Noyes FR, Barber-Westin SD: Reconstruction of the anterior and posterior cruciate ligaments after knee dislocation. Use of early protected postoperative motion to decrease arthrofibrosis, Am J Sports Med 25:769–778, 1997. 54. Nunley JA, Vertullo CJ: Classification, investigation and management of midfoot sprains: Lisfranc injuries in the athlete, Am J Sports Med 30:871–878, 2002. 55. Pagenstert GI, Barg A, Leumann AG, et al: SPECT-CT in degenerative joint disease of the foot and ankle, J Bone Joint Surg Br 91:1191–1196, 2009. 56. Palestro CJ: The current role of gallium imaging in infection, Semin Nucl Med 24:128–141, 1994. 57. Pearce MS, Salotti JA, Little MP, et al: Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study, Lancet 380:499– 505, 2012. doi:10.1016/S0140-6736(12)60815-0.

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58. Potter HG, Deland JT, Gusmer PB, et al: Magnetic resonance imaging of the Lisfranc ligament of the foot, Foot Ankle Int 19:438–446, 1998. 59. Preidler KW, Peicha G, Lajtai G, et al: Conventional radiography, CT, and MR imaging in patients with hyperflexion injuries of the foot: diagnostic accuracy in the detection of bony and ligamentous changes, AJR Am J Roentgenol 173:1673–1677, 1999. 60. Raikin SM, Elias I, Dheer S, et al: Prediction of midfoot instability in the subtle Lisfranc injury, J Bone Joint Surg Am 91:892–899, 2009. 61. Rammelt S, Zwipp H: Talar neck and body fractures, Injury 40:120–135, 2009. 62. Reiter M, Ulreich N, Dirisamer A, et al: Colour and power Doppler sonography in symptomatic Achilles tendon disease, Int J Sports Med 25:301–305, 2004. 63. Robinson P, White LM, Salonen D, Ogilivie-Harris D: Anteromedial impingment of the ankle: using MR arthrography to assess the anteromedial recess, AJR Am J Roentgenol 178:601–604, 2002. 64. Rosenberg ZS, Feldman F, Singson RD, Price G: Peroneal tendon injury associated with calcaneal fractures: CT findings, AJR Am J Roengenol 149:125–129, 1987. 65. Scheuer LB, Black S: Developmental juvenile osteology, Oxford, England, 2000, Elsevier Academic Press. 66. Schmidt H, Köhler A, Zimmer EA, et al: Borderlands of normal and early pathologic findings in skeletal radiography, ed 4, New York, 1993, Thieme Medical Publishers. 67. Schutzer SF, Gossling HR: The treatment of reflex sympathetic dystrophy syndrome, J Bone Joint Surg Am 66:625–629, 1984. 68. Shabshin N, Schweitzer ME, Morrison WB, et al: High-signal T2 changes of the bone marrow of the foot and ankle in children:

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red marrow or traumatic changes? Pediatr Radiol 36:670–676, 2006. 69. Steinbach LS, Palmer WE, Schweitzer ME: Special focus session. MR arthrography, Radiographics 22:1223–1246, 2002. 70. Stiell IG, McKnight RD, Greenberg GH, et al: Implementation of the Ottawa ankle rules, JAMA 271:827–832, 1994. 71. Takao M, Sugano N, Nishii T, et al: Different magnetic resonance imaging features in two types of nontraumatic rabbit osteonecrosis models, Magn Reson Imaging 27:233–239, 2009. 72. Trattnig S, Welsch G, Domayer S, Apprich S: MR imaging of postoperative talar dome lesions, Semin Musculoskelet Radiol 16:177–184, 2012. [Epub Jul 31, 2012]. 73. Tsai TS, Evans HA, Donnelly LF, et al: Fat necrosis after trauma: a benign cause of palpable lumps in children, AJR Am J Roentgenol 169:1623–1626, 1997. 74. Wheaton AJ, Dodge GR, Borthakur A, et al: Detection of changes in articular cartilage proteoglycan by T(1rho) magnetic resonance imaging, J Orthop Res 23:102–108, 2005. 75. Wheeless CR 3rd: Reflex sympathetic dystrophy imaging [database on the Internet]. Wheeless’ textbook of orthopaedics. Available at http://www.wheelessonline.com/ortho/rsd_role_ of_bone_scans. Accessed July 12, 2012. 76. Williams T, Cullen N, Goldberg A, Singh D: SPECT-CT imaging of obscure foot and ankle pain, Foot Ankle Surg 18:30–33, 2012. 77. Yuj WT, Corosn JD, Baraniewski HM, et al: Osteomyelitis of the foot in diabetic patients: evaluation with plain film, 99 m Tc-MDP bone scintigraphy and MR imaging, AJR Am J Roentgenol 152:795–800, 1989. 78. Zubler V, Mengiardi B, Pfirmann CW, et al: Bone marrow changes on STIR MR images of asymptomatic feet and ankles, Eur Radiol 17:3066–3072, 2007.

Chapter

Conservative Treatment of the Foot Loretta B. Chou, Keith L. Wapner

CHAPTER CONTENTS GENERAL CONSIDERATIONS FOOT ORTHOSES Over-the-Counter Inserts Custom Foot Orthoses University of California Biomechanics Laboratory (UCBL) Foot Orthoses ANKLE–FOOT ORTHOSES APPLIANCES TREATMENT OF SPECIFIC DISORDERS Arthritis Tendon Disorders Heel Pain LESSER TOE DISORDERS Calluses and Corns Neuromas Bunionettes FIRST METATARSOPHALANGEAL JOINT Hallus Valgus Deformities Hallux Rigidus Sesamoid Disorders SHOE ANATOMY Types of Uppers Types of Lasts Types of Soles Types of Heels

121 122 122 123 124 124 125 125 125 126 126 127 127 128 128 128 128 128 128 129 130 132 132 133

GENERAL CONSIDERATIONS

Conservative treatment of foot and ankle disorders is important and often successful. Nonoperative regimens are relatively inexpensive and can be easily accomplished. The treating physician and surgeon should have thorough knowledge and understanding of the interaction of the foot and the shoe or device applied. Also, the biomechanics of normal foot function and the effect of the disease entity being treated should be analyzed. The anatomy of the normal shoe, the function of each component, and the effect of modifying each of these components must be appreciated.4,5,7,23,24 Furthermore, the practitioner should be familiar with over-the-counter devices as well

as with prescribed inserts and orthoses. The desired results of these devices on the foot and ankle should be fully recognized.8,15 The majority of adult forefoot deformities are acquired and the result of ill-fitting footwear. The most common of these deformities are hallux valgus, hammer toes, hard corns, interdigital neuromas, and plantar keratoses. The foremost component of conservative treatment begins with patient education about the effects of illfitting shoes and high heels. Forefoot loading is increased by the foot sliding forward into the toe box.22 Female patients may not comply with this initial treatment because ill-fitting shoes continue to be inherent in high fashion. It is often necessary to remind patients that, for daily dress, there is no other part of the body they would consider putting in a container whose shape is so drastically different from that body part. A useful tool is comparing an outline of the patient’s foot to his or her current footwear; this is usually effective in conveying this point (Fig. 4-1). Unless the patient is willing to accept that a change in footwear is indicated, both conservative and operative intervention may be futile. A proper-fitting shoe should accommodate the variations in the person’s foot.16 A set of consumer guidelines has been developed by the National Shoe Retailers Association, the Pedorthic Footwear Association, and the American Orthopaedic Foot and Ankle Society (Table 4-1). It is imperative to measure the shoe with the foot in a standing position because the width of the foot can increase up to two sizes and length by one-half size from the sitting to standing position. In addition, the foot should be measured late in the day because the foot expands in volume as much as 4% by the end of the day. Shoes should be fitted with the normally worn socks. There should be a full finger breadth between the tip of the shoe and the end of the longest toe, with the toes fully extended. Recently, walking- and running-type athletic shoes have made proper-fitting shoes more socially acceptable. Currently, women have more choices in the appropriate and acceptable type of footwear in many workplace environments. Acceptance of proper fit over trends in style may adequately relieve a patient’s symptoms. 121

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Figure 4-1 Comparing the outline of a foot to a woman’s dress shoe demonstrates the disparity in shape.

Table 4-1 10 Points of Proper Shoe Fit

1. Sizes vary among shoe brands and styles. Do not select shoes by the size marked inside the shoe. Judge the shoe by how it fits on your foot. 2. Select a shoe that conforms as nearly as possible to the shape of your foot. 3. Have your feet measured regularly. The size of your feet changes as you grow older. 4. Have both feet measured. For most persons, one foot is larger than the other. Fit to the larger foot. 5. Fit at the end of the day when the feet are largest. 6. Stand during the fitting process and check that there is adequate space ( 3 8 to 12 inch) for your longest toe at the end of each shoe. 7. Make sure the ball of your foot fits snugly into the widest part of the shoe. 8. Do not purchase shoes that feel too tight, expecting them to stretch. 9. Your heel should fit comfortably in the shoe with a minimum amount of slippage. 10. Walk in the shoe to make sure it fits and feels right. National Shoe Retailers Association, the Pedorthic Footwear Association, and the American Orthopedic Foot and Ankle Society: 10 Points of Proper Shoe Fit. Columbia, Md, National Shoe Retailers Association, 1995.

Modification of footwear or use of orthoses can be used to treat deformities of the foot. Disease can compromise motor function, joint function, skin integrity, sensation, and proprioception. Once the effects have been assessed, the appropriate modifications should be prescribed to attempt to restore normal function or protect the affected limb from further breakdown. FOOT ORTHOSES

Foot orthoses are devices that can be placed in a shoe to help accommodate deformities or to decrease abnormal pressure or stress at a specific site on the foot or ankle. 122

Orthoses function by applying a force on the body in a controlled manner to achieve a desired result, that is, transfer of pressure or restriction of motion. These devices range from simple shoe insoles to ankle–foot orthoses (AFOs). The popularity of shoe inserts for runners has led to many anecdotal claims about the efficacy of their use. However, there are few controlled studies to confirm these claims. It should be remembered that although orthoses may correct foot position and accommodate deformity, there is no evidence that an orthosis can correct or prevent the development of a hallux valgus or other structural deformities. Also, these devices may not prevent knee, hip, or back arthritis. The goals of foot orthoses include providing shock absorption, cushioning tender areas of the foot, relieving high plantar pressure areas by redistributing weight-bearing pressures covering the entire plantar surface, supporting and protecting healed fracture using the total-contact concept, controlling and supporting flexible deformities, limiting motion of joints, and accommodating fixed deformities with soft moldable materials.17 It is not always necessary to use a custom orthosis. For the accommodation of many forefoot- and heel-related problems, over-the-counter inserts may be effective in relieving symptoms, and at a lower cost. The abuse and overprescribing of custom inserts has led most medical insurance companies to deny payment for these inserts. Familiarity with the over-the-counter devices allows the treating physician to direct the patient on how to use these devices efficaciously and may be useful for initial treatment. Over-the-Counter Inserts With the advances in materials used in shoe manufacturing, it is often possible to accomplish many of the goals of orthosis without the expense of custom-molded inlays. Several companies offer padded insoles for shock absorption and heel cushioning (Fig. 4-2). Spenco, Viscopeds, Dr. Scholl’s, and other companies provide padded insoles and inlays that can provide relief for metatarsalgia and fat-pad atrophy. The addition of metatarsal supports, such as the Hapad longitudinal metatarsal pad on a cushioned inlay or in a shoe with a soft sole, can effectively relieve metatarsalgia or neuroma symptoms. Various heel inserts, such as Visco heels or Tuli heel cups, are often helpful in treating plantar heel pain. These devices are readily available through medical supply catalogs and are often found in pharmacies and athletic shoe stores. Patients should be educated on their proper placement and use. Once the patient has been evaluated and the desired correction chosen, the proper footwear should be selected. In some instances, this may be all that is needed. If additional correction is needed, off-the-shelf items should be considered. The cost to the patient is considerable for custom orthoses, and more insurance companies now refuse payment for any orthosis that does not cross the

Conservative Treatment of the Foot ■ Chapter 4

Figure 4-2 Over-the-counter inserts. A, Viscoped. B, Combination liner and Hapad metatarsal pad. C, Visco heel cushion. D, Full-length insole. E, Three-quarter–length insole.

Figure 4-3 Common types of custom orthoses. A, Plastazote insole, a soft material ideal for patients with rheumatoid arthritis or diabetes mellitus. B, Full-length orthosis with relief for the first metatarsal head, such as for sesamoiditis. C, Three-quarter– length foot orthosis indicated for hindfoot disorders. D, Rigid foot orthosis. E, Morton carbon fiber plate used for turf toe or hallux rigidus.

ankle joint. If adequate correction cannot be accomplished, custom orthoses can be prescribed. Custom Foot Orthoses If the patient has a deformity or disorder that is not amenable to treatment with an over-the-counter device, a custom orthoses may be appropriate. There are three general types of custom inserts: soft, semirigid, and rigid (Fig. 4-3).

Soft orthoses are made with materials that may include polyurethane foam, polyvinyl chloride foam, ethylene vinyl acetate, and latex foam. These materials are used when the effect is cushioning, impact absorption, and reducing shear forces of friction. This is particularly important for use in the insensate foot. Also, soft inserts are beneficial for use with fixed deformities, especially those with bony prominences. Soft materials can be used with semirigid material underneath to gain better mechanical properties. These inserts are generally thicker 123

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than the rigid orthoses and may require the use of an extra-depth shoe, depending on the pathology. Semirigid orthoses are the most commonly prescribed inserts. Unlike rigid orthoses, they offer shock absorption and some flexibility while still providing tensile strength and durability. They are used to support and stabilize flexible deformities and relieve pressure by weight transfer. Combinations of materials are often used; the inserts are generally thicker than rigid inserts and might require the patient to wear a deeper shoe. The materials used include leather, polyethylene compounds, closed or open cellular rubber compounds, cork, felt, and viscoelastic polymers. Rigid orthoses are used to decrease or control motion, such as in the treatment of arthritis of the midfoot or forefoot. The device stiffens the shoe and functions similar to a steel shank within the shoe. Of note, patients with plantar prominences or significant fat-pad atrophy might find these too uncomfortable to wear. A rigid orthosis is often prescribed to block pronation but may be no more effective than a semirigid device and may be more difficult to tolerate. Furthermore, rigid orthoses offer no shock-absorbing properties and should be avoided in patients with impaired sensation. The materials used are thermoplastics or carbon fiber. Custom orthoses are generally made from a foam impression of the feet of patients, in which the foot is pressed into the foam box evenly. The use of plantar pressure data obtained from new technology with the EMED-D pressure platform (Novel, Munich, Germany) with four sensors/cm2 yields superior off-loading capacity of insoles.20 University of California Biomechanics Laboratory (UCBL) Foot Orthoses Another type of foot orthosis is the UCBL insert, which controls flexible postural deformities by controlling the hindfoot.15 The orthosis should be molded with the heel in neutral position. To work successfully, the orthosis must be able to grasp the heel and prevent it from moving into valgus. By keeping the calcaneus in neutral position, the orthosis stiffens the transverse tarsal joints, and pronation and forefoot abduction can be diminished. It may be necessary to add medial posting to the heel and forefoot to keep the heel out of valgus. As medial posting is added, it may be necessary to lower the medial trim line to avoid impingement on the medial malleolus. With fxed deformities, such as arthritis of the midfoot, a UCBL insert can decrease motion and reduce pain. The foot is molded in situ, and the polypropylene should have a relief over the area of bony prominence. The orthosis can be lined with a material for pressure absorption, such as polyurethane foam (PPT) in the relief, and then the entire orthosis can be covered with a material such as polyethylene foam (Plastazote) for comfort (Fig. 4-4). 124

Figure 4-4 University of California Biomechanics Laboratory (UCBL) insert. A, Posterior view. B, Medial view. C, Posterior view of a patient with posterior tibial tendon dysfunction demonstrating hindfoot valgus, pes planus, and forefoot abduction. D, UCBL insert controlling foot deformity.

ANKLE–FOOT ORTHOSES

The most common type of orthosis that has proved useful in treating foot and ankle problems is the ankle–foot orthosis (AFO), made of either molded polypropylene or double-upright construction. AFOs can be made from double uprights attached to the shoe or molded polypropylene, either as a posterior shell or incorporated into a leather lacer (Arizona brace) (Fig. 4-5). The molded AFO is more potent in most instances. The AFO can be made with a fixed or hinged ankle. The orthosis is manufactured from a positive cast of the lower limb. Modifications can be made through reliefs over bony prominences to accommodate fit, and these can be lined with material to provide comfort and protect the foot and deformity. These modifications of the orthosis allow better control of deformities and expand the use of these orthoses to rigid as well as flexible deformities.

Conservative Treatment of the Foot ■ Chapter 4

Figure 4-5 Ankle–foot orthoses (AFOs). A, Double upright AFO for solid control of the ankle. B, Dorsi-assist AFO used for patients with footdrop or foot instability. C, Posterior leaf spring AFO, prefabricated for stable foot and ankle and supports dropfoot. D, Solid ankle AFO prescribed for ankle arthritis pain and control of the foot and ankle. E, Arizona-style AFO.

The molded AFO can provide stability to one or several joints of the foot and ankle complex. The trim lines can be modified, depending on the rigidity desired. To diminish ankle motion, the trim lines should extend anteriorly to the midline of the malleoli, but the foot plate can end proximal or just distal to the metatarsal heads. If intending to control subtalar or transverse tarsal motion, the trim lines can be cut behind the malleoli to allow some ankle motion. If intending to control midfoot arthritis, it may be necessary to use a full foot plate to prevent pain during normal gait. The Arizona brace AFO can be constructed with either lace or hook-and-loop (Velcro) closures. It provides stability to the hindfoot through three-point fixation similar to a short-leg cast. It has the advantage of being lower than a standard molded AFO and might have better patient acceptance. APPLIANCES

Various appliances have been developed for the treatment of forefoot deformities. Pads and cushions can be effective in relieving pain but will not correct deformities. Padding is effective only if the shoe is the correct shape and material. Pads take up additional space within

the shoe and can increase pressure if the toe box is too small. A toe crest can be effective in relieving pressure on the tips of the toes from hammer toe and mallet toe deformities. Corn and callus pads can also relieve pressure but are more effective if the overlying callus and corn tissue is removed and the shoe is stretched over the offending prominence or a wider toe box is used. Foam or gel (Silipos) sleeves can also effectively relieve pressure (Fig. 4-6). Toe separators can be used, but lamb’s wool can be equally effective between the toes and has the advantage of better absorption of moisture than the separators have. TREATMENT OF SPECIFIC DISORDERS

Arthritis The use of orthoses can be beneficial in the conservative therapy of arthritis of the foot and ankle by decreasing the pressure and motion across the affected joint. Orthoses should be custom molded and padded appropriately over any bony deformity. The patient must understand that an orthosis does not cure the problem but can offer a good means of controlling symptoms if he or she wishes to avoid an operation. 125

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Figure 4-6 Appliances used for forefoot deformities. A, Silipos digital cap to relieve pressure on tip of toe; digital pads for hard corns and hammer toes; toe separators for soft corns and hallux valgus. B, Toe cushion digital pads. C, Toe crests to elevate tips of toes for hammer and mallet toe deformities.

Ankle arthritis is treated with a molded AFO with a fixed ankle or Arizona brace. In patients with normal ankles and arthritis restricted to the subtalar joint, a molded AFO with a hinged ankle or a UCBL with high trim lines can be prescribed. A solid ankle cushion heel (SACH) and rocker-bottom sole on the shoe can increase the beneficial results of the orthosis and afford the patient a more normal gait pattern. Also, if a full foot plate is used, a rocker-bottom sole should be considered. In patients with a normal ankle joint, a hinged ankle orthosis may be used to allow ankle motion. Midfoot arthritis can be very painful and limit weightbearing activities. In general, arthritis in this area can be treated successfully with an orthotic device. This is achieved by stabilizing affected joints and still allowing function.21 The use of the UCBL or a carbon fiber plate may be indicated. More severe cases may be treated with an AFO and accommodative arch support. Patients often need to change the lacing pattern on their shoes to avoid pressure over dorsal spurs. A rocker-bottom sole may provide additional relief of pain and improved function. Tendon Disorders Chronic tendon tears can lead to significant pain and deformity if left untreated. Although surgical reconstruction has proved successful, some patients are not candidates for surgery because of concomitant medical conditions, whereas others do not wish to undergo surgical intervention. For chronic dysfunction of the Achilles, peroneal, and anterior and posterior tibial tendons, a custom-molded AFO1,7 or Arizona brace2 is capable of controlling symptoms. A custom articulated AFO may be one of the most potent ways to produce the greatest improvement in a flexible flatfoot deformity caused by posterior tibial tendon dysfunction (stage II). It allows some correction of the deformity and yet allows ankle motion.1 If necessary, these orthoses can be combined with a good-quality running shoe, rocker-bottom heel, or SACH to yield a better gait pattern. 126

Patients should understand that the purpose of the orthosis is to control the position of the foot and hopefully prevent progression of any deformity. If significant tendon damage is present, the orthosis will not be curative, and the patient can decide between using a permanent orthosis or having reconstructive surgery. In instances of tendinitis or early tendinosis, prolonged use of a molded AFO for ambulation can allow for healing.26 Bracing is continued until the swelling and tenderness have resolved, and then progressive mobilization and physical therapy are prescribed. If the objective changes have not resolved within 6 months, bracing has proved not curative, and the patient has the option of continuing with bracing as the elected form of treatment or choosing surgical correction. If healing occurs, then a patient may progress to less restrictive devices before returning to full activity without appropriate support. This may involve the use of a flexible foot orthosis. In patients with complete tendon rupture, orthoses can be used for producing pain relief and providing improved function. With chronic tendon tears or dysfunction, there can be a fixed deformity of the foot and ankle complex. For the orthosis to give the desired result, the mold must incorporate reliefs and padding over areas of deformities. An outflare heel may be needed to support the orthosis in the shoe and provide an adequate base of support in advanced deformities. For posterior tibial tendon dysfunction (PTTD), stage I may be treated with a cast or a removeable walking boot. Once acute symptoms subside, the patient can use a foot orthosis. Stage II deformity requires a more significant support, such as an over-the-counter ankle–stirrup brace, a UCBL orthosis, or an AFO.1,2,18 For a fixed deformity, or stage III deformity, an Arizona brace or AFO may be necessary to decrease pain, increase support, and improve function. Heel Pain Orthoses are frequently used to treat chronic heel pain syndrome.3,9 Because of the difficulty in diagnosing a

Conservative Treatment of the Foot ■ Chapter 4

specific cause of heel pain, recommendations for the type of inserts vary, from the use of a rigid orthosis to soft, pliable inserts.19 Some studies cast doubt on inserts being effective in the treatment of heel pain, but this might reflect the overprescription of these devices without the proper indications.12,13 In patients with atrophy of the heel fat pad, soft inserts and a well-padded shoe would be indicated. For chronic plantar fasciitis, soft inserts may be fruitful for shock absorption if overuse is a causative factor. Over-thecounter devices and appropriate shoes can be as effective as custom devices at significantly less cost. This treatment should be combined with other treatment modalities. Night splints for the treatment of chronic plantar fasciitis maintain foot position and have been shown to be a useful treatment.27 Although the original studies were performed using a custom-molded AFO with full foot plates, over-the-counter alternatives are now readily available and appear to be equally successful. The prefabricated foot orthosis has been found to increase the midfoot contact area, resulting in greater redistribution of force, thus reducing pressure under the heel.3 Recent finite element analysis of the heel model quantified the effects of insole conformity, insole thickness, and insole material on pressure relief.14 It appears that a conforming profile insert is the most important design for reducing heel-pad plantar pressure during walking. In addition, although thicker insoles give secondary pressure relief, conforming insoles should be made from stiffer material to avoid bottoming out. Flat insoles are less potent in reducing pressure.

LESSER TOE DISORDERS

Lesser toe deformities may be caused by ill-fitting footwear, such as high heels and narrow–toe box shoes. Other etiologies include those of traumatic, arthritic, idiopathic, or neuromuscular origin. Initial treatment consists of proper footwear, that is, a deeper and wider toe box. Stretching the shoe over the deformity or use of over-thecounter insoles with metatarsal pads or bars is effective. Severe or fixed deformities may need more significant treatment, such as rocker-bottom shoes, accommodative shoes, and a custom orthosis. Calluses and Corns Callus and corn formation occurs in response to excessive pressure over a bony prominence. This may be the consequence of a loss of the normal fat pad without deformity, secondary to pressure developing in response to deformity, or improper footwear that causes pressure on a bony prominence. Adequate management of these problems requires patient education and acceptance of appropriate shoes. Removal of the overlying hyperkeratotic tissue by paring the lesion produces significant relief of symptoms (Fig. 4-7).28 To prevent recurrence of the

B Figure 4-7 A, Number 17 blade for paring callus has no sharp points but rounded edges. B, Paring callus.

lesion, the shoe must be modified to keep pressure off the affected area. With plantar callosities, recurrence can be prevented by an appropriately sized metatarsal pad placed proximal to the metatarsal heads. The pad can be placed directly in the shoe or integrated in a custom foot orthosis. Patients prefer the later because it can be transferred from shoe to shoe. For dorsal corns, after the removal of the hyperkeratotic tissue, toe sleeves or toe crests may be effective (see Fig. 4-6). Stretching the toe box above the affected toe also helps relieve pressure and decreases the rate and incidence of corn formation. The commonly found corn over the dorsal and lateral aspects of the fifth toe without deformity is seen in patients wearing pointed dress shoes. Paring is initially effective; however, the lesion recurs if the footwear is not modified. If the patient is unwilling to change his or her footwear, the shoe should be prestretched with a shoemaker’s wand over the affected toe to help decrease the pressure. In this instance, surgery is rarely successful if the patient is unwilling to change his or her shoe style. The success of shoe modifications when accepted by the patient makes surgery rarely indicated. Hammer toe deformities can be treated, in part, with a metatarsal pad to relieve plantar pain. In addition, taping can add stability to the metatarsophalangeal joint with a hammer toe deformity. A strip of 1 4 -inch tape can be looped over the base of the toe to mimic the force of the intrinsic muscles and plantar plate (Fig. 4-8). This loop should be applied in the morning and removed at the end of the day. It can help patients with crossover toe deformities and subluxating hammer toe deformities. Another method is to use an over-the-counter toe sling or toe sleeve (see Fig. 4-6). 127

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Bunionettes Bunionettes can often be treated successfully by prestretching the shoe to avoid pressure over the bony prominence. A rounded or squared toe box can help prevent progression of the deformity.

FIRST METATARSOPHALANGEAL JOINT

Hallux Valgus Deformities

Figure 4-8 Toe taped for instability of the metatarsophalangeal joint. A, Dorsal view. B, Plantar view.

Hallux valgus deformities cannot be prevented or corrected by orthotic devices, and such devices should not be prescribed for that purpose.10 In patients with excessive pronation, an orthotic device to reduce pronation may be helpful and can relieve valgus stress on the great toe. Nonoperative treatment of hallux valgus revolves around the choice of proper footwear to accommodate the present deformity and prevent increased valgus pressure on the great toe to reduce progression.10 The choice of shoes is determined by the severity of the deformity. Pre-stretching of the shoe above the first metatarsophalangeal joint can be useful to relieve pressure. In moderate-to-severe deformities, an extra-wide shoe may be required. The shoe can be pre-stretched over the bunion, and a soft leather upper should be used. Hallux Rigidus

Figure 4-9 A, Diagram of location of Morton neuroma at the level of the transverse metatarsal ligament. B, Pad placement to relieve pressure proximal to the neuroma.

Neuromas Interdigital neuromas, or Morton neuromas, can often be successfully treated with a wider shoe and appropriately placed and sized metatarsal pad (Fig. 4-9). The effect is to prevent squeezing the metatarsal heads together, as with a narrow–toe box shoe, and providing a pad to spread the metatarsals and alleviate pressure on the affected neuroma. When using these pads, the patient should be instructed to break in these devices gradually. In most cases, patients start with a small size and may increase the size of the pad if their symptoms have not been relieved once they are wearing the pad all day. Or, a custom-molded orthosis may be help decrease symptoms. If a custom orthosis is prescribed, rigid material at the distal end of the orthosis should be avoided because it may aggravate symptoms. 128

Hallux rigidus is an arthritic condition, and nonoperative management involves accommodating the dorsal exostosis in a roomy comfortable shoe.25 A computational modeling approach with a three-dimensional finite element model of the first ray showed increased hallux pressures as much as 223% with restriction of metatarsophalangeal joint dorsiflexion, as with hallux rigidus.6 The increase in pressure can be reduced using flat insoles. Therefore initial treatment consists of wearing a stiff-soled shoe. A carbon fiber plate or custom orthosis with a Morton extension can be effective in decreasing symptoms (see Fig. 4-3F). Alternatively, a shoe with a steel shank and rocker bottom can be used. Symptoms from a prominent dorsal eminence may be treated with stretching of the toe box or use of an extra-depth shoe. Sesamoid Disorders The sesamoids can be afflicted by inflammation, injury, or fracture. Inflammation of the sesamoids is known as sesamoiditis, and the pain is localized to the medial or lateral sesamoid. Treatment consists of casting to decrease the severe acute pain. Then a metatarsal pad placed just proximal to the sesamoids can be used. Some patients benefit from a custom orthosis with a metatarsal pad for relief at the sesamoid (see Fig. 4-3C). Adjustments may be needed for recovery, which is generally expected.

Conservative Treatment of the Foot ■ Chapter 4

toe box, and vamp (Fig. 4-11). First, the upper is the top portion of the shoe, while the outsole and heel form the bottom of the shoe. The outsole and heel has contact with the ground. On the inside of the shoe is the insole, which contacts the plantar aspect of the foot. The shank extends from the heel breast (the front of the heel) to the ball of the shoe. The ball is the area under the metatarsal heads. The forepart extends from the ball to the tip, or end of the shoe. The toe box describes the height of the shoe at this level. The vamp, part of the upper, extends from the tip back over the ball and instep to the quarters, which join in the back of the shoe at the back seam. The Balmoral, or Bal last, shoe has the quarters meeting at the front of the throat of the shoe, with the vamp extending as the tongue beneath them. The Blucher last has the quarters loose at the inner edge and is made to be laced over the vamp and tongue.

SHOE ANATOMY

The shoe protects the foot from the external environment. It is also used to decrease pressure with weight bearing, and in cases of disease or deformities, shoes are helpful in decreasing shear forces, while supporting and accommodating the foot. The basic shoe types used are the traditional Oxfordtype shoe, which allows for 0.25- to 0.375-inch depth.17 The extra depth will allow for deformities and can accept an insert (Fig. 4-10). The shoe can be modified to improve propulsion, improve ambulation and motion, increase stability and proprioception, and to off-load areas of high pressure. These are accomplished by using flares, extended shanks, rocker soles, and relasting. The basic anatomy of the shoe includes standard parts of the upper, outsole, heel, insole, shank, ball, forepart,

Figure 4-10 A, Extra-depth shoe to accommodate forefoot deformity or for use with an orthosis. B, Extra-depth shoe with soft material for diabetes mellitus patients.

Foxing Eyelet row Vamp

Heel

Durable rubber outersole

Perforations for decorations

Quarter Welt

Flexion grooves Variablewidth lacing

Achilles notch Bal pattern Wing tip

Out sole

Top lines Lining Tongue Eyelet row Heel

Vamp

Heel breast

Pivot point

Lace lock

Upper

Heel collar

Exposed midsole

Heel counter

Durable rubber outersole

Stabilizing bar

Toe box

Flared heel

Toe wrap

Outersole Variableheight tread Contoured midsole Multidensity midsole

Sockliner Shock-absorbing midsole material

Flex point Stabilizing straps

Welt Blucher pattern

Figure 4-11 Structural components of the shoe.

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Lasting also describes the bottoming method that is used to attach the upper to the sole. Many techniques have been used, and one shoe can be lasted with more than one method, called combination lasting. Slip lasting involves sewing the upper pieces together moccasin style and gluing this to the midsole, giving a flexible construction. With board lasting, the upper is glued to a firm board, providing a stiff shoe; this method is often used in athletic shoes to decrease pronation. A combination last can provide stability from a board-lasted heel and flexibility from a slip-lasted forefoot (Fig. 4-13).

The last is the three-dimensional form that the upper of the shoe is made from (Fig. 4-12). Historically, all lasts were made by hand with no distinction between the left and right foot until about 1820. In the 1850s, the ability to duplicate shoe lasts, mold the leather uppers, and attach them to the soles by machine allowed the shoemaker to progress from making 1 pair of shoes per day to more than 600 per day. Over the next century and a half, the technology of manufacturing has rapidly progressed, just as the materials available have.15

Heel lift

Many different materials are available for constructing the upper of the shoe. Traditionally, leather has been used because of its durability, moldability, and breathability. Athletic shoes are made from soft nylon, mesh nylon, and canvas reinforced at the counter, toe box, or vamp with leather, rubber, or plastics for added stability. This combination allows the shoe to be lighter but still stable. The nylon mesh shoe may be useful in accommodating deformities of the lesser toes. Leather uppers can be stretched to accommodate forefoot deformities, but the extent of shoe deformation is limited. The toe box should have the height and width to properly fit the foot. If friction against the skin is a concern, as in a neuropathic foot, a heat-moldable foam (Thermold) upper may be used. Several patterns of lace stays are available, and each has its own advantage (Fig. 4-14). The Blucher pattern, with no seam across the instep, has the advantage of allowing easier entry into the shoe. The Bal pattern can provide

Ball girth

Waist gir

Instep g

Types of Uppers th

irth

ir el g

Toe spring Medial curvature Heel seat

l Ba

Lateral curvature Figure 4-12 Diagram of the last, the form on which the shoe is made. (Modified from Frey C: Shoe wear and pedorthic devices. In Lutter LD, Mizel MS, Pfeffer GB, editors: Orthopedic knowledge update: foot and ankle, Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

RIB LASTING

FLAT LASTING

PREWELTED LASTING

Tacks Staples Cement

Tacks Staples Cement Goodyear welt Cement welt Silhouwelt

FORCE LASTING TURN LASTING

Tacks or holding devices

McKay McKay welt Littleway Cement Nailed

Prewelt

Tacks Thread STRING LASTING

Turns

SLIP LASTING

Strings Thread

LASTING UP

Thread Cement Stitchdown One sole Two sole Three sole

MOCCASIN SEAM LASTING

String lasted (bottom view) Thread

Tacks Cement Thread Moccasin

LASTING DOWN

Slip lasted

Figure 4-13 Lasting techniques used to attach the upper to the sole. (Modified from Gould N: Footwear: shoes and shoe modifications. In Jahss MH, editor: Disorders of the foot and ankle: medical and surgical management, ed 2, vol 3, Philadelphia, 1991, WB Saunders, p 2885.)

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Blucher

Balmoral

U-Throat

Figure 4-14 Lace stay patterns. A, Blucher pattern, with no seam across the instep, has the advantage of allowing easy entry into the shoe. B, Balmoral pattern may provide more stability, but the entry is limited and might not accept an orthotic device. C, The U-throat or lace-toe pattern allows the shoe to open even wider and may be useful in accepting an orthosis or allowing entry into the shoe after hindfoot fusion. D, Diagram of patterns of lace stays.

Figure 4-15 Patterns of lacing. A, Variable for wide fit. B, Variable for narrow fit. C, Independent, using two laces. D, Crisscross to avoid bony prominences. E, High arch pattern to avoid lacing crossing top of foot. F, Pull-up pattern to allow relief of pressure on toes. G, Crisscross loop pattern to avoid heel blisters. (Modified from Frey C: Shoe wear and pedorthic devices. In Lutter LD, Mizel MS, Pfeffer GB, editors: Orthopedic knowledge update: foot and ankle, Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons, p 78.)

more stability, but the entry is limited and might not accept an orthotic device. The U-throat and lace-toe patterns allow the shoe to open even wider and may be useful in accepting an orthosis or allowing entry into the shoe after hindfoot fusion. Many lacing patterns can secure a better fit of the shoe (Fig. 4-15). Athletic shoes often have multiple eyelets to allow different lacing techniques. By changing the lacing

Figure 4-16 A, Shoemaker’s wand. B, Stretching shoe with the wand.

to avoid crossing the dorsum of the foot, pressure can be relieved over bony prominences or a high-arched foot. Wide or narrow feet can be secured by different lacing patterns. Once the proper material, shape, and lacing pattern of the shoe have been determined, it may still be necessary to stretch the upper to avoid pressure over bony deformities. With the patient standing and bearing full weight on the affected foot, the area of impingement can be identified and marked. A shoemaker’s wand can stretch the shoe at this area (Fig. 4-16). 131

Part I ■ General Considerations

toe box. Women’s dress shoes can simulate a straight last on the medial side and have the point of the toe box at the end of the great toe. The outflare last, or reverse last, flares to the lateral side of the shoe and is often used after treatment for metatarsus adductus. The inflare last curves medially and is used in athletic shoes, with a 7-degree curve to allow greater mobility of the foot.11

Types of Lasts Shoe manufacturers have many different lasts, and there is great variation in the fit of shoes that are labeled with the same size. A shoe manufacturer might have 30 to 60 active last styles with 80 to 90 sizes for as many as 5000 different lasts.15 Thus it is difficult to define a normal last. The concept of a corrective last is not accurate because the last cannot correct a deformity. Lasts come in several general categories (Fig. 4-17). A conventional last is made in right- and left-foot shapes. A straight last has a straight medial border from heel to toe, without curving at the

Types of Soles Traditionally, soles of shoes were constructed of leather. In dress shoes, this material is still commonly used. Soles in athletic, work, and recreational shoes are generally made from rubber compounds. Microcellular blown rubber compounds and polyurethane are used for midsole and wedges. Black carbon rubber and styrene-butadiene are very hard-wearing compounds used for outsoles. Ethyl vinyl acetate is also commonly used in running shoes for its flexibility and impact-absorbing properties. Manufacturers often combine the blown rubber for impact resistance covered by black carbon rubber for wear on the outsole. The superior impact absorption of these rubber and synthetic materials can be used to decrease pressure and loading of the foot and ankle. As a result, many manufacturers now offer dress shoes with soles made of these materials. Traction between the shoe and the floor can be influenced by the material of the sole and the pattern on the outsole. Various patterns have been developed for different sports. The pattern and amount of friction can also influence how well a patient with balance or proprioceptive loss can tolerate a shoe. Too much friction can cause a patient to stumble, whereas loss of friction with a slick surface can be equally dangerous. The outsole of the shoe can be modified (Fig. 4-18). A medial wedge can be used to decrease forefoot eversion,

Figure 4-17 Lasts. A, Conventional. B, Straight. C, Outflare. D, Inflare. (Modified from Gould N: Footwear: Shoes and shoe modifications. In Jahss MH, editor: Disorders of the foot and ankle: medical and surgical management, ed 2, vol 3, Philadelphia, 1991, WB Saunders, p 2903.)

Figure 4-18 Outsole modifications. A, Lateral sole wedge. B, Medial sole wedge. C, Mayo metatarsal bar. D, Flush’s metatarsal bar. E, Denver heel. F, Hauser bar. G, Rocker sole. H, Extended rocker sole. (Modified from Gould N: Footwear: shoes and shoe modifications. In Jahss MH, editor: Disorders of the foot and ankle: medical and surgical management, ed 2, vol 3, Philadelphia, 1991, WB Saunders, p 2907.)

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and a lateral wedge can be used to decrease forefoot inversion in a flexible foot. Various metatarsal bars have been described for treating metatarsalgia. The principle is to have the bar placed proximal to the metatarsal heads to adequately relieve pressure under the area of greatest loading. Rocker soles are often useful in unloading the forefoot and decreasing the need for metatarsophalangeal joint dorsiflexion. Rocker soles allow a better gait pattern when used with rigid bracing of the foot and ankle (Fig. 4-19). There are five basic types of rocker soles.17,23 The mild rocker sole is the most popular type and results in notable improvement in mild metatarsal pressure and gait by increasing forward propulsion. The other types

include heel-to-toe, toe-only, severe angle, negative heel, and double-rocker soles. Types of Heels The materials used for the heel are similar to those used for the sole. The decision about the material used should stem from the demands placed on the foot. Many modifications of the heel have been described (Fig. 4-20). The Thomas and Stone heels were used to help prevent pronation. Medial and lateral heel wedges help block heel eversion and inversion, respectively. These wedges should be used with a rigid heel counter to effectively grip the heel and produce the desired effect. External heel wedges have

Figure 4-19 Variations of rocker soles. A, Mild rocker sole is the most common type used to relieve metatarsal pressure and assist in gait. B, Heel-to-toe sole used for increased propulsion at toe-off, decreased pressure on heel strike, and reduced need for ankle motion, such as for patients with ankle or subtalar fusion. C, Toe-only rocker sole is used for patients with forefoot problems, because it increases weight bearing proximal to the metatarsal heads. D, Severe angle is prescribed for extreme relief of metatarsal head or toe tip ulcerations. E, Negative heel accommodates a foot fixed in dorsiflexion or relieves forefoot pressures. F, Double sole is helpful for patients with midfoot pathology, such as Charcot foot. (Redrawn from Janisse DJ, Janisse E: Shoe modification and the use of orthoses in the treatment of foot and ankle pathology. J Am Acad Orthop Surg 16:152-158, 2008.)

Figure 4-20 Heel modifications. A, Thomas heel. B, Stone heel. C, Reverse Thomas and Stone heel. D, Flare heel. E, Offset heel. F, Plantar flexion heel. G, Medial wedge heel. H, Lateral wedge heel. (Modified from Gould N: Footwear: shoes and shoe modifications. In Jahss MH, editor: Disorders of the foot and ankle: medical and surgical management, ed 2, vol 3, Philadelphia, 1991, WB Saunders, p 2906.)

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an advantage over inserts by not raising the heel out of the counter, which allows for a better grasp of the heel. Flared and offset heels allow for a broader base of support in walking. These heels decrease the amount of subtalar motion in patients with arthritis. A lateral flare can help prevent ankle sprains in patients with chronic instability. The offset heel is often useful with bracing in patients with advanced hindfoot deformities. The SACH, or plantar flexion heel, is also useful with bracing when ankle motion is lost (see Fig. 4-20G and H). It uses a wedge of soft compressible material within the heel. It may be combined with a rocker sole to compensate for decreased ankle dorsiflexion and plantar flexion. The degree of rocker-bottom effect is controlled by the height of the heel, thickness of the wedge, and position of the rocker bottom. Heel lifts are used to compensate for leg-length discrepancy. These may be all external or combined with an internal device on the shoe. These are often useful as a temporary device when the opposite extremity is placed in a prefabricated walking cast. These walking casts usually have a built-in rocker bottom and are higher than the patient’s normal shoe. Patients who have difficulty with this temporary leg-length discrepancy can be helped by application of a lift to the opposite shoe to compensate. A heel lift may also be used when a SACH and rocker bottom have been applied to the opposite shoe. When the outsole and heel of the shoe for postural abnormalities are modified, the shank of the shoe should afford some flexibility to allow the foot to respond to the correction applied. When arthritic conditions of the midfoot and forefoot are treated, the shank should be stiffened to decrease the motion of the foot. The advances in shoe manufacturing and materials have led to a new popularity of running and walking shoes. In general, these shoes allow better fit of the forefoot and greater cushioning of the foot and ankle. The popularity of these shoes helps in the treatment of many foot and ankle problems without the need to prescribe the traditional orthopaedic Oxford. Patient acceptance of this type of footwear affords greater compliance with treatment. REFERENCES 1. Alvarez RG, Marini A, Schmitt C, Saltzman CL: Stage I and II posterior tibial tendon dysfunction treated by a structured nonoperative management protocol: an orthosis and exercise program, Foot Ankle Int 27:2–8, 2006. 2. Augustin JF, Lin SS, Berberian WA, Johnson JE: Nonoperative treatment of adult acquired flat foot with the Arizona brace, Foot Ankle Clin 8:491–502, 2003. 3. Bonanno DR, Landorf KB, Menz HB: Pressure-relieving properties of various shoe inserts in older people with plantar heel pain, Gait Posture 33:385–389, 2011. 4. Bordelon RL: Correction of hypermobile flatfoot in children by molded inserts, Foot Ankle Int 1:143–150, 1980. 5. Bordelon RL: Hypermobile flatfoot in children. Comprehension, evaluation, and treatment, Clin Orthop Relat Res 181:7–14, 1983.

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6. Budhabhatti SP, Erdemir A, Petre M, et al: Finite element modeling of the first ray of the foot: a tool for the design of interventions, J Biomech Eng 129:750–756, 2007. 7. Cavanagh PR, Ulbrecht JS, Zanine W, et al: A method for investigation of the effects of outsole modifications in therapeutic footwear, Foot Ankle Int 17:706–708, 1996. 8. Chao W, Wapner KL, Lee TH, et al: Nonoperative treatment of posterior tibial tendon dysfunction, Foot Ankle Int 17:736–741, 1996. 9. Drake M, Bittenbender C, Boyles RE: The short-term effects of treating plantar fasciitis with a temporary custom foot orthosis and stretching, J Orthop Sports Phys Ther 41:221–231, 2011. 10. Easley ME, Trnka HJ: Current concepts review: hallux valgus part 1: pathomechanics, clinical assessment, and nonoperative management, Foot Ankle Int 28:654–659, 2007. 11. Frey C: Shoe wear and pedorthic devices. In Lutter LD, Mizel MS, Pfeffer GB, editors: Orthopaedic knowledge update: foot and ankle, Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons. 12. Gill LH: Plantar fasciitis: diagnosis and conservative management, J Am Acad Orthop Surg 5:109–117, 1997. 13. Gill LH, Kiebzak GM: Outcome of nonsurgical treatment for plantar fasciitis, Foot Ankle Int 17:527–532, 1996. 14. Goske S, Erdemir A, Petre M, et al: Reduction of plantar heel pressures: insole design using finite element analysis, J Biomech 39:2363–2370, 2006. 15. Gould N: Footwear: Shoes and shoe modifications. In Jahss MH, editor: Disorders of the foot and ankle: medical and surgical management, ed 2, vol 3. Philadelphia, 1991, WB Saunders, pp 73–88. 16. Janisse DJ: The art and science of fitting shoes, Foot Ankle Int 13:257–262, 1992. 17. Janisse DJ, Janisse E: Shoe modification and the use of orthoses in the treatment of foot and ankle pathology, J Am Acad Orthop Surg 16:152–158, 2008. 18. Krause F, Bosshard A, Lehmann O, Weber M: Shell brace for stage II posterior tibial tendon insufficiency, Foot Ankle Int 29: 1095–1100, 2008. 19. Mizel MS, Marymount JV, Trepman E: Treatment of plantar fasciitis with a night splint and shoe modification consisting of a steel shank and anterior rocker bottom, Foot Ankle Int 17: 732–735, 1996. 20. Owings TM, Woerner JL, Frampton JD, et al: Custom therapeutic insoles based on both foot shape and plantar pressure measurement provide enhanced pressure relief, Diabetes Care 31: 839–844, 2008. 21. Patel A, Rao S, Nawoczenski D, et al: Midfoot arthritis, J Am Acad Orthop Surg 18:417–425, 2010. 22. Perera AM, Mason L, Stephens MM: The pathogenesis of hallux valgus, J Bone Joint Surg Am 93:1650–1661, 2011. 23. Perry JE, Ulbrecht JS, Derr JA, et al: The use of running shoes to reduce plantar pressures in patients who have diabetes, J Bone Joint Surg Am 77:1819–1826, 1995. 24. Rozema A, Ulbrecht MB, Pammer SE, et al: In-shoe plantar pressures during activities of daily living: implications for therapeutic footwear design, Foot Ankle Int 17:352–359, 1996. 25. Shurnas PS: Hallux rigidus: etiology, biomechanics, and non operative treatment, Foot Ankle Clin 14:1–8, 2009. 26. Solan M, Davies M: Management of insertional tendinopathy of the Achilles tendon, Foot Ankle Clin 12:597–615, 2007. 27. Wapner KL, Sharkey PF: The use of night splints for treatment of recalcitrant plantar fasciitis, Foot Ankle Int 12:135–137, 1991. 28. Young MJ, Cavanagh PR, Thomas G, et al: The effect of callus removal on dynamic foot pressures in diabetic patients, Diabet Med 9:55–57, 1992.

Chapter

Anesthesia Jeffrey Swenson, Jennifer J. Davis

CHAPTER CONTENTS OVERVIEW A CHANGING ROLE FOR OPIOIDS MULTIMODAL ANALGESIA COMPONENTS OF MULTIMODAL ANALGESIA Nonsteroidal Antiinflammatory Drugs Acetaminophen and Paracetamol Combining Paracetamol (Acetaminophen) and Nonsteroidal Antiinflammatory Drugs Pregabalin and Gabapentin Opioid Agonists Combined Opioid Agonist–Monoamine Reuptake Inhibitors PATIENTS WHO REQUIRE SPECIAL CONSIDERATION Obstructive Sleep Apnea Chronic Opioid-Consuming Patients REGIONAL ANESTHESIA Ultrasound-Guided Peripheral Nerve Blocks Continuous Peripheral Nerve Block (Video Clip 7) Nerve Blocks above the Knee (Video Clip 6) Nerve Blocks below the Knee (Video Clip 5) NERVE BLOCK COMPLICATIONS Intravascular Injection of Local Anesthetic Nerve Injury Infection SUMMARY

135 135 135 136 136 137 137 137 138 138 138 138 139 140 140 140 141 144 147 147 148 148 148

OVERVIEW

This chapter contains a review of the pharmacologic and procedural therapies available for pain control after foot and ankle surgery. The focus is on new techniques and pharmacologic agents. Recent progress in acute pain management is a product of changing patient demographics as well as advances in technology. For several years, opioids have been used as a primary therapy to provide postoperative analgesia. However, as the population ages and has a higher rate of obesity, the side effects of opioids become more concerning. Opioidinduced respiratory depression is a life-threatening risk that increases with age and obesity. Nausea, vomiting,

constipation, and pruritus are major sources of patient dissatisfaction that must be overcome as more procedures are performed in an ambulatory setting. Finally, many more patients are now treated with opioids for chronic pain conditions. For patients consuming opioids chronically, efficacy in the acute pain setting is markedly reduced. All of these factors contribute to a growing interest in finding effective methods to reduce opioid requirements by using “nonopioid” alternatives for pain control. A CHANGING ROLE FOR OPIOIDS

The American Society of Anesthesiologists and the American College of Chest Physicians have both published guidelines for the perioperative management of patients with known or suspected obstructive sleep apnea (OSA).2,45 These guidelines highlight the association of opioids with adverse respiratory events during the postoperative period. They also stress the importance of screening patients preoperatively for signs or symptoms of OSA because up to 70% of patients who suffer from this disorder have not been diagnosed at the time of surgery.37 A common theme in all guidelines for perioperative management of OSA is the need to reduce or eliminate opioid analgesics during the postoperative period. The rate of opioid prescription in the United States has changed dramatically in response to increased pressure placed on physicians to treat pain. The Centers for Disease Control and Prevention report that the distribution of prescription opioids through the pharmaceutical supply chain increased more than 600% between 1997 and 2007.73 Since 2003, opioid analgesics have been the cause of more deaths from overdose than cocaine and heroin combined.73 This increase in opioid abuse and accidental deaths has also been a catalyst for efforts to decrease the role of opioids as the primary analgesics after surgery. MULTIMODAL ANALGESIA

Multimodal analgesia is the practice of combining more than one type of analgesic to optimize pain control while minimizing the adverse effects of individual agents.70,90,109 135

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Table 5-1 Drug Categories That Can Be Used Concurrently in Multimodal Analgesia Drug Category Gabapentinoids Pregabalin

NSAIDs Ibuprofen (oral)

Mechanism of Action

Dosing

Special Considerations

Voltage-dependent calcium channels at central/ peripheral nerves

75-100 mg bid

Inhibition of cyclooxygenase (nonspecific)

400-800 mg tid

Reduces opioid use and opioid side effects May reduce chronic pain at surgery site NSAIDs (nonspecific): Potential renal toxicity Platelet inhibition Cardiovascular risk Gastric mucosa effects Potent analgesic Higher gastric mucosa Toxicity compared with other NSAIDs: Reduced platelet effect Reduced gastric toxicity Cardiovascular risk Potential renal toxicity Well tolerated Caution with hepatic disease

Ketorolac (IV)

15-30 mg qid

Celecoxib

COX-2 specific

Acetaminophen

CNS inhibition of cyclooxygenase, modulation of central serotonin

Acetaminophen (IV) (paracetamol) Acetaminophen (oral) Combined Mu Agonist/ Norepinephrine-Serotonin Reuptake Inhibitors Tramadol Tapentadol

200 mg bid

Up to 1 g qid Up to 1 g qid Mu agonist/inhibition of norepinephrine-serotonin reuptake Inhibits both serotonin and norepinephrine reuptake Norepinephrine reuptake inhibition only

Reliable plasma levels in the perioperative period May not produce therapeutic levels in perioperative period Caution with other serotonin reuptake inhibitors such as antidepressants

50-100 mg qid

Lower risk of tolerance, dependence

50-75 mg qid

Lower risk of tolerance, dependence, nausea, constipation

bid, Two times per day; COX-2, cyclooxygenase-2; CNS, central nervous system; IV, intravenous; NSAIDs, nonsteroidal antiiflammatory drugs; qid, four times per day; tid, three times per day.

It is a promising way to decrease or eliminate the role of opioids in postoperative pain control. A number of pharmacologic agents can be used concurrently to provide analgesia, including nonsteroidal antiinflammatory drugs (NSAIDs), acetaminophen, gabapentinoids, mu agonists, and serotonin/norepinephrine reuptake inhibitors (Table 5-1). Peripheral nerve blocks also provide a major component in reducing opioid requirements.48 The increased availability of high-resolution ultrasound has greatly facilitated the use of peripheral nerve blocks as a component of multimodal analgesia. COMPONENTS OF MULTIMODAL ANALGESIA

Nonsteroidal Antiinflammatory Drugs Nonsteroidal antiinflammatory drugs belong to broad class of medications used to treat pain and inflammation. The mechanism of action for these agents is to block the production of prostaglandins. This effect is achieved by the inhibition of cyclooxygenase. At least two isoenzymes 136

(COX-1, COX-2) have been identified for cyclooxygenase. The COX-1 isoenzyme has been called a “housekeeping” enzyme responsible for maintaining physiologic functions of the gastrointestinal tract, platelets, and kidneys. The COX-2 isoenzyme is involved primarily in production of prostaglandins that intensify the inflammatory response.15 Nonspecific NSAIDs are effective for relieving pain and inflammation but are also associated with platelet dysfunction, gastrointestinal toxicity, renal toxicity, cardiovascular risk, and the potential for impaired bone and connective tissue healing. The introduction of COX-2– specific NSAIDs (referred to as coxibs) has been an attempt to reduce or eliminate two of these unwanted effects, namely, gastrointestinal and platelet effects.43,88 At present, celecoxib is the only COX-2–specific NSAID available for use in the United States. Other coxibs, such as rofecoxib and valdecoxib, have been removed amid concerns that they are associated with increased cardiovascular risk. Clinicians should be mindful that all NSAIDs (COX-2–specific and nonspecific NSAIDs) must

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be used with caution in patients at increased risk of cardiovascular disease.63,85 Gastrointestinal side effects of NSAIDs are more common in older patients, those with a prior history of peptic ulcer disease, and those receiving aspirin.91 The improved gastrointestinal tolerance with celecoxib and other COX-2–specific NSAIDs is expected because these drugs were developed in part to reduce gastrointestinal side effects. When using nonspecific COX inhibitors, however, the incidence of gastrointestinal side effects can also be significantly reduced with proton pump inhibitors.52,57 Although all NSAIDs can be associated with cardiovascular risk, the COX-2–specific drugs have been the subject of most recent reports of edema, ventricular dysfunction, and cardiac ischemia. The cardiovascular risk associated with these drugs is thought to be partly the result of a relative imbalance of prostacyclin and thromboxane.49 At present, only one COX-2 inhibitor (celecoxib) remains approved for use in the United States by the Food and Drug Administration (FDA). The early clinical evidence suggesting cardiovascular risk related to NSAIDs was largely associated with prolonged use; however, recent studies suggest that increased cardiovascular risk occurs almost immediately after initiation of therapy.85 Bone and soft tissue healing are additional concerns with the use of all NSAIDs. Reviews of in vitro and animal studies document changes in bone and soft tissue healing associated with NSAID use.16,78 Although clinical data do not consistently show outcome differences in patients treated with NSAIDs,51 there is enough evidence to justify careful consideration before their use. A reasonable approach for the use of NSAIDs in the perioperative period is to limit or avoid their use in patient populations or procedures that typically have high rates of failure or nonunion.6,75 A common question that arises with the use of celecoxib is whether it can be used safely in patients who have a history of allergy to sulfonamide antibiotics. Metaanalyses suggest there is a greater incidence of allergic reactions, in general, among patients with sulfonamide hypersensitivity; however, there is not an increased risk specific to celecoxib.72,92 Acetaminophen and Paracetamol Acetaminophen and its parenteral form, paracetamol, are commonly used in conjunction with opioids for postoperative analgesia. The mechanisms of action for these drugs is not well defined but has been linked to cyclooxygenase inhibition in the central nervous system (CNS) as well as central modulation of the serotonin system.13,44 Both agents are well tolerated, with relatively few side effects. Paracetamol, the intravenous formulation of acetaminophen, was approved for use in the United States in 2011. A unique application for paracetamol is for patients

who cannot take oral acetaminophen. There seems to be little difference in analgesic efficacy between oral and parenteral forms of acetaminophen if therapeutic levels are achieved. However, at least two studies comparing plasma levels in surgical patients after preoperative dosing of oral acetaminophen or parenteral paracetamol show therapeutic plasma levels are reliably achieved only when intravenous paracetamol is used.17,99 In fact, less than 50% of subjects receiving oral doses achieved therapeutic plasma concentrations.17 Combining Paracetamol (Acetaminophen) and Nonsteroidal Antiinflammatory Drugs An important aspect of multimodal analgesia that can be easily overlooked is the simple practice of combining acetaminophen (or paracetamol) with an NSAID. This approach has been evaluated in the setting of paracetamol alone versus the combination as well as NSAIDs alone versus the combination. In both situations, there were significant reductions in both pain scores and opioid requirements.55,68 An especially appealing aspect of this practice is that many of the studies showing improved pain control involved ibuprofen and acetaminophen, which are inexpensive and easily accessible by patients. Pregabalin and Gabapentin Pregabalin and gabapentin are unique drugs that are structurally related to gamma-aminobutyric acid. They act by binding to voltage-dependent calcium channels in the central and peripheral nervous system and thereby alter the release of excitatory neurotransmitters.40 These actions produce anticonvulsant, antihyperalgesic, and anxiolytic effects.110 Although both drugs are used for pain control, pre gabalin has some unique characteristics that make it well suited for postoperative analgesia. Compared with gabapentin, pregabalin has faster onset, more predictable plasma concentrations, and fewer side effects.40 Pregabalin has been studied in a number of perioperative settings and found to reduce opioid requirements as well as opioid-related side effects.4,14,35,97 The most commonly reported side effects of pregabalin are dizziness and somnolence. Clinical effect is achieved rapidly after oral administration of pregabalin. There is early onset of analgesia, and peak plasma concentrations are reached within 1 hour.10 Pregabalin has been studied in a range of doses as an adjunct for postoperative pain control. Although a typical starting dose is 75 mg bid, effective doses for reducing perioperative opioid requirements ranged up to 150 mg bid.58,110 A unique finding in patients treated with pregabalin in the perioperative period is a lower incidence of chronic pain associated with surgery. For example, patients treated with pregabalin after total knee arthroplasty had a significantly lower incidence of chronic neuropathic pain 137

Part I ■ General Considerations

at 6 months compared with controls.20 Likewise, functional outcomes and pain scores at 3 months after lumbar diskectomy were improved in patients treated perioperatively with pregabalin.19 Opioid Agonists Opioids produce analgesia through agonist activity at mu receptors in the central nervous system. However, in addition to analgesia, all opioids are associated with abuse potential, respiratory depression, nausea, constipation, and pruritus. Despite these unwanted side effects, opioids still are the primary analgesics prescribed by most clinicians. Anecdotal differences with respect to nausea, pruritus, and analgesic efficacy are a common reason for “opioid swapping” in clinical practice. However, the continued publication of reviews on the management of opioidrelated side effects suggests that no particular opioid has emerged as “clearly superior” with respect to side-effect profile.8,93 Opioids such as oxycodone, hydrocodone, and hydromorphone may differ with respect to potency and dosing interval; however, they are surprisingly similar in terms of analgesic efficacy and side-effect profile when compared in equipotent doses. The most successful measures for reducing opioidrelated side effects have resulted from reducing their dose requirements through multimodal analgesia.61 Combined Opioid Agonist–Monoamine Reuptake Inhibitors Tramadol and tapentadol are analgesics that act through a dual mechanism of opioid receptor activity and monoamine reuptake inhibition.67 In the case of tramadol, reuptake of both serotonin and norepinephrine are inhibited.32 For tapentadol, only norepinephrine levels are affected.38 A notable difference between tramadol and tapentadol and equipotent doses of traditional opioids is their potential for respiratory depression. These drugs do not rely on mu agonist activity as their sole mechanism for analgesia. As such, there is some evidence to suggest they may associated with less respiratory depression than conventional opioids at doses providing comparable levels of analgesia.53,76,77,87 Respiratory depression is always a concern when treating postoperative pain, and certain patient populations are especially at risk. Thus tramadol and tapentadol, while still associated with respiratory depression, may be preferable for patients at risk for obstructive sleep apnea or with other specific risk factors for respiratory depression. A unique characteristic of tapentadol is its low incidence of gastrointestinal side effects. Compared with other commonly prescribed opioids, tapentadol causes significantly less nausea, vomiting, and constipation.47,67 Thus, in patients in whom these symptoms are problematic, tapentadol may be especially advantageous. This 138

decrease in nausea and other gastrointestinal side effects has not been observed to the same degree for tramadol. Serotonin and norepinephrine reuptake inhibition have been shown to produce analgesia even in the absence of mu receptor activity. Duloxetine, a selective serotonin and norepinephrine reuptake inhibitor, has been reported to significantly reduce opioid requirements by more than 30% after knee arthroplasty.50 In light of their effect on monoamine reuptake inhibition, caution should be used before prescribing tramadol or tapentadol in combination with other drugs that might increase CNS serotonin or norepinephrine concentrations. Serotonin syndrome is a potentially life-threatening condition that may develop in patients treated with drugs whose mechanism of action involves increased CNS serotonin and norepinephrine levels.67 This syndrome is also known to be associated with the use of this class of drugs in patients treated with opioid analgesics. PATIENTS WHO REQUIRE SPECIAL CONSIDERATION

Obstructive Sleep Apnea Obstructive sleep apnea is a breathing disorder that is often not diagnosed until surgery. In a recent review, it was reported that more than 70% of patients with OSA were not diagnosed until their preoperative eval uation.2 Unfortunately, OSA may first be detected in the perioperative period as a result of a respiratory or cardiac complication. After surgery, OSA may manifest as hypoxemia, cardiac ischemia, delirium, and arrhythmias. Because of its association with obesity and increased age, the prevalence of OSA has increased steadily in recent years. The American College of Chest Physicians and the American Society of Anesthesiologists (ASA) have outlined treatment guidelines for screening and perioperative management of OSA patients.2,45 Their recommendations include specific aspects of the preoperative, intraoperative, and postoperative care. In the preoperative evaluation, it is important to conduct a directed history and physical examination in all patients because many with OSA are undiagnosed at the time of surgery. Specific questionnaires have been developed to screen for OSA. These include the STOPBANG and ASA questionnaires that stratify patients as low or high risk for OSA. The STOP-BANG scoring system uses a mnemonic to present an eight-point evaluation validated by Chung et al.27 Specifically, the questionnaire identifies loud snoring (S), daytime tiredness (T), observed apnea during sleep (O), and treatment for high blood pressure (P). The other characteristics associated with OSA are body mass index (BMI) greater than 35 kg/ m2 (B), age greater than 50 years (A), neck circumference greater than 40 cm (N), and male gender (G). Patients with three or more of these eight criteria are considered high risk for OSA.

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The intraoperative management of patients with OSA is focused on avoiding anesthetics that have a prolonged effect on recovery of spontaneous ventilation. Thus it seems reasonable to favor regional over general anesthesia and to use short-acting anesthetics whenever possible. However, despite the logic of these strategies, there are no prospective trials showing improved outcomes with any specific anesthetic technique.28 There is consensus, however, about the practice of minimizing the use of opioids in the perioperative period. Patients with OSA have an increased sensitivity to respiratory depression caused by opioid analgesics compared with controls without OSA.18,103 An important question with respect to postoperative management of OSA patients is whether they should be candidates for ambulatory surgery. There is little prospective information on outcome for OSA patients having outpatient surgery. The ASA has suggested that management of OSA patients should be based on three factors. These factors include the severity of their OSA symptoms, the scale of surgery/anesthesia performed, and the anticipated need for postoperative opioid analgesics. Only patients who have minimally invasive procedures requiring little or no postoperative opioids are considered for ambulatory surgery. Table 5-2 contains a summary of the preoperative, intraoperative, and postoperative considerations in patients at risk for OSA. Chronic Opioid-Consuming Patients In recent years, there has been a significant increase in the number of patients treated chronically with opioids. These patients present a unique challenge in the perioperative period for several reasons. First, tolerance can develop very rapidly after initiating therapy with opioid analgesics.25,46,100 There is considerable evidence to suggest that chronic opioid use may even cause a hyperalgesic state in some patients.60 Thus, during the postoperative period, chronic opioid-consuming patients may report higher pain scores despite having higher levels of sedation when compared with opioid-naïve controls.79 In fact, the incidence of severe sedation postoperatively in opioidtolerant patients is more than twice that of opioid-naïve controls. It has been suggested that lethal overdoses of opioid in chronic users may be due to a narrowing of the ratio between analgesic and lethal plasma concentrations.104 As with OSA patients, nonopioid analgesics and peripheral nerve blocks should be utilized wherever possible to provide improved pain control. Use caution when trying to achieve a specific “pain score.” As previously stated, chronic opioid-consuming patients typically report higher pain scores at rest and with movement despite having higher levels of sedation.79 Thus an objective measure of opioid effect, such as respiratory rate, is appropriate for maintaining safety. When dosing opioids in the postoperative period, it should be noted that opioid-tolerant patients may require

Table 5-2 Perioperative Management of Patients with Obstructive Sleep Apnea Preoperative Management Screen all patients for signs/symptoms of obstructive sleep apnea (OSA) with a validated protocol such as STOP-BANG.27 S—Loud Snoring T—Daytime Fatique, Tiredness O—Observed Apnea during Sleep P—High Blood Pressure B—Body Mass Index (BMI) > 35 kg/m2 A—Age > 50 years N—Neck Circumference > 40 cm G—Male Gender Patients with a documented history of OSA or with three or more positive findings on STOP-BANG screening should be identified as high risk for OSA and informed of the likely need for hospital admission after surgery. Patients with a known history of OSA who are already treated with continuous positive airway pressure (CPAP) should bring their device from home. Intraoperative Management Where reasonable, regional anesthesia or peripheral nerve block for anesthesia and postoperative analgesia should be provided. Use short-acting anesthetics and minimize the use of opioids. Postoperative Management Ambulatory surgery may be appropriate for the following patients: Those who have had only regional or local anesthesia Those who require minimal or no postoperative opioid analgesics For Hospitalized Patients Consider nonopioid analgesia and peripheral nerve blocks wherever possible. Maintain patient in semiupright position to avoid airway obstruction (avoid supine position). Continue the use of CPAP for patients already on this therapy at home. Monitor with continuous pulse-oximetry. See references 2, 27, 28, and 45.

significantly greater doses than opioid-naïve patients.31,71 Patients should have their preoperative opioid doses restarted as soon as it is practical. Additional analgesia should be provided ideally with nerve blocks and non opioid analgesics. Additional opioids should be available “prn” but not as long-acting, scheduled doses. Practical considerations for the postoperative management of opioid tolerant patients are found in Table 5-3. Because of the increased potential for opioid-related respiratory depression, inpatient monitoring and supplemental oxygen should be considered for opioid-tolerant patients having surgery associated with significant postoperative pain. Consideration should also be given to scheduling these patients earlier in the day to allow adequate time in the perioperative anesthetic care unit (PACU) to safely determine appropriate postoperative care and disposition (inpatient or ambulatory). 139

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Table 5-3 Practical Considerations for Chronic OpioidConsuming Patients

1. Instruct the patient and family that safety is the primary goal. For that reason, respiratory rate and level of consciousness will be used to regulate opioid administration rather than by pain score alone. 2. Preoperative opioid doses should restarted as soon as is practical. Additional opioids to treat acute pain should be prescribed as immediate-release only and scheduled on a “prn” basis. 3. Schedule these patients early in the day to allow adequate time in the perioperative anesthetic care unit and in the patient’s room (if hospitalized) to observe the planned analgesic regimen and adjust as needed during normal working hours. 4. Utilize all additional elements of multimodal analgesics where appropriate, including nonsteroidal antiiflammatory drugs, pregabalin, acetaminophen (paracetamol), peripheral nerve blocks, and mixed mu agonist/monoamine reuptake inhibitors (tramadol/ tapentadol). 5. Patients requiring large doses of opioids should be cared for in a monitored setting with continuous pulse oximetry and supplemental oxygen.

REGIONAL ANESTHESIA

Recent advances in technology have had a significant impact on regional anesthesia. The introduction of portable, high-resolution ultrasound (US) is largely responsible for a resurgence of interest in peripheral nerve blocks. Ultrasound use has increased dramatically as a result of the combined effects of decreased equipment cost and remarkable improvement in image quality. In addition, imaging platforms are now extremely portable, with many devices being as small as hand-held computers. Significant advances have also been made in the use of continuous peripheral nerve blocks. As more complex procedures are performed on an outpatient basis, there is an increased need to provide safe and effective analgesia without relying solely on opioid analgesics. Continuous peripheral nerve blocks can facilitate pain man agement in a number of patients for whom opioids are unsuitable. Ultrasound-Guided Peripheral Nerve Blocks For many years, electrical nerve stimulation (NS) was the “gold standard” technique for performing nerve blocks. Despite an absence of data showing a consistent relationship between the stimulating needle current and the distance to the nerve,12,81,82,98 NS remained popular due to the lack of any alternative method to guide needle placement. A troubling aspect of NS-guided blocks is the frequency with which they result in unintentional needle trauma and intraneural injection.82 In a recent study of sciatic nerve (SN) blocks performed using NS guidance, 94% of 140

patients experienced unintended nerve penetration and intraneural injection.83 This high rate of intraneural injection reflects the inability to consistently produce motor response from the stimulating needle even when it is positioned on or within the target nerve.82,98 There is considerable disparity in the rate of neurologic complications reported for patients having NS-guided blocks. For example, in the previously mentioned study, where the authors described a 94% rate of intraneural injection, there were no reported neuropathies.83 By contrast, in a larger series of NS-guided SN catheters placed for foot and ankle surgery, 41% of patients reported postoperative neuropathic symptoms. Of these patients, 11% required extra hospital visits specifically for treatment of neurologic symptoms.41 Thus, although the actual incidence of nerve injury associated with NS block may vary, laboratory and clinical data confirm that needle trauma and intraneural injection are not only uncomfortable for the patient36 but injurious to the nerve as well.29,39,80,86,106 The introduction of high-resolution US has been an important development in regional anesthesia. Although initially viewed by some as a novelty or merely a supplement to NS techniques,11 US is now established as the preferred method for performing nerve blocks. Indeed, when compared with NS techniques, blocks performed using US have higher success rates, less procedure-related pain, fewer vascular punctures, fewer needle passes, lower local anesthetic requirements, and shorter performance times.1,42,59,62,64,74 Perhaps even more compelling, when NS is used in an attempt to supplement US guidance, nerve blocks take longer to perform and require more needle passes.34,89 Continuous Peripheral Nerve Block (Video Clips 7) After orthopedic surgery, severe pain may persist for 2 to 3 days. Although single-injection nerve blocks (SINB) can provide analgesia for up to 24 hours, blocks of this duration require large volumes of concentrated local anesthetics and are associated with dense motor and sensory effect. By contrast, continuous peripheral nerve block (CPNB) can be used to provide prolonged analgesia by using low volumes of dilute local anesthetic. Thus flexibility with respect to duration and block density can be achieved while avoiding the need for large and potentially toxic doses of local anesthetic. The ability to provide prolonged analgesia without dense motor and sensory effect is appealing because many patients report decreased satisfaction when the extremity is “too numb” or “immobile.” Limb neglect caused by dense motor and sensory block may also result in positioning injury and falls.84,94,107 Emerging data for dilute local anesthetic infusions suggest that lower concentrations are associated with improved motor function without compromise in pain scores or patient satisfaction. After shoulder surgery, low concentration interscalene blocks (0.125% vs. 0.25% bupivacaine) provided

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comparable analgesia and patient satisfaction but with improved diaphragm function and higher oxygen saturation.96 Continuous nerve block can facilitate outpatient management for procedures that historically have required hospital admission for pain control. In one series, patients were successfully treated as outpatients after open treatment of calcaneus fracture.54 This resulted in a cost savings of more than $4000 per patient. Thus CPNB may not only provide excellent analgesia, but may also result in reduced health care costs. The benefits of CPNB are increasingly apparent as more complex procedures are performed on an outpatient basis. It should be noted, however, that there is considerable variability between institutions regarding placement and management of continuous peripheral catheters. Some common trends, however, include a dominant influence of ultrasound to guide catheter placement and recognition that patients can manage and remove their catheters at home with minimal supervision. Equipment costs are important in all aspects of patient care. With this in mind, it should be noted that a wide variety of infusion pumps are available for continuous peripheral nerve blocks. Although some very costly pumps are programmable and feature variable infusion rates with bolus capability,56 excellent results can be obtained using less expensive fixed-rate elastomeric pumps.94,105 In comparisons between simple, fixed-rate elastomeric pumps and pumps featuring variable-rate and bolus capability, fixed-rate elastomeric pumps were associated with higher patient satisfaction and fewer technical problems.23 Thus many institutions experienced in the use of CPNB have adopted the use of simple elastomeric pumps for both economic and patient satisfaction reasons. Nerve Blocks above the Knee Sciatic Nerve Block at the Level of the Popliteal Fossa (Video Clips 6) Sciatic nerve block at the level of the popliteal fossa is widely used because the nerve is easily visualized with US at this level. Moreover, a single injection can block all the nerves of the foot and ankle, with the exception of the saphenous nerve. The sciatic nerve, popliteal artery, and popliteal vein are easy to visualize within the popliteal fossa by using US guidance. As seen in Figure 5-1, the popliteal fossa is bordered medially by the semimembranosus/semitendinosus muscles and laterally by the biceps femoris muscle. This nerve can be located by imaging superficial and lateral to the popliteal artery and vein, which are useful landmarks when imaging with ultrasound. Division of the sciatic nerve into the tibial and peroneal nerves occurs approximately 5 to 7 cm superior to the popliteal crease.101 Many early techniques for sciatic nerve block are based on the belief that the nerve is closely enveloped within the popliteal space by an impermeable connective tissue sheath.102 This would require the injecting needle to

SM/ST

Medial

Lateral

TN/PN

PA/PV

Figure 5-1 The tibial (TN) and peroneal nerves (PN) are displayed within the popliteal fossa distal to the division of the sciatic nerve. The popliteal artery (PA) and popliteal vein (PV) are medial to the nerves and are marked with a vessel loop. The biceps femoris (BF) muscle forms the lateral border of the popliteal fossa. Its medial border is formed by a confluence of the semimembranosus/semitendinosis (SM/ST) muscles.

penetrate this sheath to achieve successful nerve block. However, in Figure 5-2, the distribution pattern of methylene blue dye injected 0.5 cm medial to the sciatic nerve is demonstrated. It is clear from this image that methylene blue dye spreads from the medial to lateral border of the space as well as for a considerable distance proximal to the injection point. This extensive distribution of injectate suggests that successful sciatic nerve block at the level of the popliteal fossa can be performed without contact or immediate proximity between the injecting needle and the sciatic nerve. Clinical and laboratory outcomes confirm the efficacy of this technique.54,94 Excellent analgesia is achieved while injecting a safe distance from the nerve. In Figure 5-3, an ultrasound image of the sciatic nerve within the popliteal fossa is demonstrated. In this view, the biceps femoris muscle is visible at the lateral border of the space, while the semimembranosus/semitendinosus muscles are seen medially. The popliteal artery and vein are hypoechoic (black) structures seen deep and medial to the nerve. Figure 5-4 demonstrates the ultrasound appearance of local anesthetic injected 0.5 cm medial to the sciatic nerve. An extensive black (hypoechoic) area of local anesthetic surrounds the nerve. 141

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SM/ST

Medial

Lateral PV/PA

Figure 5-2 The distribution of methylene blue dye throughout the popliteal space from a single injection point within the popliteal space demonstrates how successful sciatic nerve block does not require immediate proximity to the nerve. The sciatic nerve (SN) is shown proximal to its division into the tibial (TN) and peroneal nerves (PN). The biceps femoris (BF) muscle as well as the semimembranosus/ semitendinosus (SM/ST) muscles are also labeled as borders of the popliteal fossa.

Lateral

Medial SN

SM/ST

Figure 5-3 Axial ultrasound image of the popliteal space approximately 5 cm superior to the popliteal crease. The popliteal artery (PA) and vein (PV) are visible medial and deep to the sciatic nerve (SN). The borders of the popliteal space are formed by the biceps femoris muscle (BF) laterally and the semimembranosus/semitendinosis muscles (SM/ST) medially. The white arrows highlight the superficial border of the SN.

142

Figure 5-4 Axial image of the popliteal space approximately 5 cm superior to the popliteal crease during ultrasound-guided injection. The white arrow represents the position of the needle approximately 1 cm medial to the superficial surface of the sciatic nerve (SN). The hypoechoic (black) area superficial and lateral to the nerve is local anesthetic. The popliteal artery (PA) and vein (PV) are visible medial and deep to the SN.

The Saphenous Nerve above the Knee The saphenous nerve is a pure sensory branch of the femoral nerve. At the level of the superior pole of the patella, it exits the adductor canal in a tissue plane between the vastus medialis and sartorius muscles (Fig. 5-5). Figure 5-6 demonstrates the tissue plane between the vastus medialis and the sartorius that is readily visible with ultrasound. Although the saphenous nerve itself is rarely visible within this tissue plane, it can be reliably blocked by injection of local anesthetic into this compartment. In Figure 5-7, the fascial plane between the vastus medialis and the sartorius muscles has been distended with local anesthetic. This will effectively block the saphenous nerve. Nerve Blocks below the Knee Historically, nerve blocks below the knee have been limited to the ankle, where surface landmarks can be used to identify injection sites. With US guidance, nerves can be visualized and blocked for a considerable distance proximal to the ankle if necessary. This greatly increases the versatility of block placement in cases where traditional landmarks for injection at the ankle might be affected by edema, erythema, or skin breakdown. Another advantage of US is the ability to inject local anesthetic without needle trauma to nerves or blood vessels. Thus

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Patella Saphenous nerve Vastus medialis VM

Adductor muscles

SM Sartorius

Figure 5-5 This image shows the medial aspect of the thigh immediately superior to the patella. The sartorius muscle has been transected and reflected medially to expose the saphenous nerve. The saphenous nerve passes superficial to the tendinous insertion of the adductor muscles to a fascial plane between the vastus medialis and the sartorius muscle.

Figure 5-7 Axial ultrasound view of the medial aspect of the thigh immediately after injection of 15 mL of local anesthetic into the fascial plane between the sartorius (SM) and the vastus medialis (VM) muscles. The saphenous nerve itself is not usually visible at this level but can be reliably blocked by injection within this fascial plane.

Saphenous vein

Inferior pole patella Infrapatellar branch of saphenous nerve

Pes anserinus

Fascial plane with saphenous nerve

Figure 5-6 Ultrasound image showing an axial view of the medial aspect of the thigh at the level of the superior pole of the patella. The fascial plane between the sartorius (SM) and the vastus medialis (VM) contains the saphenous nerve. The saphenous nerve itself is not usually visible in this plane.

ultrasound provides an added degree of versatility because nerves of the foot and ankle can be visualized along most of their length and blocked where most appropriate. The Saphenous Nerve The saphenous nerve can be blocked below the knee at the level of the tibial plateau. Figure 5-8 shows the saphenous nerve as it emerges from beneath the pes

Saphenous nerve

Figure 5-8 The relationship of the saphenous vein, saphenous nerve, and the pes anserinus. Inferior to the pes anserinus, the saphenous vein and nerve are in close proximity to one other within the subcutaneous tissue. Proximally, the nerve passes deep to the pes anserinus, while the vein remains in the subcutaneous tissue. When using the saphenous vein as a landmark for saphenous nerve block, injection should be immediately inferior to the pes anserinus.

anserinus. After emerging from deep to the pes anserinus, the saphenous nerve travels in the subcutaneous tissue with the saphenous vein see (see Fig. 5-8) on the medial aspect of the tibia. A common mistake in blocking the saphenous nerve at this level is to inject only in an anterior direction across the medial tibial plateau. Although this will effectively block the infrapatellar branch of the saphenous nerve, the more distal portion should be 143

Part I ■ General Considerations

Flexor retinaculum Achilles tendon Tibial artery

Tibial nerve

Saphenous vein

Figure 5-9 Ultrasound image of the medial aspect of the leg shows the appearance of the saphenous vein (SV) immediately inferior to the pes anserinus. Note the saphenous nerve is not visible in this image, and injection is performed using the vein as a marker for the position of the saphenous nerve. This image must be obtained using extremely light pressure with the ultrasound transducer, to avoid compression of the saphenous vein.

Figure 5-11 A dissection of the medial aspect of the right ankle shows the flexor retinaculum, which has been cut away inferiorly. The tibial nerve is seen posterior to the tibial artery.

Anterior Local anesthetic

TA Posterior

Figure 5-10 Axial view of local anesthetic (hypoechoic) after infiltration around the saphenous vein. Injection is performed using the saphenous vein inferior to the pes anserinus as a landmark.

blocked by infiltration around the saphenous vein as shown in Figures 5-9 and 5-10. Note in these US images that the saphenous nerve is not visible and that successful block is achieved by injecting in proximity to the saphenous vein. The Tibial Nerve (Video Clip 5) The tibial nerve is readily visualized with US at the level of the medial malleolus. Here, it is located deep to the flexor retinaculum and posterior to the tibial artery (Fig. 5-11). Using ultrasound, the injecting needle can be advanced either anterior or posterior to the nerve and 144

Figure 5-12 Ultrasound image of the medial aspect of the left ankle immediately superior to the malleolus. The image shows the relationship between the tibial artery (TA) and the tibial nerve (TN) (whose borders are defined by yellow arrows). Note that both structures are deep to the flexor retinaculum that is outlined by white arrows.

deep to the flexor retinaculum (Fig. 5-12). The proximal course of the tibial nerve can be followed as it runs with the tibial artery in a plane between the flexor digitorum longus anteriorly and the flexor hallucis longus posteriorly. Figure 5-13 shows the ultrasound appearance of the tibial nerve at the level of the midtibia. It is readily visualized adjacent to the tibial artery in a tissue plane between the flexor digitorum longus and the flexor hallucis longus. Injection can be made in the tissue plane between the flexor digitorum longus and the flexor hallucis longus.

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SP Anterior

FDL

rio

FHL

rI M

Posterior

EDL

Fibula

Figure 5-13 The medial aspect of the left leg is at the level of the midtibia. The tibial nerve (TN) and tibial artery (TA) continue in close proximity to one another. They are bordered anteriorly by the flexor digitorum longus (FDL) and posteriorly by the flexor hallucis longus (FHL).

Figure 5-15 Ultrasound image of the lateral aspect of the right leg at the level of the midfibula. The superficial peroneal nerve (SPN) at this level is deep to the investing fascia of the leg and lies on the superficial surface of the peroneus brevis muscle (PB). The anterior intermuscular septum is a useful landmark because the nerve lies immediately posterior to this septum. The extensor digitorum longus muscle (EDL) borders the anterior surface of the intermuscular septum.

Figure 5-14 In this dissection of the right lower leg, the superficial peroneal nerve is seen as it pierces the investing fascia near the anterior intermuscular septum. As it passes distally to the ankle, it divides extensively over the dorsum of the foot.

The Deep Peroneal Nerve The deep peroneal nerve can be visualized at the superior level of the malleoli, where it lies on the anterior surface of the tibia immediately lateral to the anterior tibial artery. At this level, both the artery and the nerve pass between the tendons of the extensor hallucis longus and the extensor digitorum longus (Fig. 5-16). When using ultrasound, the pulsatile anterior tibial artery is easily visualized and is a useful point of reference for the deep peroneal nerve at the level of the ankle (Fig. 5-17). If more a proximal block is required, the artery and nerve can be followed proximally, where they lie on the anterior surface of the interosseous membrane (Fig. 5-18). At this level, the nerve is rarely visible but can be successfully blocked by injecting in a plane between the interosseous membrane and the anterior tibial artery.

The Superficial Peroneal Nerve The superficial peroneal nerve branches extensively as it passes in the subcutaneous tissue from the lower leg to the ankle (Fig. 5-14). It is typically not visible with ultrasound at this level but can be blocked at the ankle with a subcutaneous injection between the medial and lateral malleoli. At the level of the midfibula, the nerve pierces the investing fascia of the leg. Using ultrasound at this level, the nerve can be visualized immediately deep to the investing fascia of the leg on the surface of the peroneus brevis muscle and lateral to the anterior intermuscular septum (Fig. 5-15).

The Sural Nerve At the level of the lateral malleolus, the sural nerve can be identified, using ultrasound, by its proximity to the small saphenous vein. The vein and nerve are adjacent to one another in the subcutaneous tissue between the Achilles tendon posteriorly and the tendons of the peroneus longus and brevis anteriorly (Fig. 5-19). The nerve and vein can be traced proximally to a position midline between the medial and lateral heads of the gastrocnemius muscle. At this level, the nerve pierces the investing fascia of the leg (Fig. 5-20). In Figure 5-21, the small saphenous vein and the sural nerve are visible in the midline between the medial and lateral heads of the gastrocnemius muscle. Here the nerve is still in the

Superficial peroneal nerve

Lateral malleolus

145

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Extensor hallucis longus

EDL

Extensor digitorum longus

Anterior tibial artery

EHL AT DPN

Deep peroneal nerve

Distal tibia

Medial malleolus

Lateral malleolus

Figure 5-17 Ultrasound image immediately superior to the malleoli shows the anterior tibial artery (AT) medial to the deep peroneal nerve (DPN). Both structures are on the anterior surface of the tibia. The extensor digitorum longus (EDL) and extensor hallucis longus (EHL) muscles are superficial to the nerve and artery.

Figure 5-16 In this dissection of the ankle, the extensor retinaculum has been removed to reveal the deep peroneal nerve in a position lateral to the anterior tibial artery. These two structures are between the extensor hallucis longus and extensor digitorum longus tendons. AT SSV

PL/PB

TA In t m ero em ss br eou an s e

Fibula

ATA

Tibia

Figure 5-18 The deep peroneal nerve is not usually visible above the ankle when using ultrasound. However, because this nerve travels in close proximity to the anterior tibial artery (ATA), this vessel can be used as a marker for successful injection. Injection between the interosseous membrane and the ATA will result in successful block at this level. The tibialis anterior muscle (TA) is seen in this view anterior to the artery and nerve.

146

Figure 5-19 Ultrasound image at the level of the lateral malleolus, the sural nerve (SN) is seen adjacent to the small saphenous vein (SSV). Both the vein and the nerve are in the subcutaneous tissue between the Achilles tendon (AT) posteriorly and the tendons of the peroneus longus and peroneus brevis (PL/PB) anteriorly. The small saphenous vein (SSV) is a useful landmark that is consistently adjacent to the sural nerve (SN) at this level.

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LH-GM

subcutaneous tissue and has not pierced the investing fascia of the leg.

MH-GM

NERVE BLOCK COMPLICATIONS

Sural nerve Achilles tendon

Lateral malleolus

Medial malleolus

Figure 5-20 In this image of the posterior aspect of the lower leg, the proximal sural nerve is visible in the midline between the medial (MH-GM) and lateral (LH-GM) heads of the gastrocnemius muscle. The distal position of the nerve is between the Achilles tendon and the lateral malleolus.

MH-GM

SSV

LH-GM

Figure 5-21 Ultrasound image of the posterior aspect of the lower leg shows the small saphenous vein (SSV) and the sural nerve (SN) in a position midline between the medial (MH-GM) and lateral (LH-GM) heads of the gastrocnemius muscle.

Peripheral nerve blocks provide excellent pain relief after surgery, but are not considered an indispensible component of perioperative care. Because all medical procedures are associated with the risk of injury, it is appropriate to reserve nerve blocks for patients in whom there is a clear benefit. The obvious goal for regional anesthesia is to reduce the risk of nerve blocks to a level that is favorable for all patients experiencing moderate-to-severe postoperative pain. Complications occurring during the performance of nerve blocks include intravascular injection of local anesthetic, nerve injury, and vascular injury. However, injury may also result from the loss of motor and sensory function in the affected extremity. For example, patients are vulnerable to compression injuries and falls during any period of dense motor and sensory block.84,94,107 Thus it is important to take appropriate safety measures both during nerve block placement and for the duration of its effect. Intravascular Injection of Local Anesthetic Accidental intravascular injection of local anesthetic can manifest as symptoms and signs ranging from perioral numbness and agitation to grand mal seizures and cardiovascular collapse. A local anesthetic dose that is completely safe for injection into tissue can be toxic if injected intravascularly. Thus it is important to recognize that published guidelines for “allowable doses” of local anesthetic do not apply to rapid intravascular administration.33 The use of ultrasound has introduced new methods for detecting intravascular injection. First, blood vessels can be visualized during the procedure, and needle position can be adjusted accordingly. Next, injection of even small volumes of local anesthetic (0.5-1.0 mL) within a blood vessel causes turbulence that can be seen on the ultrasound image as “hyperechoic contrast,” alerting the operator to intravascular injection. Finally, during normal injection, there should be obvious displacement of tissue by the injectate that is visibly hypoechoic (black). Examples of the hypoechoic appearance of injectate are seen in Figures 5-4 and 5-10. If tissue displacement is not apparent during injection, the procedure is halted until intravascular injection can be ruled out. Studies comparing ultrasound guided nerve blocks with nerve stimulator techniques demonstrate that fewer vascular punctures as well as fewer seizures caused by intravascular injection occur when using ultrasound guidance.1,69 Thus ultrasound has already had a significant impact on one of the most serious complications of regional anesthesia. 147

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Nerve Injury The reported incidence of injury after peripheral nerve block in the lower extremity varies greatly. This is due to several factors, including what defines “nerve injury.” Transient sensory changes, lasting days or weeks after nerve block, have been reported in up to 41% of patients treated with peripheral nerve block performed using nerve stimulator guidance.41 By contrast, prolonged neurologic deficits are reported to be as low as 0.05% in other large series.3 The cause of perioperative nerve injury is often difficult to identify. Some recognized factors related to nerve block include needle trauma, intraneural injection, and toxicity of injectate.5,65 Equally important, however, are injuries related to trauma or compression of the extremity during a period of dense motor and sensory block. Thus the postoperative care of patients with long-acting nerve blocks should include precautions with respect to limb positioning, padding of the extremity, and assessing perfusion. Several studies show superiority of ultrasound over nerve stimulation when comparing success rate, patient acceptance, efficiency, and local anesthetic requirements.1,59,74 However, there is little evidence confirming a decreased incidence of nerve injury for blocks placed using ultrasound compared with nerve stimulation. The apparent lack of improvement with respect to nerve injury when blocks are placed with ultrasound may reflect reluctance on the part of anesthesiologists to modify existing block techniques. Before the availability of ultrasound, nerve stimulation was used to position the injecting needle in contact with or in immediate proximity to the nerve. With the transition away from nerve stimulation, many practitioners have simply converted ultrasound into the visual equivalent of a nerve stimulator. In other words, ultrasound rather than nerve stimulation is used to position the needle in immediate proximity or contact with the nerve. The result of this practice has been a continued high rate of nerve penetration and intraneural injection that is the subject of considerable discussion and investigation.9,26,95 Because needle trauma and intraneural injection are known to be associated with nerve injury,29,39,80,86,106 it would seem wise to use every possible tool to avoid these risk factors. In fact, existing anatomic studies demonstrate that most nerves such as the brachial plexus, femoral nerve, and the sciatic nerve are all contained within distinct fascial compartments.7,30,108 Moreover, these nerves can be successfully blocked by injection into these fascial compartments and without immediate proximity to the nerve. Ultrasound is particularly suited for these techniques because it can be used to position the needle in the correct fascial compartment for successful block without proximity to the nerve. Thus two of the known causes of nerve injury—needle trauma and intraneural injection—can be avoided. Recent clinical data confirm success rates approaching 100% for blocks performed 148

using ultrasound to guide fascial compartment injection without proximity to the nerve.94 Infection Although infection can occur with any type of nerve block, this complication is most commonly associated with continuous indwelling catheters. The majority of studies reporting infection associated with indwelling catheters are from hospitalized patients. In these reports, the infection rate ranges from 0% to 3.2%.24,66 For outpatients, the reported rates are less than 1%.21,94 Guidelines for sterile precautions during catheter placement are largely extrapolations from data pertaining to central venous access techniques. In addition to sterile precautions for catheter placement, it is important to follow all pharmacy standards and sterile precautions during the preparation and filling of infusion pumps used with continuous catheter techniques. At least one report of deep cellulitis has been attributed to an infusion pump that was not filled under sterile conditions.22 Although tunneling of peripheral nerve catheters has been recommended to reduce bacterial colonization, this has not been proven to reduce infection. Specific risk factors identified with catheter infection include duration of catheter use longer than 48 hours, lack of antibiotic prophylaxis, and position in the axillary or inguinal region.21 SUMMARY

The postoperative management of surgical patients has undergone important developments in recent years. These developments are the result of changing patient demographics as well as technologic advances in medical devices and pharmaceuticals. An aging and more obese population has increased the risk of perioperative respiratory events in patients with diagnosed and undiagnosed obstructive sleep apnea. The increasing use and abuse of opioids in the overall population changes the safety and efficacy of this widely prescribed class of drugs. Lastly, economic pressures to perform more complex procedures on an ambulatory basis have steadily increased. Fortunately, the tools to provide safe and effective patient care in the face of these challenges are developing as well. Of necessity, the greatest paradigm shift will be away from a reliance on opioids as the dominant analgesic for postoperative pain control. REFERENCES 1. Abrahams MS, Aziz MF, Fu RF, Horn JL: Ultrasound guidance compared with electrical neurostimulation for peripheral nerve block: a systematic review and meta-analysis of randomized controlled trials, Br J Anaesth 102:408–417, 2009. 2. Adesanya AO, Lee W, Greilich NB, Joshi GP: Perioperative management of obstructive sleep apnea, Chest 138:1489–1498, 2010.

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3. Auroy Y, Benhamou D, Bargues L, et al: Major complications of regional anesthesia in France: the SOS Regional Anesthesia Hotline Service, Anesthesiology 97:1274–1280, 2002. 4. Balaban F, Yagar S, Ozgok A, et al: A randomized, placebocontrolled study of pregabalin for postoperative pain intensity after laparoscopic cholecystectomy, J Clin Anesth 24:175–178, 2012. 5. Barrington MJ, Snyder GL: Neurologic complications of regional anesthesia, Curr Opin Anaesthesiol 24:554–560, 2011. 6. Beck A, Salem K, Krischak G, et al: Nonsteroidal antiinflammatory drugs (NSAIDs) in the perioperative phase in traumatology and orthopedics effects on bone healing, Oper Orthop Traumatol 17:569–578, 2005. 7. Beck GP: Anterior approach to sciatic nerve block, Anesthesiology 24:222–224, 1963. 8. Benyamin R, Trescot AM, Datta S, et al: Opioid complications and side effects, Pain Physician 11(Suppl 2):S105–S120, 2008. 9. Bigeleisen PE, Chelly J: An unsubstantiated condemnation of intraneural injection, Reg Anesth Pain Med 36:95, 2011; author reply 95–97, 98–99. 10. Bockbrader HN, Radulovic LL, Posvar EL, et al: Clinical pharmaco*kinetics of pregabalin in healthy volunteers, J Clin Pharmacol 50:941–950, 2010. 11. Boezaart AP: Perineural infusion of local anesthetics, Anesthesiology 104:872–880, 2006. 12. Bollini CA, Urmey WF, Vascello L, Cacheiro F: Relationship between evoked motor response and sensory paresthesia in interscalene brachial plexus block, Reg Anesth Pain Med 28:384–388, 2003. 13. Bonnefont J, Courade JP, Alloui A, Eschalier A: [Antinociceptive mechanism of action of paracetamol], Drugs 63(Spec No 2):1– 4, 2003. 14. Bornemann-Cimenti H, Lederer AJ, Wejbora M, et al: Preoperative pregabalin administration significantly reduces postoperative opioid consumption and mechanical hyperalgesia after transperitoneal nephrectomy, Br J Anaesth 108:845–849, 2012. 15. Botting RM: Inhibitors of cyclooxygenases: mechanisms, selectivity and uses, J Physiol Pharmacol 57(Suppl 5):113–124, 2006. 16. Boursinos LA, Karachalios T, Poultsides L, Malizos KN: Do steroids, conventional non-steroidal anti-inflammatory drugs and selective Cox-2 inhibitors adversely affect fracture healing? J Musculoskel Neuronal Interact 9:44–52, 2009. 17. Brett CN, Barnett SG, Pearson J: Postoperative plasma paracetamol levels following oral or intravenous paracetamol administration: a double-blind randomised controlled trial, Anaesth Intensive Care 40:166–171, 2012. 18. Brown KA, Laferriere A, Lakheeram I, Moss IR: Recurrent hypoxemia in children is associated with increased analgesic sensitivity to opiates, Anesthesiol 105:665–669, 2006. 19. Burke SM, Shorten GD: Perioperative pregabalin improves pain and functional outcomes 3 months after lumbar discectomy, Anesth Analg 110:1180–1185, 2010. 20. Buvanendran A, Kroin JS, Della Valle CJ, et al: Perioperative oral pregabalin reduces chronic pain after total knee arthroplasty: a prospective, randomized, controlled trial, Anesth Analg 110:199–207, 2010. 21. Capdevila X, Bringuier S, Borgeat A: Infectious risk of con tinuous peripheral nerve blocks, Anesthesiology 110:182–188, 2009. 22. Capdevila X, Jaber S, Pesonen P, et al: Acute neck cellulitis and mediastinitis complicating a continuous interscalene block, Anesth Analg 107:1419–1421, 2008. 23. Capdevila X, Macaire P, Aknin P, et al: Patient-controlled perineural analgesia after ambulatory orthopedic surgery: a comparison of electronic versus elastomeric pumps, Anesth Analg 96:414–417, 2003.

24. Capdevila X, Pirat P, Bringuier S, et al: Continuous peripheral nerve blocks in hospital wards after orthopedic surgery: a multicenter prospective analysis of the quality of postoperative analgesia and complications in 1,416 patients, Anesthesiology 103:1035–1045, 2005. 25. Chia YY, Liu K, Wang JJ, et al: Intraoperative high-dose fentanyl induces postoperative fentanyl tolerance, Can J Anaesth 46:872– 877, 1999. 26. Choquet O, Morau D, Biboulet P, Capdevila X: Where should the tip of the needle be located in ultrasound-guided peripheral nerve blocks? Curr Opin Anaesthesiol 25:596–602, 2012. 27. Chung F, Yegneswaran B, Liao P, et al: STOP questionnaire: a tool to screen patients for obstructive sleep apnea, Anesthesiology 108:812–821, 2008. 28. Chung SA, Yuan H, Chung F: A systemic review of obstructive sleep apnea and its implications for anesthesiologists, Anesth Analg 107:1543–1563, 2008. 29. Cohen JM, Gray AT: Functional deficits after intraneural injection during interscalene block, Reg Anesthesia Pain Med 35:397– 399, 2010. 30. Dalens B, Vanneuville G, Tanguy A: Comparison of the fascia iliaca compartment block with the 3-in-1 block in children, Anesth Analg 69:705–713, 1989. 31. Davis JJ, Johnson KB, Egan TD, et al: Preoperative fentanyl infusion with pharmaco*kinetic simulation for anesthetic and perioperative management of an opioid-tolerant patient, Anesth Analg 97:1661–1662, 2003. 32. Dayer P, Desmeules J, Collart L: [Pharmacology of tramadol], Drugs 53(Suppl 2):18–24, 1997. 33. Dillane D, Finucane BT: Local anesthetic systemic toxicity, Can J Anaesth 57:368–380, 2010. 34. Dingemans E, Williams SR, Arcand G, et al: Neurostimulation in ultrasound-guided infraclavicular block: a prospective randomized trial, Anesth Analg 104:1275–1280, 2007. 35. Durkin B, Page C, Glass P: Pregabalin for the treatment of postsurgical pain, Expert Opin Pharmacother 11:2751–2758, 2010. 36. Fanelli G, Casati A, Garancini P, Torri G: Nerve stimulator and multiple injection technique for upper and lower limb blockade: failure rate, patient acceptance, and neurologic complications. Study Group on Regional Anesthesia, Anesth Analg 88: 847–852, 1999. 37. Finkel KJ, Searleman AC, Tymkew H, et al: Prevalence of undiagnosed obstructive sleep apnea among adult surgical patients in an academic medical center, Sleep Med 10:753–758, 2009. 38. Frampton JE. Tapentadol immediate release: a review of its use in the treatment of moderate to severe acute pain, Drugs 70:1719–1743, 2010. 39. Fredrickson MJ: Case report: neurological deficit associated with intraneural needle placement without injection, Can J Anaesth 56:935–938, 2009. 40. Gajraj NM: Pregabalin: its pharmacology and use in pain management, Anesth Analg 105:1805–1815, 2007. 41. Gartke K, Portner O, Taljaard M: Neuropathic symptoms following continuous popliteal block after foot and ankle surgery, Foot Ankle Int 33:267–274, 2012. 42. Gelfand HJ, Ouanes JP, Lesley MR, et al: Analgesic efficacy of ultrasound-guided regional anesthesia: a meta-analysis, J Clinl Anesth 23:90–96, 2011. 43. Graff J, Skarke C, Klinkhardt U, et al: Effects of selective COX-2 inhibition on prostanoids and platelet physiology in young healthy volunteers, J Thromb Haemost 5:2376–2385, 2007. 44. Graham GG, Scott KF: Mechanism of action of paracetamol, Am J Ther 12:46–55, 2005. 45. Gross JB, Bachenberg KL, Benumof JL, et al: Practice guidelines for the perioperative management of patients with obstructive

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sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea, Anesthesiology 104:1081–1093, 2006; quiz 117–118. 46. Guignard B, Bossard AE, Coste C, et al: Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement, Anesthesiology 93:409–417, 2000. 47. Hartrick C, Van Hove I, Stegmann JU, et al: Efficacy and tolerability of tapentadol immediate release and oxycodone HCl immediate release in patients awaiting primary joint replacement surgery for end-stage joint disease: a 10-day, phase III, randomized, double-blind, active- and placebo-controlled study, Clin Ther 31:260–271, 2009. 48. Hebl JR, Dilger JA, Byer DE, et al: A pre-emptive multimodal pathway featuring peripheral nerve block improves perioperative outcomes after major orthopedic surgery, Reg Anesth Pain Med 33:510–517, 2008. 49. Hinz B, Renner B, Brune K: Drug insight: cyclo-oxygenase-2 inhibitors—-a critical appraisal, Nat Clin Pract Rheumatol 3:552–560, 2007. 50. Ho KY, Tay W, Yeo MC, et al: Duloxetine reduces morphine requirements after knee replacement surgery, Br J Anaesth 105:371–376, 2010. 51. Hofmann AA, Bloebaum RD, Koller KE, Lahav A: Does celecoxib have an adverse effect on bone remodeling and ingrowth in humans? Clin Orthop Rel Res 452:200–204, 2006. 52. Hooper L, Brown TJ, Elliott R, et al: The effectiveness of five strategies for the prevention of gastrointestinal toxicity induced by non-steroidal anti-inflammatory drugs: systematic review, BMJ 329:948, 2004. 53. Houmes RJ, Voets MA, Verkaaik A, et al: Efficacy and safety of tramadol versus morphine for moderate and severe postoperative pain with special regard to respiratory depression, Anesth Analg 74:510–514, 1992. 54. Hunt KJ, Higgins TF, Carlston CV, et al: Continuous peripheral nerve blockade as postoperative analgesia for open treatment of calcaneal fractures, J Orthop Trauma 24:148–155, 2010. 55. Hyllested M, Jones S, Pedersen JL, Kehlet H: Comparative effect of paracetamol, NSAIDs or their combination in postoperative pain management: a qualitative review, Br J Anaesth 88:199– 214, 2002. 56. Ilfeld BM, Enneking FK: Continuous peripheral nerve blocks at home: a review, Anesth Analg 100:1822–1833, 2005. 57. Jacobsen RB, Phillips BB: Reducing clinically significant gastrointestinal toxicity associated with nonsteroidal antiinflammatory drugs, Anns Pharmacother 38:1469–1481, 2004. 58. Kim JC, Choi YS, Kim KN, et al: Effective dose of peri-operative oral pregabalin as an adjunct to multimodal analgesic regimen in lumbar spinal fusion surgery, Spine 36:428–433, 2011. 59. Koscielniak-Nielsen ZJ: Ultrasound-guided peripheral nerve blocks: what are the benefits? Acta Anaesthesiol Scand 52:727– 737, 2008. 60. Lee M, Silverman SM, Hansen H, et al: A comprehensive review of opioid-induced hyperalgesia, Pain Physician 14:145–161, 2011. 61. Maheshwari AV, Blum YC, Shekhar L, et al: Multimodal pain management after total hip and knee arthroplasty at the Ranawat Orthopaedic Center, Clin Orthop Rel Res 467:1418– 1423, 2009. 62. Mariano ER, Loland VJ, Sandhu NS, et al: Comparative efficacy of ultrasound-guided and stimulating popliteal-sciatic perineural catheters for postoperative analgesia, Can J Anaesth 57:919– 926, 2010. 63. McGettigan P, Henry D: Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of populationbased controlled observational studies, PLoS Med 8:e1001098, 2011.

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64. McNaught A, Shastri U, Carmichael N, et al: Ultrasound reduces the minimum effective local anaesthetic volume compared with peripheral nerve stimulation for interscalene block, Br J Anaesth 106:124–130, 2011. 65. Neal JM, Bernards CM, Hadzic A, et al: ASRA Practice Advisory on Neurologic Complications in Regional Anesthesia and Pain Medicine, Reg Anesth Pain Med 33:404–415, 2008. 66. Neuburger M, Buttner J, Blumenthal S, et al: Inflammation and infection complications of 2285 perineural catheters: a prospective study, Acta Anaesthesiol Scand 51:108–114, 2007. 67. Nossaman VE, Ramadhyani U, Kadowitz PJ, Nossaman BD: Advances in perioperative pain management: use of medications with dual analgesic mechanisms, tramadol and tapentadol, Anesthesiol Clin 28:647–666, 2010. 68. Ong CK, Seymour RA, Lirk P, Merry AF: Combining paracetamol (acetaminophen) with nonsteroidal antiinflammatory drugs: a qualitative systematic review of analgesic efficacy for acute postoperative pain, Anesth Analg 110:1170–1179, 2010. 69. Orebaugh SL, Williams BA, Vallejo M, Kentor ML: Adverse outcomes associated with stimulator-based peripheral nerve blocks with versus without ultrasound visualization, Reg Anesth Pain Med 34:251–255, 2009. 70. Parvizi J, Miller AG, Gandhi K: Multimodal pain management after total joint arthroplasty, J Bone Joint Surg Am 93:1075–1084, 2011. 71. Patanwala AE, Jarzyna DL, Miller MD, Erstad BL: Comparison of opioid requirements and analgesic response in opioidtolerant versus opioid-naive patients after total knee arthroplasty, Pharmacotherapy 28:1453–1460, 2008. 72. Patterson R, Bello AE, Lefkowith J: Immunologic tolerability profile of celecoxib, Clin Therap 21:2065–2079, 1999. 73. Centers for Disease Control and Prevention (CDC): CDC grand rounds: prescription drug overdoses—a U.S. epidemic, MMWR Morb Mortal Wkly Rep 61:10–13, 2012. 74. Perlas A, Brull R, Chan VW, et al: Ultrasound guidance improves the success of sciatic nerve block at the popliteal fossa, Reg Anesth Pain Med 33:259–265, 2008. 75. Pountos I, Georgouli T, Calori GM, Giannoudis PV: Do nonsteroidal anti-inflammatory drugs affect bone healing? A critical analysis, Scientific World Journal 2012:606404, 2012. 76. Prommer EE: Tramadol: does it have a role in cancer pain management? J Opioid Manag 1:131–138, 2005. 77. Radbruch L, Grond S, Lehmann KA: A risk-benefit assessment of tramadol in the management of pain, Drug Safety 15:8–29, 1996. 78. Randelli P, Randelli F, Cabitza P, Vaienti L: The effects of COX-2 anti-inflammatory drugs on soft tissue healing: a review of the literature, J Biol Regul Homeostatic Agents 24:107–114, 2010. 79. Rapp SE, Ready LB, Nessly ML: Acute pain management in patients with prior opioid consumption: a case-controlled retrospective review, Pain 61:195–201, 1995. 80. Rice AS, McMahon SB: Peripheral nerve injury caused by injection needles used in regional anaesthesia: influence of bevel configuration, studied in a rat model, Br J Anaesth 69:433–438, 1992. 81. Rigaud M, Filip P, Lirk P, et al: Guidance of block needle insertion by electrical nerve stimulation: a pilot study of the resulting distribution of injected solution in dogs, Anesthesiology 2008;109:473–478. 82. Robards C, Hadzic A, Somasundaram L, et al: Intraneural injection with low-current stimulation during popliteal sciatic nerve block, Anesth Analg 109:673–677, 2009. 83. Sala-Blanch X, Lopez AM, Pomes J, et al: No clinical or electrophysiologic evidence of nerve injury after intraneural injection during sciatic popliteal block, Anesthesiology 115:589–595, 2011.

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84. Saporito A, Sturini E, Petri J, et al: Case report: unusual complication during outpatient continuous regional popliteal analgesia, Can J Anaesth 59:958–962, 2012. 85. Schjerning Olsen AM, Fosbol EL, Lindhardsen J, et al: Duration of treatment with nonsteroidal anti-inflammatory drugs and impact on risk of death and recurrent myocardial infarction in patients with prior myocardial infarction: a nationwide cohort study, Circulation 123:2226–2235, 2011. 86. Selander D, Dhuner KG, Lundborg G: Peripheral nerve injury due to injection needles used for regional anesthesia. An experimental study of the acute effects of needle point trauma, Acta Anaesthesiol Scand 21:182–188, 1977. 87. Shipton EA: Tramadol—present and future, Anaesth Intensive Care 28:363–374, 2000. 88. Silverstein FE, Faich G, Goldstein JL, et al: Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial. Celecoxib Long-term Arthritis Safety Study, JAMA 284:1247–1255, 2000. 89. Sites BD, Beach ML, Chinn CD, et al: A comparison of sensory and motor loss after a femoral nerve block conducted with ultrasound versus ultrasound and nerve stimulation, Reg Anesth Pain Med 34:508–513, 2009. 90. Skinner HB: Multimodal acute pain management, Am J Orthop 33(Suppl 5):5–9, 2004. 91. Sostres C, Gargallo CJ, Arroyo MT, Lanas A: Adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs, aspirin and coxibs) on upper gastrointestinal tract, Best Pract Res Clin Gastroenterol 24:121–132, 2010. 92. Strom BL, Schinnar R, Apter AJ, et al: Absence of cross-reactivity between sulfonamide antibiotics and sulfonamide nonantibiotics, N Engl J Med 349:1628–1635, 2003. 93. Swegle JM, Logemann C: Management of common opioidinduced adverse effects, Am Fam Physician 74:1347–1354, 2006. 94. Swenson JD, Bay N, Loose E, et al: Outpatient management of continuous peripheral nerve catheters placed using ultrasound guidance: an experience in 620 patients, Anesth Analg 103:1436– 1443, 2006. 95. Swenson JD, Davis JJ: No clinical or electrophysiologic evidence proving intraneural injection is safe, Anesthesiology 116:1152, 2012; author reply 1153–1154. 96. Thackeray EM, Swenson JD, Gertsch MC, et al: Diaphragm function after interscalene brachila plexus block: a doubleblind, randomized comparison of 0.25% and 0.125% bupivacaine, J Shoulder Elbow Surg 2012. [Epub ahead of print.]

97. Tiippana EM, Hamunen K, Kontinen VK, Kalso E: Do surgical patients benefit from perioperative gabapentin/pregabalin? A systematic review of efficacy and safety, Anesth Analg 104:1545– 1556, 2007. 98. Urmey WF, Stanton J: Inability to consistently elicit a motor response following sensory paresthesia during interscalene block administration, Anesthesiology 96:552–554, 2002. 99. van der Westhuizen J, Kuo PY, Reed PW, Holder K: Randomised controlled trial comparing oral and intravenous paracetamol (acetaminophen) plasma levels when given as preoperative analgesia, Anaesth Intensive Care 39:242–246, 2011. 100. Vinik HR, Kissin I: Rapid development of tolerance to analgesia during remifentanil infusion in humans, Anesth Analg 86:1307– 1311, 1998. 101. Vloka JD, Hadzic A, April E, Thys DM: The division of the sciatic nerve in the popliteal fossa: anatomical implications for popliteal nerve blockade, Anesth Analg 92:215–217, 2001. 102. Vloka JD, Hadzic A, Lesser JB, et al: A common epineural sheath for the nerves in the popliteal fossa and its possible implications for sciatic nerve block, Anesth Analg 84:387–390, 1997. 103. Waters KA, McBrien F, Stewart P, et al: Effects of OSA, inhalational anesthesia, and fentanyl on the airway and ventilation of children, J Appl Physiol 92:1987–1994, 2002. 104. White JM, Irvine RJ: Mechanisms of fatal opioid overdose, Addiction 94:961–972, 1999. 105. White PF, Issioui T, Skrivanek GD, et al: The use of a continuous popliteal sciatic nerve block after surgery involving the foot and ankle: does it improve the quality of recovery? Anesth Analg 97:1303–1309, 2003. 106. Whitlock EL, Brenner MJ, Fox IK, et al: Ropivacaine-induced peripheral nerve injection injury in the rodent model, Anesth Analg 111:214–220, 2010. 107. Williams BA, Kentor ML, Bottegal MT: The incidence of falls at home in patients with perineural femoral catheters: a retrospective summary of a randomized clinical trial, Anesth Analg 104:1002, 2007. 108. Winnie AP: Interscalene brachial plexus block, Anesth Analg 49:455–466, 1970. 109. Young A, Buvanendran A: Recent advances in multimodal analgesia, Anesthesiol Clin 30:91–100, 2012. 110. Zhang J, Ho KY, Wang Y: Efficacy of pregabalin in acute postoperative pain: a meta-analysis, Br J Anaesth 106:454–462, 2011.

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Chapter

Hallux Valgus Michael J. Coughlin, Robert B. Anderson

CHAPTER CONTENTS OVERVIEW ANATOMY PATHOANATOMY PATHOPHYSIOLOGY DEMOGRAPHICS Age of Onset Gender Bilaterality Handedness Frequency of Occurrence ETIOLOGY Extrinsic Causes Footwear Occupation Trauma Intrinsic Causes Heredity Pes Planus Hypermobility of the Metatarsocuneiform Joint Ligamentous Laxity Achilles Contracture Miscellaneous Factors ANATOMIC AND RADIOGRAPHIC CONSIDERATIONS Angular Measurements Hallux Valgus Angle 1–2 Intermetatarsal Angle Hallux Interphalangeal Angle Distal Metatarsal Articular Angle Metatarsophalangeal Joint Congruency Medial Eminence Metatarsus Primus Varus Hallux Valgus Interphalangeus First Metatarsal Length Metatarsophalangeal Joint Shape Joint Congruity Distal Metatarsal Articular Angle and Proximal Articular Set Angle First Metatarsocuneiform Joint Intermetatarsal Facet/Os Intermetatarseum Metatarsus Adductus Blood Supply to the First Metatarsal Head Open Epiphysis

155 156 158 159 164 164 165 166 166 166 166 166 166 167 167 168 168 168 171 175 176 177 177 177 177 177 177 177 180 180 181 182 182 183 184 186 187 189 190 191 192

JUVENILE HALLUX VALGUS CLASSIFICATION PATIENT EVALUATION History and Physical Examination CONSERVATIVE TREATMENT Considerations with Surgical Intervention Anesthesia and Pain Control Miscellaneous Factors SURGICAL TREATMENT Decision Making Surgical Procedures (Video Clips 33-36 and 52-62) Complications of Hallux Valgus Surgery Causes of Surgical Failure Soft Tissue Problems Complications Affecting the Metatarsal Shaft Complications Affecting the Metatarsal Head Complications Involving the Proximal Phalanx Complications Associated with Capsular Tissue of the First Metatarsophalangeal Joint Complications Involving the Sesamoids Recurrent Hallux Valgus Deformity Distal Soft Tissue Procedure Chevron Procedure Proximal Metatarsal Osteotomy Akin Procedure Scarf Procedure Keller Procedure Preoperative Conditions HALLUX VARUS (Video Clip 61) PAIN AROUND THE FIRST METATARSOPHALANGEAL JOINT AFTER BUNION SURGERY PROSTHESES

193 194 195 195 197 198 198 199 199 199 201 279 279 281 284 289 291 294 295 297 298 298 298 298 298 298 298 300 307 307

OVERVIEW

The term bunion is derived from the Latin word bunio, meaning turnip, which has led to some confusing misapplications regarding disorders of the first metatarsophalangeal (MTP) joint. The word bunion has been used to denote any enlargement or deformity of the MTP joint, including such diverse diagnoses as an enlarged bursa, overlying ganglion, gouty arthropathy, and hallux valgus, as well as proliferative osseous changes that can develop secondary to MTP joint arthrosis (Fig. 6-1). 155

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Figure 6-1 A, Appearance of hallux valgus deformity. B, Gouty arthropathy with a similar appearance. C, Intraoperative appearance with gouty tophi causing medial enlargement. D, Ganglion over the medial eminence causing enlargement. E, Enlargement due to hallux rigidus. F and G, As the cristae is worn, full-thickness cartilaginous erosions occur on the plantar aspect of the first metatarsal head. These are largely not observed, unless exposed during the dissection. They can be a source of postoperative diminished motion and intraarticular pain.

The term hallux valgus was introduced by Carl Hueter230 to define a static subluxation of the first MTP joint characterized by lateral deviation of the great toe and medial deviation of the first metatarsal. It is now recognized, particularly in juvenile patients, that a hallux valgus deformity can originate because of lateral deviation of the articular surface of the metatarsal head without subluxation of the first MTP joint.97-99 A hallux valgus deformity can also be associated with abnormal foot mechanics, such as a contracted Achilles tendon; severe pes planus; generalized neuromuscular disease, such as cerebral palsy or a cerebrovascular accident (CVA, stroke); or an acquired deformity of the hindfoot secondary to rupture of the posterior tibial tendon. It can likewise be associated with various inflammatory arthritic conditions, such as rheumatoid arthritis (Fig. 6-2).

ANATOMY

The specialized articulation of the first MTP joint of the great toe differs from that of the lesser toes in that it has a sesamoid mechanism. The head of the first metatarsal is round and covered by cartilage and articulates with the 156

Figure 6-2 Hallux valgus deformity after a cerebral vascular accident (A1 and A2), rheumatoid arthritis (B), and ruptured posterior tibial tendon (C).

Hallux Valgus ■ Chapter 6

Collateral ligament

Sesamoid

Figure 6-3 Collateral ligament structure around the first metatarsal head.

Plantar plate Adductor hallucis

Abductor hallucis

somewhat smaller, concave elliptic base of the proximal phalanx. A fan-shaped ligamentous band originates from the medial and lateral metatarsal epicondyles and constitutes the collateral ligaments of the MTP joint (Fig. 6-3). These ligaments interdigitate with ligaments of the sesamoids. The strong collateral ligaments run distally and plantarward to the base of the proximal phalanx, whereas the sesamoid ligaments fan out plantarward to the margins of the sesamoid and the plantar plate. The two tendons of the flexor hallucis brevis, the abductor and adductor hallucis, the plantar aponeurosis, and the joint capsule condense on the plantar aspect of the MTP joint to form the plantar plate (Fig. 6-4A). Located on the plantar surface of the metatarsal head are two longitudinal cartilage-covered grooves separated by a rounded ridge (the crista). A sesamoid bone is contained in each tendon of the flexor hallucis brevis and articulates by means of cartilage-covered convex facets on its superior surface, with the corresponding longitudinal grooves on the inferior surface of the first metatarsal head. Distally, the two sesamoids are attached by the fibrous plantar plate (sesamoid-phalangeal ligament) to the base of the proximal phalanx; thus the sesamoid complex is attached to the base of the proximal phalanx rather than the metatarsal head. The sesamoids are connected by the intersesamoidal ligament, and this recess conforms to the crista on the plantar surface of the metatarsal head (Fig. 6-4B). The tendons and muscles that move the great toe are arranged around the MTP joint in four groups. The dorsal group is composed of the long and short extensor tendons, which pass dorsally, with the extensor hallucis longus anchored, medially and laterally by the hood ligament (Fig. 6-5). The extensor hallucis brevis inserts beneath the hood ligament into the dorsal aspect of the base of the proximal phalanx. The plantar group contains the long and short flexor tendons, which pass across the plantar surface, with the tendon of the flexor hallucis longus coursing through a centrally located tendon sheath on the plantar aspect of the sesamoid complex. This tendon is firmly anchored by this tunnel within the sesamoid complex. The last two groups are composed of the tendons of the abductor and adductor hallucis, which pass medially and laterally, respectively, but closer to the plantar surface than the dorsal surface. Thus the dorsomedial and dorsolateral aspects of the joint capsule are covered only

Flexor hallucis brevis

Abductor hallucis

Adductor hallucis Intersesamoidal ligament

Crista

Flexor hallucis brevis

B Figure 6-4 A, Dorsal view of first metatarsophalangeal (MTP) joint with the toe in plantar flexion. B, Cross section through the MTP joint demonstrating the relationship of the sesamoids and tendons to the first metatarsal head.

Extensor hallucis brevis Extensor hallucis longus

Hood ligament Collateral ligament

Sesamoid ligament

Figure 6-5 Collateral ligament structure and extensor mechanism around the first metatarsophalangeal joint.

by the hood ligaments, which maintain alignment of the extensor hallucis longus tendon. The adductor hallucis, arising from the lesser metatarsal shafts, is made up of two segments, the transverse and the oblique heads, which insert on the plantar lateral aspect of the base of the proximal phalanx and also blend with the plantar plate and the sesamoid complex. The 157

Part II ■ Forefoot

adductor hallucis balances the abductor forces of the abductor hallucis (Fig. 6-6). Acting in a line parallel to this bone and using the head of the first metatarsal as a fulcrum, the abductor hallucis pushes the first metatarsal toward the second metatarsal. The base of the first metatarsal has a mildly sinusoidal articular surface that articulates with the distal articular surface of the first cuneiform. The joint has a slight medial plantar inclination. The medial lateral dimension is approximately half the length of the dorsoplantar dimension. The joint is stabilized by capsular ligaments and is bordered laterally by the proximal aspect of the second metatarsal, which extends more cephalad and offers a stabilizing lateral buttress to the first metatarsocuneiform (MTC) articulation. ElSaid et al,146 in a cadaveric evaluation of 239 specimens, observed a facet to be present in 25% of cases; however, these were not specimens with

hallux valgus. Coughlin and Jones101 observed the radiographic presence of a facet between the proximal first and second metatarsals in 7% of 122 cases review with a bunion deformity (Fig. 6-7). The orientation of the MTC joint may determine the amount of metatarsus primus varus, and the shape of the articulation may affect metatarsal mobility. A medial inclination of up to 8 degrees at the MTC joint is normal. Increased obliquity at this joint can increase the degree of metatarsus primus varus. The axis of motion of the MTC joint is aligned to permit motion in a dorsal-medial to plantar-lateral plane. The tarsometatarsal articulation is quite stable in the central portion because of interlocking of the central metatarsals and cuneiforms (Fig. 6-8). This is not necessarily the case for the first and fifth metatarsals, where stability is determined not only by the inherent stability of the tarsometatarsal articulation but also by the surrounding capsular structures. Therefore, when ligamentous laxity is present, the first metatarsal may deviate medially and the fifth metatarsal laterally in the development of a splay foot deformity (Fig. 6-9). PATHOANATOMY

Because no muscle inserts on the metatarsal head, it is vulnerable to extrinsic forces, in particular, constricting Transverse head adductor hallucis Oblique head adductor hallucis Abductor hallucis Figure 6-6 Normal anatomic configuration of the first metatarsophalangeal joint demonstrating the stabilizing effect of the abductor and adductor hallucis muscles.

Figure 6-8 Stability of the tarsometatarsal articulation is maintained by interlocking of the central metatarsals.

Figure 6-7 A, Anteroposterior radiograph demonstrating the irreducibility of the 1–2 intermetatarsal (IM) angle because of IM facet. B, Close-up demonstrating facet between proximal first and second metatarsal. C, Anatomic specimen showing close-up of the first metatarsal proximal facet (M) (on right) and cuneiform articular surface (C) on left. The first metatarsal has been folded back, exposing the cuneiform and metatarsal articular surfaces and the corresponding facets. The accessory facet is noted with three arrows. (Courtesy Faustin R. Stevens, MD.)

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deformity occurs, the medial eminence often becomes more prominent (Fig. 6-11). The hallux and the first MTP joint play a significant role in the transfer of weight-bearing forces during locomotion. The plantar aponeurosis also plays a key role in this process by plantar flexing the first metatarsal as weight is transferred to the hallux. As the hallux is dorsiflexed at the first MTP joint, the first metatarsal is depressed, which results in increased weight bearing beneath the first metatarsal head and stabilization of the medial longitudinal arch (Fig. 6-12). Certain pathologic conditions, either acquired or iatrogenic, diminish the ability of the first MTP joint and hallux to function as weight-bearing structures. This results in transfer of weight to the lateral aspect of the forefoot, which often leads to the development of a transfer lesion beneath the second or third metatarsal head. As less weight is borne by the first ray, transfer metatarsalgia and lesser toe deformities may develop. Coughlin and Jones100 reported a 48% incidence of second MTP joint symptoms in a prospective study of adult patients undergoing repair of moderate and severe hallux valgus deformity.

footwear. Once the metatarsal becomes destabilized and begins to subluxate medially, the tendons about the MTP joint drift laterally. The muscles that previously acted to stabilize the joint become deforming forces because their pull is lateral to the longitudinal axis of the first ray. The plantar aponeurosis and the windlass mechanism contribute significantly to stabilization of the first ray450,460; with progression of a hallux valgus deformity, their stabilizing influence is diminished (Fig. 6-10).102,190 As the hallux valgus deformity progresses, the soft tissues on the lateral aspect of the first MTP joint become contracted, and those on the medial aspect become attenuated. The metatarsal head is pushed in a medial direction by the lateral deviation of the proximal phalanx, thereby progressively exposing the sesamoids, which are anchored in place by the transverse metatarsal ligament and the adductor hallucis muscle. As the metatarsal head continues to deviate medially off the sesamoids, the crista, which normally acts to stabilize the sesamoids, is gradually eroded (see Fig. 6-1F and G).35,449,496 These lesions are rarely seen on the plantar surface of the first metatarsal unless an effort is made intraoperatively to inspect this area. Bock et al35 reported on a large series of patients treat for hallux valgus, and found that 57% had significant plantar erosive lesions. Roukis et  al,449 reporting on 166 feet that underwent bunion surgery, noted that almost every joint had some element of articular cartilage erosion on the plantar metatarsal head. In more severe deformities, this erosion becomes more pronounced and extensive.35,449 As the sesamoid sling slides beneath the first metatarsal head, the hallux gradually pronates. As this dynamic joint

PATHOPHYSIOLOGY

The dynamics of the hallux valgus deformity can best be understood by first examining the articulation where the deformity occurs, that is, the MTP and MTC joints. The most stable MTP articulation has a flat articular surface, and conversely, the most unstable has a rounded head (Fig. 6-13).88,139,155,336 Coughlin and Jones101 noted this in 71% of patients in a large series of cases of hallux valgus

B Figure 6-9 Splayed foot deformity. A, Clinical appearance. B, Radiograph.

159

B B Figure 6-10 A, Medial view of the plantar aponeurosis. B, From beneath, the insertion into the hallux stabilizes the first ray.

Figure 6-12 Dynamic function of the plantar aponeurosis. A, Foot at rest. B, Dorsiflexion of the metatarsophalangeal joints, which activates windlass mechanisms and brings about elevation of the longitudinal arch, plantar flexion of the metatarsal heads, and inversion of the heel.

Figure 6-11 Sesamoid (A1) and anteroposterior (AP) (A2) views of a normal foot. Sesamoid (B1) view and AP (B2) views of moderate deformity. Sesamoid (C1) and AP (C2) views of severe deformity.

Figure 6-13 Anteroposterior radiographs demonstrating varying shapes of the metatarsophalangeal (MTP) articular surface. A, Flat MTP joint surface. Chevron-shaped surface in a juvenile (B) and in an adult (C) without subluxation. D and E, A rounded articular surface is more prone to subluxation of the MTP joint (D, mild subluxation (arrow denotes lateral subluxation of proximal phalanx); E, moderate subluxation). F, Congruent MTP joint with hallux valgus.

Hallux Valgus ■ Chapter 6

they examined. Okuda et al394 also observed an increased incidence of a rounded first metatarsal head associated with hallux valgus. A congruent MTP joint likewise is more stable than an incongruent or subluxated joint. A congruent joint tends to remain stable, whereas once a joint has begun to subluxate, the deformity tends to progress with the passing of time (Fig. 6-14). A patient with more than 10 to 15 degrees of lateral deviation of the distal metatarsal articular surface may have a significant hallux valgus deformity that is symptomatic because of the presence of a prominent medial eminence, even though the joint is congruent and tends to be stable. In some circ*mstances, alignment of the first MTP joint is normal but a valgus deformity is present because of a deformity within the proximal phalanx, and a hallux valgus interphalangeus (HVI) deformity results (Fig. 6-15). No muscle inserts into the first metatarsal head, and as a result its position is influenced by the position of the proximal phalanx. Because medial and lateral movement of the first metatarsal is to a great extent controlled by the position of the proximal phalanx, a certain degree of mobility at the MTC joint must exist for this to occur. A horizontal orientation tends to resist an increase in the intermetatarsal (IM) angle, whereas an oblique orientation is a less stable articulation.

Figure 6-14 A, Subluxated metatarsophalangeal (MTP) joint with a hallux valgus deformity. B, Moderate metatarsus adductus with a congruent MTP joint (distal metatarsal articular angle, 37 degrees; hallux valgus angle, 37 degrees).

Figure 6-15 Hallux valgus interphalangeus. A, Clinical photo. B, Radiographic appearance. C, Schematic diagram of the abnormality. D, Clinical appearance of the distal interphalangeus. E, Radiographic appearance. F, Clinical appearance. G, Radiographic appearance of the interphalangeus that developed after an epiphyseal injury in adolescence.

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Extensor hallucis longus tendon

Head width stays normal

Adductor hallucis

Flexor hallucis brevis

Figure 6-16 Pathophysiology of hallux valgus deformity. Normally, the metatarsal head is stabilized within the sleeve of ligaments and tendons, which provide stability to the joint. As the proximal phalanx deviates laterally, it places pressure on the metatarsal head, which deviates medially. This results in attenuation of the medial joint capsule and contracture of the lateral joint capsule.

The pathophysiology of a hallux valgus deformity varies, depending on the nature of the deformity. With a congruent hallux valgus deformity, the basic deformity consists of the prominent medial eminence (the bunion), which results in pressure against the shoe and thus a painful bursa or cutaneous nerve over the prominence. The MTP joint itself is stable, and the deformity does not usually progress in adults. With an incongruent or subluxated hallux valgus deformity, there is usually a progressive deformity. As the proximal phalanx moves laterally on the metatarsal head, it exerts pressure against the metatarsal head, which pushes it medially and results in an increased IM angle. As this process occurs, there is progressive attenuation of the medial joint capsule, as well as a progressive contracture of the lateral joint capsule (Figs. 6-16 and 6-17). While this deformity is occurring, the sesamoid sling, which is anchored laterally by the insertion of the adductor hallucis muscle and the transverse metatarsal ligament, remains in place as the metatarsal head moves medially and thereby creates pressure on the medial joint capsule. The weakest portion of the medial joint capsule lies just above the abductor hallucis tendon, and with chronic pressure, this portion of the capsule gives way; as a result, the abductor hallucis muscle gradually slides beneath the medially deviating metatarsal head. As this process slowly progresses, atrophy of the crista occurs beneath the first metatarsal head, which normally helps stabilize the sesamoids (Fig. 6-18). Once the abductor hallucis slides beneath the first metatarsal head, two events occur. First, the intrinsic muscles no longer act to stabilize the MTP joint but actually help enhance the deformity. Second, as the abductor hallucis rotates beneath the metatarsal head, because it is connected to the proximal phalanx, it will spin the proximal phalanx around on its long axis and give rise to 162

Figure 6-17 Progression of both hallux valgus and a 1–2 intermetatarsal angular deformity over a 5-year period. A, Initial radiograph. B, Twenty years later, a simultaneous increase in both angular deformities has occurred.

varying degrees of pronation (Fig. 6-19). It has been well established that as the hallux valgus deformity progresses, so does the degree of pronation.336,344 Because of this abnormal rotation, calluses may develop along the medial aspect of the interphalangeal (IP) joint. Ultimately, as the MTP joint becomes less stable, the hallux carries less weight, body weight is transferred laterally in the forefoot, and callus may develop beneath the second, third, or both metatarsal heads. Increased pressure may lead to capsulitis, instability, or deviation of the second MTP joint as well. With severe hallux valgus deformities, the extensor hallucis longus tendon is displaced laterally as the medial

Hallux Valgus ■ Chapter 6

Tendon of adductor hallucis muscle Tendon of abductor hallucis muscle

Sesamoids

Tendon of flexor hallucis brevis muscle

Figure 6-18 Relationship of the sesamoids to the metatarsal head. A, Diagram demonstrating the sesamoids stabilized by the crista, followed by atrophy of the crista as the metatarsal head deviates medially off the sesamoids. B, Normal relationship of the sesamoids to the crista. C, Moderate hallux valgus deformity. D, Severe hallux valgus deformity.

hood ligament and capsule become stretched. As a result, when the extensor hallucis contracts, it not only extends the toe but also tends to adduct it, thus further aggravating the deformity. The abductor hallucis tendon, by migrating plantarward, loses its remaining abduction power. The flexor hallucis longus tendon, which retains its relationship to the sesamoids, moves laterally and also becomes a dynamic deforming force. In rare circ*mstances, if the progressive deformity of the MTP joint continues unabated, dislocation of the MTP joint may occur over time, with the fibular and tibial sesamoids becoming dislocated into the first IM space (Fig. 6-20). Normally, a small eminence is present on the medial aspect of the first metatarsal head. The size of the medial eminence varies, and sometimes most of the enlargement is on the dorsomedial aspect of the head and is thus not apparent on anteroposterior (AP) radiographs. Volkman540 and Truslow527 both suggested that new bone formation occurred with bunion formation, whereas Lane293 and Haines and McDougall200 suggested that merely a segment of the first metatrsal head had become exposed with lateral deviation of the hallux. Thordarson and Krewer515 and Coughlin and Jones101 have both demonstrated that the size of the medial eminence was similar in subjects with and without bunions, and the authors concluded that bony proliferation was not a component of bunion formation. The overall width of the distal metatarsal head does not enlarge with progression of a hallux valgus deformity. Thordarson and Krewer reported an average width of the medial eminence of 4.4 mm, whereas Coughlin and Jones101 reported the mean width to be 4.6 mm in subjects with bunions (Fig. 6-21). The medial eminence develops with lateral migration of the proximal phalanx, but it is not characterized by new bone formation or hypertrophy of the medial first metatarsal head. As the hallux valgus deformity develops, progressive medial deviation of the metatarsal head occurs and becomes symptomatic because of pressure against the shoe. Individuals who wear a broad, soft shoe or sandal are not usually bothered by the enlarged medial eminence, in contrast to persons who wear dress or highheeled shoes. At times, an inflamed or thickened bursa

EHB MEDIAL

ABH

ADH FHBM

FHBL

A EHB LATERAL ADH FHBL ABH

FHBM

B Figure 6-19 Schematic representation of tendons around the first metatarsal head. A, Normal articulation in a balanced state. B, Relationship of the tendons in hallux valgus deformity. ABH, abductor hallucis; ADH, adductor hallucis; EHB, extensor hallucis brevis; FHBL, flexor hallucis brevis lateral head; FHBM, flexor hallucis brevis medial head.

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Spokes

Hub

Figure 6-20 A, Diagram of severe hallux valgus. B, Severe end-stage hallux valgus deformity with dislocation of metatarsophalangeal joint and sesamoid mechanism into first web space.

because the first metatarsal head is no longer contained within the sesamoid sling and is displaced in a medially deviated position. The middle metatarsals do not splay because of the stable articulation at their tarsometatarsal joints. On occasion, the fifth metatarsal lacks stability and drifts laterally, thereby completing the appearance of a splayed foot. As the hallux drifts laterally, the lesser toes, particularly the second toe, are under increasing pressure. In response to this pressure, the second MTP joint may remain stable, and the great toe may drift beneath the second toe or occasionally on top of it. At other times, progressive subluxation or complete dislocation of the second MTP joint occurs. On occasion, no subluxation affects the second MTP joint; rather, all the lesser toes are pushed into lateral deviation or a “wind-swept” appearance resulting from extrinsic pressure from the hallux.

Figure 6-21 Technique of measuring the medial eminence. A, A longitudinal line is drawn along the medial diaphyseal shaft of the first metatarsal. A perpendicular line (A) is then drawn at the widest extent on the medial eminence and measured. B, Radiograph.

Age of Onset

may aggravate the problem. On rare occasions and usually in older patients, the skin over the medial eminence can break down and result in a draining sinus. On other occasions, a ganglion arising from the medial side of the joint can erode the joint capsule and make the eventual hallux valgus repair technically much more difficult (see Fig. 6-1D). The splayed appearance of the forefoot in more severe cases of hallux valgus (see Fig. 6-9) occurs primarily

Piggott414 reported on a series of adult patients evaluated for hallux valgus deformities. Fifty-seven percent of the patients interviewed recalled an onset of the deformity during their adolescent years, whereas only 5% recalled development of the bunion deformity after 20 years of age. In a long-term review of patients with hallux valgus deformities, Hardy and Clapham208 reported that 46% of bunion deformities occurred before the age of 20. Although Scranton471 stated that a hallux valgus deformity rarely develops before 10 years of age, Coughlin95 reported on a series of juvenile patients with bunions in whom the

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average age at onset was 12 years; 40% of these patients noted that the onset of their deformity occurred at the age of 10 years or younger. Thus development probably occurs much earlier than has previously been appreciated.* In contrast, Coughlin91 reported onset by decade in a group of men and noted that 21 of 34 (62%) patients dated the development of their bunion to the third to fifth decade of life. Only 7 of 34 (20%) recalled onset in the adolescent years. Later, Coughlin and Jones101 stated that 65% of adults reported the onset of their deformity in the third through fifth decades and only 4% in the first decade. Although the onset of hallux valgus indeed peaked during the third decade, the incidence of occurrence was almost equal throughout the second through fifth decades. There was not relationship between the severity of the deformity and the decade of onset. At what age a patient recognizes a hallux valgus deformity is obviously dependent on understanding the deformity, the symptoms, magnitude of the deformity, family history, and keenness of a patient’s observation skills. Many deformities can begin in the adolescent years but progress in magnitude in later decades when they become more symptomatic. The date when surgery was performed should not be confused with the age at onset. Coughlin and Jones101 noted that although patients recalled the onset of their bunion deformity at a mean age of 31 years, the average age at which surgery was performed was 50 years. Increasing age was not associated with increasing magnitude of angular deformity. In a retrospective study, Coughlin and Thompson112 reviewed more than 800 cases and reported the mean age at surgery to be 60 years. Of importance is the fact that late development after skeletal maturity occurs in a foot that at one point most likely had a normal structure, whereas an early onset in the juvenile years occurs before maturation in a foot that most likely “never had a normal structure.” Coughlin95 observed, in a series of patients with juvenile hallux valgus, that early onset of hallux valgus (before 10 years of age) was associated with a much higher distal metatarsal articular angle (DMAA), a finding that would probably alter the choice of operative technique in these patients. Gender Although several studies have provided statistical data showing some predilection in the female population for the development of hallux valgus, this may be merely a reflection of a specific person’s choice of footwear. Wilkins,552 in a study of schoolchildren’s feet, reported a female preponderance of 2 : 1. Hewitt et al221 and Marwil and Brantingham,350 in investigating male and female military recruits, found a predilection of approximately 3 : 1 in the female population. Creer114 and Hardy and Clapham,207 in reporting statistics from their surgical practices, found this ratio to be approximately 15 : 1 in

B Figure 6-22 A, Normal foot on the left, foot in a fashionable shoe on the right. B, Photograph of the foot and shoe.

adult patients. The reported incidence of females in the juvenile population undergoing surgical correction for hallux valgus deformities varies from 84% to 100%.* Several studies on adult patients report females make up 90% or more of the patient population.† Coughlin and Jones101 found that the proportion of females in their report on moderate and severe hallux valgus deformities was 92% (P < .01). Certainly, shoes worn by women are generally less physiologic than those worn by men, and shoes of any type can lead to hallux valgus in susceptible persons; however, it is also likely that heredity plays a substantial role in the development of bunion deformities (Fig. 6-22). On the contrary, Akinbo et al,3 in a study of young Nigerians, reported close to equal female (56%) and male (44%) involvement in an adolescent population. Pique-Vidal et al419 observed that gender did not *References 73, 217, 370, 513, 514, and 526. References 34, 38, 73, 74, 112, 207, 255, 312, 318, 336, 352, 370, and 414. †

*References 10, 58, 170, 195, 364, 471, and 472.

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effect the severity of the angular deformity. Pique-Vidal419 did not note an association between gender and severity of deformity in his series of 350 subjects. Bilaterality The authors previously believed that hallux valgus deformities commonly occurred as unilateral deformities.339 This notion was based on reports of the results of surgical procedures in which a majority of patients underwent unilateral surgery.* However, this information does not truly document the incidence of bilaterality. Patients may have bilateral deformities yet have surgery performed on only one side. They may undergo bilateral surgery yet have only the index surgery performed during the period of study. Even though many reports cite unilateral occurrence, the author’s prospective evaluation of moderate and severe hallux valgus deformities demonstrated that although 84% of patients had bilateral hallux valgus deformities, only 18% had both feet corrected during the study period.101 The remaining surgery occurred either before or after the reported study. There was no association between bilateral deformities and handedness, family history, or the magnitude of the preoperative deformity. There was a strong correlation between bilateralism and a family history of bunions (P < .01). Symptoms and varying magnitudes of deformity may lead a person to desire unilateral correction despite having bilateral hallux valgus deformities. The authors believe that the majority of patients have bilateral hallux valgus deformities of differing magnitude.

ETIOLOGY

Extrinsic Causes Footwear Hallux valgus occurs almost exclusively in persons who wear shoes but does occasionally occur in unshod people (Fig. 6-23). The notion of footwear being the principal

Handedness Ninety percent of the population is right handed,550 but how this translates to foot dominance is unknown.549 Coughlin and Jones101 reported that 91% of patients who underwent bunion surgery were right handed and were unable to find a correlation between handedness and foot side involved, age of onset, or severity of the hallux valgus deformity. Although most series report the number of right and left feet involved, it is unknown whether handedness makes a difference in development of the deformity.

Frequency of Occurrence Myerson384 has suggested that hallux valgus deformities develop in 2% to 4% of the population. Although no published study has reported the frequency of development or the rate of surgical correction of hallux valgus deformities in the United States, Coughlin and Thompson112,513 estimated that more than 200,000 hallux valgus corrections are performed in the United States each year. This figure is probably an underestimate of both the incidence of the deformity and the frequency of surgical correction. *References 73, 140, 344, 348, 454, and 535.

166

C Figure 6-23 A, Normal feet of young woman during weight bearing. B, Feet in shoes during weight bearing. Note the developing hallux valgus. C, Effects of different types of shoes. The left shoe permits freedom of forefoot function; the right shoe restricts function of the four lesser toes.

Hallux Valgus ■ Chapter 6

contributor to the development of hallux valgus was substantiated by a study of Sim-f*ck and Hodgson487 in which 33% of shod persons had some degree of hallux valgus as compared with 2% of unshod persons. Owoeye et al3,398 reported a very low incidence of hallux valgus in Nigerian youth in a typically unshod population. Hallux valgus deformities were also extremely rare in the Japanese because of the nature of their traditional footwear, the tabi sandal (Fig. 6-24). When the manufacture of fashionable leather shoes greatly exceeded the manufacture of traditional sandals in the 1970s, the incidence of hallux valgus deformity increased substantially.259 Conversely, physicians in France referred to the development of hallux valgus deformities as early as the 18th century. Before that time, the common footwear was a GrecoRoman style, flat-soled sandal. Studies by Maclennan322 in New Guinea, Wells547 in South Africa, Barnicot and Hardy21 in West Africa, Engle and Morton148 in the Belgian Congo, and James239 in the Solomon Islands found some element of metatarsus primus varus and an occasional asymptomatic hallux valgus deformity in the indigenous populations (Fig. 6-25). Cho et al67 has reported in a study from a rural Korean community, that female subject

Figure 6-24 Traditional Japanese sandal.

in the fourth through seventh decades had a higher incidence of deformity. One can conclude from these studies that an asymptomatic hallux valgus deformity in an unshod person may be attributed to hereditary causes. In shoe-wearing populations, however, a symptomatic and painful bunion would be expected to develop more commonly.113,221 A wide or splayed forefoot forced into a constricting shoe might thus lead to symptoms over the medial eminence. Although shoes appear to be an essential extrinsic factor in the development of hallux valgus, the deformity does not develop in many people who wear fashionable footwear. Therefore some intrinsic predisposing factors must make some feet more vulnerable to the effect of footwear and likewise predispose some unshod feet to the development of hallux valgus. Although high-fashion footwear has been implicated in the progression of hallux valgus deformities in adults,* Hardy and Clapham207 and others95,249 have suggested that in most cases a juvenile hallux valgus deformity does not appear to be influenced by a history of constricting footwear. Poorly fitting shoes play a small role in juvenile hallux valgus. In a prospective study of adults with hallux valgus, Coughlin and Jones101 reported that only 34% of patients undergoing surgical correction implicated constricting footwear as a cause of their deformity. In an earlier report, Coughlin91 found that 60% of men with hallux valgus who had undergone surgical correction implicated ill-fitting shoes as a cause of their deformity. Occupation Cathcart62 and Creer114 have implicated occupation as a cause of hallux valgus. Again, objective evidence in the small percentage of patients who claim that their occupation contributed to their hallux valgus deformity is lacking. Coughlin and Jones101 reported that patients considered occupation an infrequent cause of their deformity, with 17% implicating their job as a cause of their hallux valgus deformity. However, there was not a correlation between the magnitude of the angular deformity and those who attributed their deformity to either occupation or constricting shoewear. Trauma Trauma to the forefoot may be a cause of acute deformity or chronic deviation to the MTP joint. Rupture of the medial joint capsule has been recognized as a cause leading to development of a bunion deformity.151 Johal et al241 reported a bunion deformity that followed a tibial shaft fracture with entrapment and injury to the medial plantar nerve. Bohay et al37 reported seven cases in which a Lisfranc joint injury led to first MTC joint instability and later bunion deformity. Surgical correction with a standard bunion correction in several of these cases led to realignment of the first ray.

Figure 6-25 Kenyan tribesman with an asymptomatic hallux valgus deformity. (Courtesy J.J. Coughlin, MD.)

*References 5, 105, 164, 361, 471, and 487.

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Intrinsic Causes Heredity The notion that a hallux valgus deformity is inherited has indeed been suggested by many authors.* A positive family history of hallux valgus in 58% to 88% has been reported in five different series of adult patients.73,184,207,370,427 Coughlin and Jones101 stated that 86 of 103 adult patients (84%) reported a family history (parents, grandpartents) of hallux valgus deformities. In 1956, Johnston248 reported an in-depth genetic history on subjects with hallux valgus. Based on a singlefamily case report, he proposed that this trait was autosomal dominant with incomplete penetrance. Juvenile hallux valgus deformities have been characterized by their familial tendency. Coughlin95 reported a family history in 72% of patients in his retrospective study on juveniles and noted that a bunion was identified in 94% of 31 mothers of children with a family history of hallux valgus deformity. Of the 31 patients with a positive family history for the deformity, four females noted an unbroken fourgeneration history of hallux valgus transmission from maternal great-grandmother to maternal grandmother to mother to patient (Fig. 6-26). Eleven females reported a three-generation history of transmission from maternal grandmother to mother to patient, and 11 patients noted a two-generation history of mother-to-patient transmission. Of three males with hallux valgus in this same series, two reported their mothers to have had a bunion and one reported a three-generation history of maternal transmission to the patient. Thus 29 of 31 patients (94%) with a family history showed a pattern consistent with maternal transmission. The preoperative hallux valgus deformity in these patients was reported to be 5 degrees greater in those with a family history, although the average postoperative hallux valgus correction was similar in patients with and without a family history. Pique-Vidal et al,419 in a report of 350 patients with hallux valgus, constructed a three-generation pedigree. The gender ratio was male : female 1 : 15; juveniles comprised only 5% of the series. Ninety percent of the subjects had at least one other relative with a bunion; 70% of the subjects had at least three relatives with bunion involvement. The authors also observed that severity of the deformity was not affected by gender or the magnitude of deformity in other relatives. Both Bonney and Macnab38 and Coughlin95 observed an earlier onset of deformity in patients with a family history of hallux valgus. The high rate of maternal transmission noted in previous reports95,207 makes it difficult to avoid a conclusion that there is a genetic predisposition for hallux valgus deformities in the female population. However, the chapter authors believe that although this trait can be associated with X-linked dominant transmission or polygenic transmission, it more commonly is *References 38, 58, 95, 101, 110, 138, 145, 170, 184, 197, 201, 318, 419, 472, and 514.

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Figure 6-26 A family history of juvenile hallux valgus is common. A, Hallux valgus in a 16-year-old girl. B, Hallux valgus of long-standing duration in her 33-year-old mother. C, Hallux valgus in her 60-year-old grandmother. D, Hallux valgus in her 85-year-old great-grandmother, present since her youth.

an autosomal dominant transmission with incomplete penetrance.95,419 Pes Planus The association of pes planus with the development of a hallux valgus deformity is controversial. A low incidence of advanced pes planus in adults with hallux valgus led Mann and Coughlin to conclude that the occurrence of hallux valgus with pes planus is uncommon in patients without neuromuscular disorders.336 The incidence of pes planus in the general population was defined in a review of normal adult military recruits by Harris and Beath.210 They reported a 20% incidence of pes planus. Half of these cases represented an asymptomatic “simple depression of the longitudinal arch.” In general, pes planus may be no more common in those with hallux valgus than in the general population.* Pouliart et al427 did not observe any relationship between the degree of pes planus and the severity of hallux valgus. Kilmartin and Wallace272 found that the incidence of pes planus in the normal *References 95, 101, 110, 272, 336, 459, and 526.

Hallux Valgus ■ Chapter 6

MFA

+4 +3 +2 +1 0 -1 -2 -3 -4 -5 -6

+4 +3 +2 +1 0 -1 -2 -3 -4 -5

Figure 6-27 A, Pes planus deformity. B, Lateral talometatarsal angle demonstrating pes planus. Harris mat imprint (C) demonstrating a normal arch and a pes planus deformity (D) (MFA, midline foot axis, a line drawn from the middle of the second toe imprint to the center of the heel imprint. An imprint medial to the MFA represents a low-arched foot or pes planus). (C and D, Used with permission from Grebing B, Coughlin M: Evaluation of Morton’s theory of second metatarsal hypertrophy. J Bone Joint Surg Am 86:1375-1386, 2004.)

population and in those with a hallux valgus deformity was essentially the same. They concluded that pes planus in juveniles had no significant association either with the magnitude of the preoperative hallux valgus deformity or with the postoperative success or failure rate of a surgical repair. This finding was confirmed by Coughlin95 and Trott,526 and McCluney and Tinley,359 who all noted no increased incidence of pes planus in juvenile patients. Studies by Canale et al,58 Coughlin95 and Kilmartin and Wallace272 have reported no correlation between pes planus and the success rate of surgical repair of a hallux valgus deformity. Coughlin and Jones100,101 reported a 15% incidence of moderate and severe pes planus in their surgical series of 122 feet with hallux valgus. Arch height has been quantified by both Harris mat imprints and radiographic measurements (Fig. 6-27).103,110 Coughlin and Kaz103 reported good correlation between Harris mat imprints and physical examination and angular measurements, such as the lateral talometatarsal angle, lateral talocalcaneal angle, calcaneal pitch, and the AP taolnavicular angle. Grebing and Coughlin192 used Harris mat imprints to assess arch height and demonstrated that a low arch was significantly more common in an adult group with hallux valgus than in a control group. They reported an 11% incidence of pes planus in a normal control group and a 24% incidence in a group with hallux valgus but also found no correlation between the hallux valgus angle and pes planus or between pes planus and first-ray mobility. Saragas and Becker459 did not find an increased incidence of pes planus when they examined

the calcaneal pitch angle and found no association between the degree of pes planus and the severity of hallux valgus deformity. King and Toolan275 observed an association between the hallux valgus angle and both the Meary line (lateral talometatarsal angle) and the AP talonavicular coverage angle in those with pes planus. Other authors have suggested that a hallux valgus deformity tends to develop in a pronated foot.* Hohmann225 was the most definitive and asserted that hallux valgus was always associated with pes planus and that pes planus is always a causative factor in hallux valgus. In attempting to resolve this contradiction, the chapter authors believe that a patient with a pes planus deformity in whom hallux valgus develops will have more rapid progression of the deformity. However, hallux valgus does not develop in most patients with pes planus. Models and radiographs can demonstrate the role of pronation in the pathophysiology of hallux valgus in a normal foot (Figs. 6-28 to 6-31). Although an excellent demonstration of the effect of pronation on the foot and hallux. They do not enable determination of what initiates a hallux valgus deformity. In Figure 6-28, a pendulum has been attached to the nail of the great toe. As the foot is pronated, rotation of the first ray around its longitudinal axis is clearly seen. In Figure 6-29, a skeletal model has been photographed. With longitudinal rotation of the *References 9, 28, 73, 89, 90, 113, 138, 150, 165, 205, 223, 230, 235, 254, 255, 353, 354, 385, 444, 462, 466, 486, 503, and 534.

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Figure 6-28 Longitudinal rotation of the first ray. A, Supination. B, Pronation. A pendulum is attached to the toenail of the great toe.

Figure 6-29 Skeletal model of the demonstration in Figure 6-28. A, Supination. B, Pronation.

B A

Figure 6-30 Foot during weight bearing. A, Supination. B, Pronation. Note the apparent lateral displacement of the sesamoids.

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Figure 6-31 Tangential views of the sesamoids during weight bearing. A, Supination. B, Pronation. The degree of longitudinal rotation of the metatarsal is clearly demonstrated by the position of the sesamoids, which still retain a normal relationship to their facets beneath the metatarsal head.

Hallux Valgus ■ Chapter 6

first metatarsal head, the fibular sesamoid becomes visible on the lateral side of the first metatarsal head. Figure 6-30 shows a dorsoplantar weight-bearing radiograph; with the pronated position of the sesamoids, they appear to have been displaced laterally. The fibular sesamoid is now visible in the interval between the first and second metatarsals, as would be anticipated from the skeletal model in Figure 6-31. Tangential or sesamoid views of the foot show that this appearance is caused solely by longitudinal rotation of the first metatarsal, not by actual lateral displacement; the sesamoids remain in a normal relationship with their facets located on the plantar surface of the metatarsal head (see Fig. 6-31). Pronation of the foot imposes a longitudinal rotation of the first ray (metatarsal and phalanges) that places the axis of the MTP joint in an oblique plane relative to the floor. In this position, the foot appears to be less able to withstand the deforming pressures exerted on it by either shoes or weight bearing.255 No data are available on the relationship between the degree of pes planus and the degree of hallux valgus in the small percentage of unshod persons in whom the condition develops. Furthermore, authors who have noted a relationship between pes planus and hallux valgus in shod people have presented no quantitative data.* To discount pronation entirely, however, is not appropriate because in some cases it can play a substantial role in the development and progression of specific hallux valgus deformities. Pronation of the foot does alter the axis of the first ray.258 With weight bearing, the first MTP joint assumes an oblique orientation with the ground. In some pronated feet, especially in patients with ligamentous laxity, pressure exerted on the medial capsule of the first MTP joint can lead to progression of a hallux valgus deformity because the soft tissue supporting structures are unable to withstand these deforming forces. In such pathologic situations, a physician should be aware of possible progression of deformity, as well as postoperative recurrence. The use of prefabricated or custom orthoses in these patients may be beneficial. Persons with a mild hallux valgus deformity may experience rapid progression of the deformity if instability of the hindfoot secondary to rupture of the posterior tibial tendon, hindfoot valgus secondary to rheumatoid arthritis, or instability of the first MTC joint develops. Therefore pronation of the foot can be a factor predisposing to hallux valgus in certain conditions because the medial capsular structures offer limited resistance to the strong deforming forces. Hypermobility of the Metatarsocuneiform Joint The concept of hypermobility of the first ray was introduced by Morton in 1928.376,377 Later, Lapidus294-296 suggested an association between increased mobility of the first MTC joint and hallux valgus. Many reports dealing with correction of hallux valgus implicate first-ray hypermobility as a cause yet offer no proof regarding the *References 28, 73, 138, 205, 225, 235, 246, and 466.

magnitude of preoperative or postoperative mobility.* The notion of this theory has been advanced by Hansen, Sangeorzan, and others.73,205,456 Others have disputed the significance of first-ray mobility as a cause of hallux valgus.† In reports on series involving the treatment of hallux valgus, Dreeben and Mann136 and others99,110 have found no evidence of firstray hypermobility after surgical correction of a hallux valgus deformity. Wanivenhaus and Pretterklieber544 reported a 7% incidence of MTC joint instability. Coughlin and Jones100 reported that 23 of 122 patients (10%) with moderate or severe halllux valgus preoperatively were observed to have increased first-ray mobility. Clinical assessment of sagittal plane mobility of the first ray was described by Morton,376,377 who suggested that with the ankle in neutral position, the examiner stabilize the lateral aspect of the forefoot with one hand and then grasp the first ray with the other hand (Fig. 6-32). The first ray was translated in a dorsal plantar direction until a soft end point was reached. First-ray hypermobility was defined as excess motion on this examination. The biomechanical axis of the first MTC joint is obliquely placed, which permits motion of the metatarsal head to occur in a dorsomedial to plantar-lateral direction (Fig. 6-33). This oblique motion of the joint can indeed be qualitatively observed on physical examination, but attempting to quantify it clinically has been difficult. Although Morton claimed that first-ray hypermobility led to a multitude of foot problems,376,377 he concluded that there was no reliable method by which he could quantify the magnitude of first-ray hypermobility.377 Efforts to quantify MTC mobility have proved difficult,162,386,456 and surprisingly, no report of the results of first MTC joint arthrodesis has provided data on the preoperative and postoperative magnitude of first-ray mobility.386,456 Attempts to quantify first-ray mobility have measured motion in either degrees152,236,544 or millimeters of either dorsal displacement or total excursion176-181 (Fig. 6-34). Efforts to accurately measure first-ray mobility have evolved to the use of external calipers in recent years. Klaue, Hansen, and Masquelet279 described a noninvasive caliper consisting of a modified ankle–foot orthosis and an external micrometer to quantify first-ray mobility. The authors found measurable, repeatable values for both normal and hypermobile first rays and concluded that hypermobility was often associated with the development of hallux valgus. They reported that normal adult patients had approximately 5 mm of flexibility at the MTC joint, and patients with hallux valgus had 9 mm or more of mobility. Although the applied force is not standardized when using this device, both the examination and the position of the foot and ankle are actually quite similar to the manual examination as originally described by Morton.377,539 Jones et al252 have substantiated that the *References 14, 28, 73, 88, 204, 205, 219, 279, 305, 383, 385, 386, 456, and 466. † References 110, 111, 136, 190, 208, 448, and 492.

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Figure 6-32 Examination for metatarsophalangeal (MTC) instability of the first ray. A and B, The lesser metatarsals are grasped between the index finger and the thumb of one hand, and the first metatarsal is grasped with the other hand. With the ankle in neutral position, the first metatarsal head is moved in the dorsoplantar direction. With a stable MTC joint, the distal ray does not become excessively elevated. C and D, With hypermobility, the first metatarsal head can be pushed in a dorsal direction above the sagittal plate axis of the lesser metatarsal heads. E and F, The ankle must be maintained in neutral position, or “false hypermobility” may be diagnosed.

Figure 6-33 The mechanical axis of the first metatarsocuneiform joint is from plantar lateral to dorsomedial.

Klaue device is reliable and gives reproducible measurements of first-ray excursion.252 Glasoe et al179,180 demonstrated comparability of both the Klaue device and the Glasoe device for external measurement of first-ray mobility. Other reports have also demonstrated that external calipers are reliable in quantifying first-ray motion.84,176-178,181 172

Klaue et al279 and others176,192 used external calipers to measure first-ray mobility and reported greater mobility in patients with hallux valgus deformities than in control subjects. However, both Glasoe et al177 and Cornwall et al84 reported that the manual testing technique, as described by Hansen204 and others,* was quite unreliable and not reproducible when compared with mechanical testing techniques. Using the Klaue device to assess postoperative first-ray mobility after treatment with various hallux valgus surgical techniques, Coughlin et al99 reported that the measured mobility was 4 mm after MTP arthrodesis and 5 mm after distal soft tissue reconstruction with proximal first metatarsal osteotomy.110 In both series, no first-ray hypermobility was observed after correction of the bunion. However, in neither of these studies were measurements made before correction of the hallux valgus (because this measurement device had not been available). Sarrafian460 observed that the position of the ankle secondarily affects tension on the plantar aponeurosis (Fig. 6-35). Rush et al450 suggested that first-ray motion could affect tension on the plantar aponeurosis and windlass mechanism, thus secondarily diminishing first-ray mobility. *References 28, 73, 144, 204, 383, 385, 386, 456, and 262.

Hallux Valgus ■ Chapter 6

A A

B Figure 6-35 Plantar aponeurosis in neutral position (A) and plantar flexion of the ankle (B). Lax aponeurosis may play a significant role in first-ray hypermobility when the examination is conducted with the ankle in plantar flexion.

B Figure 6-34 Two examples of external devices used to quantify first-ray hypermobility. A, Klaue device. B, Glasoe device. (Courtesy Ward Glasoe.)

It was Grebing and Coughlin190 who defined the position of manual examination by investigating a group of patients with a modified Klaue device that enabled them to dorsiflex and plantar flex the ankle while measuring first-ray mobility (Fig. 6-36). A control group (mean mobility, 5 mm), a group with moderate and severe hallux valgus (mean mobility, 7.0 mm), a group that had previously undergone first MTP arthrodesis (mean mobility, 4.4 mm), and a group that had previously undergone plantar fasciectomy (mean mobility, 7.4 mm) were studied. When the ankle was placed in 5 degrees of dorsiflexion, first-ray mobility was significantly diminished in all four groups. When the ankle was placed in 30 degrees of plantar flexion, there was significantly increased mobility in the first three groups; however, the group that previously underwent plantar fasciectomy did not experience an increase in first-ray mobility. Of interest is that in the hallux valgus group, when examined in neutral position, 21% were considered hypermobile, but when they

B Figure 6-36 Modified Klaue device in dorsiflexion (A) and plantar flexion (B) demonstrating a substantial difference in first-ray mobility.

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IMT

MCT

Figure 6-37 A, Anteroposterior radiograph of an asymptomatic foot with medial cortical hypertrophy. B, Measurements of medial cortical thickness (MCT), intramedullary thickness (IMT), and shaft thickness (ST) demonstrate no correlation with hypermobility of the first ray and hallux valgus. (B, Used with permission from Grebing B, Coughlin M: Evaluation of Morton’s theory of second metatarsal hypertrophy. J Bone Joint Surg Am 86:1375-1386, 2004.)

were examined in plantar flexion, 92% were considered hypermobile. Thus the position of the ankle substantially influences the perceived first-ray mobility. When the ankle is plantar flexed 30 degrees, the amount of first-ray mobility is increased almost twofold. Coughlin et al,102 in a cadaver study of specimens with hallux valgus, reported that first-ray mobility as measured with the Klaue device was 11 mm preoperatively. After distal soft tissue repair and proximal osteotomy to correct the deformity, mean first-ray mobility was 5 mm. In a follow-up prospective study in which a similar operative repair was performed on 122 feet with moderate and severe hallux valgus deformities, Coughlin and Jones100,101 reported first-ray mobility to have a preoperative mean of 7.3 mm that was reduced to a mean of 4.5 mm after surgical correction. Thus, with the ability to actually quantify first-ray mobility, the authors concluded that first-ray mobility is an effect of the hallux valgus deformity rather than a cause in most cases. The fact that it is reduced to a normal level after distal surgical realignment or proximal first metatarsal osteotomy that spares the MTC joint101,102,110 makes a strong case for increased firstray mobility being a secondary rather than a primary cause. First-ray stability is probably a function of first-ray alignment and the effectiveness of the intrinsic and extrinsic muscles and the plantar aponeurosis and not an intrinsic characteristic of the first MTC joint. Coughlin and Jones101 reported no correlation between first-ray mobility and the magnitude of the hallux valgus angular deformities. Although Morton377 claimed that first-ray hypermobility was characterized by increased mobility on manual clinical examination, he concluded that the most notable structural feature of first-ray hypermobility was hypertrophy of the second metatarsal diaphysis as demonstrated 174

on an AP radiograph (1928). Prieskorn et al429 attempted to relate mobility of the first MTC joint to thickening of the second metatarsal shaft and found no correlation. Grebing and Coughlin192 analyzed second metatarsal shaft width and medial cortical hypertrophy (in a series of 172 patients, with 25,000 data points) and found no association with hallux valgus, first-ray mobility, or first metatarsal length. They concluded that using second metatarsal cortical hypertrophy or shaft width was an inappropriate indication for first MTC joint arthrodesis in the treatment of a hallux valgus deformity (Fig. 6-37). Opsomer et al,396 in a later study of second-ray medial cortical thickness after hallux valgus correction, reported osseous diminution of the cortical thickness in as little as 11 months after surgery. In their series of 13 patients in which differences were measured in hundreths of millimeters, their claim that redistribution of weight-bearing patterns led to cortical thinning is questionable. The significance of the preoperative measurement, as well as the postoperative changes will require a much more rigorous process with a larger study, and longer-term follow-up. Coughlin and Jones101 and Cooper et al81 have reported no correlation between measured first-ray mobility and any radiographic angular measurements defining pes planus (Meary’s line, calcaneal pitch, AP talonavicular coverage, lateral talocalcaneal angle). Myerson384 and King and Toolan275 suggested that a radiographic gap on the plantar aspect of the first MTC joint is associated with both hallux valgus and first MTC joint instability. The incidence of this finding is unknown. Coughlin and Jones,100 in a prospective study of moderate and severe hallux valgus deformities, reported a 23% incidence of plantar gapping. Of those 122 cases, the average first-ray mobility as measured by the Klaue device was 7.2 mm. The mean hallux valgus angle for these cases was 30

Hallux Valgus ■ Chapter 6

B Figure 6-38 A, The first metatarsal lift is the difference in the perpendicular distance between the inferior border of the base of the first metatarsal and the inferior border of the first cuneiform. B, The first metatarsal–medial cuneiform angle is demonstrated on the lateral radiograph. (Courtesy Chris Coetzee, MD.)

degrees. With respect to the preoperative presence of plantar MTC joint gapping, there was no significant difference in first-ray mobility between those with and without gapping. Of interest, one third of those joints with a gap resolved after distal realignment of the bunion deformity. It is likely that the plantar gapping as seen on the lateral radiograph is indicative of sagittal plane instability, just as metatarsus primus varus is indicative of axial plane instability. King and Toolan,275 in a small series (25 cases), described the first metatarsal medial cuneiform angle (MMCA) as a possibly being a reliable measure of dorsiflexion or plantar wedging of the first MTC joint (Fig. 6-38). All patients in King and Toolan’s series were considered to have first-ray instability when assessed by manual examination, although the magnitude of mobility was not quantified or reported. They described increased dorsiflexion through the first MTC joint (hallux valgus patients, 2 degrees; controls, 0.2 degree) and concluded that this demonstrated an association between the clinical and radiographic findings of first-ray hypermobility and hallux valgus. In the Coughlin study,100 in which a much larger cohort was examined, no evidence was found to support King and Toolan’s notion275 that an increase in first metatarsal-cuneiform angle was associated with increased first-ray mobility. If increased sagittal motion of the first ray is a primary factor that predisposes to the onset of a hallux valgus deformity, one would not expect a substantial reduction

in first-ray mobility after a surgical realignment distal to the first MTC joint. Postcorrection measurements of firstray mobility (using Klaue device measurements) after a distal realignment procedure (both in vivo and in vitro) demonstrate consistent and regular reduction of first-ray mobility.91,99,100,102,274 Sarrafian460 has suggested that the plantar aponeurosis plays a key role in first-ray stability. The chapter authors believe that realignment of the first ray restores normal anatomic relationships (intrinsic and extrinsic muscles, plantar aponeurosis) and that this, in turn, leads to a diminution in first-ray mobility. Thus the stability of the first ray, in most cases, is a function of the alignment of the first ray and is not an intrinsic characteristic of the first MTC joint. Ligamentous Laxity Carl et al59 observed mild generalized ligamentous laxity in a small series of patients with hallux valgus. Clark et al,73 in a report on juveniles, noted that 69% of patients in their series had generalized laxity on physical examination. Others88,336,385 have mentioned ligamentous laxity as an etiologic factor. Beighton and Bird29 defined ligamentous laxity with a 9-point scale in which 2 points were awarded for hyperextension of both elbows beyond 10 degrees (1 point for only one elbow), 2 points for hyperextension of both knees beyond 10 degrees (1 point for only one knee), 2 points for extension of the little finger beyond 90 degrees (1 point for each hand), 2 points for extension of the thumb flat with the wrist (1 point for each hand), and 1 point for the ability to place the hands flat on the ground with the knees extended. A total of 9 points can be accumulated on the examination. A score greater than 6 points indicated generalized ligamentous laxity or hypermobility. Beighton noted that most individuals (94% of males and 80% of females) score 2 or fewer points (Fig. 6-39). Although studies88,336,385 have correlated hyperflexibility of the thumb with hypermobility of the first ray, no study has documented the preoperative and postoperative laxity of patients with Beighton and Bird’s method. In one retrospective study99 of a group of patients with moderate and severe hallux valgus deformities treated by first MTP arthrodesis (mean hallux valgus angle, 42 degrees), 17 of 19 patients demonstrated no evidence of any laxity on the 9-point examination (0 points). Although postoperative recurrence may be a concern in treating patients with ligamentous laxity, the incidence is most likely quite low. Grimes and Coughlin196 evaluated a series of subjects treated with first MTP joint arthrodesis for previously failed hallux valgus surgery. They closely evaluated this series of 29 patients (33 feet) with the Beighton examination and found only 5 of 29 (14%) had confirmed ligamentous laxity. Of interest, only two patients had first-ray hypermobility as confirmed on the Klaue apparatus. Nonetheless, attention should be addressed to ligamentous laxity in any evaluation before correction of hallux valgus. Although the finding of ligamentous laxity is probably uncommon in the typical adult patient with 175

Part II ■ Forefoot

hallux valgus, patients with Ehlers-Danlos or Marfan syndrome may be better treated conservatively because they may have an increased risk of postoperative recurrence. Achilles Contracture Morton377 defined normal ankle dorsiflexion as requiring 15 degrees. Mann and Coughlin336 and others28,88,89,205

D Figure 6-39 Beighton criteria for ligamentous laxity. The 9-point scoring system awards points for hyper-laxity: able to touch palms of hands on the floor with knees extended = 1 point for each side (A), able to touch thumb to radial forearm = 1 point for each side (B), able to touch index finger to extensor surface of forearm = 1 point for each side (C), and elbow hyperextension = 1 point for each side (D). Values over 5 points are considered to indicate ligamentous laxity in the patient.

have suggested that on occasion, a contracted Achilles tendon is associated with the development of hallux valgus. In contrast, Coughlin and Shurnas110 noted an absence of heel cord tightness in their series and found no correlation between ankle dorsiflexion and hallux valgus (Fig. 6-40). DiGiovanni et al,134 when using 10 degrees or less of ankle dorsiflexion as a guideline, noted that 44% demonstrated “restricted dorsiflexion.” When using 5 degrees or less of ankle dorsiflexion as a guideline for surgical intervention, they observed that 8 of 34 normal subjects (24%) had restricted dorsiflexion and recommended surgical lengthening of the Achilles complex. Grebing and Coughlin192 studied the incidence of ankle range of motion in normal subjects and patients with hallux valgus. In the control group, the mean ankle dorsiflexion was 9 degrees, and in the hallux valgus group it averaged 11 degrees. They reported that 19% of normal patients they studied had ankle dorsiflexion of 5 degrees or less. In a similarly sized group of patients with hallux valgus, 21% demonstrated ankle dorsiflexion of 5 degrees or less. Grebing and Coughlin noted that 81% of controls and 67% of those with hallux valgus had 10 degrees or less of ankle dorsiflexion. No correlation was found between ankle dorsiflexion and the magnitude of hallux valgus. In the report by Coughlin and Jones,101 no correlation was demonstrated between ankle dorsiflexion and the hallux valgus angle. Gastrocnemius lengthening has been recommended for patients with a limitation of 5 degrees or more.204 However, none of the patients in the series reported by Grebing and Coughlin192 were symptomatic, and no Achilles tendon lengthening were performed in the course of their treatment. An Achilles tendon contracture secondary to any cause can produce a gait pattern in which the person slightly externally rotates the foot or tends to roll off the medial border of the foot. This repetitive stress against the hallux has been postulated to lead to a hallux valgus deformity. This can be observed in patients with

B C A Figure 6-40 Ankle range of motion is quantified with the hindfoot in neutral position (A) and the knee both extended (B) and flexed (C).

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neuromuscular disorders (e.g., cerebral palsy, poliomyelitis) or patients who have had a CVA. Although DiGiovanni et al134 suggested that gastrocnemius lengthening be performed in patients undergoing foot surgery with dorsiflexion of less than 5 degrees, the fact that 81% of subjects demonstrated less than 10 degrees of ankle dorsiflexion suggests that this finding may not be abnormal. Furthermore, Coughlin and Jones101 reported an incidence of 12% to 54% in patients with moderate and severe hallux valgus who had either less than 5 degrees (14 feet, 12%) or less than 10 degrees (66 feet, 54%) of ankle dorsiflexion. Of the 122 feet in the series, in no case was an Achilles tendon lengthening or gastrocnemius slide procedure performed in conjunction with the bunion correction. There was no correlation between the success of surgery and the tightness of the gastrocnemius–soleus complex. Although on occasion a gastrocnemius–soleus contracture may accompany a hallux valgus deformity, the chapter authors believe this to be uncommon, and lengthening is recommended in the uncommon patients with substantial restriction in ankle dorsiflexion. Miscellaneous Factors Obesity or an increased body mass index (BMI) has been shown to present an increased risk factor for tendonitis, plantar fasciitis, and degenerative arthritis of the lower extremity, but has not been associated with an increased risk of hallux valgus.160 Amputation of the second toe often results in a hallux valgus deformity, probably from loss of the support afforded by the second toe (Fig. 6-41). Mild hallux valgus may be seen after resection of the second metatarsal head. Syndacylization of the first and second toes has been reported to occur with a hallux valgus deformity.432 Cystic degeneration of the medial capsule of the first MTP joint can occur. The resulting ganglion formation may sufficiently attenuate the capsule to permit the development of a hallux valgus deformity (see Fig. 6-1D). Hallux valgus has been reported to occur with the development of a space occupying mass in the first IM space (Fig. 6-42).566

Figure 6-41 A, Clinical appearance. B, Radiograph of severe hallux valgus after amputation of the second toe.

ANATOMIC AND RADIOGRAPHIC CONSIDERATIONS

Angular Measurements Radiographs of the foot should always be taken with the patient in the weight-bearing position. The basic studies should include AP, lateral, and oblique views. The AP radiographs are obtained with a tube-to-film distance of 1 m and the x-ray tube centered on the tarsometatarsal joint and angled 15 degrees toward the ankle joint, relative to the plantar aspect of the foot.106 Hallux Valgus Angle On an AP weight-bearing radiograph, axes are drawn on the first metatarsal and proximal phalanx so that they bisect metaphyseal reference points in the proximal and distal metaphyseal regions that are equidistant from the medial and lateral cortices of the proximal phalanx and the first metatarsal. The angle created by the intersection of these axes forms the hallux valgus angle. A normal angle is less than 15 degrees,207 mild deformity is less than 20 degrees, moderate deformity is 20 to 40 degrees, and severe deformity is greater than 40 degrees88 (Fig. 6-43). 1–2 Intermetatarsal Angle On an AP weight-bearing radiograph, reference points are placed in the proximal and distal metaphyseal regions equidistant from the medial and lateral cortices of the first and second metatarsals.106 The angle created by the intersection of these axes forms the 1–2 intermetatarsal angle. Normal is less than 9 degrees,207 mild deformity is 11 degrees or less, moderate deformity is greater than 11 and less than 16 degrees, and severe deformity is greater than 16 degrees88 (Fig. 6-44). Hallux Interphalangeal Angle On an AP weight-bearing radiograph, reference points are placed in the proximal and distal metaphyseal regions equidistant from the medial and lateral cortices of the proximal phalanx to create an axis of the proximal phalanx.108 Reference points are placed at the center of the base of the distal phalanx and at the tip of the distal phalanx, and a second axis is drawn. The intersection of these two axes forms the hallux IP angle (Fig. 6-45). Distal Metatarsal Articular Angle On an AP weight-bearing radiograph, the DMAA defines the relationship of the distal first metatarsal articular surface to the longitudinal axis of the first metatarsal.98 Points are placed at the most medial and lateral extent on the distal first metatarsal articular surface. A line connecting these points defines the lateral slope of the articular surface. Another line is drawn perpendicular to this articular line. The angle subtended by this perpendicular line and the longitudinal diaphyseal axis of the first metatarsal defines the DMAA. Normal is regarded as 6 degrees or less of lateral deviation (Fig. 6-46).438 177

Part II ■ Forefoot

E Figure 6-42 A, Clinical photograph demonstrating hallux valgus deformity on left. B, Anteroposterior radiograph showing large osseous lesion on second metatarsal creating widening of the 1–2 intermetatarsal (IM) angle. C, Intraoperative photograph showing bony lesions. D, Resected specimen. E, After removal of the mass, a marked reduction in the IM angle has occurred. (Courtesy Young Koo Lee, MD. Used with permission. From Young KW, Lee KT, Kwak JJ, et al: Mass-induced unilateral hallux valgus. Orthopedics 33:927, 2010.)

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A B

Hallux valgus ( 20 degrees correction or an IM angle > 15 degrees), a proximal metatarsal osteotomy has been recommended in conjunction with a distal soft tissue realignment.* In a subsequent review of 72 feet in 47 patients undergoing distal soft tissue realignment, Mann and Pfeffinger343 reported postoperative satisfaction in 92% of patients. The main reason for satisfaction was pain relief, decreased deformity, and diminution in bunion size. Unrestricted footwear was possible in 20% of patients preoperatively and 53% postoperatively. This still left 47% of patients unable to wear the shoes of their choice. The overall level of activity increased in 66% of patients and was unchanged in 34%. Table 6-1 presents the preoperative and postoperative hallux valgus and IM angles for the entire group, and Table 6-2 lists the results by severity of the deformity. These results once again confirm that a satisfactory outcome can be obtained in the treatment of mild and *References 69, 82, 101, 122, 136, 140, 142, 153, 167, 168, 186, 233, 303, 306, 344, 387, 392, 409, 416, 443, 457, 481, 508, 516, and 535.

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Table 6-2 Summary of Results of Distal Soft Tissue Procedures by Severity of Deformity Varus

Mild (40°)

Patients with Postoperative Hallux

4 51

57 55

11 57

6 56

Mean Hallux Valgus Angle Preoperative 18° Postoperative 11°

31° 15°

46° 19°

37° −7.5°

Mean First/Second Intermetatarsal Angle Preoperative 10.7° Postoperative 8.5°

14° 8.6°

17° 10°

17° 5°

Number of feet Mean age (yr)

From Reference 343.

Table 6-3 Postoperative Correction before and after Distal Soft Tissue Procedures Preoperative Intermetatarsal Angle Hallux Valgus Angle Preoperative Postoperative Correction

≤15°

>15°

28 11 17

38 18 20

From Reference 343.

moderate hallux valgus deformities. However, with a severe deformity, a distal soft tissue procedure alone will not usually result in a satisfactory outcome. Table 6-3 compares the results in patients with an IM angle of less than 15 degrees and greater than 15 degrees and demonstrates that with severe deformity, a distal soft tissue procedure alone is routinely incapable of achieving satisfactory realignment. In the entire series, only 41% of feet had a residual hallux valgus angle of less than 16 degrees. This figure emphasizes that the reliability of this procedure, particularly for a more advanced deformity, is not good, and the procedure is indicated mainly for mild and low-end moderate deformities. Complications Recurrence of Deformity. Recurrence may be related to one or more of the following factors: ■ ■ ■

■ ■ ■

Inadequate postoperative dressings Insufficient plication of the medial joint capsule Inadequate release of the lateral joint contracture, which may include the capsule, adductor hallucis tendon, or transverse metatarsal ligament Insufficient medial capsular tissues secondary to degenerative changes or cyst formation Failure to recognize and treat metatarsus primus varus Failure to recognize a congruent joint

Arthrofibrosis. Slight loss of motion occurred after surgery.343 Range-of-motion measurements demonstrated 67 degrees of dorsiflexion and 8 degrees of plantar flexion, compared with 75 and 16 degrees, respectively, in the uninvolved foot. Arthrofibrosis may be caused by the following: 212

■

Postoperative infection Unrecognized arthrosis of the MTP joint ■ Unrecognized causes ■ Realignment of a congruent joint ■

Peripheral Nerve Entrapment. On occasion, the dorsal or plantar cutaneous nerve to the great toe becomes injured or entrapped, which can cause pain if a large neuroma develops. Use of the incisions as described in this section reduces this complication to a minimum. Hallux Varus. The major complication encountered in the series of Mann et al344 was an 8% incidence of hallux varus deformity, which averaged 7.5 degrees (Fig. 6-101). The position of the proximal phalanx influenced the IM angle; the IM angle was corrected 12 degrees in feet with hallux varus versus 5 degrees in those without overcorrection. In all cases of hallux varus, the tibial sesamoid subluxated medially; however, in only half the feet with medial sesamoid subluxation did a hallux varus deformity develop. Preoperatively, the feet in which a hallux varus deformity developed were characterized by more severe deformities. Mann and Coughlin339 recommended that release of the lateral MTP joint capsule be performed without a lateral sesamoidectomy. After this modification, a reduced rate of hallux varus was reported.335,337 Use of the stump of conjoined adductor tendon and cuff of the lateral MTP capsule to reinforce the lateral capsule at the time of surgical correction may also help minimize the incidence of postoperative hallux varus.93 See page 300 at the end of this chapter for a discussion of hallux varus. Intermetatarsal (Interosseous) Fixation. There have been several reports of second metatarsal stress fractures with the use of cerclage suture techniques and with suturebutton fixation devices.261,265,323,422 This has lead to modifications of the technique, not only downsizing the device but also placing it in a more proximal location in the second metatarsal. The technique is avoided in those patients with osteopenia. AKIN PROCEDURE An Akin procedure2 achieves correction of a hallux valgus deformity by means of a medial capsulorrhaphy, resection of the medial eminence, and medial closing-wedge

Hallux Valgus ■ Chapter 6

Figure 6-101 Hallux varus deformity after a distal soft tissue procedure with excision of the fibular sesamoid. A, Mild. B, Moderate. C, Severe deformity with medial deviation of the lesser toes. D and E, Postoperative radiographs demonstrating moderately severe hallux varus deformity with subluxation of the medial sesamoid.

phalangeal osteotomy (Video Clips 52 and 53).11,404,476,520,538 This procedure can produce a satisfactory result in the treatment of specific types of deformities but is not indicated in the presence of MTP joint subluxation. Indications The primary indication for this procedure is a hallux valgus interphalangeus (HVI) deformity (Fig. 6-102).420 In the presence of a congruous MTP joint with a significant hallux valgus deformity and an increased IM angle, extraarticular repair can be achieved by a combination of proximal phalangeal osteotomy and first metatarsal osteotomy (Fig. 6-103).80,371,404,520 The use of an extraarticular repair may prevent disturbance of a congruent MTP articulation.97,186 It is also useful to achieve derotation of a pronated hallux,404,447,468 and shortening in patients with a long proximal phalanx.224,447 After an initial surgical procedure complicated by recurrent deformity, if any residual lateral deviation of the hallux results in pressure against the second toe, a phalangeal osteotomy can angulate the hallux medially away from the adjacent second toe. The procedure can also be used in conjunction with almost any bunion

Figure 6-102 Hallux valgus interphalangeus: clinical (A) and radiographic (B) appearance.

correction in which some valgus of the hallux is still present.80,101,371,404,520 A phalangeal osteotomy can be combined with a more proximal first-ray osteotomy (Fig. 6-104).101,404,520 On occasion, a phalangeal osteotomy can be used without a medial eminence resection and medial capsular reefing if only an osteotomy is indicated to realign the great toe. 213

Part II ■ Forefoot

Figure 6-103 Moderate hallux valgus deformity. A, Preoperative radiographic appearance. B, Radiograph after a chevron osteotomy with correction of the hallux valgus angle. C, Twelve-year follow-up after the procedure.

Figure 6-104 A, Preoperative radiograph. B, After a Mann-Akin procedure.

Contraindications The Akin procedure is contraindicated as a primary procedure to correct a hallux valgus deformity if there is any subluxation of the MTP joint. An Akin procedure does not decrease the 1–2 IM angle; therefore, with a significant metatarsus primus varus deformity, an Akin procedure alone is insufficient to correct the deformity. This procedure can actually lead to destabilization of the MTP joint if used as a primary procedure to correct a hallux valgus deformity characterized by a subluxated MTP joint.420 Technique The surgical technique for the Akin procedure is divided into exposure, performance of the osteotomy, and reconstruction of the joint capsule and osteotomy. 214

Surgical Exposure 1. A medial longitudinal skin incision is centered over the medial eminence, just proximal to the IP joint and extended 1 cm proximal to the medial eminence. Dorsal and plantar full-thickness skin flaps are created, with care taken to protect the dorsomedial and plantar medial cutaneous nerves. 2. An L-shaped, distally based capsular flap is created. With this L-shaped flap, the dorsal and proximal MTP joint capsular attachments are released while the distal and plantar capsular attachments remain intact. The capsule is carefully dissected off the medial eminence (see Fig. 6-91D). 3. Through this same exposure, subperiosteal dissection is used to expose the phalangeal metaphyseal region, with care taken to protect the distally based capsular flap. The soft tissue is not stripped past the dorsomedial and plantar medial surfaces of the proximal phalanx. Alternative to Step 2: A vertical capsulotomy is made with a No. 11 blade, starting 2 to 3 mm proximal to the base of the proximal phalanx. A second cut is made parallel to the first, with no more than 2 to 4 mm of capsular tissue removed. The amount of capsular excision depends on the size of the medial eminence (see Fig. 6-91B). Technique of Resection of the Medial Eminence and Phalangeal Osteotomy 1. With an oscillating saw, the medial eminence is resected in line with the first metatarsal medial cortex. The osteotomy is begun slightly medial to the sagittal sulcus and extended proximally along the medial border of the first metatarsal. The remaining edges,

Hallux Valgus ■ Chapter 6

particularly on the dorsomedial aspect of the metatarsal head, are smoothed with a rongeur. 2. A small, medially based wedge of bone is resected in the metaphyseal, diaphyseal-metaphyseal, or diaphyseal region. The location of the osteotomy depends on the site of maximal deformity, which in the proximal phalanx may be central, proximal, or distal (Figs. 6-105A and B and 6-106).447 (A mini–image intensifier can be used to check the location of the phalangeal osteotomy site in reference to the location of the MTP joint, IP joint, and, in a juvenile patient, open epiphysis.)

3. The lateral cortex of the phalanx is left intact (minimally), and the osteotomy site is closed. Routinely, a 2- to 3-mm–wide resection is performed with the apex at the lateral base; however, depending on the magnitude of the deformity, the closing-wedge osteotomy may be smaller or larger (see Fig. 6-105C and D). In addition, the surgeon must keep in mind that the phalangeal surface of the MTP joint is concave. When performing the initial osteotomy, there is a risk of penetrating the joint with the saw blade. A second cut is made slightly distal to the first, and usually 3 to 4 mm of bone is removed at the medial aspect of the

Figure 6-105 Technique of Akin phalangeal osteotomy. Preoperative clinical (A) and radiographic (B) appearance. C, Operative incision for just phalangeal osteotomy. D, Two parallel cuts are made for the medially based closing-wedge osteotomy. E, The wedge is removed. F, The osteotomy is closed and fixed with two Kirschner wires. Postoperative clinical (G) and radiographic (H1 and H2) appearance after osteotomy. (An interdigital neuroma and Weil osteotomy was performed as well.)

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compression pin (Fig. 6-107D), or screws (Fig. 6-107E) may be used to stabilize the osteotomy site. 4. The skin is approximated with interrupted sutures and a compression dressing applied.

Figure 6-106 A, Proposed phalangeal osteotomy. B, After the osteotomy.

osteotomy site. One should attempt to maintain a periosteal hinge laterally. If pronation of the hallux is present, the hallux can be derotated at the osteotomy site before placement of fixation to correct any remaining deformity (see Fig. 6-105E). Reconstruction of the Joint Capsule and Osteotomy 1. The medial joint capsule is repaired because, after this step, one can predict how much correction must be gained from the phalangeal osteotomy. The MTP capsule is repaired with interrupted absorbable suture. If insufficient capsule is present on the dorsal proximal aspect of the MTP joint, a small hole can be drilled in the metaphysis to anchor the capsular flap. 2. After capsular repair, the osteotomy site is approximated medially to assess alignment of the hallux. If the alignment is inadequate, more bone can be resected. The osteotomy site is stabilized with one or two 0.062-inch Kirschner wires (K-wires) (see Fig. 6-105F-H). The pin or pins are placed obliquely from a distal medial location. Care is taken to avoid penetration of the IP and MTP joints. Intraoperative fluoroscopy or intraoperative radiography can be used to visualize the final position of the K-wire. The pins are cut flush with the level of the skin to aid in later removal. 3. An alternative method of fixation of the osteotomy site can be achieved by using a staple, heavy suture, or wire placed through two pairs of medial drill holes, one on the dorsomedial aspect and one on the plantar medial aspect of the osteotomy site. This suture is passed through the drill holes and tied to stabilize the osteotomy (Fig. 6-107A). A compression staple520 can also be used (Fig. 6-107B); multiple K-wires (Fig. 6-107C), 216

Postoperative Care A gauze-and-tape toe spica compression dressing is applied after surgery (Fig. 6-108). The patient is permitted to ambulate in a postoperative shoe with weight borne on the outer aspect of the foot. The dressing is changed 1 to 2 days after surgery and then on a weekly basis. The toe is held in a neutral or slight varus position during this healing phase to allow the capsular tissues and osteotomy site to heal adequately. Rarely is casting necessary after a phalangeal osteotomy. The dressing is maintained until the osteotomy site has healed, which typically takes 6 to 8 weeks. If K-wires were used for internal fixation, they are removed 3 to 6 weeks after surgery. Motion of the IP and MTP joints is initiated at this time. Results The best indication for the use of an isolated Akin phalangeal osteotomy is hallux valgus interphalangeus (Fig. 6-109). There are no studies that report the results of isolated Akin osteotomies for interphalangeal deformities alone. When used to correct a mild residual deformity after a previous hallux valgus correction, a phalangeal osteotomy can produce a satisfactory result, provided that the MTP joint is congruent and the residual valgus is caused by lateral sloping of the distal phalangeal articular surface (Fig. 6-110). The use of internal fixation is helpful in maintaining the operative correction and should achieve rigid stabilization of the osteotomy; malunion and nonunion are uncommon (Fig. 6-111).473 The Akin procedure achieves little correction of the 1–2 IM angle.185,420 In reporting on a series of 22 adult patients, Plattner and Van Manen420 initially observed an average 13-degree correction of the hallux valgus angle; however, at long-term follow-up, this correction diminished to only 6 degrees of correction. Seelenfreund et al473 and Goldberg et al185 reported high recurrence rates (16%21%) and a high rate of postoperative dissatisfaction and concluded that isolated phalangeal osteotomy as treatment of a hallux valgus deformity does not have a sound biomechanical basis and is contraindicated as an isolated procedure (Figs. 6-112 and 6-113). Toth et al520 reported on 22 consecutive Akin osteotomies and noted an average correction of 9 degrees at the osteotomy site. All were done in combination with a first metatarsal osteotomy. No delayed or nonunions were noted. The average shortening of the phalanx was 2  mm. Shannak et al,476 who suggested the Akin procedure can reliably achieve approximately 10 degrees of angular correction, recommended locating the osteotomy 5 mm distal to the apex of the proximal phalangeal MTP articular surface. Although Akin2 and Colloff and Weitz80 advocated lateral MTP capsular release, the chapter authors believe

Hallux Valgus ■ Chapter 6

Figure 6-107 Alternative means of osteotomy fixation. A, Osteotomy site. Heavy suture material has been placed through drill holes on either side, after which the osteotomy site is closed and the sutures tied to secure the osteotomy in place. B, Small compression staple. C, Akin osteotomy fixed with multiple Kirschner wires. D, Fixation with compression pin. E, Fixation with cross-compression screws.

that, in general, a wide capsular release should be avoided because it has the potential for devascularizing the proximal phalangeal fragment or the epiphysis in a younger patient. Extensive soft tissue stripping of the proximal phalanx should be avoided because it may lead to vascular compromise of the proximal fragment. Intraarticular extension of the osteotomy with subsequent arthritis occurs infrequently.447 Complications Overcorrection can develop because of an excessively large medial-wedge resection.476,538 Shannak et al476 advised a wedge resection of approximately 3 mm, although they cautioned that males (with typically increased width of the proximal phalanx) required a larger wedge than females. Vilas et al538 reported performing a medial exostectomy of the IP joint after overcorrection with an Akin ostetomy.

The main complication of the Akin procedure is recurrence or progression of a deformity when the procedure was used to treat a deformity characterized by an incongruent or subluxated MTP joint (see Fig. 6-112). On occasion, when a phalangeal osteotomy is used to treat a hallux valgus deformity characterized by a congruent joint, the MTP joint may sublux postoperatively. Significant loss of IP joint plantar flexion of the great toe may occur, especially if the osteotomy is carried out distal to the midportion of the phalanx. If care is not taken, the tendon of the flexor or extensor hallucis longus could be inadvertently severed, particularly when the osteotomy is performed in the distal portion of the phalanx. AVN of the proximal phalanx may occur after excessive soft tissue stripping or excessive retraction of the soft tissues (Fig. 6-114). Other reported complications with this procedure include a poor cosmetic appearance and a high rate of subjective dissatisfaction postoperatively.42,185,473 217

Part II ■ Forefoot DISTAL METATARSAL OSTEOTOMY (CHEVRON PROCEDURE) The technique for a distal chevron osteotomy was initially described by Austin and Leventen12,13 and Corless.83 With a chevron osteotomy, resection of the medial eminence,

distal metatarsal osteotomy, and medial capsulorrhaphy are used to realign the hallux, thereby producing some narrowing of the forefoot (Video Clip 54). Since its initial description, several modifications in the technical part of the procedure have been made, including the angle of the osteotomy and the use of various alternative methods of internal fixation. An Akin procedure has been added by some371 to augment the angular correction. There have been numerous modifications made in an attempt to use this technique for more moderate bunion deformities* Indications In general, a chevron osteotomy is indicated for mild and low-moderate hallux valgus deformities (hallux valgus angle < 30 degrees or 1–2 IM angle < 13 degrees) with subluxation of the first MTP joint.92,222,365,415 When used in patients with a greater deformity, particularly the IM angle, the procedure’s capability of achieving correction diminishes. The limits of the osteotomy rest in the width of the metatarsal neck available for displacement. A chevron osteotomy provides an extraarticular correction and can also be used for the treatment of a hallux valgus deformity with a congruous first MTP joint if the DMAA is 15 degrees or less. For the occasional patient with a DMAA greater than 15 degrees or in the presence of a congruent or minimally subluxated hallux valgus deformity, the end result can be enhanced by removal of a small wedge of bone from the medial aspect of the chevron cut to enable the articular surface to be rotated more perpendicular to the long axis of the metatarsal (Fig. 6-115) (Video Clip 62).71 Modifications have been described for this scenario as well, allowing reproducible biplanar correction to diminish an increased DMMA.85,128,408,517,518 Likewise, moving the apex of the

B Figure 6-108 A, Immediate postoperative dressing. B, Dressing used for the remainder of treatment.

*References 17, 220, 301, 307, 382, 393, 400, 402, 408, 517, and 518.

Figure 6-109 A, Preoperative radiograph demonstrating an irregularly shaped metatarsal head. This metatarsal head will not permit correction by medial displacement because an incongruent articular surface will result. B, Postoperative radiograph demonstrating satisfactory alignment after an Akin procedure, with removal of the medial eminence without affecting the articular surface. Preoperative (C) and postoperative (D) radiographs of hallux valgus demonstrate correction with the Akin procedure and excision of the medial eminence.

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Figure 6-110 A, Preoperative radiograph of mild recurrence of hallux valgus deformity. B, Correction of recurrence with the Akin procedure. Preoperative (C) and postoperative (D) radiographs demonstrate correction of hallux valgus interphalangeus with the Akin procedure. Note that the osteotomy site is near the apex of the deformity, whereas in a routine Akin procedure, it is carried out in the proximal portion of the phalanx.

B Figure 6-111 A, Rigid internal fixation holds the osteotomy. B, Dorsiflexion malunion resulting from early weight bearing.

osteotomy slightly proximal tends to increase the angular correction that can be achieved. A chevron osteotomy does not correct hallux pronation and only partially corrects sesamoid subluxation. The indications for a chevron osteotomy, when combined with a phalangeal osteotomy,371 include a hallux valgus deformity with a congruous first MTP joint (DMAA < 20 degrees), as well as mild or moderate pronation of the hallux. Whereas Hattrup and Johnson213 initially suggested that postoperative patient satisfaction seemed to decrease somewhat in patients older than 60 years, Trnka523,524,525 reported high levels of satisfaction in even older age groups.

Contraindications The main contraindication to a traditional chevron osteotomy is a moderate-to-severe deformity, with the hallux valgus angle exceeding 35 degrees, the IM angle exceeding 15 degrees, and a congruous first MTP joint with a DMAA greater than 15 degrees. Moderate or severe pronation of the hallux is difficult to correct with the chevron procedure. Advanced age is only a relative contraindication, but it may be associated with decreased MTP joint motion. In patients with moderate or advanced joint arthrosis, stiffness usually develops after a chevron procedure, and thus an alternative procedure should be considered. Medial Approach and Exposure of the Metatarsal Head 1. A longitudinal incision is centered over the medial eminence beginning at the midportion of the proximal phalanx and extending 1 cm proximal to the medial eminence (Fig. 6-116A). The dissection is carried down to the joint capsule, and full-thickness dorsal and plantar skin flaps are created. As the dorsal flap is created, caution is exercised to avoid damage to the dorsomedial cutaneous nerve. As the plantar flap is created, the surgeon must avoid the plantar medial cutaneous nerve. 2. An L- or V-shaped, distally based capsular flap is developed as previously described for a distal soft tissue procedure (Fig. 6-116B and C), with detachment of the dorsal and proximal capsular attachments.309 Alternative Technique: A vertical capsular incision is made approximately 2 to 3 mm proximal and parallel to the base of the proximal phalanx. A second capsular incision is made 2 to 4 mm more proximal but parallel to the first cut. The two capsular incisions are joined dorsally by an inverted-V cut (see Fig. 6-91B and C). The capsular flap is then grasped with forceps and dissected plantarward, and a second V cut is made through 219

Part II ■ Forefoot

Figure 6-112 A, Preoperative radiograph demonstrating moderate hallux valgus deformity in a 25-year-old woman. B, After an Akin osteotomy and resection of the medial eminence, the 1–2 intermetatarsal angle has not been corrected. C, At final follow-up, the radiograph demonstrates recurrence of the deformity with subluxation of the metatarsophalangeal joint.

Figure 6-113 A, Preoperative radiograph demonstrating a hallux valgus interphalangeus deformity. B, Radiograph after an Akin phalangeal osteotomy. C, Seven years later, a radiograph demonstrates acceptable long-term alignment. (Note: medial capsulorrhaphy and medial eminence resection were not performed.)

the abductor hallucis tendon. With this inferior cut, the knife blade must remain inside the joint and come to rest against the tibial sesamoid at the apex of the plantar cut, to prevent damage to the plantar medial cutaneous nerve. (Rarely is more than 4 mm of capsule removed.) An incision is made along the dorsomedial aspect of the metatarsal head to create a capsular flap, which when retracted exposes the medial eminence. Soft tissue reflection should be limited to a degree necessary for exposure of the medial prominence and sulcus. Care should also be taken to avoid excessive soft tissue stripping with Hohmann retractors.

Figure 6-114 Complications after the Akin procedure. A, Delayed union or nonunion of the osteotomy site. B, Avascular necrosis.

220

Technique of Osteotomy 1. The medial eminence is resected with an oscillating saw (or osteotome) in a line parallel with the medial border of the foot (Fig. 6-116D). The plane of the osteotomy through the medial eminence is not parallel to the metatarsal shaft but rather slightly oblique,

Hallux Valgus ■ Chapter 6

Figure 6-115 Biplanar chevron osteotomy. With an increased distal metatarsal articular angle, a biplanar chevron osteotomy is performed. A transverse chevron osteotomy is placed in a similar location. A, However, more bone is removed from the dorsomedial and plantar medial limb of the osteotomy to allow realignment (B and C) of a congruent metatarsophalangeal joint articulation with lateral translation of the capital fragment. D, Closing-wedge osteotomy. E, Closure of the osteotomy site. F, Preoperative radiograph. G, Postoperative radiograph after a biplanar chevron osteotomy. H and I, With screw fixation.

which creates a broad base of the capital fragment that adds stability to the osteotomy site as it is displaced laterally. The cut begins at the lateral edge of the sagittal sulcus and is carried proximally (Fig. 6-117A). Any osteophytes, including the medial ridge of the sagittal sulcus, are removed with a rongeur. 2. Although the authors do not routinely release the adductor tendon and lateral capsular structures, others have successfully performed a release in conjunction with a chevron osteotomy.193,281,410,421,523 Some surgeons reach through the joint and release the lateral capsule,307,505 whereas others choose an open exposure with a separate intermetatarsal dissection.* Excessive soft tissue stripping is avoided because it may endanger circulation to the metatarsal head. Most of the *References 19, 63, 193, 410, 464, 523, and 524.

blood supply emanates from the dorsal and plantar aspects of the metatarsal head.410 The authors believe, however, that if the deformity is so severe as to require a formal lateral release, rather than stretching the indications for a chevron osteotomy, another procedure might be preferable because the risk for vascular compromise would be eliminated. 3. The distal chevron osteotomy is carried out in the metaphyseal region because this area provides a large surface area for bone contact that is quite stable and aids in rapid healing (Fig. 6-117B). A 2-mm drill hole is useful to mark the apex of the osteotomy on the metatarsal head. The drill hole is placed at the center of an imaginary circle in which the radius is the distal articular surface (see Fig. 6-116E). The hole is made in a lateral direction, parallel to the bottom of the foot and articular surface. A horizontal osteotomy is 221

Part II ■ Forefoot

J Figure 6-116 Technique for the chevron procedure. A, The skin incision is centered over the medial aspect of the metatarsophalangeal joint, starting at the midportion of the proximal phalanx and carried proximally about 6 cm. B, An L-shaped capsular flap is used to expose the medial eminence and is retracted (C). D, The medial eminence is resected. E, A hole is drilled in the center of the metatarsal head to mark the apex of the osteotomy. F, The chevron osteotomy is performed at a 60-degree angle. G, The osteotomy is fixed with a dorsoplantar pin. H, Care is taken to avoid excess plantar placement of the pin. I, The medial flare is resected. J, Skin closure.

created with an oscillating saw blade that has a fine in-line tooth configuration so as to avoid excessive bone resection. The angle of the chevron cut diverges at approximately a 60-degree angle; the base is oriented proximally (see Fig. 6-116F). The plantar cut must exit proximal to the sesamoids, which places it just proximal to the synovial fold, thereby making it extraarticular. As the osteotomy is performed, the surgeon can feel the saw blade meet and penetrate the lateral cortex; care must be taken to not overpenetrate the cortex and enter the lateral soft tissues, which may damage the blood supply to the metatarsal head (Fig. 6-117E).71 It is critical that the osteotomy arms do not venture proximally, because this would create 222

further shortening and the risk of transfer metatarsalgia. Badwey et al15 reported that the capital fragment can be displaced laterally up to 6  mm in males and 5  mm in females, which constitutes displacement of approximately 30% of the metatarsal’s width. To displace the osteotomy, it is sometimes useful to hold the proximal portion of the metatarsal with a small towel clip while pushing the metatarsal head laterally (Fig. 6-117C). 4. Alternative Technique: The authors have also used a vertical distal osteotomy with a longitudinal plantar cut as an alternative to a chevron osteotomy. This enables placement of a dorsoplantar screw and is also more adaptable for a biplanar osteotomy (Fig. 6-118).

Hallux Valgus ■ Chapter 6

Sagittal groove

Medial approach A

Osteotomy MEDIAL B

Chevron osteotomy

LATERAL

DSTP osteotomy

C Lateral soft tissue release (contraindicated)

Figure 6-117 A, With a chevron osteotomy, resection of the medial eminence proceeds in line with the medial border of the foot. (With a distal soft tissue repair, the resection is in line with the medial border of the first metatarsal.) B, A drill hole is placed equidistant from the dorsal, distal, and plantar metatarsal articular surface. This point marks the apex of the osteotomy, with the chevron osteotomy oriented in a mediolateral plane. C, The capital fragment is translated laterally (arrow). D, The osteotomy is stabilized with a Kirschner wire, and the capsule is anchored by suture through the metaphyseal drill hole. E, Dorsal view of the first metatarsal demonstrating the vascular supply to the first metatarsal head. Distal metatarsal osteotomy (B) combined with extensive lateral soft tissue release (C) and medial capsulorrhaphy (A) may compromise the vascularity of the capital fragment. DSTP, distal soft tissue procedure.

Figure 6-118 A, Through a medial approach, the eminence is resected. B, A longitudinal osteotomy is made parallel to the plantar surface of the foot, exiting above the sesamoid articulation. C, A vertical cut is made proximal to the articular surface. D, If biplanar correction is necessary, a single medial-based wedge is removed. E, A compression screw is placed. F, The medial flare is shaved with a saw.

Reconstruction of the Joint 1. Once the osteotomy is displaced and the proximal phalanx centered on the articular surface of the metatarsal head, if a significant degree of valgus still remains, a uniplanar or biplanar chevron osteotomy is added to produce a medial closing-wedge effect128 (Figs. 6-119 and 6-120). Two to 3 mm of bone can be removed from the medial aspect of the metatarsal cut to produce this medial closing osteotomy and realignment of the

articular surface. Rarely is it necessary to remove more than this amount of bone. After the initial chevron osteotomy, the surgeon retracts the capital fragment distally by grasping the osteotomized surface with a small, two-pronged bone hook. An oscillating saw is then used to resect a small, medially based wedge of bone from the medial superior (and medial inferior surfaces if biplanar), with the resection beveled toward the lateral aspect of the metatarsal metaphysis. When 223

Part II ■ Forefoot

Figure 6-119 Intraoperative fluoroscopic anteroposterior (A) and lateral (B) radiographs illustrating internal fixation of a distal metatarsal osteotomy with 3-mm bicortical screw. Note the modified osteotomy, in this case a longer dorsal arm (C), to allow for screw fixation.

Figure 6-120 Combined chevron-Akin procedure. Preoperative clinical (A) and radiographic (B) appearance. C and D, Phalangeal osteotomy. E, Kirschner wire fixation. F, Internal fixation. G, Postoperative clinical appearance. H, Final radiographic appearance.

the osteotomy site is closed, the capital fragment is angulated in a more medial direction than with a routine chevron osteotomy. 2. With either technique (standard or biplanar), the capital fragment is then impacted on the proximal fragment and fixed with a 0.062-inch K-wire, or 2.5- to 3.0-mm screw, directed from a dorsal to plantar direction (see Figs. 6-116G and 6-118E). The use of a screw will typically require a longer osteotomy arm (either 224

dorsal or plantar) to allow perpendicular and bicortical fixation (see Fig. 6-119A-C). Care is taken to avoid penetrating the MTP joint with the fixation device (see Fig. 6-116H). 3. The prominent metaphyseal flare created by displacement at the osteotomy site is beveled with an oscillating saw (see Fig. 6-116I). 4. The medial capsular flap is repaired with interrupted absorbable sutures, with the toe held in neutral to

Hallux Valgus ■ Chapter 6

slight varus position. If correction is incomplete because of inadequate excision of capsular tissue, more capsule should be removed. Intraoperative fluoroscopic imaging is helpful in confirming desired joint alignment. When there is insufficient dorsomedial capsule with which to repair the capsular flap, a dorsal metaphyseal drill hole can be used to anchor the capsular repair (see Fig. 6-91F). The skin is closed in routine fashion (see Fig. 6-116J). 5. Inadequate correction of valgus results from one of three anatomic problems: More capsular tissue may need to be removed from the medial joint capsule, the DMAA may be increased and should be corrected by the addition of a medial closing osteotomy at the chevron site, or an HVI deformity may be present and requires correction via a phalangeal osteotomy (see Fig. 6-120). 6. Before placing a compression dressing, the foot is inspected to ensure that there is no excessive skin tension over the pin site, if used. If present, a small incision should be made in the skin to release this tension. Postoperative Care The gauze-and-tape compression dressing applied at surgery is removed 1 to 2 weeks later, after which the foot is covered in a firm toe-spica dressing consisting of 2-inch Kling gauze and 1 2 -inch adhesive tape, similar to that used after a distal soft tissue procedure (see Fig. 6-108). If any pronation is present, the dressing must be wrapped in such a way that the toe is held in correct alignment to eliminate or minimize the pronation. The dressing is changed weekly. Sutures are removed 2 to 3 weeks after surgery. The patient is allowed to ambulate in a postoperative shoe with weight borne on the heel and outer aspect of the foot. At initial follow-up, a radiograph is obtained to assess alignment of the first ray, and subsequent dressings are used to correct any residual varus or valgus deformity. The dressing is changed at 10-day intervals over an 8-week period after surgery, assuming that the alignment is satisfactory. If used, the K-wire is removed 4 weeks after surgery in an office setting, and dressings can be discontinued 6 weeks after the procedure. Patients are started on a program of active and passive range-ofmotion exercises, as pain permits; they are permitted to ambulate in a soft shoe 6 to 8 weeks after surgery. Results After a chevron osteotomy the satisfaction rate is relatively high, with the reported average correction of the hallux valgus angle being 12 to 15 degrees* and the average correction of the 1–2 IM angle varying from 4 to 5 degrees† (see Fig. 6-103). Reported postoperative narrowing of the forefoot varies from 3 to 6 mm after a chevron osteotomy. Zimmer et al569 published a report on the *References 129, 213, 220, 222, 245, 310, 410, 421, 461, and 523. † References 213, 220, 222, 245, 309, 310, and 421.

effectiveness of the chevron procedure in juvenile patients and reported a 20% recurrence rate. Extrapolating from these results, the limits of the procedure for a consistently reproducible outcome are a hallux valgus angle of less than 30 degrees and an IM angle of less than 12 to 13 degrees. Expansion of the indications for this procedure to more severe deformities appears to increase the risk of patient dissatisfaction and complications. Reporting on 50 adults who underwent distal metatarsal osteotomy for hallux valgus, Meier and Kenzora365 noted a 74% satisfaction rate when the 1–2 IM angle was greater than 12 degrees and a 94% satisfaction rate when the 1–2 IM angle was 12 degrees or less. In general, Harper209 noted that 1 degree of correction is obtained for every 1 mm of lateral translation of the capital fragment. Greater correction has been achieved by Trnka et al524 and Stienstra et al,505 who reported 18 degrees of correction of the hallux valgus angle. In both studies, a lateral release was performed. Stienstra et al505 reported that they translated the capital fragment almost 10 mm laterally. No cases of delayed union, nonunion, or AVN developed. Trnka et al524 performed a retrospective study on 100 feet treated with a chevron osteotomy and translation of the capital fragment 3 to 6 mm, and they achieved 87% good or excellent results. They also released the lateral capsule, the adductor tendon, and the transverse intermetatarsal ligament. In a follow-up study,523 there was no deterioration of the results or subjective satisfaction at 5-year follow-up. In a series of 17 patients and 23 feet, Mann and Donatto340 carefully analyzed the degree of correction of the hallux valgus angle, IM angle, and the fibular sesamoid position to carefully define the true correction after a chevron procedure. They measured the hallux valgus and IM angles by drawing lines that bisected the shafts of the first and second metatarsals and then compared the results with those from the center-of-head method, which measures the angle formed by a line drawn from the center of the first metatarsal head and middle of the metatarsal base and a line bisecting the second metatarsal shaft.106 In the method in which both metatarsals were bisected, the preoperative and postoperative IM angle was 11 degrees. In the center-of-head method, the IM angle was 9 degrees preoperatively and 7 degrees postoperatively. When the hallux valgus angle was measured with one line through the longitudinal axis of the first metatarsal and the other through the proximal phalanx, as opposed to one line through the center of the first metatarsal head, the results demonstrated a correction of 5 degrees for the former and 8 degrees for the latter. Basically, this demonstrates that the degree of correction possible with the chevron procedure is quite small, which must be considered when selecting patients for this procedure. The position of the fibular sesamoid was essentially unchanged. The chevron osteotomy has limited capability to correct a hallux valgus deformity with an increased DMAA.95 Because of the limited correction achieved with a chevron osteotomy, it must be reserved for mild and 225

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Figure 6-121 Malunion can occur in any plane. Medial (A), lateral (B), and dorsal (C) displacement because of lack of internal fixation. D, Plantar displacement with internal fixation.

Figure 6-122 Malunion because of poor alignment of the osteotomy. A, Preoperative. B, Poor postoperative malalignment. C, Salvage with metatarsophalangeal joint arthrodesis.

moderate hallux valgus deformities. Chou et al71 reported on 14 patients who had undergone a biplanar chevron osteotomy for mild and moderate hallux valgus deformities in which an average 7-degree correction of the DMAA was achieved. Postoperative displacement of the osteotomy site varied from 1.8% of 225 cases reported by Hattrup and Johnson213 to 12% reported by Johnson et al244 and can lead to overcorrection or undercorrection (Fig. 6-121).222 The incidence of postoperative displacement of the capital fragment medially or laterally or deviation dorsally or plantarward can be minimized by the use of some form of internal fixation rather than relying on impaction of 226

the osteotomy site as was initially recommended,13,245,524 especially in those for whom greater displacement of the osteotomy is desired (Fig. 6-122). Most surgeons have transitioned from wire fixation to a variety of screws to decrease the inherent risks of loosening, skin irritation, and infection. Early reports on internal fixation with absorbable implants demonstrated evidence of a foreign body reaction.406 Recent reports using poly-L-lactic acid19,54,129,222,375,406 demonstrated less common side effects of osteolysis or granuloma formation. Gill et al173 reported a 10% incidence of pin-tract osteolysis when using polydioxanone (PDS) bioabsorbable pins to internally fix a chevron osteotomy.

Hallux Valgus ■ Chapter 6 Complications Complications after the chevron procedure are similar to those noted with other osteotomy procedures: pain, recurrence of the hallux valgus deformity, transfer metatarsalgia secondary to shortening, MTP joint arthrofibrosis, nonunion, and postoperative neuritic symptoms secondary to entrapment of a cutaneous nerve. The most frequent complications reported with the chevron osteotomy are recurrence and undercorrection of a hallux valgus deformity, which vary in frequency from 10% to 20% (Fig. 6-123).12,222,310 Recurrence of hallux valgus deformity occurs in about 10% of cases.6,164 The 10% recurrence rate can probably

Figure 6-123 A, Recurrence after the chevron procedure. B, Salvage with metatarsophalangeal joint arthrodesis.

be significantly lessened if the indications for the procedure are not overextended. In the series reported by Hirvensalo et al,222 the deformity recurred when the preoperative hallux valgus averaged 37 degrees, and the IM angle averaged 13 degrees. Hattrup and Johnson213 noted recurrence of the deformity in 18 of 225 procedures; they reported that the average preoperative hallux valgus angle of 37 degrees was corrected to an average of 31 degrees postoperatively. Other authors have not documented the severity of the preoperative hallux valgus deformity when discussing recurrence. If there are no intraarticular symptoms or advanced degeneration, recurrent hallux valgus can be managed with an Akin osteotomy (Fig. 6-124A and B). Mean shortening of the first metatarsal averaged 2 to 2.5 mm in two series222,340 and was as high as 6 mm in 28 cases reported by Pring et al.430 Shortening can develop as a result of excessive bone loss12,222,365 or be due to bone necrosis or resection at the osteotomy site. Klosok et al281 reported the development of postoperative transfer lesions in 12% and postoperative metatarsalgia in 43% of patients after a chevron osteotomy (Fig. 6-125). Although cutaneous nerve injury can occur with this procedure, the use of a medial midline surgical approach substantially reduces the incidence of nerve entrapment when compared with performance of the osteotomy through a dorsal or dorsomedial incision. Excessive soft tissue stripping and and overpenetration of the lateral cortex at the level of the osteotomy should be avoided to minimize the risk for nonunion (Fig. 6-126A and B). The location of the two limbs of the osteotomy, particularly the plantar limb, is critical. The plantar limb should be extraarticular, if possible, both to avoid injury to the sesamoids and to minimize the development of MTP joint adhesions between the sesamoids and the metatarsal head, which can lead to resultant loss of MTP joint motion. Trnka et al523 noted that passive range

Figure 6-124 A, Preoperative anteroposterior standing radiograph in a patient with recurrent hallux valgus after a distal metatarsal osteotomy. B, Postoperative radiograph 7 weeks after correction, using a medial closing-wedge osteotomy of the proximal phalanx.

B 227

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of motion was 72 degrees preoperatively and 61 and 62 degrees at the 1-year and 2-year follow-up after a chevron osteotomy. A patient should be counseled that decreased MTP range of motion may occur after the procedure (Fig. 6-127). Hallux varus may develop because of lateral displacement of the capital fragment, medial subluxation of the tibial sesamoid, excessive excision of the medial eminence resulting in inappropriate narrowing of the metatarsal head, and AVN of the medial aspect of the capital fragment. Although these complications are uncommon, awareness of them may help in their prevention (Fig. 6-128). The most serious complication after a chevron osteotomy is AVN (Fig. 6-129). The incidence of AVN varies

Figure 6-125 A, After a combined chevron-Akin procedure. B, Stress fracture of the second metatarsal 4 months after surgery.

from 4% to 20%.193,227,244,410 In an early report, Meier and Kenzora365 noted AVN in 20% of patients after a chevron osteotomy, and this figure increased to 40% when combined with an adductor tenotomy. Shereff et al478 cautioned that lateral release increases the risk of AVN (Fig. 6-130). No AVN, however, was observed in a series of chevron procedures reported by Hattrup and Johnson.213 Green et al193 identified no evidence of first metatarsal AVN after release of the conjoined adductor tendon, sesamoidal ligament, and fibular sesamoid ligament through an intermetatarsal incision. Although excessive capsular dissection has been implicated in the development of AVN, careful surgical technique and preservation of the distal vascular structures can help avoid AVN. Peterson et al410 reported a case of AVN after lateral release. They suggested that a carefully performed chevron procedure preserves the dorsal and plantar blood supply and did not believe that a lateral capsular release above the sesamoids or an adductor tendon release interrupted the vascular supply. Trnka et al524 performed a lateral release through a separate incision; after dissecting out and releasing the tarsometatarsal ligament and the lateral capsule, they reported no evidence of AVN at final follow-up. Trnka et al523 then reviewed the combined series of Pochatko, Trnka, and Peterson410,421,524,525 of 224 chevron procedures and found that only four cases of AVN developed (2%), and in three of these cases, excessive stripping was documented. Most recently, Pontenza’s series426 noted only one case of asymptomatic AVN and concluded that a lateral release was safe in those patients with mild-tomoderate hallux valgus. AVN is a potential problem that may not be preventable in certain cases because of peculiarities in the blood supply to the capital fragment,328 but this does not necessarily preclude a successful end result.477 When performing a chevron procedure, however, excessive soft tissue stripping should be minimized. Excess lateral penetration of the saw blade should also be avoided because it can damage the lateral capsular circulation to the metatarsal head (Fig. 6-131). Malal recommended a longer plantar osteotomy arm to avoid the plantar-lateral corner of the metatarsal neck, where blood supply enters the metatarsal

Figure 6-126 Anteroposterior (A) and lateral (B) radiographs depicting a nonunion of a distal chevron osteotomy.

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Figure 6-127 Patient with severe restriction of metatarsophalangeal (MTP) joint motion. A, Degenerative arthritis versus avascular necrosis 2 years after a chevron procedure. B, Increased uptake on bone scan at the MTP joint. C, Salvage with MTP joint arthrodesis.

Figure 6-128 A, Hallux varus after a chevron procedure. B, Salvage with metatarsophalangeal arthrodesis. (Same patient as shown in Fig. 6-123 after recurrence on the contralateral side.)

head—a finding contrary to the work of Shereff.478 Release of the lateral structures may enable greater correction but, if done extensively, can increase the risk of AVN.238,309,365,555 Thomas et al511 performed lateral soft tissue release and, frequently, fibular sesamoidectomy through a plantar incision. In a review of 80 of their chevron procedures, the radiographic changes suggested vascular compromise in 76% (61 of 80) of the feet, but at follow-up, none had progressed to AVN. Wilkinson et al554 postoperatively evaluated 20 patients with magnetic resonance imaging after chevron osteotomy. Fifty percent had evidence of AVN, mostly in the dorsal metatarsal head, although none of the patients were symptomatic. The authors also

performed McBride procedures as controls, and none showed evidence of decreased vascularity to the metatarsal head. The question of whether to release the lateral capsular structures when performing a chevron procedure depends on the perceived risk of AVN. Based on the literature,* careful, meticulous release of contracted lateral structures at the level of the joint is probably safe because it is distal to the blood supply to the metatarsal head. However, in the presence of a more severe deformity, it may be a better alternative to choose another procedure that does not have any risk of development of AVN. More extensive dissection along the lateral aspect of the metatarsal head, such as with excision of the fibular sesamoid, should be avoided because this dissection carries a higher risk of disturbing the blood supply along the lateral aspect of the metatarsal head. DISTAL METATARSAL OSTEOTOMY (MITCHELL, BOSCH TYPES) Correction of a hallux valgus deformity by means of a distal first metatarsal osteotomy was first described by Reverdin436 in 1881 and later by both Peabody407 and Hohmann.225 However, it was Mitchell214,370 who described and popularized the technique of a biplanar metaphyseal osteotomy, which achieves lateral and plantar displacement of the capital fragment, as well as shortening of the first metatarsal. Wilson558 and others188,374,463,530 described an oblique metaphyseal osteotomy, Bosch42,43 and Kramer,283 a transverse osteotomy, and Magnan,26,330,331 a percutaneous osteotomy. The Mitchell procedure, as described by Hawkins et al,214 is a double step-cut osteotomy through the neck of the first metatarsal. Several modifications have been made to this procedure through the years, including changes in the design of *References 12, 281, 328, 410, 421, 511, and 524.

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Figure 6-129 Avascular necrosis of the metatarsal head after distal osteotomy. A, Preoperative radiograph. B, After surgery. C, Five years after surgery, complete chondrolysis and avascular necrosis have developed.

of late as one324 amenable to minimally invasive techniques.26,330,331 Minimal incision surgery has also been applied to the chevron and other distal first metatarsal osteotomies. Arthroscopic-assisted surgeries have also been described.321,484

Figure 6-130 A, Avascular necrosis after a chevron procedure. B, Computed tomography scan demonstrating marked cystic degeneration.

the medial capsulorrhaphy,49,369,374,463 the osteotomy technique,* the method of internal fixation,† and postoperative care.49,374,507 The changes described make the eponym Mitchell somewhat inadequate to describe the procedure as now performed in many series. Nonetheless, Mitchell’s important principles remain—that shortening should be kept to a minimum, plantar flexion of the capital fragment should consistently be achieved, and rotation of the capital fragment to realign the distal articular metatarsal surface is occasionally indicated. The Bosch osteotomy is much like the Mitchell in principle. However, it has received considerable attention *References 42, 43, 49, 284, 330, 331, 374, 425, 463, 530, 558, 561, and 562. † References 49, 127, 158, 290, 342, 366, 372, 374, 425, 463, 507, 561, and 562.

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Indications Distal metatarsal osteotomies (whether oblique or transverse) are indicated for a moderate or moderately severe hallux valgus deformity with a subluxed MTP joint. If the DMAA is not substantial ( 15 degrees)93,312,516 because recurrence, degenerative arthrosis, or postoperative stiffness could result. Coughlin91 reported that the final angulation of the MTP joint mirrored the magnitude of the DMAA preoperatively; thus, with substantial sloping of the metatarsal articular surface, soft tissue realignment of the MTP joint is contraindicated. Technique: Crescentic Osteotomy A crescentic osteotomy has been advocated as the means to correct an increased 1–2 IM angle without significantly altering the length of the first metatarsal.93,335 The osteotomy is located in the first metatarsal metaphysis because this area provides a broad contact area, which promotes rapid healing, and a relatively large surface area, which affords stability in a dorsoplantar direction. Initially, the crescentic osteotomy was performed with the concavity directed distally toward the great toe.95,335 The authors noted, however, that if the osteotomy site was inadvertently displaced medially and the metatarsal head was translated too far laterally, an incongruent MTP joint and, in some cases, hallux varus resulted (Fig. 6-146). This prompted a reverse of the direction so that the concavity was directed toward the heel (Fig. 6-147), a technique now commonplace.140,344,409 With the concavity oriented proximally, the center of the rotational axis of the osteotomy is centered at the MTC joint,452 thus making this correction much more anatomic and biomechanically sound. This also reduces the possibility of displacing the metatarsal head too far laterally or creating a malunion. Distal soft tissue reconstruction is performed in association with a proximal first metatarsal osteotomy and in a manner as previously described. After the lateral capsular tissues have been released, the medial capsule opened, and the medial eminence resected, the IM angle is tested to see whether an osteotomy is indicated. The first metatarsal head is pushed laterally toward the second metatarsal. A tendency for these two metatarsals to spring apart indicates insufficient mobility at the MTC joint to permit 241

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Figure 6-146 Overcorrection of a proximal osteotomy. A, Preoperative radiograph demonstrating a moderate hallux valgus deformity. B, Overcorrection of the 1–2 intermetatarsal angle with a proximal metatarsal osteotomy and resection of excessive medial eminence. C, Six-year follow-up radiograph demonstrating a mild hallux varus deformity. The patient had no symptoms, but progression of varus deformity is possible.

Figure 6-147 Proximal crescentic metatarsal osteotomies. A, With the concave surface oriented distally. B, With the concave surface oriented proximally. C, After osteotomy with the concavity oriented distally, overcorrection and hallux varus have resulted; medial displacement of the osteotomy results in excessive lateral displacement of the metatarsal head. Before (D) and after (E) osteotomy with the concavity oriented distally. Note that this orientation prevents medial displacement of the osteotomy site and therefore prevents overcorrection of the metatarsal head. For this reason, the authors now always carry out the crescentic osteotomy with the concavity directed (proximally) toward the heel.

reduction of the IM angle, and an osteotomy is indicated (see Fig. 6-93B and C). 1. Following the two distal incisions on the medial aspect of the MTP joint, and in this first inter space, a third incision is made on the dorsal aspect of the base of the first metatarsal over the extensor hallucis longus tendon. The incision starts just proximal to the MTC joint and is carried distally for about 3 cm. It is deepened through 242

the subcutaneous tissue to expose the extensor tendon. The extensor tendon is retracted medially or laterally to expose the metatarsal shaft (Fig. 6-148). 2. The MTC joint is identified with the tip of the knife blade, and the osteotomy site is located approximately 1 cm distal to the MTC joint (Fig. 6-148B). A screw (and K-wire) is generally used for fixation of the osteotomy site and is inserted approximately 1 cm distal to the osteotomy site.

Hallux Valgus ■ Chapter 6

Medial eminence resection

Skin incisions

Figure 6-148 A, Incisions for distal soft tissue realignment with a proximal first metatarsal osteotomy. B, The incision for the osteotomy is made 1 cm distal to metatarsocuneiform joint. C, Saw blade used for crescentic osteotomy. D, Orientation of the saw blade with the concave surface oriented proximally. E, Orientation of the saw blade with the concave surface oriented distally.

Figure 6-149 Errors in position of the saw blade. The crescentic osteotomy is placed 1 cm distal to the metatarsocuneiform joint or 8 mm distal to the open epiphysis in a juvenile. A lateral view of the osteotomy demonstrates the angle of the cut. The concave surface is proximal. A, This angle is incorrect because the blade is perpendicular to the floor. B, Incorrect angle of the osteotomy because the angle is too oblique. There is less contact at the osteotomy site. C, Correct angle of the osteotomy. The correct angle is neither perpendicular to the first metatarsal shaft nor perpendicular to the plantar aspect of the foot.

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3. If a screw is used to fix the osteotomy, the initial glide hole is created at this time. A 3.5-mm drill bit is used to make a hole at an angle of about 45 to 50 degrees to the metatarsal shaft, with the bit passing into the metatarsal approximately 5 mm (Fig. 6-150H). A countersink is used to lower the screw head. If a 4.0-mm cannulated screw is used, the guide pin is inserted and overdrilled later in the procedure. 4. The osteotomy is created with a crescentic blade so that the concavity is directed proximally (see Fig. 6-148CE). The plane of the osteotomy is perpendicular to neither the first metatarsal nor the bottom of the foot; rather, it is halfway between (see Fig. 6-149). In the coronal plane, it is critical that the saw blade be neither medially nor laterally rotated. Medial rotation can lead to elevatus. Often, the leg of the patient externally rotates, and if care is not taken, inadvertent medial rotation of the saw blade may occur. To help avoid this error a vertical 0.045-inch K-wire can be placed in the medial cuneiform as a guide while holding the foot in a plantigrade position (see Fig. 6-212). The saw blade is held parallel to the wire during the osteotomy, thus minimizing malrotation of the blade.250 As the osteotomy is performed, the saw blade must exit the lateral aspect of the metatarsal shaft to ensure that the osteotomy is completed along this margin of the

metatarsal. If it is not, it is difficult to complete the osteotomy in this narrow area, and the communicating artery may be damaged. If the osteotomy is not completed along the medial side, it is simple to finish the cut with a 4-mm osteotome. Once the osteotomy is complete, a Freer elevator is used to ensure that it is completely mobile and that any periosteal hinge that might prevent displacement of the osteotomy is released. The crescentic saw blade comes in two lengths, one 4 mm longer than the other. As the osteotomy is being performed, if the shoulder of the blade impinges on the skin just proximal to the osteotomy site, the longer blade (No. 2296-31-416S7, 277-31-415, or 277-31-416S1, Stryker, Kalamazoo, Mich., or No. 5053-176, Zimmer, Wausau, Ind.) is used. The surgeon should not undertake this osteotomy without having both blades available. Again, care must be taken to avoid either medial or lateral rotation of the saw blade because such rotation may lead to plantar flexion or dorsiflexion at the osteotomy site. 5. A Freer elevator is used to displace the proximal portion of the metatarsal base in a medial direction as far as possible (Fig. 6-150B and C). The index finger is used to push the metatarsal head in a lateral direction, which displaces the osteotomy site laterally. The displacement at the osteotomy site is usually only 2 to

Figure 6-150 A, Exposure of the osteotomy site in the proximal portion of the metatarsal. A rongeur is used to remove the lateral spike of bone that frequently prevents displacement of the osteotomy. B, Diagram demonstrating that the proximal fragment is displaced medially as far as the metatarsocuneiform joint will permit while the metatarsal head is pushed laterally against the second metatarsal. C, Intraoperative photograph demonstrating the Freer elevator pushing the proximal fragment medially and the surgeon’s hand pulling the first metatarsal head laterally against the second metatarsal. D, Kirschner wire stabilizes the osteotomy site. E, Note that the osteotomy site is displaced 2 to 3 mm laterally. F, The hole is drilled at a 45-degree angle to the long axis of the metatarsal. G, The screw is placed approximately 1 cm distal to the osteotomy site. H, After placement of the wire and screw.

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Figure 6-151 Fixation of the osteotomy site with an oblique 5 64 -inch Steinmann pin. Because of the high infection rate, this is rarely used except with unsuccessful internal fixation. A, Radiograph demonstrating the pin driven into the tarsal bones for added stability. Note that when the osteotomy site was reduced, the proximal fragment was not displaced medially on the cuneiform. B, After removal of the pin, the proximal fragment drifted in the medial direction on the cuneiform, which resulted in incomplete correction of the intermetatarsal angle and recurrence of the hallux valgus deformity because of the lack of medial displacement of the proximal fragment.

3 mm because a small degree of translation proximally accounts for much movement distally. Care must be taken to not overcorrect the osteotomy site. If the osteotomy site does not move freely, some medial periosteum is still attached and must be released so that the osteotomy can be rotated laterally. On occasion, a small spike of bone on the lateral aspect of the distal fragment must be removed to allow rotation of the osteotomy (Fig. 6-150A). At this point, the distal fragment can be slightly displaced plantarward (about 2 mm) to compensate for any possible dorsiflexion angulation at the osteotomy site. To ensure that the osteotomy site is not being held in a dorsiflexed position, the metatarsal head is pushed slightly plantarward until the osteotomy site just begins to open up. However, excessive plantar flexion may displace the MTC joint and should be avoided.510 6. While holding the osteotomy in a corrected position, the osteotomy is generally fixed with both a 0.062inch K-wire (Fig. 6-150D and E) and a 4.0-mm smallfragment compression screw to provide rotational stability, as well as compression (Fig. 6-150F-H). The screw hole is also countersunk to lower the profile of the screw head and to prevent cracking the island of bone between the screw and osteotomy site. Other than revision cases or in patients with osteopenia, the wire may be removed before closure, which will reduce the risk of postoperative infection (Fig. 6-151). There have been recent reports of fixing the crescentic osteotomy with a plate construct as opposed to screw fixation for improved stability. The use of a plate also avoids penetration of the MTC joint.72,532 Technique: Medial Opening Osteotomy Many surgeons have found the crescentic osteotomy to be a challenging technique requiring an appreciation of spatial positioning. The medial opening osteotomy is a

single-plane transection and easier for the occasional bunion surgeon to conceptualize. The technique typically uses wedge-plate fixation to maintain the medial opening while providing stability for this inherently unstable osteotomy. 1. The medial based incision used for exposure of the MTP joint is extended proximally to the MTC joint, with care taken to avoid transecting superficial nerves. Periosteum is sharply reflected off of the medial aspect of the proximal one third of the metatarsal. The MTC joint does not require exposure. 2. The osteotomy is made approximately 1.5 cm distal to the MTC joint, as confirmed using fluoroscopic imaging. The angle of the bone cut is generally made perpendicular to the axis of the metatarsal, but some surgeons will make the cut oblique proximally, which will minimize the lengthening effect of the opening wedge (Fig. 6-152A). 3. Fluoroscopic imaging is used to follow the osteotomy to, but not through, the lateral cortex (Fig. 6-152B). The osteotomy is then gradually opened using a spreader device, joy stick, or osteotome (Fig. 6-152C). The soft tissues progressively stretch, and the lateral cortex fatigues as a greenstick. 4. Four hole plates, locked and nonlocked, are available with multiple options for wedge length. The wedge size is determined intraoperatively and based on the severity of the IM angle. The 3- and 4-mm sizes are the most commonly used. Larger sizes may create a distraction effect along the lateral cortex, negating the medial opening-wedge correction, and should be avoided. The plate is usually positioned directly medial on the first metatarsal (Fig. 6-153). However, in cases of metatarsalgia or overload on the lesser metatarsals (as may occur with hypermobility, pes planus), the plate can be placed more dorsal to create plantar flexion at the osteotomy. 245

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C Figure 6-152 A, Medial approach to the proximal first metatarsal. Saw blade is positioned perpendicular to the long axis of the bone, approximate 15 mm from the metatarsocuneiform joint. B, Fluoroscopic image confirms proper level of the bone cut and is also used to advance the blade just short of the lateral cortex. C, An osteotome can be used to gently greenstick the lateral cortex and reduce the intermetatarsal 1–2 angle.

5. Bone graft obtained from the medial eminence previously resected is used to fill the opening in the osteotomy. In revision cases, autogenous calcaneal bone graft or allografts can be used. Long Oblique Osteotomy (Mau, Ludloff) In the case of a long first metatarsal, the surgeon may use a long oblique proximal osteotomy to avoid the lengthening effect of the opening-wedge technique. Multiple types and modifications have been described.16,388,446,455,522 The modified Mau technique has been advocated by Glover et al.183 Their medial approach is similar to the medial opening technique described previously, and the modification uses a shorter osteotomy than in the traditional Mau technique (Fig. 6-154A). 1. The periosteum is elevated in line with the osteotomy, with the proximal portion of the osteotomy placed at least 1 cm distal to the first MTC joint. The saw blade is kept parallel to the weight-bearing surface of the foot to prevent unwanted dorsal angulation of the first metatarsal head, which could occur after completion of the osteotomy (Fig. 6-154B and C). 2. To maintain complete control of the osteotomy, a guidewire for the cannulated screw is placed 246

perpendicular in the completed proximal portion of the osteotomy. The osteotomy can then be completed dorsal-distally without fear of losing the orientation. 3. Reduction can be achieved with large reduction clamps or by using a Freer elevator on the lateral portion of the proximal fragment and placing counterpressure on the first metatarsal head. Intraoperative fluoroscopy is recommended after placing temporary fixation to achieve an IM angle less than 9 degrees (Fig. 6-154D). 4. Placing a screw too distal may cause fracture of the dorsal portion of the osteotomy site. Allow adequate space between the screws and the distal aspect of the osteotomy to prevent fracture (Fig. 6-154E-G). Reconstruction of Hallux Valgus Deformity 1. After the proximal osteotomy is completed and before fixation, (regardless of the specific type of osteotomy chosen) attention is directed to the first web space, where two sutures are placed to approximate the adductor hallucis tendon to the lateral capsular tissues along the border of the first metatarsal head (see Fig. 6-94). If such approximation is not accomplished at this time, it is difficult to later expose the adductor tendon in the depths of the interspace after the osteotomy site has been displaced and stabilized.

Hallux Valgus ■ Chapter 6

Figure 6-153 A, A 3-mm wedge plate is applied to the medial aspect of the first metatarsal, with option for locking screws. B, Preoperative radiograph of a 50-year-old woman with a symptomatic bunion deformity. Postoperative standing anteroposterior (C) and lateral (D) radiographs at 5 weeks, illustrating correction with medial opening-wedge technique and healing of the osteotomy.

2. Once the osteotomy site is stabilized, the sutures in the first web space are tied and the medial capsular tissue is repaired as previously described for the distal soft tissue procedure. The skin is approximated in routine manner (Fig. 6-155). 3. Intraoperative fluoroscopy may be beneficial to evaluate the correction of the IM angle, as well as to evaluate the position of the internal fixation. In addition, fluoroscopic imaging is recommended to evaluate alignment of the first MTP joint, ensuring that there is no overcorrection into varus. 4. Postoperatively, the foot is wrapped in a gauze-andtape compression dressing to hold the hallux in correct alignment or in slight overcorrection if a severe deformity has been corrected (Fig. 6-156A). Postoperative Care As previously described for the distal soft tissue procedure, the foot is re-dressed weekly for 6 to 8 weeks (Fig. 6-156B). It is unusual to cast the foot postoperatively,

although a cast may be necessary in an unreliable patient or one with precarious internal fixation. Radiographs are obtained at the first office visit after surgery. Based on this radiograph, the toe is dressed in a neutral position, varus, or valgus. The patient is allowed to ambulate in a stiffsoled postoperative shoe, with weight bearing mainly on the heel and outer aspect of the foot for 8 weeks after surgery. After the final dressings are removed, the patient is permitted to ambulate, as tolerated, in a sandal or soft, wide shoe. Sutures are removed 2 to 3 weeks after surgery. MTP joint range-of-motion exercises are initiated 3 to 4 weeks after surgery, while the foot is still maintained in a postoperative dressing. An intensive walking program is begun 7 to 8 weeks after surgery. Should the MTC joint be penetrated with internal fixation, as with the crescentic procedure, the hardware can be removed after successful healing at the osteotomy site, typically 6 to 8 weeks after surgery. Coughlin and Shurnas110 reported that internal fixation crossed the MTC joint in 13 of 35 proximal crescentic cases. The hardware 247

Part II ■ Forefoot

Figure 6-154 A, The modified osteotomy exits more proximal than the traditional line of the osteotomy (in red). B, Medial approach to the first metatarsal and the marking of the osteotomy, with the metatarsocuneiform (MTC) joint identified. C, Note that the proximal cut exits distal to the MTC joint. D, The correction and reduction of the intermetatarsal 1–2 angle can be obtained with a clamp while the osteotomy is temporarily secured with guide wires. E, The osteotomy is fixed with two screws. F, Screws are positioned away from the thin dorsal distal cortex to avoid fracturing. G1, Preoperative standing anteroposterior (AP) radiograph of a moderate bunion deformity. Postoperative standing AP (G2) and lateral (G3) showing correction obtained.

was removed 6 weeks after surgery, and at long-term follow-up, they did not identify degenerative arthritis in the MTC joint. The degree of swelling varies among patients, but usually within 4 to 5 months after surgery, the thickening about the joint and swelling of the foot have subsided. Results Reported patient satisfaction rates after proximal first metatarsal osteotomy vary from 78% to 93%.* Most of what has been written has dealt with the crescentic *References 63, 101, 344, 435, 452, 488, and 516.

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technique as popularized by Mann. Mann et al344 reviewed 109 feet in which a distal soft tissue procedure and proximal crescentic osteotomy were performed. The major preoperative complaint was pain over the medial eminence in 75% of patients, around the first MTP joint or sesamoids in 7%, in the lesser toes in 7%, and from other causes in 11%. Ninety-three percent of patients were satisfied postoperatively. Of the 7% dissatisfied, half complained of pain and half complained of the varus or valgus position of the hallux. At final follow-up, 39% of patients believed that they could perform more activities on their feet, 57% thought that their level of activity was unchanged, and 4% said that their level of activity was

Hallux Valgus ■ Chapter 6

Figure 6-155 Distal soft tissue realignment with first metatarsal osteotomy. Preoperative clinical appearance (A) and radiograph (B) demonstrating a moderate hallux valgus deformity with metatarsophalangeal (MTP) subluxation (hallux valgus angle, 34 degrees; 1–2 intermetatarsal (IM) angle, 15 degrees; distal metatarsal articular angle, 10 degrees) and a subluxated MTP joint. Postoperative clinical appearance (C) and radiograph (D) 5 years after a distal soft tissue procedure with a proximal metatarsal osteotomy. The alignment has been corrected (hallux valgus angle, 5 degrees; 1–2 IM angle, 4 degrees).

Table 6-4 Summary of 109 Feet before and after Distal Soft Tissue Procedures with Proximal Crescentic Osteotomy Angle Average hallux valgus Average first/second intermetatarsal

Preoperative

Postoperative

30° 13°

9° 5°

From reference 344.

B Figure 6-156 A, Immediate postoperative dressing. B, Dressing used for the remainder of treatment.

diminished. Preoperatively, 30% of patients could wear any shoe that they desired, and postoperatively, 59% could. Still, 41% were unable to wear the shoe of their choice. The average correction of the hallux valgus angle is consistently reported to be 23 to 24 degrees,* (Fig. 6-155) with the degree of improvement being directly proportional to the severity of the preoperative deformity (Fig. 6-157).41,344 Mann334 reported that with more severe deformities, an average hallux valgus correction of 30 degrees was achieved. Average correction of the 1–2 IM angle is 8 to 11 degrees after a crescentic osteotomy,95,101,335,344,516 3 to 6 degrees after a closing-wedge osteotomy,435,472 and 7 degrees after an opening-wedge osteotomy.312,488 Tables 6-4 and 6-5 summarize correction of the hallux valgus and IM angles achieved in the series and by subgroups. Reporting on 33 cases of correction of a juvenile hallux valgus deformity with distal soft tissue reconstruction and proximal first metatarsal osteotomy, Coughlin95 noted an average 23-degree correction of the hallux valgus angle and an average 8-degree correction of the 1–2 IM angle, results identical to those reported by Mann335 in adult patients. In the only prospective study of this procedure published, Coughlin and Jones101 *References 101, 136, 335, 344, 435, and 516.

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Figure 6-157 Correction of severe deformity. Preoperative clinical (A) and radiographic (B) appearance. Postoperative clinical (C) and radiographic (D) appearance. E, Follow-up radiograph 5 years after surgery.

Table 6-5 Summary of Results by Severity of Deformity in Distal Soft Tissue Procedures with Proximal Crescentic Osteotomy Mild (< 20°)

Moderate (21°-40°)

Severe (> 40°)

9 48

87 52

13 59

30° 9°

46° 13°

Mean First/Second Intermetatarsal Angle Preoperative 11° 13° Postoperative 5° 6°

16° 5°

Number of feet Mean age (yr)

Mean Hallux Valgus Angle Preoperative 17° Postoperative 3°

Hallux Varus Mean deformity 5.4° 6°, 5 cases (2 dissatisfied) From reference 344.

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reported an average 20-degree correction of the hallux valgus angle and an average 10-degree correction of the IM angle. Mann et al344 further observed that before surgery, 48 feet (44%) had a symptomatic callus beneath the second metatarsal head and that postoperatively, 30 of these calluses had resolved, 13 were unchanged but no longer painful, and 5 remained painful but no new lesions had developed. Coughlin and Jones101 reported a 47% incidence of concomitant lateral metatarsalgia in patients who were scheduled to undergo surgical correction for moderate and severe hallux valgus deformities. Overall, the first metatarsal was shortened an average of 2.2 mm, a finding identical to that in other reports in the literature on proximal first metatarsal osteotomies.309,348,409,454 Rather than shortening, there is a risk of lengthening with the opening-wedge osteotomy technique. This may alter plantar forefoot pressures as well as create increased joint surface compression at the hallux metatarsophalangeal

Hallux Valgus ■ Chapter 6

level. Studies have shown that the lengthening effect is minimal and the risk of creating joint degeneration is minimal.53,433,458,483,563 It is recommended that the opening-wedge technique be avoided in those patients with long first metatarsals and hallux metatarsophalangeal stiffness.563 As Easley et al140 observed, in patients with moderate and severe hallux valgus deformities, evaluation of transfer lesions is hampered by the fact that forefoot problems are not isolated to the hallux and frequently involve the second and third MTP joints as well. Whereas some have suggested a relationship between first metatarsal shortening and metatarsalgia543 or elevatus and metatarsalgia,543 others have found no correlation.* When the metatarsal is already short before surgery, Schemitsch and Horne463 found a positive correlation between further shortening of the first metatarsal and metatarsalgia. Dorsiflexion at the osteotomy site should be avoided with all proximal osteotomy techniques. Brodsky et al51 found that sagittal-plane correction is difficult with the crescentic osteotomy in particular, thus resulting in unpredictable plantar forefoot pressures. Mann et al344 observed on lateral weight-bearing radiographs that 28% of the feet demonstrated the first metatarsal to be slightly dorsiflexed, although the magnitude was not quantified. With the crescentic procedure, saw position and rigid internal fixation are important principles in avoiding elevatus.88,93,313,501 Lippert and McDermott313 found that medial or lateral rotation of the saw blade altered the eventual position of the distal first metatarsal head after the osteotomy was displaced. Medial rotation of the saw led to elevation, and lateral rotation led to plantar angulation after displacement of the osteotomy. Jones et al,250 in a cadaveric and laboratory study, demonstrated a linear relationship between metatarsus elevatus and saw blade orientation. For every 10 degrees of saw blade angulation, a 2-mm change in the sagittal position of the distal first metatarsal was noted. They then used a K-wire to help orient the saw blade to avoid malrotation of the saw and substantially improved the accuracy of the osteotomy in a cadaveric study. Rigid fixation to prevent malunion, *References 44, 188, 266, 344, 348, 370, 427, and 435.

preferably with locking screws, is also mandatory with the inherently unstable wedge osteotomies.82,497 Joseph256 quantified MTP joint range of motion in normal subjects and reported total MTP motion of 87 degrees with an average dorsiflexion of 67 degrees and average passive plantar flexion of 20 degrees. In reports documenting postoperative MTP range of motion after proximal osteotomy and distal soft tissue repair, total passive motion ranged from 64 to 86 degrees.91,95,535 Coughlin95 noted an average loss of 12 degrees when compared with the nonoperated side in juveniles and an average loss of 11 degrees in adults.91 Mann et al344 reported that patients demonstrated 55 degrees of dorsiflexion and 9 degrees of plantar flexion for a total range of 64 degrees at midterm follow-up after surgery. Veri et al535 reported that preoperative total range of motion averaged 86 degrees; at a minimum 1-year follow-up, range of motion averaged 69 degrees; however, at a mean follow-up of 8 years, total motion averaged 86 degrees. In a cadaver study in which range of motion was measured immediately before and after a distal soft tissue procedure and proximal metatarsal osteotomy, Coughlin et al102 reported that the total range of MTP joint motion decreased from 85 to 62 degrees. There was a significant loss of dorsiflexion motion but not plantar flexion motion. Thus there appears to be an initial loss of motion after the realignment procedure that is probably due to intrinsic muscle tightness. Initiation of early range-ofmotion activities may help diminish the eventual loss of motion, but patients should be counseled that it is not unusual to lose some motion as a consequence of the procedure (Fig. 6-158). Two reports in the literature compared proximal crescentic osteotomy with proximal chevron osteotomy for the correction of hallux valgus (Fig. 6-159).140,348 In both reports, the results were essentially the same with regard to correction of the hallux valgus deformity and IM angle and relief of lateral metatarsalgia. The main difference was the lack of dorsiflexion at the osteotomy site, as noted occasionally after proximal crescentic osteotomy, but statistically, it did not appear to affect either the incidence of new transfer lesions or the resolution of existing lesions. The chapter authors believe that either procedure

Figure 6-158 Passive dorsiflexion (A) and plantar-flexion (B) range-of-motion exercises are important in regaining motion. Pressure placed on the proximal phalanx stretches the metatarsophalangeal (MTP) joint. C, Incorrect stretching places stress on the interphalangeal joint instead of the MTP joint.

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will result in satisfactory correction of the hallux valgus deformity, and it is the surgeon’s preference which of these osteotomies should be used. Although Lian et al311 reported proximal chevron and crescentic osteotomy to be of equal strength in resisting failure with dorsiflexion, criticism of the strength of the osteotomy and its fixation has been presented by McCluskey et al360 and by Campbell et al.57 These groups found both proximal chevron and oblique closing-wedge osteotomy to be stronger constructs. Chiodo et al66 reported the results of 70 cases in which a Ludloff oblique osteotomy was performed for moderate and severe hallux valgus deformities. The average hallux valgus angle was corrected 20 degrees, and the 1–2 IM

Complications Potential complications after a distal soft tissue procedure have been listed previously. Complications after proximal osteotomy include shortening, metatarsalgia, failure of internal fixation, overcorrection (hallux varus) (Fig. 6-160), undercorrection (or recurrence) (Fig. 6-161), delayed union, and malunion (Figs. 6-162 and 6-163). Shortening or dorsiflexion at the osteotomy site predisposes to the development of lateral metatarsalgia (Fig. 6-164), whereas lengthening the first metatarsal through an opening-wedge osteotomy may lead to stiffness and degeneration of the hallux metatarsophalangeal joint. Mann et al344 reported a 28% incidence of dorsiflexion at the osteotomy site (although some deformities were

Figure 6-159 A1 and A2, Ludloff osteotomy. B, Proximal chevron osteotomy (base proximal). C, Proximal chevron osteotomy (base distal).

angle was corrected 9 degrees. In the sagittal plane, the first metatarsal was plantar flexed 1 mm. No transfer lesions were reported; varus occurred in 4 of 70 patients and delayed union in 3 of 70. The authors suggested that the plane of the osteotomy and the rigidity of the internal fixation placed the osteotomy site at minimal risk of dorsiflexion malunion. Glover et al182 compared the modified Mau technique to the crescentic and found similar healing, correction, and patient satisfaction rates but with fewer complications. Coughlin95 noted that, in general, proximal osteotomy techniques are less successful in correcting a congruent joint but, with a subluxated joint, have a relatively high success rate. Mild residual deformity or degenerative arthritis may develop if one fails to appreciate the presence of an increased DMAA (see Figs. 6-56 to 6-59). Mild degenerative arthritis has been reported at both the MTP joint344,535,543 and the MTC joint,101,543 although it is rarely symptomatic. Correction has been found to be more reproducible in those with “moderate” as opposed to “severe” preoperative deformities.395

Figure 6-160 Hallux varus after a distal soft tissue procedure and proximal metatarsal osteotomy. A and B, Preoperative and postoperative radiographs, respectively, demonstrating 5 degrees of varus. C and D, Preoperative and postoperative radiographs, respectively, demonstrating 9 degrees of hallux varus. Hallux varus of this magnitude is rarely of clinical significance and represents mainly a radiographic finding.

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Figure 6-161 Clinical (A) and radiographic (B) examples of severe recurrence. Clinical (C) and radiographic (D) appearance of severe varus. E, Salvage with metatarsophalangeal joint arthrodesis.

Figure 6-162 Delayed union after proximal crescentic osteotomy. A, Preoperative anteroposterior radiograph. B, Postoperative radiograph demonstrating delayed union. C, After below-knee casting for 6 weeks, successful union has occurred.

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A A

B Figure 6-164 A, Elevatus after proximal oblique. B, Salvage with an opening-wedge osteotomy and interposition dorsal graft.

B Figure 6-163 Nonunion after proximal crescentic osteotomy. A, Preoperative anteroposterior (left), oblique (right), and lateral (centered) radiographs demonstrating nonunion. B, Postoperative repair demonstrating satisfactory union after internal fixation and local bone graft.

minimal) when using a single Steinmann pin for internal fixation. Various methods of internal fixation have been used to fix proximal osteotomies, including Steinmann pins,335,344,435,535 a single screw,154,348,409 a screw and pin,92,101,140 and a dorsal plate.445,533 Mann et al344 noted that superficial inflammation around the pin site developed in approximately 10% of patients in whom the osteotomy site was fixed with an oblique Steinmann pin, another reason why this method of fixation was discontinued (see Fig. 6-151). Other alternatives to proximal cresecentic osteotomies include a proximal oblique osteotomy16,66,320,384,446 and a proximal chevron osteotomy348,452,454 (see Fig. 6-159). Markbreiter and Thompson348 and Sammarco et al452 254

reported excellent correction with proximal chevron osteotomies of differing orientations. Complication rates were similar to those experienced with proximal crescentic osteotomy. Rigid internal fixation appears to increase the stability at the osteotomy site. Thordarson and Leventen516 reported less shortening with the use of a more stable internal fixation construct and emphasized that adequate internal fixation was vital to avoid dorsiflexion malunion. Malunion is an extremely difficult complication to treat and may require extensive and complex salvage techniques (see Fig. 6-164). Mann et al344 reported that the most frequent complication of this procedure was hallux varus, which occurred in 14 (13%) of 109 feet and averaged 5.6 degrees. None of the patients complained of pain, and none had a co*ck-up deformity of the first MTP joint. Three patients were dissatisfied because of the position of the toe, whereas the others had essentially no functional complaints and were satisfied with the result. Simmonds and Menelaus488 and Mann and Coughlin336 cautioned that a lateral sesamoid should rarely if ever be removed. This amount of varus is typically a minimal deformity and is more a radiographic finding than a clinical entity (see Fig. 6-160). Frequently, a hallux varus deformity of less than 10 degrees is asymptomatic and is considered by patients to be a subjectively satisfactory result.516 Easley et al140 reported a 12% (5 of 43 patients) incidence of hallux varus after proximal chevron osteotomy. In most cases, hallux varus develops because of

Hallux Valgus ■ Chapter 6

lateral translation of the metatarsal head after medial displacement of the proximal osteotomy. This was a much more frequent occurrence in the cresecentic procedure before changing the osteotomy from being oriented concave distal to concave proximal (see Figs. 6-146 and 6-161D and E).344 In a retrospective study, Trnka et al525 presented a long-term follow-up of a group of patients in whom hallux varus developed (average deformity of 10 degrees of varus). In a series of 16 feet with a follow-up averaging 18 years, 12 (75%) of 16 patients still rated their result as excellent. Only those with a severe hallux varus deformity were dissatisfied or required further surgery. In most patients, the varus deformity was usually 15 degrees or less, a finding similar to that reported by Mann et al344 (see Fig. 6-160). Nonunion is rarely reported after osteotomy in the proximal metaphyseal region. Mann et al observed two nonunions in a series of 1500 cases.344 Both were corrected with an interposition bone graft and internal fixation (see Fig. 6-163). Even though such treatment resulted in some shortening of the metatarsal, no symptomatic transfer lesion developed. Cedell and Astrom63 reported a 10% nonunion rate with an opening-wedge osteotomy, and Sammarco and Russo-Alesi454 reported three cases in a series of 72 operations involving a proximal chevron osteotomy. More recent studies evaluating the openingwedge technique found a low nonunion rate, and several authors feel that the use of a locking plate may be beneficial.433,483,497,563 Epiphyseal injury can occur with a proximal first metatarsal osteotomy in the skeletally immature and lead to growth arrest and ultimately to a short first metatarsal (see Fig. 6-70). Care must be taken in an adolescent to protect the proximal first metatarsal epiphysis. In the treatment of moderate and severe hallux valgus deformities with subluxation of the MTP joint, proximal first metatarsal osteotomy combined with distal soft tissue reconstruction can lead to a successful outcome, although it is well recognized that this procedure is technically difficult.344,360,409 MULTIPLE OSTEOTOMIES The incidence of congruent hallux valgus deformities is unknown. Coughlin and Carlson97 reviewed a series of 878 consecutive bunions over a 12-year period and determined that 18 patients (21 feet) qualified as having congruent deformities of such magnitude that they warranted extraarticular correction (2%). These authors noted that although 12 of the 18 patients underwent surgery before 20 years of age, it should be stressed that with deferred surgery, these deformities can present during the adult years. Thus congruent hallux valgus deformities, although decidedly uncommon (Fig. 6-165), may be seen and treated at any age. A soft tissue intraarticular reconstruction is contraindicated for repair of a hallux valgus deformity with a congruent MTP joint (DMAA > 15 degrees).95 For this deformity, extraarticular correction can be achieved with either a double or triple first-ray

osteotomy.* An Akin osteotomy can diminish phalangeal angulation because of an increased PPAA. A proximal first metatarsal osteotomy or cuneiform osteotomy can decrease an increased 1–2 IM angle. In some situations, an increased DMAA requires a medial closing-wedge osteotomy of the distal first metatarsal.164,225,407,436 Mitchell and Baxter371 reported on the combination of a chevron osteotomy and phalangeal osteotomy to achieve an extraarticular repair. The magnitude of the DMAA and the 1–2 IM angle determines the necessity for multiple firstray osteotomies and the magnitude of realignment. In their radiographic analysis, Richardson et al438 reported that the average normal DMAA was 6 to 7 degrees. Coughlin95 has observed that this angle increases as the magnitude of the congruent hallux valgus deformity increases. Likewise, he has also reported that the final hallux valgus angle closely mirrors the underlying DMAA. Thus any procedure that attempts to realign an MTP joint with an increased DMAA or lateral slope of the distal metatarsal articular surface has a substantial risk of reverting to the preoperative inclination determined by the underlying DMAA (Video Clip 58).91,401 First Cuneiform Osteotomy Riedel439 (in 1886), according to Kelikian,263 first reported the use of a first cuneiform osteotomy for the correction of metatarsus primus varus. Young565 used a first cuneiform osteotomy, and Bonney and Macnab38 and Coughlin and Mann92,105 reported on the use of a medial cuneiform osteotomy for realignment of the MTC joint to avoid disturbing an open proximal first metatarsal epiphysis. Up to now, no long-term series has been published on the use of this technique. All reports deal with individual case studies. A medial cuneiform opening-wedge osteotomy is most commonly indicated in a juvenile patient with an open proximal first metatarsal epiphysis and a hallux valgus deformity characterized by an abnormally widened 1–2 IM angle. An opening-wedge first cuneiform osteotomy is an alternative that can effectively reduce metatarsus primus varus or an increased 1–2 IM angle without exposing the proximal first metatarsal epiphysis to an iatrogenic injury. Jawish et al240 reported on 63 patients (101 feet) treated with a distal soft tissue realignment combined with an opening-wedge cuneiform osteotomy by using a 5- to 10-mm–wide allograft wedge. A 16-degree correction of the hallux valgus angle and a reduction of the 1–2 IM angle of 4 degrees was achieved at an average follow-up of almost 8 years. Technique 1. A medial longitudinal incision is centered over the first cuneiform. (The medial cuneiform is approximately 2 to 2.5 cm long, and the osteotomy is centered in the middle of the first cuneiform.) *References 5, 95, 105, 123, 138, and 472.

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26° 23° 35 23

Figure 6-165 Congruent joint with a sloped distal metatarsal articular angle. A, Preoperative radiograph. B, After a distal soft tissue procedure, no improvement of the hallux valgus angle was achieved. C, Congruent joint as seen on a regular radiograph. D, Computed tomography scan. E, Magnetic resonance image.

2. The naviculocuneiform and the MTC joints are identified. 3. The osteotomy is directed in a medial-lateral plane and carried to a depth of 1.5 cm. The osteotomy must transect both the dorsal and the plantar cortices. A vertical osteotomy is positioned in the center of the first cuneiform, and the osteotomy site is opened medially (Fig. 6-166A and B). 4. Although the medial eminence can be used as an interposition graft, often little medial eminence remains with a juvenile bunion deformity. Therefore it is best to use a wedge-shaped bicortical graft from the iliac crest. The iliac crest graft is removed in a routine manner. Because of the height of the first cuneiform, a 2-cm–long graft is used. The base of the graft should be approximately 1 cm or less and should taper to a fine point at the apex. Once the osteotomy site has 256

been distracted, a triangular bicortical iliac crest bone graft is impacted into place and stabilized with two 0.062-inch K-wires (Fig. 6-166C). 5. With a hallux valgus deformity and a subluxated first MTP joint, a distal soft tissue realignment is performed with the cuneiform osteotomy (Fig. 6-167). 6. With a hallux valgus deformity and a congruent first MTP joint, a concomitant distal first metatarsal closingwedge osteotomy is an option (Fig. 6-168). 7. The wound is closed routinely. Postoperative Care A gauze-and-tape compression dressing or a below-knee cast is applied at surgery. Frequently, the osteotomy is combined with a distal soft tissue realignment or multiple other first-ray osteotomies. The osteotomy will usually heal by 6 weeks after surgery. Internal fixation is

Hallux Valgus ■ Chapter 6

removed after successful healing of the osteotomy site (Fig. 6-169). Distal First Metatarsal Closing-Wedge Osteotomy First described by Reverdin436 and later by Peabody407 and others,95,138,164,411,451 a distal first metatarsal closing-wedge osteotomy can be used for the treatment of a juvenile hallux valgus deformity or in an adult with a congruent hallux valgus deformity. It is especially useful in the presence of an increased DMAA to reorient the metatarsal articular surface more perpendicular to the longitudinal axis of the first metatarsal.

Cuneiform osteotomy

C Line of osteotomy

B Figure 6-166 Technique of cuneiform osteotomy. A, Anteroposterior diagram of a cuneiform osteotomy before distraction. B, Lateral diagram of a cuneiform osteotomy. C, After distraction of the osteotomy site and bone grafting, alignment has been improved. Internal fixation with Kirschner wires is typically used.

Technique 1. A medial longitudinal incision is centered over the MTP joint, beginning at the midproximal phalanx and extending 2 cm above the medial eminence. 2. The medial MTP joint capsule is released on the dorsal proximal aspect with an L-shaped, distally based capsular flap (see Fig. 6-91D). 3. At a point 1.5 cm proximal to the MTP joint, an osteotomy of the proximal metatarsal metaphysis (just proximal to the sesamoids) is performed. A second osteotomy proximal to the first is located 6 to 10 mm proximal to the initial osteotomy. It converges at its apex at the lateral cortex with the distal osteotomy. The magnitude of the medial closing-wedge osteotomy depends on the magnitude of the DMAA (1-mm resection = 5 degrees of correction of the DMAA) (Fig. 6-170).299 4. Care is taken to avoid injury to the sesamoid complex on the plantar aspect at the osteotomy site. 5. Once the wedge has been excised, the osteotomy site is closed. Medial translation of the capital fragment may be necessary. The osteotomy site is fixed with two oblique 0.062-inch K-wires.

Figure 6-167 Cuneiform osteotomy technique. A, Preoperative radiograph demonstrating a juvenile hallux valgus deformity with metatarsus primus varus and an open epiphysis. B, Radiograph after opening-wedge cuneiform osteotomy and distal soft tissue repair. C, Two-year follow-up radiograph after cuneiform osteotomy and distal soft tissue realignment.

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Figure 6-168 A, Juvenile hallux valgus with open epiphysis and distal metatarsal articular angle of 30 degrees. B, Radiograph after opening-wedge cuneiform osteotomy and closing-wedge distal first metatarsal osteotomy. C, Eight-year follow-up radiograph demonstrating successful long-term repair. D, Clinical photograph at 8-year follow-up.

6. The medial eminence is resected with an oscillating saw. 7. The medial capsule is approximated and secured to the first metatarsal with suture placed through a medial metaphyseal drill hole. The dorsal and proximal capsular incisions are repaired with interrupted absorbable suture. 8. After completion of this osteotomy, the hallux should be oriented in slight varus because the articular surface now closely parallels the longitudinal axis of the first metatarsal shaft. This situation creates a need for a proximal first-ray osteotomy to decrease the 1–2 IM angle. An Akin osteotomy can also be added when necessary to create a triple osteotomy (Fig. 6-171). Other Osteotomies Another alternative is to combine a distal first metatarsal closing-wedge osteotomy with a proximal crescentic osteotomy. Although this technique may be quite effective, careful dissection is necessary to protect the first metatarsal shaft from devascularization (Fig. 6-172). This interval may be rather small, thus increasing the risk of a vascular insult to the first metatarsal diaphysis. A better alternative may be to combine a distal first metatarsal osteotomy with a first cuneiform osteotomy, even though a first cuneiform osteotomy is more difficult. A proximal osteotomy of the first metatarsal may be considered but should be approached with caution because extensive soft tissue stripping of the first metatarsal can lead to AVN. Alternative osteotomies have been described by Loretz et al317 and Kramer et al.284 Z-shaped osteotomies (scarf type) of the distal first metatarsal that both protect the sesamoid mechanism and allow realignment of the distal metatarsal articular angle are an alternative as well. Amarnek et al5 used a crescentic distal phalangeal and 258

a distal metatarsal crescentic osteotomy to realign the first ray. Results Funk and Wells164 and others225,407,436 have reported success with distal first metatarsal osteotomies, as have Durman138 and Goldner and Gaines186 with double firstray osteotomies. Kramer et al284 and Day et al121 both reported an average 15-degree correction of the DMAA with a Z-shaped rotational osteotomy, and Loretz et al317 reported similar correction of the hallux valgus deformity with an increase in the DMAA. Funk and Wells164 reported an average 7.2-degree correction of the 1–2 IM angle with a distal first metatarsal closing-wedge osteotomy. A biplanar and triplanar osteotomy has been used to correct an increased DMAA.71,408 Chou et al71 used a biplanar distal chevron osteotomy to correct the DMAA 4 degrees with this procedure. A variety of double osteotomies have been advocated, including proximal phalangeal and first metatarsal osteotomy,5,95,97,186 double metatarsal osteotomy,95,97,138 phalangeal and chevron osteotomy,371 and phalangeal and cuneiform osteotomy.206 Reporting on the use of double and triple osteotomies for the treatment of juvenile hallux valgus with congruous MTP joints, Coughlin95 noted an average 23-degree correction of the hallux valgus angle and an average 8.3-degree correction of the 1–2 IM angle. This correction occurred in the presence of an average DMAA of 19 degrees. These results are similar to those noted by Peterson and Newman,411 who reported on 10 adolescent patients with an average 24-degree correction of the hallux valgus angle and an average 8-degree correction of the 1–2 IM angle after double osteotomy. A high rate of subjective satisfaction was reported in both series. Coughlin and Carlson97 reported on the results of 21 feet

Hallux Valgus ■ Chapter 6 Complications Complications after multiple metatarsal osteotomies may include loss of correction, malunion, loss of fixation, AVN, intraarticular injury from an associated fracture with the osteotomy, and degenerative arthrosis of the IP or MTP joints. These procedures are technically difficult and should be reserved for the occasional case of hallux valgus characterized by a congruent first MTP joint with a DMAA greater than 15 degrees. When possible, a simpler and technically easier procedure is preferable to a more complex and difficult technique. Degenerative arthritis has been reported by Bock et al,35 who noted both metatarsal head and metatarsal sesamoid cartilaginous lesions, with increased occurrence related to the severity of the preoperative hallux valgus deformity.

1 1

3 2 1

Medial exostectomy Bone resection

Figure 6-169 Technique of multiple first-ray osteotomies. Multiple first-ray osteotomies can be used to achieve extraarticular correction of a hallux valgus deformity, especially with an increased distal metatarsal articular angle. A, 1, Closing-wedge osteotomy; 2, closing-wedge osteotomy of the distal first metatarsal with resection of the medial eminence; 3, opening-wedge osteotomy of the first cuneiform. B, Lateral view demonstrating the location of the osteotomies. C, A triple osteotomy improves the overall alignment of the first ray.

with congruent hallux valgus deformities (with an increased DMAA) treated by periarticular osteotomies. Both double and triple first-ray osteotomies were performed in the series. The average correction of the hallux valgus angle was 23 degrees, the average correction of the IM angle was 9 degrees, and the average correction of the DMAA was 14 degrees postoperatively. In a laboratory study, Lau and Daniels299 determined that the size of the wedge to be resected to reduce an abnormally high DMAA in a congruent hallux valgus deformity can be easily calculated preoperatively. They suggested that for every 1 mm of bone resected from the distal metaphysis in the process of performing a closingwedge osteotomy, the DMAA was decreased by 4.7 degrees.

METATARSOCUNEIFORM ARTHRODESIS AND DISTAL SOFT TISSUE PROCEDURE Arthrodesis of the first MTC joint in conjunction with a distal soft tissue procedure for correction of hallux valgus was popularized by Lapidus, although it was conceived by Albrecht,4 Kleinberg,280 and Truslow.527 The procedure is predicated on the principle that metatarsus primus varus must be corrected to obtain satisfactory correction of the hallux valgus deformity. Initially, Lapidus294 specified that a suitable patient preferably should be “young and robust,” with an IM angle of 15 degrees or greater and a “fixed” deformity of the MTC joint. In time, Lapidus294 narrowed his indications substantially for the use of MTC joint fusion. If there was “adequate mobility of the first MTC joint to allow approximation of the first and second metatarsal heads,” Lapidus indicated that a simple bunionectomy was sufficient treatment rather than MTC joint arthrodesis. Although Lapidus did not specifically use the procedure for the so-called hypermobile first ray, currently this appears to be one of the main indications (Video Clip 57).* Indications The major indication for this procedure is a moderate or severe hallux valgus deformity79,199,204,456 (a hallux valgus angle of at least 30 degrees and a 1–2 IM angle of at least 16 degrees). Other indications include juvenile hallux valgus,28,73,172,186,383 recurrent hallux valgus,383,456 severe deformity,28,45,77,383,456 a hallux valgus deformity in the presence of generalized ligamentous laxity,28,383 and degenerative arthritis of the first MTC joint,28,383 Hypermobility of the first ray associated with a hallux valgus deformity is probably the most frequently listed condition for which the Lapidus procedure is indicated,† yet none of these reports give any objective data on the preoperative or postoperative quantification of first-ray hypermobility. There remains continued difficulty in identifying patients who have substantial first-ray *References 21, 54, 140, 141, 174, 218, 248, 271-273, 298, and 307. † References 21, 33, 43, 140, 141, 174, 248, 271-273, and 298.

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Figure 6-170 A, Anteroposterior (AP) radiograph demonstrating a mild hallux valgus deformity in an 11-year-old girl. B, AP radiograph of a 14-year-old girl demonstrating progression of the deformity. C, After distal first metatarsal closing-wedge osteotomy and proximal crescentic osteotomy, alignment is improved. D, A 2-year follow-up radiograph shows acceptable alignment.

Figure 6-171 A, Preoperative radiograph demonstrating moderate hallux valgus deformity with a congruent metatarsophalangeal (MTP) joint (see Fig. 6-59A and B for early preoperative images when the patient was 10 years old). B, At skeletal maturity, a congruent MTP joint and moderate hallux valgus deformity are present. C, Triple osteotomy (closing-wedge phalangeal osteotomy, closing-wedge distal first metatarsal osteotomy, opening-wedge cuneiform osteotomy) has achieved realignment. D, Four-year follow-up radiograph demonstrating excellent correction of a juvenile hallux valgus deformity with a congruent MTP articulation.

instability190,192 as well as the location of this instability. Recent studies by Cooper et al,81 Ellinton et al,144 and Kazzaz et al262continue to cite first-ray instability as an indication for the lapidus procedure, although it has been unequivocably demonstrated by Smith and Coughlin,100,102,190,192,492 that the metatarsal cuneiform joint is uncommonly the site of first-ray hypermobility. 260

Proponents of the Lapidus procedure using it to address first metatarsocuneifrom instability have as yet failed to identify this joint as the cause of this increased mobility; the fact that it diminishes to a normal range of mobility after a distal correction without an MTC joint fusion100 leads the chapter authors to question this particular indication. Ellington et al144 suggested in their study that 96%

Hallux Valgus ■ Chapter 6

Figure 6-172 A, Preoperative radiograph in 40-year-old man who underwent unsuccessful juvenile hallux valgus correction. Note the congruent metatarsophalangeal joint (distal metatarsal articular angle of 30 degrees). B, Triple osteotomy (closingwedge phalangeal osteotomy, closing-wedge distal first metatarsal osteotomy, crescentic proximal first metatarsal osteotomy) has achieved realignment of the first ray. C, One-year follow-up radiograph demonstrating improved alignment. (A suture anchor was used to stabilize a medial capsular disruption found at surgery.)

of subjects had first-ray hypermobility but did not quantify it. They did observe gapping of the plantar MC joint in 52% of lateral radiographs preoperatively. Of interest, Cooper et al81 also reported on 85 feet in which they suggested clinical instability was present. They observed, as did Coughlin and Jones,101 that radiographic plantar gapping was an inconsistent finding. Further study needs to be carried out to identify the location of increased firstray mobility and the significance and reliability of radiographic findings, such as plantar gapping of the first MTC joint. The authors believe that this procedure is useful in about 5% to 10% of patients with an advanced or severe hallux valgus deformity. On the other hand, for those comfortable with this procedure, it can be used for a broader spectrum of cases (in the moderate range of hallux valgus deformities) if a surgeon’s results substantiate its effectiveness. The procedure is also used as a salvage procedure after failed repair of a previous hallux valgus deformity.* Contraindication The main contraindications are a short first metatarsal,383 juvenile hallux valgus with an open epiphysis,88 a mild hallux valgus deformity without excessive first-ray hypermobility (in which a lesser procedure could be performed),88 and the presence of degenerative arthritis of the MTP joint.325 There is probably a relative contraindication to using this procedure in a young person who is active in sports because of the stiffness that follows loss of first MTC joint function. *References 28, 77, 149, 202, 383, and 456.

Technique The surgical technique consists of a distal soft tissue procedure with lateral release of the first web space, excision of the medial eminence, and preparation of the medial joint capsule. Then the first MTC joint arthrodesis is performed, after which the first MTP joint is reconstructed. Distal Soft Tissue Procedure The distal soft tissue procedure is carried out in the same manner as discussed previously. (See pages 203 to 212). Metatarsocuneiform Joint Arthrodesis 1. The MTC joint is approached through a 5-cm dorsomedial, slightly curved incision centered over the first MTC joint.77 The joint capsule is opened dorsally and medially to expose the joint (Figs. 6-173 and 6-174A). 2. With a small curet, ring curet, or osteotome, the articular cartilage is removed in its entirety from the MTC joint (Fig. 6-174B-D). This is a sinusoidal-shaped articular surface 30 mm in height, and it is important to remove the cartilage completely from the joint’s plantar lateral aspect (Fig. 6-175). The inferior lateral portion of the medial cuneiform, as well as the lateral base of the first metatarsal, is resected with an osteotomy.28 This allows correction of both excess valgus and mild plantar flexion. The adjoining lateral surfaces of the proximal first metatarsal and medial second metatarsal are denuded as well.77 If a facet is present on the proximal lateral aspect of the base of the first metatarsal, it is also resected. 3. The joint is gently manipulated from a dorsomedial to a plantar lateral position while bringing the first metatarsal head into a plantar lateral position (see 261

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Bone resection

Figure 6-173 Technique of Lapidus (metatarsocuneiform [MTC] fusion). A, Biplanar wedge resection of the MTC joint, anteroposterior (AP) plane. B, The lateral view demonstrates more plantar bone resection to plantar flex the first metatarsal. The AP (C) and lateral (D) views after placement of internal fixation demonstrate plantar flexion of the osteotomy site. (A third screw can be placed from the first cuneiform through the first metatarsal in a proximal distal direction.)

Figure 6-174 Technique for the Lapidus procedure. A, Operative incision. B, Resection of the articular surfaces. C1, C2, and D, Minimal resection of the articular surfaces. E, More extensive resection to reduce the intermetatarsal angle. F, After removal of the triangular resected segment. G, Closure of the arthrodesis site. (Courtesy Chris DiGiovanni, MD.)

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C Figure 6-175 Exposure of the metatarsocuneiform joint. A, Wide exposure is necessary to prevent dorsiflexion malunion. B, Anatomic dissection demonstrates the depth of the joint. C, Care must be taken to avoid injury to the peroneus longus tendon on the plantar surface of the joint. (A, Courtesy Chris Coetzee, MD.)

Fig. 6-174E-G). Moving the joint in this manner respects the joint’s biomechanical axis. Placing the metatarsal head in a plantar lateral position corrects the IM angle so that often little if any bone needs to be resected from the joint to achieve this alignment. Although some have advocated the use of an iliac crest bone block to realign the joint, the authors believe that this is rarely necessary and technically makes the procedure much more complex. On the other hand, placement of local bone graft obtained from the medial eminence into the interval between the first and second metatarsals may be advantageous.28,77 Likewise, cutting a small dorsal slot and filling it with local bone graft is thought by some to aid the fusion process as well.28,204,205 4. Sutures are placed into the first web space to secure the adductor tendon into the lateral side of the first metatarsal. 5. The first MTC joint is “feathered” with a 4-mm osteotome to increase the bony surfaces. Alternatively, multiple small holes are drilled to perforate the subchondral plate on both adjoining surfaces. The first metatarsal

Figure 6-176 Lapidus procedure. A, Preoperative radiograph demonstrating a severe hallux valgus deformity. B and C, Postoperative correction has been achieved. Internal fixation is routinely removed 12 to 16 weeks after successful arthrodesis to avoid breakage of the intermetatarsal screw.

is then reduced so that it is parallel with the second metatarsal to close the IM angle. As this is done, the first metatarsal can be overreduced into excess plantar direction or underreduced and excessive dorsiflexion left. This is a key maneuver, and the surgeon must continuously assess the relationship of the first to the second metatarsal when displacing the first MTC joint. When proper alignment appears to be achieved, a guide pin is placed across the MTC joint, after which a 4.0-mm cannulated self-tapping screw is inserted from the first cuneiform into the first metatarsal and a second screw is placed from the first metatarsal into the cuneiform. Usually, two79 or three screws are used to gain rigid interfragmentary compression (Fig. 6-176). Fixation can also be achieved by placing a small plate along the joint’s dorsomedial aspect that has been molded to hold the metatarsal in its corrected position. (Fig. 6-177). A derotational lag screw can be placed between the first and second metatarsals.28 If used, it is typically removed 12 weeks after surgery. Reconstruction of the Metatarsophalangeal Joint 1. The capsular tissues on the medial side of the MTP joint are plicated to place the hallux in satisfactory 263

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Figure 6-177 Anteroposterior (A) and lateral (B) radiographs after fixation with dorsal lateral compression plate. (Courtesy Keith Wapner, MD.)

alignment. Any pronation is corrected when the sutures are placed along the joint’s medial aspect. 2. The wounds are closed with interrupted sutures, and a compression dressing is applied. Postoperative Care In the office, 1 to 2 days after surgery, the compression dressing is removed and another gauze-and-tape dressing applied, similar to that described for the distal soft tissue procedure. The patient is kept non–weight bearing on the affected extremity. This type of dressing is changed weekly for 8 weeks. The extremity is initially placed in a belowknee cast. Coetzee and Wickum79 recommend a slipper cast for 6 weeks, with weight bearing only on the heel. One to 3 weeks after surgery, the sutures are removed, a radiograph is obtained, and based on alignment of the hallux, a determination is made about how to align the MTP joint with the postoperative dressings. Weight bearing is allowed 4 to 6 weeks after surgery. After 8 weeks, if adequate fusion has occurred at the MTC joint, the patient is permitted to progress to ambulation in a sandal or shoe as tolerated. If the arthrodesis is not complete, the dressings are removed from the foot so that the patient can start range-of-motion exercises for the hallux. The patient is maintained in a short-leg removable cast until the fusion is complete. More recently, Kazzaz and Singh262 reported on 27 feet in which a postoperative shoe rather than a below-knee cast was used for immobilization. All MTC joints successfully fused. Results Patient satisfaction rates vary from 74% to 92%.* Many of the reports on the Lapidus procedure are marked by no or little follow-up186,325,472,527; short-term follow-up of less than 1 year73,280,295; insufficient data on the demographics, method, or criteria of assessment or radiographic information280,294-296,383; inclusion of patients with *References 28, 56, 73, 77, 352, 362, 383, 385, and 456.

264

varying preoperative diagnoses28; or use in combination with a silicon great toe implant.14,42 The average correction of the hallux valgus angle varies from 10 to 22 degrees28,77,352,383,385 and the 1–2 IM angle from 6 to 9 degrees.* Various nonunion rates reported include Kazzaz and Singh262 (0%), Coetzee and Wickum79 (6.6%), Sangeorzan and Hansen456 and Faber et al152 (10%), and McInnes and Bouche362 (15.6%). Nonetheless, Coetzee and Wickum79 reported on their results with the Lapidus procedure. Of 105 patients, only 7 had a fibrous union. The hallux valgus angle was reduced from 37 to an average of 16 degrees; the 1–2 IM angle was reduced from 18 to 8 degrees at final follow-up. An 85% satisfaction level was reported by the cohort of patients. Hass et al199 compared the Lapidus procedure with a proximal first metatarsal closing-wedge osteotomy and noted excellent correction with the Lapidus procedure. In another study of failed bunion procedures treated with the Lapidus procedure as a salvage reconstruction procedure. Complications Reported complications after the Lapidus procedure include a prolonged healing time,456 malunion,383,385,456 prolonged swelling,383,456 continued pain,456 nonunion,† stiffness,28,295,383,385 recurrence,28,77,295 and postoperative varus deformity (Fig. 6-178).352 The pseudoarthrosis rate at the MTC joint varies from approximately 0% to 75%,‡ with symptoms in about half these patients (Fig. 6-179). The 5% to 24% pseudoarthrosis rate reported by most authors attests to the MTC joint being a difficult joint in which to obtain a satisfactory arthrodesis; however, Mauldin et al352 reported a 74% incidence of nonunion. *References 28, 45, 73, 204, 205, 246, 316, 383, 385, 386, and 441. † References 28, 73, 204, 205, 246, 316, 352, 383, 385, 386, and 441. ‡ References 28, 56, 73, 77, 144, 352, 362, 383, 385, and 456.

Hallux Valgus ■ Chapter 6

Figure 6-178 A, Severe hallux valgus deformity with metatarsalgia and instability of the metatarsocuneiform joint. B, After the Lapidus procedure, severe hallux varus deformity has resulted.

Figure 6-179 Preoperative (A) and postoperative (B) radiographs of painful nonunion after attempted metatarsocuneiform joint fusion.

Lombardi et al316 noted a mean shortening of 8 mm after the procedure. Sangeorzan and Hansen456 reported a 13% revision rate and a 20% overall failure rate. Mauldin et al352 reported a 16% incidence of postoperative hallux varus, Myerson383 and others73,456 observed that the procedure was technically challenging, and Clark et al73 noted a high rate of complications. More recent reports77,79 with improved surgical technique have demonstrated a much higher level of success with this procedure. Most authors agree that first MTC joint arthrodesis with a distal soft tissue procedure is technically difficult and should not be used in patients with the typical bunion but rather advocate it in those with marked hypermobility of the first ray and significant widening of the 1–2 IM angle or in salvage situations.77,79 Postoperative

MTP range of motion was reported by McInnes and Bouche362 to be 62 degrees. In a prospective study, Coetzee and Wickum79 observed preoperative dorsiflexion of 66 degrees and no significant diminution at almost 4 years’ follow-up. Plantar flexion was not affected by the procedure. Rink-Brune441 reported that it took longer than 3 months to resolve the swelling and subjective complaints in 16% of patients. McInnes and Bouche362 reported that only 30% of athletes returned to their preoperative level of activity, whereas 75% of more sedentary patients achieved this goal. The chapter authors believe that because of the stiffness that results after the procedure, it is less often indicated in younger and more active individuals. When the procedure results in shortening because of bone resection, the metatarsal must be placed in sufficient plantar flexion to accommodate for this shortening. Myerson383 noted, however, that 9% of the first metatarsals in his series were dorsiflexed, half of which resulted in transfer lesions beneath the second metatarsal. More recently, the use of dorsal plating of the first MTC joint appears to have alleviated the tendency for dorsiflexion at the arthrodesis site, and can be used to increase the compression across the joint.149,378,470 Scranton et al,470 in a cadaveric study, found a dorsal-compression locking plate was 25% stronger than cross-compression screws in the fixation of the first MTC joint. The use of the Lapidus procedure has gained favor in the salvaging of prior failed bunion surgery.79,202 Hamilton et al202 reported success in 14 of 17 (82%) feet treated for failed prior halux valgus surgery using either crossed screws or a compression plate and augmented with a bone stimulator. The three nonunions occurred in patients who smoked. Ellington et al144 reported on successful salvage in 24 of 25 feet (96%) and at final follow-up, 87% of patients reported good or excellent results. With an overall failure rate reported to be as high as 28%,456 this is not the procedure of choice for the occasional foot surgeon. METATARSOPHALANGEAL JOINT ARTHRODESIS Arthrodesis of the first MTP joint for treatment of hallux valgus deformity was described in 1852 by Broca50 and subsequently by Clutton.75 Many authors have recommended the use of first MTP joint arthrodesis as a primary procedure either to correct a severe hallux valgus deformity* or for rheumatoid arthritis (Fig. 6-180 and Video Clip 36),† hallux rigidus (Video Clip 33),‡ or traumatic arthritis.96,108 It can be used as a salvage procedure for failed bunion surgery or previous infection196 (Video Clip 34).§ *References 99, 116, 143, 187, 242, 288, 300, 314, 434, 506, and 521. † References 27, 64, 86, 94, 96, 218, 342, 345, 346, 379, 512, 528, 529, 541, and 553. ‡ References 109, 157, 175, 266, 335, 363, 453, 493, 494, 512, 528, 529, 541, 559, and 568. § References 104, 175, 196, 215, 347, 453, 528, and 541.

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9°

Figure 6-180 Rheumatoid arthritis with hallux valgus. A, Preoperative radiograph. B, Postoperative radiograph. C, Follow-up at 1 year. Note the diminution of the intermetatarsal angle as well.

procedure, it is indicated for a recurrent hallux valgus deformity, following a failed implant, and after an unsuccessful cheilectomy. Contraindications Few contraindications to arthrodesis of the first MTP joint exist. Relative contraindications include arthrosis of the IP joint or an insensate foot. Another relative contraindication is lack of motion at the MTP joint, which in some cases is annoying to patients. A thorough discussion about the trade-off between reduced MTP joint motion and realignment of the first ray is important preoperatively.

Figure 6-181 Severe hallux valgus. A, Preoperative radiograph with a widened intermetatarsal (IM) angle as well. B, After metatarsophalangeal arthrodesis, correction of both hallux valgus and the IM angle.

First MTP joint arthrodesis is also useful in a patient with neuromuscular instability secondary to a cerebral vascular accident, head injury, or cerebral palsy.341,342,512,528 The rationale for the procedure is that the length of the first metatarsal is preserved and stability of the first ray is maintained, thereby allowing weight to be transferred to the hallux. Indications Arthrodesis is indicated in a patient with a severe hallux valgus deformity, usually with an angle greater than 50 degrees (Fig. 6-181), in a rheumatoid patient with hallux valgus, in an older patient with moderate or severe hallux valgus, in advanced cases of hallux rigidus, for primary arthritis or arthritis after trauma, and in a patient with a hallux valgus deformity after a CVA or head injury, or with an underlying diagnosis of cerebral palsy. As a salvage 266

Technique The surgical technique is divided into the surgical approach, preparation of the joint surfaces, and fixation of the arthrodesis. Surgical Approach 1. The MTP joint is approached through a dorsal longitudinal incision just medial to the extensor hallucis longus tendon. The 5-cm incision extends from a point just proximal to the IP joint to above the MTP joint (Fig. 6-182A). 2. The incision is deepened through the extensor retinaculum, which is reflected along with the joint capsule. In this way, the dorsomedial cutaneous nerve is protected. The extensor tendon is usually retracted laterally. A complete synovectomy of the MTP joint is performed, after which the medial and lateral collateral ligaments are transected. Preparation of Curved Concentric Surfaces Curved concentric surfaces permit easy positioning and adjustment of the MTP joint surfaces for the arthrodesis. This process is less involved technically than cutting two flat surfaces.490 Flat cuts may lead to excessive shortening if further resection is necessary to

Hallux Valgus ■ Chapter 6

Figure 6-182 Technique of metatarsophalangeal arthrodesis. A, Longitudinal dorsal incision. B, A cannulated concave metatarsal head reamer (C) is used to prepare the metatarsal surface. D, Power-driven convex phalangeal reamers are used to prepare the phalanx. E, Bone slurry from the reamers is placed in the joint. F, Temporary fixation of the arthrodesis site with a Kirschner wire. G, Dorsal titanium plate fixation. H, Cross-screw placement. I, Final appearance of the foot.

achieve adequate position. The following technique for preparation of congruous curved surfaces uses cup-shaped power reamers.* 1. After soft tissue release has been performed medially and laterally, to expose the metatarsal and phalangeal articular surfaces, the medial eminence is removed with a small sagittal saw. A small wafer of bone can be resected from the base of the proximal phalanx and metatarsal head to decompress the joint or shorten the first ray if shortening is desired. If the procedure is being carried out in a rheumatoid patient *References 87, 107, 109, 143, 187, 288, and 506.

and significant shortening is necessary, more of the metatarsal head can be removed at this time. If length is to be preserved, only the articular surface should be removed. On the other hand, preparation of the joint surfaces can be accomplished without initial bone excision, and one can proceed directly to the reaming process. 2. A 0.062-inch K-wire is driven into the center of the first metatarsal head. The size of the metatarsal metaphysis is estimated and a corresponding reamer of the appropriate size is chosen (Fig. 6-182B and C). (Reamers vary from 14 to 20 mm in size, although 16 to 18 mm is the most common diameter used.) A cannulated metatarsal head reamer is used to reduce the 267

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metatarsal head and metaphysis and to shape the articular surface area into a convex cup-shaped surface, after which the wire is removed. 3. The K-wire is then driven into the base of the proximal phalanx. A convex male reamer is used to create a concave, cup-shaped surface. Typically, the smallest reamer is initially used. Reaming is continued with progressively larger reamers until the surface size matches the prepared metatarsal surface (Fig. 6-182D). The K-wire is then removed. 4. The two curved congruent surfaces are rotated into proper alignment, which is 15 degrees of valgus and 15 to 20 degrees of dorsiflexion in relation to the first metatarsal shaft (Fig. 6-182E). The hallux is derotated so that there is no pronation. A 0.062-inch K-wire is driven across the proposed arthrodesis site through a plantar medial stab wound and exits dorsolaterally (Fig. 6-182F). Alternative Method of Joint Preparation There are ways to create surfaces for the arthrodesis other than the curved surfaces just described. 1. The distal portion of the first metatarsal is cut with an oscillating saw, and only the articular surface is removed to create a flat surface that is angulated slightly dorsally and laterally. If the procedure is being carried out in a rheumatoid patient and significant shortening is necessary, more of the metatarsal head can be removed at this time, but if length is to be preserved, only the articular surface should be removed (Fig. 6-183A). 2. Longitudinal traction is placed on the hallux, and all the tissues inserting into the base of the proximal phalanx are released by sharp dissection. 3. The hallux is positioned with one hand holding it in approximately 15 degrees of valgus and 10 to 15 degrees of dorsiflexion in relation to the plantar aspect of the foot. The surgeon then carefully notes the relationship between the base of the proximal phalanx and the initial cut made in the metatarsal head. With

the initial cut as a guide, another cut is made parallel to it to resect the entire articular surface and subchondral bone, while leaving, if possible, the metaphyseal flare of the proximal phalanx intact (Fig. 6-183B). 4. The two parallel cuts are placed together, and their alignment is carefully observed. If the position is not correct, another cut is made, this time in the metatarsal head to adjust the alignment. If the procedure is being done in conjunction with a rheumatoid foot repair, no further shortening of the MTP joint should be undertaken until the metatarsal heads are resected and the final length of the first metatarsal can be determined. 5. The hallux is derotated so that there is no pronation. A 0.062-inch K-wire is driven across the proposed arthrodesis site through a plantar medial stab wound and exits dorsolaterally. Internal Fixation of the Arthrodesis 1. The prepared surfaces are apposed and the alignment carefully checked. On occasion, if the lesser toes tend to deviate slightly medially, the arthrodesis site is aligned in slightly more valgus. As a general rule, the desired alignment is 15 degrees of valgus, 15 to 20 degrees of dorsiflexion, and neutral rotation. With the curved congruous surfaces, these dimensions can be easily altered by merely changing the position of the hallux. With flat surfaces, further resection of the prepared surfaces is necessary to achieve the desired alignment. A 0.062-inch K-wire is inserted as temporary fixation to hold the prepared surfaces (see Fig. 6-182F). A second cross K-wire can be placed if further stabilization is necessary before placement of internal fixation. 2. A dorsal six-hole titanium plate is then placed on the dorsal aspect of the distal first metatarsal and proximal phalanx (see Fig. 6-182G). This preformed plate has 15 degrees of valgus and 20 degrees of dorsiflexion built into it to help align the first ray in the appropriate position. It is stabilized with six dorsal plantar bicortical screws. The K-wire is removed and a cross screw

Figure 6-183 A, Phalangeal osteotomy to create flat surfaces. B, The joint is distracted before arthrodesis.

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placed to further fix the arthrodesis site (see Fig. 6-182H and I). 3. Alternatively, an interfragmentary 4.0-mm cannulated screw can be inserted across the proposed arthrodesis site in a medial to lateral direction. The guide pin is placed slightly below the midline of the proximal phalanx and angled in a proximal to lateral direction. The cortex on the medial side of the phalanx is drilled and the hole countersunk. A 24- to 30-mm–long screw is inserted. As the screw is cinched down, the K-wire, which is at a right angle to the screw, is removed to permit as much interfragmentary compression as possible. 4. Any remaining prominent bone or remnants of the medial eminence are resected with a rongeur. 5. The wound is closed in two layers, with the capsule closed beneath the extensor tendon. The skin is closed with fine interrupted sutures, and a compression dressing is applied. The patient is permitted to ambulate in a postoperative shoe, with weight bearing as tolerated on the heel and other aspect of the foot. Alternative Method of Fixation Fixation of the arthrodesis site can be carried out in a variety of ways. The authors’ philosophy is to obtain fixation that is as rigid as possible so that the patient can ambulate without a cast while achieving a satisfactory rate of fusion. At times, inadequate bone stock is present in the proximal phalanx when attempting to salvage a Keller procedure104,536 or after removal of a prosthesis. On occasion, in a rheumatoid patient with severe osteopenia, the plate-and-screw technique cannot be used. In these circ*mstances, the authors prefer to use threaded Steinmann pins to gain fixation of the arthrodesis site (Video Clip 35).86 These pins have the disadvantage of crossing the IP joint, although in two large series, this did not create a significant clinical problem.342,346 The surgical technique follows. 1. The joint surfaces are prepared in the same manner as initially described or through the creation of congruous curved surfaces (Fig. 6-184; see also Fig. 6-183). 2. A 1 8 -inch, double-pointed Steinmann pin is drilled in a proximal to distal direction out the tip of the hallux (Fig. 6-185A). 3. A second pin is drilled out parallel to the first one. 4. One of the pins protruding through the end of the proximal phalanx is cut about in half so that the chuck can be placed onto the distal end of the longest Steinmann pin. 5. The MTP joint is reduced in proper alignment (varus/ valgus, dorsiflexion/plantar flexion, rotation), and with the other hand holding the handle of the drill, the Steinmann pin is slowly drilled across the arthrodesis site into the metatarsal. It should be drilled in until the surgeon feels it penetrating the cortex of the proximal first metatarsal or until it reaches the proximity of the MTC joint. The first pin is then cut off

15o

A 20 o

B Figure 6-184 The fusion site is placed in 15 to 20 degrees of valgus (A), dorsal view and about 20 degrees of dorsiflexion (B), lateral view in relation to the metatarsal shaft, which is approximately 10 to 15 degrees of dorsiflexion in relation to the floor.

approximately 5 mm from the tip of the skin; the second pin is drilled across the arthrodesis site in a similar manner (Fig. 6-185B). 6. The wound is closed with interrupted sutures and a compression dressing applied. The patient is permitted to ambulate as tolerated. 7. Postoperative care is the same as for other forms of arthrodesis (Fig. 6-185C-F). On rare occasions, because of loss of significant bone stock, it becomes necessary to add an interposition bone graft to gain more length at the first MTP joint arthrodesis site. As a general rule, a slightly shorter great toe does not create a significant problem, but if circ*mstances indicate that a bone graft is needed, it can be placed between the proximal phalanx and the metatarsal head as a flat piece of tricortical iliac crest or an oval “football-type” graft (Fig. 6-186 and Video Clip 34). Whenever a bone graft is added, the morbidity of the procedure increases substantially, and the healing time is usually doubled from 3 months to often 5 to 6 months. These patients should usually be kept non–weight bearing to avoid stress on the fixation device and to promote healing of the graft. Postoperative Care In the office, 1 or 2 days after surgery, the compression dressing is removed, and a firm 2-inch Kling gauze dressing with 1 2 -inch adhesive tape is applied. The patient is permitted to ambulate in a postoperative shoe, as tolerated, with weight borne on the heel and lateral aspect of the foot. The patient is evaluated with radiographs every 4 weeks until successful fusion occurs. At this time, the postoperative shoe is discontinued. As a general rule, 10 to 12 weeks is required for complete fusion. If longitudinal Steinmann pins have been placed, they are easily removed under a digital block in an office setting. 269

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Figure 6-185 First metatarsophalangeal joint fusion technique using threaded Steinmann pins. A, A Steinmann pin is driven out through the tip of the great toe in retrograde manner. B, Pins are brought back across the attempted fusion site while manually compressing the bony surfaces together. C, Preoperative radiograph. D, After intramedullary Steinmann pin fixation. E, Fifteen years after surgery, a successful arthrodesis is observed. F, Fifteen years after surgery, the patient is able to walk on tiptoe.

Results The reported rate of patient satisfaction after MTP arthrodesis varies from 78% to 93%.* In the only five studies reporting on the treatment of idiopathic hallux valgus by MTP arthrodesis,99,187,231,434,521 subjective satisfaction was noted in more than 90% of patients (Fig. 6-187). The rate of fusion varies, depending on the operative technique, the method of internal fixation, and the preoperative diagnosis. MTP joint fusion generally occurs in most patients between 10 and 12 weeks. Reported success rates vary from 77% to 100%, with an average rate of 90%† Coughlin86 reported a 10% failure rate in a review of 1451 cases in the literature. In the largest series, Riggs and Johnson440 reported a 91% fusion rate in 309 procedures. With the use of a dorsal compression plate, the reported success rate ranged from 92% to 100%.‡ *References 27, 64, 87, 94, 96, 187, 218, 288, 342, 345, 346, 379, 506, 512, 528, 529, 541, and 553. † References 99, 116, 143, 187, 288, and 506. ‡ References 87, 96, 99, 116, 143, 187, 196, 288, 332, 506, and 541.

270

Coughlin and Abdo96 reported subjective good and excellent results in 93% of cases. Inadequate fixation is the more commonly cited reason for nonunion,174,434,440,529 but true failure of fixation is uncommon.440 As McKeever363 noted, an unsuccessful arthrodesis or pseudoarthrosis may still give a painless and successful result (Fig. 6-188). Coughlin,99 in a series of 21 arthrodeses, reported 3 asyptomatic nonunions (14%). In another series of 49 patients, Goucher and Coughlin187 reported 4 nonunions (8%), three of which were asymptomatic. Hope et al226 reported on 11 nonunions from a large series of otherwise successful arthrodeses and observed that 7 of the 11 were successfully treated with removal of the failed hardware and debridement of the wound. Only four patients required eventual redo arthrodesis or arthroplasty. The final alignment of the fusion is very important for patient satisfaction. The recommended angle of valgus ranges from 5 to 30 degrees, with an average of 15 degrees.* Fitzgerald157 warned that fusion in less than 20 degrees of valgus is associated with a threefold incidence *References 99, 104, 157, 196, 346, 434, and 440.

Hallux Valgus ■ Chapter 6

Figure 6-186 A, Preoperative radiograph demonstrating a failed single-stem prosthesis. B, Postoperative radiograph of fusion after removal of the prosthesis. C, Preoperative radiograph with a failed double-stemmed prosthesis. D, Postoperative radiograph after removal of the prosthesis and insertion of a bone graft. E, Successful arthrodesis. F, Preoperative radiograph after a failed Keller arthroplasty. G and H, After arthrodesis with the Steinmann pin technique. I, After removal of the pins.

Figure 6-187 A, Preoperative radiograph demonstrating recurrent hallux valgus deformity with increased 1–2 intermetatarsal angle. Postoperative anteroposterior (B) and lateral (C) radiographs demonstrating precontoured titanium dorsal plate.

271

Part II ■ Forefoot

Figure 6-188 A, Severe hallux valgus associated with rheumatoid arthritis. B, Painful nonunion with a decrease in angular deformity in a satisfied patient. C, Broken Steinmann pins portend a nonunion.

Figure 6-189 Degenerative arthritis of the interphalangeal joint is rarely symptomatic.

of IP joint arthritis. The literature reports a 6% to 33% rate of degenerative arthritis of the IP joint after arthrodesis of the MTP joint (Fig. 6-189).99,187,218,379,440 Coughlin et al 99 reported at an average 8-year follow-up and noted little progression of IP joint arthritis and negligible IP joint pain. Grimes and Coughlin196 reported that 8 of 33 feet showed progression of IP joint arthritis; however, in this and the previous study,99,196 corresponding arthritis in the contralateral foot IP joint was relatively symmetric and may have been related to patient age and the longterm follow-up of each study (8 years). Mann and Oates,342 using Steinmann pins that crossed the IP joint for internal fixation, reported a 40% incidence of degenerative changes at the IP joint. Few of these patients had any clinical symptoms at final follow-up. 272

Degenerative arthritis in the first MTC joint can also be a concern. Coughlin et al99 reported on 21 feet followed for an average of 8 years after MTP arthrodesis. Four MC joints showed progression of arthritis, but four contralateral MTC joints showed similar changes. Grimes and Coughlin,196 in a review of failed bunion surgery in which MTP joint arthrodesis was used to salvage 33 feet, noted 5 feet with degenerative changes, but 4 were observed in the contralateral foot. Thus, again, in this 8-year follow-up study, arthritic changes of the first MTC joint may have been a function of the length of follow-up as opposed to the ipsilateral MTP joint arthrodesis. After arthrodesis, the increased 1–2 IM angle associated with a severe hallux valgus deformity is routinely reduced,* and rarely, if ever, is a first metatarsal osteotomy necessary.212,231,341 The authors do not believe that any attempt should be made to correct the IM angle when carrying out an arthrodesis. If for some reason the IM angle is unacceptable, it can be corrected with a basal osteotomy at another time, rather than creating a situation in which, besides attempting to obtain an arthrodesis at the MTP joint, the surgeon is simultaneously attempting to heal an osteotomy at the metatarsal base. Cronin et al116 reported an average 1–2 IM angle correction of 8.2 degrees after MTP joint arthrodesis. The average preoperative 1–2 IM angle was 17 degrees, and the average hallux valgus angle was 47 degrees. Thus the more severe the preoperative angular deformity, the more correction achieved with the arthrodesis procedure. In the sagittal plane, the recommended angle of dorsiflexion for the fusion varies from 10 to 40 degrees† (in relation to the shaft of the first metatarsal), with 20 to 25 degrees being the most commonly recommended position.86 The conical shape of the proximal phalanx creates a dorsal slope to the phalanx that influences the final *References 33, 99, 104, 116, 157, 174, 187, 196, 212, 231, 242, 332, 342, 346, 363, 434, 440, 528, 553, 558, and 559. † References 96, 99, 187, 242, 342, 346, 512, and 529.

Hallux Valgus ■ Chapter 6

15°–25°

10°

10° 15°–25°

Figure 6-190 Aspects of metatarsophalangeal (MTP) joint arthrodesis. A, The dorsiflexion angle of arthrodesis. The dorsiflexion angle of arthrodesis is calculated using middiaphyseal reference points. These, as show in the diagram, may measure 10 to 25 degrees of dorsiflexion; the plate, to fit this angulation may only have a dorsal bend of 10 degrees. B, The dorsal flare of the phalanx can lead to malalignment C, Removal with a rongeur can assist in the alignment. D, Using the undersurface of an irrigation pan, or using a fingertip beneath the tip of the toe E, these methods allow a surgeon intraoperatively to gauge that there is adequate dorsiflexion present are both methods to avoid excessive plantar flexion at the MTP arthrodesis site.

position of the arthrodesis.300 Precontoured plates, to a certain extent, take this into account; however, the final position of the arthrodesis is effected by the plantar inclination of the first metatarsal. A patient with a flatfoot may have much more dorsal inclination with a precontoured plate than a patient with a cavus foot. Thus, intraoperatively, a surgeon should ensure that the position of the arthrodesis is correct in a sagittal as well as a coronal plane (Fig. 6-190). Coughlin94 reported that there was a marked increase in IP joint arthritis when the dorsiflexion angle of fusion was less than 20 degrees. Fusion in excessive dorsiflexion leads to pressure beneath the sesamoids, whereas fusion in excess plantar flexion leads to pressure beneath the tip of the great toe. Use of a dorsal mini-fragment or titanium compression plate is relatively easy and has been associated with reasonably high success rates of fusion.187,288 Whereas the larger and bulky small-fragment compression plates have frequently required removal,87,332,541 the low-profile Vitallium plates96 and titanium plates107,109 have not required removal. Other reports on the use of compression screws for fixation have demonstrated their reliability as well and a high level of patient satisfaction.242 The main advantage of rigid internal fixation is that it permits immediate ambulation with a postoperative shoe, thereby eliminating the need for a walking cast. However, protected ambulation is important. Ellington et al143 reported a lower fusion rate in those who had unprotected ambulation as opposed to those who did heel weight bearing for the first 6 weeks (86% vs. 93% fusion rate, respectively). In an older patient, particularly a rheumatoid patient, the

ability to walk postoperatively without a cast is extremely important (Fig. 6-191). The surgical technique used for MTP arthrodesis should be simple and achieve a predictable result (Fig. 6-192). Shaping of the curved congruous joint surfaces to enable the surgeon to easily adjust the metatarsal and phalanx to the desired position of valgus, extension, and rotation is a key part of this procedure. The use of rigid internal fixation is important in obtaining and maintaining the desired fusion until osseous fusion has occurred. As McKeever363 said, however, “it is the [fusion] and its position that is important and not the method by which it is obtained.” Complications The main complications after MTP joint arthrodesis are nonunion, malalignment, and degenerative arthrosis of the IP joint of the great toe. With the use of an interfragmentary screw and dorsal plate, the authors believe that a fusion rate of 95% can probably be achieved. In some cases of hallux rigidus in which the bone ends are extremely sclerotic, the surgeon may anticipate difficulty in obtaining fusion, and possibly weight bearing should be delayed in these patients. In some cases, the authors have found it necessary to make multiple drill holes through the sclerotic bone in an attempt to improve blood flow across the attempted arthrodesis site. Certain situations present increased risk for a successful arthrodesis. Ellington et al143 reported the nonunion rate for those with rheumatoid arthritis was 23%, although those without rheumatoid arthritis had a 7% nonunion 273

Part II ■ Forefoot

A A

Figure 6-191 First metatarsophalangeal joint arthrodesis. A, Preoperative radiograph demonstrating varus with a decrease in the intermetatarsal (IM) angle. B and C, After arthrodesis, the IM angle is actually increased to a normal value. Preoperative (D) and postoperative (E) radiographs demonstrate fusion with advanced arthrosis.

rate. Hope et al226 noted the nonunion rate in males was 19% and in females was 2.4%. They also noted that with prior failed surgery, the nonunion rate was 24%. On the other hand, Grimes and Coughlin196 reported a successful fusion rate of 86%. 274

Figure 6-192 A, Preoperative radiograph demonstrating severe hallux valgus and a dislocated second metatarsophalangeal joint. B, Second toe amputation is possible with a fused hallux because there is no progression of deformity.

Nonunion, when it occurs, is often not pain ful.99,187,196,226,363 If the patient has pain, repair is necessary, either by bone grafting if the fixation is adequate or by removal of the fixation device, bone grafting, and the application of new fixation if indicated. Malunion in any plane is poorly tolerated by patients. This emphasizes the importance of close attention to the final position of the arthrodesis. As Coughlin88 said, “no bunion procedure requires a technique that is more exacting and unforgiving than that required in arthrodesis of the first MTP joint.”

KELLER PROCEDURE Riedel,439 in 1886, was the first to perform a resection of the base of the proximal phalanx and arthroplasty of the MTP joint as treatment of hallux valgus. Davies-Colley,120 in 1887, described this same procedure for the treatment of hallux rigidus. It was popularized by Keller’s reports in 1904 and 1912.264 The purpose of the procedure in the treatment of hallux valgus is to decompress the MTP joint by resection of about a third of the proximal phalanx, thereby relaxing the contracted lateral structures (Video Clip 60). Although the Keller procedure was probably once the most widely used bunion procedure, with the development of other surgical techniques and critical clinical evaluation of results of the Keller procedure, its limitations and indications have been better defined. Indications The Keller procedure is indicated in an older patient in whom extensive surgery is contraindicated and who is essentially considered housebound ambulatory531 or in an older patient with a severe hallux valgus deformity and marginal circulation that has resulted in chronic skin breakdown. It is often considered a salvage technique

Hallux Valgus ■ Chapter 6

for treatment of a failed previous surgical procedure.135,464,531,536 It is indicated for moderate hallux valgus deformities in which the hallux valgus angle is less than 30 degrees associated with degenerative arthritis of the MTP joint. The Keller procedure can also be used to treat hallux rigidus in patients in whom cheilectomy or arthrodesis cannot be performed. In this procedure, medial eminence resection, partial proximal phalangectomy, and medial capsulorrhaphy are performed to realign the hallux.*

B A

Contraindications This procedure is contraindicated in younger, more active individuals318 in whom MTP joint mobility and function remain important because the stability of the first MTP joint is impaired by the Keller procedure.104 Likewise, in older individuals in whom MTP joint function is important, who have substantial lateral metatarsalgia, or who have a severe deformity for which a subtotal correction is unacceptable, this procedure is contraindicated. Technique The surgical technique is divided into the surgical approach, resection of bone, and reconstruction of the MTP joint. Surgical Approach 1. The first MTP joint is exposed through a medial approach that begins at the IP joint and extends proximally 1 cm beyond the medial eminence. A proximally based capsular flap is developed to create full-thickness dorsal and plantar skin flaps for exposure of the medial eminence (Figs. 6-193 and 6-194A; see Video Clip 60). 2. The medial eminence is exposed by sharp dissection to create a flap of medial capsule based proximally. 3. The base of the proximal phalanx is exposed subperiosteally. Resection of Bone 1. The medial eminence is removed in line with the medial aspect of the metatarsal shaft. Any osteophytes along the dorsal aspect of the metatarsal head are removed (Fig. 6-194B). 2. The proximal third of the phalanx is removed (Fig. 6-194C; see Fig. 6–193A). 3. Resection of the lateral sesamoid is thought to release the lateral contracted structures, which aids in realignment of the hallux (Fig. 6-194D).135 Reconstruction of the Metatarsophalangeal Joint 1. To reestablish flexor function, an attempt is made to reapproximate the plantar aponeurosis and plantar plate to the proximal phalanx through two or three small drill holes in the remaining diaphyseal portion of the proximal phalanx.88,542 Flexor function can also *References 31, 255, 338, 437, 480, and 542.

C Figure 6-193 The Keller procedure. A, The medial eminence is removed in line with the medial aspect of the metatarsal shaft. The proximal third of the proximal phalanx is excised. B, An attempt is made to reapproximate the plantar and medial capsular structures to the remaining base of the proximal phalanx. C, Fixation of the metatarsophalangeal joint with a 5 64 -inch Steinmann pin.

be enhanced by suturing the plantar aponeurosis to the flexor hallucis longus tendon, which helps prevent a co*ck-up deformity of the MTP joint (Fig. 6-195A). 2. A 5 64-inch Steinmann pin or two 0.062-inch K-wires135 are introduced at the joint and driven distally; they are then drilled in a retrograde direction across the joint into the metatarsal head to provide stability in the postoperative period and to create a 5-mm gap between the base of the phalanx and the metatarsal head. The tip of the pins should be bent to prevent proximal migration (see Figs. 6-193C and 6-194E). 3. The medial capsular flap is sutured to the periosteum of the proximal phalanx and, in some cases, folded across the MTP joint to create an interposition arthroplasty (see Fig. 6-194F). 4. The skin is closed with interrupted sutures, and a compression dressing is applied. Postoperative Care In the office, 1 to 2 days after surgery, the compression dressing is removed and the patient placed in a firm dressing of 2-inch Kling gauze and 1 2-inch adhesive tape. The patient is permitted to ambulate in a postoperative shoe. The dressings are maintained for 6 weeks. The pins are removed 3 weeks after surgery, at which point gentle motion of the MTP joint is begun. 275

Part II ■ Forefoot

Figure 6-194 A, A midline incision is used to expose the medial eminence. Dorsal and plantar flaps are developed. B, The medial eminence is excised. C, The base of the proximal phalanx is resected with a power saw. D, The lateral sesamoid is excised. E, An intramedullary Kirschner wire is used to stabilize the toe. F, The medial capsule and intrinsics are reattached when possible to the base of the proximal phalanx. (Courtesy E. Greer Richardson, MD.)

Figure 6-195 co*ck-up deformity after the Keller arthroplasty. A and B, Clinical photographs. C, Radiographic appearance.

Results After excisional arthroplasty, the hallux valgus angle is typically reduced approximately 50% or less,327,530,531,536 and the 1–2 IM angle is diminished very little.437,444,530 Satisfactory results occur more reliably when the hallux valgus angle does not exceed 30 degrees so that correction can be achieved by resection of less than a third of the base of the proximal phalanx (Fig. 6-196). Reduction of pain after the procedure can be attributed to a diminution in size of the medial eminence, which enables the use of more comfortable shoes, as well as decompression of an osteoarthritic joint. Satisfaction rates after a Keller procedure, judged mainly on the basis of relief of “bunion pain” as opposed to relief of metatarsalgia, vary from 72% to 96%.74 Rogers and Joplin444 reported generally poor results with this procedure: marked improvement in 9%, no change in 71%, and postoperative deterioration in 20%. Bonney and Macnab38 observed 276

that the functional results tend to deteriorate with time. Henry et al218 observed that after excisional arthroplasty, the hallux was unable to bear weight, and resultant metatarsalgia developed. Donley et al135 and Richardson437 both reported an average total MTP joint range of 40 to 50 degrees, most of which was dorsiflexion. Love et al318 reported less than 10 degrees in 18 feet. When assessing the results of a Keller procedure, the surgeon must remember that for the procedure to be successful, it should be used in older patients, who by nature are less demanding of their feet. When the procedure is used in this group, a satisfactory result can be anticipated. If, however, the procedure is used in more active persons, dissatisfaction results because of the lack of push-off of the great toe, transfer metatarsalgia (usually beneath the second metatarsal head), co*ck-up deformity of the first MTP joint, and recurrence of the deformity. The Keller procedure cannot correct a

Hallux Valgus ■ Chapter 6

Figure 6-196 Results of the Keller procedure. A, Preoperative radiograph. B, Postoperative radiograph demonstrating pin fixation. C, Radiograph after pin removal. D, Position of the toe 9 months after surgery.

Figure 6-197 Intractable plantar keratosis beneath the second metatarsophalangeal joint after the Keller procedure.

significant hallux valgus deformity or IM angle, and other procedures should be strongly considered. Berner et al31 have reported successful use of the Keller resection arthroplasty in the treatment of recalcitrant ulceration of the hallux in diabetic patients. Complications Coughlin and Mann104 and others* have reported a high incidence of metatarsalgia after excisional arthroplasty (Fig. 6-197; see Fig. 6-195). Postoperative varus and valgus deformity may occur because of lack of intrinsic control (Figs. 6-198 and 6-199). The magnitude of phalangeal resection appears to play a role in the level of satisfaction. Although excision of half of the phalanx has *References 74, 135, 218, 255, 437, 444, 530, and 536.

B Figure 6-198 Varus deformity after the Keller procedure. A and B, Clinical photographs. C, Radiographic appearance.

been recommended,38,74,255 limited phalangeal resection is associated with higher rates of postoperative satisfaction.531 Henry et al218 reported an association between greater phalangeal resection and increased weight bearing beneath the lateral metatarsals, as well as an increased incidence of lateral metatarsalgia. On analyzing the 277

Part II ■ Forefoot

Figure 6-199 Valgus deformity after the Keller procedure. Clinical (A) and radiographic (B) appearance. (A, Courtesy E. Greer Richardson, MD.)

Figure 6-200 Unstable hallux after a Keller resection arthroplasty.

length of the remaining phalanx, they noted that weight bearing on the hallux was present in 73% of feet, from which a third or less of the proximal phalanx had been resected, whereas it was present in only 9% when more than a third of the phalanx was resected. In patients with more severe deformities, there is a tendency to resect a greater amount of the proximal phalanx to realign the hallux. Vallier et al531 observed that excessive resection tended to leave a short, flail, functionless great toe (Figs. 6-200 and 6-201). Donley et al135 reported that patients lost two thirds of plantar flexion, and 40% lost plantar flexion power. Range of motion is often diminished after the Keller procedure. Postoperative metatarsalgia has been reported in most series*; other reported *References 74, 218, 318, 437, 444, 480, and 531.

278

Figure 6-201 Short hallux after a Keller procedure. A and B, Clinical photographs. C, Radiograph.

complications include impaired control and function of the hallux,104,218 diminished flexor strength,104,327,480,530,531 marked shortening of the digit,104,218 IP joint stiffness,104,218 and co*ck-up deformity of the great toe.* Because of the high incidence of incomplete correction and the *References 264, 318, 327, 444, 480, and 530.

Hallux Valgus ■ Chapter 6

Figure 6-202 Failed Keller procedure—shortened and arthritic hallux. A, Clinical appearance. B, After arthrodesis with intramedullary Steinmann pins. C, Intraoperative photograph. D, After successful fusion.

associated postoperative lateral metatarsalgia, excisional arthroplasty is recommended only for elderly sedentary patients with osteoarthritis of the first MTP joint in the absence of metatarsalgia preoperatively.327 As Henry et al218 concluded, “any operation for hallux valgus should attempt to restore (or at least not destroy) the ability of the big toe to bear weight.” Salvage of a failed Keller arthroplasty can be a difficult procedure and may require an interposition bone graft104 (Figs. 6-202 and 6-203). Coughlin and Mann104 and Vienne et al536 have both reported on series in which MTP joint arthrodesis was used to salvage a painful failed Keller arthroplasty. The arthrodesis led to improved weight bearing of the first ray and a correction of recurrent hallux valgus deformities. A high rate of fusion was achieved in both studies, although both authors cautioned that although salvage was successful, and pain reduction and deformity correction was achieved, function of the hallux was still impaired. Complications of Hallux Valgus Surgery To discuss complications of bunion surgery, the goals of treating hallux valgus deformities should first be clarified.

The main goal is to produce the most functional foot possible after surgery. This will vary, depending on the severity of the deformity and the functional capability of the patient. In a young patient with bunion pain secondary to a prominent medial eminence, a fully functional, a painless foot is the goal; in a rheumatoid patient, a foot with satisfactory overall alignment that allows reasonable footwear and an ability to walk without pain is a realistic goal. The algorithms that are found in Figures 6-78, 6-79, and 6-82 can help the clinician decide which type of surgical procedure will produce the best surgical results. However, this does not address a patient’s expectations. The patient and clinician must have the same goals in mind when surgery is being contemplated. The authors see many patients in consultation who have been misled regarding their surgery, and although the result obtained was within the normal spectrum for a specific procedure, the patient was extremely dissatisfied. If patients are made aware of the various complications associated with each specific procedure (e.g., loss of motion, residual joint pain, sensitivity about the scar), although they may not be totally satisfied, at least they face no surprises. It is important to not “sell” a patient on a procedure but rather to be sure the patient believes that all types of conservative management have been attempted and that surgery will offer a realistic solution to the problem. If the patient has no pain, it is difficult to improve the situation. To a certain extent, each age group has specific goals for correction of a foot problem. With the wide selection of leisure and sport shoes available today, people can wear a shoe that will not place excessive pressure over the painful area. Several age groups have specific problems. For example, women in their second and third decade tend to have a ligher level of dissatisfaction with the results of bunion surgery. Their goal is usually to be able to fit into a more stylish shoe, but many of these women have a wide forefoot, so even after satisfactory correction of the deformity, they are still unable to wear their desired shoes. If they believed that the surgery would permit them to do so, they will often be quite dissatisfied. This is basically a problem in preoperative communication between the surgeon and patient. An athlete or dancer, particularly if professional, should always receive the most conservative treatment plan possible.84 A general rule is that until such patients are significantly hampered in their ability to perform in their given profession, surgical intervention should be delayed because of the concern that after an unsuccessful surgical procedure, a painful foot will bring an end to their athletic career. Causes of Surgical Failure The following results represent an ideal hallux valgus repair: ■ ■

Correction of the hallux valgus and 1–2 IM angles Creation of a congruent MTP joint with sesamoid realignment 279

Part II ■ Forefoot

Figure 6-203 Salvage of a failed Keller procedure with an interposition bone graft. A, Preoperative clinical appearance. B, An iliac crest graft is harvested and inserted as an interposition graft. C, Graft is placed between prepared surfaces. D, Placement of Steinmann pin fixation. Preoperative (E) and postoperative (F) radiographs. G, After removal of internal fixation.

■

Removal of the medial eminence Retention of functional range of motion of the MTP joint ■ Maintenance of normal weight-bearing mechanics of the foot ■

With this ideal type of repair in mind, the authors now examine some of the factors that result in failure of a hallux valgus repair. If an inappropriate procedure is selected for the pathologic condition present, the outcome will often be suboptimal. As pointed out in the algorithms in Figures 6-78, 6-79, and 6-82, each hallux valgus deformity needs to be carefully analyzed before selecting the appropriate surgical procedure. If a patient has a congruent joint and an attempt is made to correct the hallux valgus deformity by realigning the proximal phalanx over the metatarsal head, an incongruent joint may result. This in turn can lead to either joint stiffness, if the phalanx does not slide back into its former congruent alignment or there is recurrence of the deformity. If significant arthrosis is present in the joint and a realignment is carried out, restricted joint motion is a common result. Therefore the first step in avoiding a complication is selection of the correct surgical procedure. 280

If the indications for a procedure are “stretched,” a suboptimal result will be obtained. This may occur when choosing a “simple bunionectomy” when a metatarsal osteotomy should be performed as well. Although the hallux is initially well aligned, recurrence of the deformity quickly results. If a chevron procedure is used to correct a severe hallux valgus deformity, full correction is rarely achieved. When performing hallux valgus surgery, a surgeon must remember that a single procedure will not result in satisfactory correction of all deformities. Inadequate or inappropriate postoperative management may result in failure even when technically the procedure was properly performed. Soft tissues need to be carefully and meticulously supported and protected after surgery to ensure a satisfactory result. After many orthopaedic procedures, meticulous postoperative management is unnecessary, but after most hallux valgus procedures, careful follow-up is necessary to ensure a successful result. Other causes of failure that may result from soft tissue, neurologic, or bone problems are discussed in detail next. Postoperative sepsis, though infrequent, can be a cause of failure and result in significant joint stiffness, chronic swelling, and possibly even nonunion of the osteotomy.

Hallux Valgus ■ Chapter 6

Finally, unrealistic patient expectations may be the cause of a failed surgical procedure. If the patient does not understand the possible limitations of the procedure preoperatively, both the patient and the surgeon may be unhappy afterward. In selecting the surgical procedure, the surgeon must consider the options for a salvage procedure if a complication develops. The following typical complications can occur after specific procedures: soft tissue realignment resulting in a hallux varus deformity; arthrodesis resulting in nonunion; proximal first metatarsal osteotomy resulting in nonunion or malunion; and distal metatarsal osteotomy resulting in malunion, nonunion, or AVN. In the treatment of a hallux varus deformity, adequate soft tissue realignment can usually be achieved frequently, but on occasion, an arthrodesis may be necessary. After nonunion of an arthrodesis, an interposition bone grafting procedure will frequently result in successful fusion. With malunion of a metatarsal osteotomy, a corrective osteotomy can often achieve satisfactory realignment. With AVN of the metatarsal head, an arthrodesis with an interposition bone block may be necessary to achieve a satisfactory result. The authors believe that patients should have a general understanding of the type of complication that may develop so that if a second procedure is required, they will have some basic knowledge of what may be necessary. The more common complications of hallux valgus surgery are presented here to acquaint the surgeon with the various types of problems that may arise. It is hoped that with a familiarity with these problems, the surgeon will take precautions to prevent them. A certain degree of risk is associated with any type of surgical procedure, and complications can occur regardless of the precautions taken. Soft Tissue Problems INFECTION A postoperative infection may be superficial or deep. The clinician must be constantly aware of the possibility of postoperative infection and treat it vigorously if it develops. It is very important to determine as quickly as possible whether an infection is superficial to the MTP joint or whether it involves the joint itself (Fig. 6-204). Generally speaking, a superficial infection is manifested by local cellulitis and, on occasion, evidence of ascending lymphangitis. The skin over the involved area may be red and warm, but motion of the joint will not usually cause significant pain. Attempts at aspiration of the MTP joint through an area of cellulitis are discouraged because of the risk of spreading a superficial infection into the joint space. Clinically, fever will usually develop in a patient with a superficial infection. Hematologic data may indicate an increase in the white blood cell (WBC), sedimentation rate, and C-reactive protein. Clinical judgment is important in choosing treatment, and the use of either oral or systemic antibiotics is indicated (Fig. 6-205).

Figure 6-204 Infection after bunion surgery with ascending lymphangitis, treated with warm moist soaks and intravenous antibiotics.

A deep infection involving the MTP joint is much more severe and is usually manifested as a marked increase in pain and swelling about the MTP joint. There may be evidence of purulent discharge from the wound. MTP joint motion will typically cause discomfort, as will palpation of the joint itself. Often a fever is present, and the WBC count, C-reactive protein, and sedimentation rate are generally elevated. Management should be directed toward obtaining a specific culture and sensitivity of the offending organism. Prompt treatment with parenteral antibiotics is indicated. With purulent drainage, a decision must be made expeditiously regarding whether prompt irrigation and debridement of the joint are indicated. After a severe joint space infection, marked intraarticular joint fibrosis and degenerative arthritis may ensue due to destruction of the articular cartilage. Changes in periarticular soft tissues after the infection may lead to recurrence of the original deformity. DELAYED WOUND HEALING On occasion after foot surgery, the operative wound edges appear to be locally reddened and slightly separated. There is no evidence of surrounding cellulitis or purulent drainage. The joint itself is not usually particularly swollen, and motion of the joint does not cause increased discomfort. Such cases are often caused by a superficial fungal infection. Carbolfuchsin (Carfusin) painted on the wound on one or two occasions will generally result in prompt wound healing with no further sequelae. In the presence of increasing evidence of cellulitis, a more serious problem should be suspected and treated accordingly. SKIN SLOUGH On occasion after surgery, a partial- or full-thickness slough about the wound may occur. Sloughing usually 281

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Figure 6-205 Postoperative infection. A, Cellulitis has developed 1 week after surgery. B, One week after initiation of oral antibiotics. C, At 3 weeks, the cellulitis is largely resolved.

Figure 6-206 Skin slough. A, Full-thickness skin slough on the plantar aspect of foot covered by skin graft, which unfortunately necrosed. B, With time and local wound care, the area of skin loss contracted and healed.

develops 7 to 14 days after surgery and, depending on its size, may create a significant problem. The cause of the sloughing is devascularization of the involved tissue (Fig. 6-206), which can result from insufficient circulation secondary to a dysvascular foot, excessive retraction on the skin edge at surgery, placement of the skin under tension after correction of a severe deformity, or pressure from the postoperative dressing (Fig. 6-207). Treatment varies depending on the severity of the tissue loss. In the case of a minor partial-thickness skin slough, local treatment and the passage of time usually result in a satisfactory outcome. Sloughing caused by a 282

dysvascular foot may require revascularization of the extremity before satisfactory wound healing can occur. Other larger, full-thickness skin sloughs may eventually require skin grafting after a satisfactory granulating bed has been achieved or could even require amputation. ADHERENT SCAR On occasion after a successful surgical procedure, a scar forms that is quite adherent to the underlying tissue. If a full-thickness dissection includes the underlying fatty tissue when skin flaps are developed at the time of the initial surgery, an adherent scar seldom occurs. As a

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general rule, an adherent scar may actually soften over time, thus rendering it less bothersome to the patient. Soft tissue and underlying fatty tissue are generally somewhat limited on the foot, and excision of a persistent, adherent scar will not usually result in significant improvement of

B Figure 6-207 A, Skin slough after bunion surgery in a patient with vascular insufficiency. B, Above-knee amputation was eventually required.

the situation. Persistent massage of an adherent scar may in time help mobilize the restricted tissue. PARESTHESIAS OF THE HALLUX Entrapment or severance (partial or complete) of a cutaneous nerve may result in either dysesthesia or anesthesia distal to the involved nerve. Protection of sensory nerves at the time of surgery is paramount; however, once a nerve injury occurs, desensitization of the involved area is managed by frequent massaging, rubbing, or tapping. This will often produce a satisfactory result over a period of several months. On occasion, it is necessary to reexplore the injured nerve and further resect the nerve proximally to an area of soft tissue to diminish the symptoms. The use of a transcutaneous nerve stimulator may be effective if surgical intervention fails. On rare occasions, a regional pain syndrome may develop (see Chapter 14). One of the most frequently involved nerves is the dorsomedial cutaneous nerve to the great toe (Fig. 6-208AC). An incision on the dorsomedial aspect of the first MTP joint unfortunately overlies this cutaneous nerve. On occasion, this nerve can be severed at the time of surgery or later become entrapped in scar tissue (Fig. 6-209). As a general rule, neurolysis is rarely helpful, particularly if the nerve has been partially severed. Exploration of the injured nerve through a long, dorsomedial incision enables the identification of normal and injured nerve. After carefully freeing the nerve from surrounding scar tissue and sectioning the nerve more proximally, the nerve is then transferred beneath and sutured under minimal tension to the abductor hallucis muscle. In this way, the nerve is transferred from an area of painful scar tissue to an area where there is little or no pressure. Although an area of numbness over the dorsomedial aspect of the great toe remains, the dysesthetic area is no longer present. The plantar medial cutaneous nerve just plantar to the abductor hallucis tendon can also be injured. Symptoms develop with ambulation as the MTP joint dorsiflexes with plantar pressure over the neuroma, and often a

Figure 6-208 Iatrogenic injuries to nerves at surgery can lead to numbness and paresthesias. A, Dorsal medial cutaneous nerve to the hallux. B, Common digital nerve to the first web space. C, Injury to the superficial peroneal nerve.

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Figure 6-209 Exposure of the dorsal cutaneous nerve of the hallux. A, The nerve is contained in the cuff of subcutaneous tissue. B, The common digital nerve is identified and protected during the hallux valgus surgery but may inadvertently injured with the capsulorraphy.

patient transfers weight to the lateral border of the foot. Again, surgical treatment consists of exposing the plantar medial cutaneous nerve through a long medial incision just dorsal to the weight-bearing surface. The nerve is identified and traced proximally to normal nerve tissue. After the nerve has been freed and sectioned, it is buried proximally beneath the abductor hallucis muscle. At the time of transposition, the sectioned nerve is sutured with a minimum of tension so that as the toes are brought into dorsiflexion, symptoms will not be exacerbated. After sectioning of the injured nerve, there is residual numbness along the plantar medial aspect of the great toe. On occasion, the common digital nerve to the first web space is partially or completely transected with exploration of the first web space. If a neuroma develops, there may be sensitivity on the plantar aspect of the foot, as well as dysesthesias on the plantar aspect of the first web space (see Fig. 6-208B). Surgical treatment involves exposure through a dorsal first web-space incision. The transverse metatarsal ligament is sectioned and the common digital nerve identified and carefully freed from surrounding tissue. If a significant neuroma is identified and transection of the nerve is necessary, it should be performed with as much length of the nerve left as possible. This ensures that the remaining stump can be elevated to an area alongside the first metatarsal so that the nerve end (where another neuroma will form) is removed from the plantar aspect of the foot. Proximal transection of the common digital nerve without elevation of the stump frequently results in a painful neuroma located more proximally in the foot. At times the common digital nerve can be freed from the adjacent soft tissue; if the nerve appears to be abnormal, it can be elevated off the plantar aspect of the foot and transferred above a portion of the adductor hallucis muscle so that the nerve is not exposed to the trauma of weight bearing. DELAYED WOUND BREAKDOWN On occasion after successful surgery and wound healing, the wound will once again become swollen and sensitive. 284

This usually occurs 4 weeks or more postoperatively but may occur many months after surgery. Frequently, the cause is a foreign body reaction to the underlying suture material. It frequently involves silk, but other suture materials (e.g., cotton, chromic, newer synthetic materials) may be involved. The area of the reaction forms a sterile abscess, the skin breaks down, and a suture granuloma develops. With time, the involved foreign material is usually extruded. On occasion, exploration of the wound may be necessary to excise the foreign material. Once removed, prompt wound healing generally occurs, although cauterization of the remaining granulation material with silver nitrate is often required. Complications Affecting the Metatarsal Shaft After any metatarsal osteotomy, malposition or loss of position of the osteotomy site is possible. To avoid this problem, a broad stable osteotomy, rigid internal fixation, adequate postoperative immobilization, and protected ambulation are necessary. Some osteotomies are inherently more stable than others. Surgical judgment is required to determine which sites are sufficiently stable for ambulation and which are not. The same surgical procedure in two different patients may require a different method of fixation and postoperative weight-bearing precautions. The following are the most common types of problems seen after metatarsal osteotomy. SHORTENING Shortening occurs after most metatarsal osteotomies. After the chevron procedure, an average shortening of 2.2  mm (range, 0-8) has been reported222,430 (Fig. 6-210A). After the Mitchell procedure, even more shortening has been reported (Fig. 6-210B).* The most shortening seems to follow the Wilson procedure, with an average of 11  mm (Fig. 6-210C and D).430 After a distal soft tissue procedure and proximal osteotomy, *References 60, 158, 184, 214, 370, and 463.

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Figure 6-210 Shortening after hallux valgus surgery. A, Preoperative radiograph of moderate hallux valgus deformity. B, After chevron osteotomy. Ten years after surgery, avascular necrosis has led to substantial shortening of the first ray. C, Preoperative radiograph. D, Shortening after a Wilson or Mitchell procedure. E, Preoperative radiograph. F, Shortening after a proximal metatarsal osteotomy. Shortening of the first metatarsal may result in a transfer lesion.

approximately 2-mm shortening has been reported (Fig. 6-210E and F).101,344 The main problem associated with shortening is the development of a transfer lesion beneath the second metatarsal head. It is difficult to assign a specific amount of shortening that will produce metatarsalgia because a number of factors play a role, including the original length of the first metatarsal and whether dorsiflexion is associated with the shortening. The degree of hallux valgus correction, range of motion, and stability of the MTP joint are factors because weight is normally transferred to the great toe at the end of stance phase. This, in turn, unloads the second metatarsal head. With insufficient stability or inadequate correction of the hallux, the first metatarsal will not carry its share of the weight. After procedures that destabilize the MTP joint, such as the Keller procedure,218 or with a prosthesis in which significant weight bearing no longer occurs beneath the great toe, the incidence of metatarsalgia is increased. Certain procedures (e.g., Mitchell, Wilson, closingwedge proximal metatarsal osteotomy) have the potential for transfer metatarsalgia.214,276,370,561 In these cases, it is imperative that the length of the first and second metatarsals be carefully assessed when planning a surgical procedure to decide whether an alternative procedure that would produce less shortening should be used. Those experienced with the Mitchell procedure emphasize that plantar flexion of the distal fragment should be carried out to help alleviate the potential for metatarsalgia.* However, if the first metatarsal is significantly short to begin with and more shortening ensues after surgery, metatarsalgia will inevitably result. Once shortening of the first metatarsal and metatarsalgia occur, further surgical treatment is often required. Surgical treatment of this condition is difficult, and the results are often less than optimal. Lengthening of a metatarsal is difficult to achieve both anatomically and technically. Metatarsals do not “stretch” well, and even if an interposition bone block is used, some resorption may occur and subsequent tilting of the distal portion of the metatarsal may develop. If the second metatarsal is significantly longer than the first and third, shortening of the second metatarsal to achieve a normal weight-bearing pattern can be beneficial. On rare occasions, both the second and the third metatarsals can be shortened to realign the weight-bearing pattern of the foot. On occasion, a plantar-flexion osteotomy of the first metatarsal can be used to increase its weight-bearing function. DORSIFLEXION Dorsiflexion of the first metatarsal can occur after a proximal osteotomy of almost any type. It can also occur distally after a chevron, Mitchell, or Wilson osteotomy. After MTC fusion, dorsiflexion of the metatarsal has been reported as well.383,456 *References 34, 184, 214, 366, 371, 561, and 562.

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Dorsiflexion, as with shortening of the metatarsal, should be avoided if possible. Unfortunately, dorsiflexion of an already short metatarsal only compounds the problem of transfer metatarsalgia. At times, dorsiflexion occurs with minimal shortening, and rarely does a problem result. Exactly how much dorsiflexion versus how much shortening can be tolerated after a surgical procedure varies from foot to foot. It probably depends on the overall rigidity of a foot, the relationship of the length of the first and second metatarsals, and a patient’s activity level. When substantial dorsiflexion occurs, however, it creates a difficult management problem and is probably best handled by a plantar-flexion first metatarsal osteotomy rather than by shortening or elevating the second metatarsal. Elevation of the second metatarsal often leads to a transfer lesion beneath the third metatarsal. After a lateral closing-wedge first metatarsal osteotomy, a dorsiflexion deformity usually develops because more bone is removed dorsally than plantarward at the osteotomy site. As the osteotomy is closed, the metatarsal moves laterally and dorsally. This combination of shortening and dorsiflexion can cause significant metatarsalgia. Furthermore, internal fixation must be adequate to maintain the desired position of the osteotomy (Fig. 6-211A and B). If dorsiflexion of the first metatarsal results in a symptomatic transfer lesion beneath the first metatarsal or results in flattening of the longitudinal arch because of loss of support by the first metatarsal head, a plantarflexion osteotomy can be performed. There are many techniques with which to plantar flex the first metatarsal. The authors prefer to make a crescentic-shaped cut in the plantar half of the first metatarsal about 1 cm distal to the MTC joint. With this cut, the blade must exit plantarward. The top of the blade does not penetrate the dorsal surface, and the osteotomy is completed vertically with a sagittal saw (Fig. 6-211C). In performing a proximal metatarsal ostetomy (crescentic or closing wedge), elevation of the capital fragment can occur because of malalignement of the actually osteotomy. The operative leg often externally rotates on the surgical table, and if the osteotomy is not perpendicular to the shaft of the first metatarsal (in a dorsal plantar plane), elevation can occur (Fig. 6-212). After a proximal crescentic osteotomy, dorsiflexion can occur with inadequate internal fixation. This osteotomy offers a broad cancellous surface, which is quite stable with screw fixation. At times, if the bone is osteopenic or if a screw of inadequate length is chosen, dorsal angulation may develop. Mann et al344 reviewed a series of 109 cases and reported postoperative dorsiflexion in approximately 28% of cases, although the magnitude of the deformity was not quantified. Some of the cases of dorsiflexion were quite minor. In none of these patients, however, did a transfer lesion develop. The explanation for this is that the first MTP joint was adequately realigned, and thus the hallux continued to 286

bear weight in a normal manner. This appears to compensate for the dorsiflexion that developed (see Fig. 6-211D and E). Shortening of the first metatarsal is an inherent part of the Mitchell procedure. The osteotomy is designed so that the shortening is compensated for by plantar flexion or plantar displacement (or both) of the distal fragment. Inadequate fixation of the distal fragment, however, can lead to postoperative dorsiflexion. With a dorsiflexed short first metatarsal, weight is transferred to the lesser metatarsals. Prevention of this complication is far simpler than later treatment. Salvage often entails placement of a proximal interposition bone block to both plantar flex and lengthen the first metatarsal. If only dorsiflexion ensues, correction can be achieved with a bone graft placed in the distal third of the metatarsal, closer to the apex of the deformity (see Fig. 6-211F). After a distal oblique or Wilson-type osteotomy, both shortening and dorsiflexion occur because of inadequate fixation of the capital fragment. This presents a challenging salvage situation. Frequently, shortening of the second and, on occasion, the third metatarsal is necessary to relieve lateral metatarsalgia. After a chevron osteotomy, dorsiflexion of the capital fragment may result in transfer metatarsalgia. Dorsal displacement of the capital fragment can be prevented by intraoperative internal fixation. When dorsiflexion of the distal fragment results in transfer metatarsalgia, it is preferable to treat the second metatarsal with a shortening osteotomy rather than attempt to realign the first metatarsal head because of the risk of AVN (see Fig. 6-211G). After MTC joint arthrodesis, dorsiflexion may develop at the MTC joint, particularly if a bone graft has been added to the procedure. When dorsiflexion is of such magnitude that a transfer lesion develops, a plantarflexion osteotomy of the first metatarsal can achieve realignment distal to the fused joint. PLANTAR FLEXION A plantar-flexion deformity of the first metatarsal occurs infrequently and is caused by inadequate internal fixation of the osteotomy site. It frequently leads to increased weight bearing beneath the first metatarsal head, with the subsequent development of a diffuse callus. An orthotic device that transfers weight laterally to the lesser metatarsal head region will often alleviate the symptoms. With a severe deformity, however, a corrective osteotomy to dorsiflex the first metatarsal can be performed (Fig. 6-213). EXCESSIVE VALGUS (LATERAL DEVIATION) OF THE FIRST METATARSAL On occasion, the IM angle will be overcorrected, and a negative angle will be created (Fig. 6-214). If the deformity is minimal, no significant sequelae will develop. If the overcorrection is excessive, the articular surface slopes laterally, and as the proximal phalanx is relocated on the

Hallux Valgus ■ Chapter 6

G Figure 6-211 Complications resulting from dorsiflexion of a first metatarsal osteotomy. A, Dorsiflexion and shortening after lateral closing-wedge osteotomy. B, Dorsiflexion and marked shortening after lateral closing-wedge osteotomy. Preoperative (C1) and postoperative (C2) radiographs demonstrating correction of the dorsiflexion posture of the first metatarsal. C3, The dotted line demonstrates a curved plantar osteotomy with a dorsal straight cut used for this correction. D, Dorsiflexion of the first metatarsal after proximal crescentic osteotomy. E, Dorsiflexion and shortening after infection of a proximal metatarsal osteotomy. F, Dorsiflexion of the metatarsal head after the Mitchell procedure. G, Dorsiflexion of the capital fragment resulting in a transfer lesion, following a chevron osteotomy.

metatarsal head, an incongruent joint surface is created. In time, the MTP joint will become painful and degenerative arthritis may develop. After a proximal crescentic osteotomy, if the concavity of the saw blade faces distally, there is a tendency to displace the metatarsal shaft medialward as the osteotomy is rotated. When this occurs, the metatarsal head may be

translated too far laterally (Fig. 6-215). Concurrently, if the medial eminence is excessively resected, an unstable situation develops that is at risk for the development of a hallux varus deformity. Therefore, when a distal soft tissue procedure and proximal crescentic osteotomy are performed, the osteotomy to resect the medial eminence is performed 2 mm medial to the sagittal sulcus to leave 287

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B B

Figure 6-212 Performing a first metatarsal ostetomy may lead to elevatus because of saw position. A, Note lateral rotation of right leg. If a saw cut is made in this plane, displacement or closing of the ostetomy will elevate the distal fragment. B, A vertical Kirschner wire is placed perpendicular to the longitudinal axis of the first metatarsal. Note the saw blade in this photograph is too far medially rotated. C, The saw blade is rotated to parallel the Kirschner wire, and then with the osteotomy, the cut will be vertical to the shaft (neither elevating or depressing the distal fragment).250

C Figure 6-213 Complications after plantar flexion of a first metatarsal osteotomy. A, Plantar-flexion deformity after the Mitchell procedure. B, Correction after dorsal osteotomy. C, Severe plantar-flexion deformity after a chevron osteotomy.

Figure 6-214 Complications associated with excessive adduction of the first metatarsal after proximal osteotomies. A, Hallux valgus associated with adduction of all metatarsals. B, Correction of hallux valgus with a proximal metatarsal osteotomy resulted in a negative intermetatarsal (IM) angle but a congruent metatarsophalangeal (MTP) joint. To gain this correction, a negative IM angle was necessary. C, Preoperative radiograph. D, Postoperative radiograph demonstrating the effects of a proximal metatarsal osteotomy with creation of an incongruent MTP joint. E, Creation of an incongruent joint from excessive lateral displacement of the proximal metatarsal osteotomy. When a congruent joint is present preoperatively, it must be appreciated. Any attempt to rotate the proximal phalanx on the metatarsal head will result in an incongruent joint.

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tissue procedure, the authors advocate moving 1 to 2 mm medial to the sagittal sulcus to ensure that an adequate medial buttress is left in place to prevent a varus deformity. The absence of articular cartilage just lateral to the sagittal sulcus may invite further excision, but this will lead to the removal of an excessive amount of the metatarsal head and result in an unstable joint, which in turn can lead to a hallux varus deformity. Other times, excessive excision of the metatarsal head results in an incongruent articular surface, which leads to early degenerative arthritis (Fig. 6-217). Treatment of excessive resection of the medial metatarsal head is difficult because insufficient metatarsal head remains to support the proximal phalanx. The most common means of salvage is an MTP arthrodesis to both realign the joint and eliminate the pain. A

Figure 6-215 A and B, Excessive lateral displacement of the metatarsal head after a proximal crescentic osteotomy caused by medial deviation of the osteotomy site.

a “medial buttress” so that the risk of overcorrection is reduced. Correction of this complication, if long-standing, is difficult because degenerative arthritis of the MTP joint commonly develops. Prevention, if possible, is desirable, and the use of intraoperative fluoroscopy helps minimize this complication. On occasion, it is necessary to revise the osteotomy of the metatarsal to realign the first ray. However, in most circ*mstances, correction of the first metatarsal must be combined with realignment of the soft tissues about the MTP joint. With advanced first MTP joint degenerative arthritis, an arthrodesis is sufficient to realign the joint and attain successful salvage. NONUNION OF THE FIRST METATARSAL Nonunion of the first metatarsal (proximal or distal) can occur after any osteotomy. With the improved methods of internal fixation, this complication is not common. On occasion, delayed union develops. Given sufficient time (even 4-6 months), successful healing will usually occur with adequate immobilization (see Fig. 6-162). Nonunion can generally be prevented by adequate preparation of the bone surfaces and adequate interfragmentary compression, which promotes rapid healing. The problem that often arises as a result of nonunion is loss of position of the metatarsal shaft, shortening, or both. Treatment of this complication is determined by the nature of the problem and may vary from bone grafting the nonunion site to performing a corrective osteotomy and rigidly fixing the nonunion site (Fig. 6-216). Complications Affecting the Metatarsal Head EXCESSIVE EXCISION When most bunion procedures are performed, the medial eminence is excised. When carrying out the distal soft

DISPLACEMENT A distal metatarsal osteotomy can become displaced in the coronal or sagittal plane. After a distal metatarsal osteotomy, especially of the chevron type, stability is not usually an issue. Displacement of the capital fragment can occur, and most authors now advocate some form of internal fixation to prevent this complication. The metatarsal head may shift dorsally, which can result in decreased weight bearing and a transfer lesion beneath the second metatarsal (Fig. 6-218A). Rarely does plantar displacement of the capital fragment occur after a chevron procedure (Fig. 6-218B and C). If the head deviates into excessive lateral deviation, the tibial sesamoid is often uncovered and a hallux varus deformity or MTP joint incongruity results (Fig. 6-218D and E). If the head deviates medially, the hallux valgus deformity may recur, and an incongruent joint may result as well (Fig. 6-218F). If internal fixation is not used in conjunction with a chevron procedure, serial postoperative radiographs should be obtained to ensure that displacement does not occur. If displacement does occur, it should be promptly recognized and treated. After the Mitchell procedure, the transverse osteotomy has inherent instability that can result in displacement of the capital fragment. Although plantar displacement can occur, most commonly, dorsal displacement develops because of the dorsal pressure applied with weight bearing (see Fig. 6-218F). With dorsal displacement, metatarsalgia can result from both shortening and dorsiflexion, whereas with plantar displacement, pain usually develops beneath the first metatarsal. Lateral displacement of the capital fragment leads to a varus deformity, whereas medial displacement leads to a recurrent valgus deformity. Adequate internal fixation of the osteotomy site can prevent most of these problems. After a distal oblique osteotomy or Wilson bunion procedure, where mild-to-moderate shortening of the first ray is permitted, the incidence of elevatus was reported to be as high as 20% in one series.430 The pressure of weight bearing presents a significant risk to an osteotomy with inadequate internal fixation. 289

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Figure 6-216 Nonunion affecting the metatarsal. A, Nonunion after a chevron procedure. B, Delayed union of a chevron osteotomy 6 months after surgery. Subsequent casting for 10 weeks resulted in union of the osteotomy site. C, Nonunion after an oblique proximal osteotomy. D, Nonunion after an oblique proximal metatarsal osteotomy. Anteroposterior (E) and lateral (F) radiographs of nonunion of a proximal crescentic osteotomy. G, Nonunion of a proximal metatarsal osteotomy.

Realignment of a malunited distal metatarsal osteotomy is associated with many technical difficulties. Realignment of the osteotomy site may require extensive soft tissue stripping, which increases the risk of AVN. Successful realignment can be achieved, yet significant joint arthrofibrosis may develop because of soft tissue adhesions. MTP joint arthrodesis is probably the most reliable method to salvage this condition. AVASCULAR NECROSIS The blood supply to the metatarsal head must be protected with a distal osteotomy (see Figs. 6-67 and 6-68). Interruption of the vascular supply to the capital fragment after extensive dissection around the MTP joint with a distal metatarsal osteotomy can result in partial or complete AVN of the metatarsal head.477 The development of AVN does not necessarily mean that the joint will become symptomatic. For some methods of distal osteotomy in which various techniques of internal fixation are used (i.e., 290

screws instead of pins), more soft tissue stripping is necessary to gain adequate exposure for insertion of the fixation device. Although fixation is vitally important, the magnitude of soft tissue dissection should be minimized to prevent problems with AVN (Figs. 6-219 and 6-220). The incidence of AVN, particularly after distal osteotomies, varies considerably. Meier and Kenzora365 reported an incidence of 20% in 60 patients and pointed out that 40% of patients in whom AVN developed had also undergone some type of lateral release; however, only 15% of the patients were deemed symptomatic. Johnston244 demonstrated cystic changes in 7 of 50 chevron procedures, along with 1 case of complete and 1 of partial AVN. Other authors of large series reported no cases of AVN.193,213,410,421,523 Although it is difficult to determine the incidence of this complication,333 it is probably uncommon (see Figs. 6-119 to 6-121). Three separate studies describe a lateral soft tissue release with the chevron procedure. Peterson et al410 reviewed 58 cases and reported 1 case of AVN. Pochatko

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Figure 6-217 Complications after excessive excision of the metatarsal head. A, Excessive excision resulting in an unstable metatarsophalangeal (MTP) joint caused medial subluxation of the tibial sesamoid and a hallux varus deformity. B, Preoperative hallux valgus repair. C, Postoperative radiograph demonstrating excessive excision of the medial eminence, which resulted in a painful, unstable MTP joint. D and E, Excision of an excessive amount of metatarsal head resulted in an unstable, painful MTP joint.

et al421 reported on 23 cases with no AVN. Thomas et al511 reviewed 80 cases in which lateral capsular release was carried out through a plantar incision along with excision of the fibular sesamoid and found no AVN. On the basis of these studies, a careful lateral release that respects the metaphyseal and capital blood supply should avoid damage to the vascularity of the metatarsal head. AVN may be accompanied by marked pain and arthrofibrosis of the joint. Treatment of this complication usually requires MTP arthrodesis. When the arthrodesis is performed, every effort should be made to excise the avascular portion. This may leave the toe somewhat shortened, but it is preferable to placement of an interpositional bone graft, which may take much time to unite. AVN is reported after the Mitchell procedure (see Fig. 6-136I). Blum34 reported a 2% incidence of AVN. Salvage with MTP joint arthrodesis is the procedure of choice. Of historical interest, after the LeLeivre bunion procedure, a 20% incidence of AVN has been reported.237,436 Currently, this procedure is rarely performed because of the unacceptably high incidence of AVN.

Complications Involving the Proximal Phalanx Complications involving a proximal phalangeal osteotomy are uncommon. Some are related to placement of the osteotomy, whereas others result from inadequate fixation of the osteotomy site.420 When malunion or nonunion occurs, a salvage procedure may be technically difficult because of the small size of the phalanx. NONUNION Delayed union or nonunion of the phalanx seems to occur most frequently when the osteotomy is in the midshaft or distal phalanx rather than within the proximal third of the phalanx. The diaphyseal region may be at risk for delayed healing; however, with the passage of time, most phalangeal osteotomies do heal. In the presence of phalangeal nonunion, waiting for a period of 4 to 5 months may allow healing to occur (Fig. 6-221). MALUNION Malunion of the proximal phalanx usually occurs as a result of loss of fixation or inadequate internal fixation at 291

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Figure 6-218 Complications secondary to displacement of the metatarsal head. A, Dorsal displacement after a chevron osteotomy. B and C, Plantar displacement after a distal metatarsal osteotomy. D, Excessive lateral deviation of the head results in an incongruent joint with a varus deformity. E, Lateral displacement of the metatarsal head results in recurrence of hallux valgus and an incongruent joint. F, Medial displacement of the capital fragment.

Figure 6-219 A and B, Sequence of radiographs demonstrating the development of central avascular necrosis (AVN) after placement of a screw for internal fixation. C, Close-up of AVN.

the osteotomy site. Loss of position is not generally of sufficient magnitude to require corrective surgery (see Fig. 6-110B). AVASCULAR NECROSIS Although AVN generally occurs in the metatarsal head, on occasion it occurs in the proximal phalanx. After a proximal phalangeal osteotomy, AVN may develop because of excessive soft tissue and capsular stripping or excessive manipulation of the osteotomy site. AVN presents a difficult salvage situation; typically, a Keller 292

procedure or arthrodesis is required to correct the problem. ADHESIONS OF THE FLEXOR HALLUCIS LONGUS After a proximal phalangeal osteotomy, particularly if done in the midportion of the phalanx, the flexor hallucis longus tendon may be disrupted or become adherent to the osteotomy site. Flexion of the IP joint is either absent or significantly diminished. This complication can usually be avoided by adequately mobilizing and retracting the flexor hallucis longus tendon before performing the

Hallux Valgus ■ Chapter 6

C Figure 6-220 Treatment of avascular necrosis with arthrodesis of the metatarsophalangeal joint. A–C, Central avascular necrosis corrected by arthrodesis.

osteotomy to avoid inadvertent damage when the osteotomy is performed. It may be treated with an interphalangeal joint (IP) arthrodesis (see Chapter 19). VIOLATION OF THE METATARSOPHALANGEAL JOINT With a proximal phalangeal osteotomy, the osteotomy may inadvertently violate the MTP joint. The proximal phalanx has a concave articular surface. When the osteotomy is performed, care must be taken to ensure that the proximal cut is distal to the articular surface. With this complication, arthrofibrosis or degenerative arthritis may develop and require MTP joint arthrodesis. INSTABILITY AFTER RESECTION OF THE BASE (KELLER PROCEDURE) With resection of the base of the proximal phalanx after a Keller procedure, the intrinsic muscle insertion to the toe is sacrificed. Attempts to restabilize the MTP joint involve reattachment of the intrinsic muscles to the proximal phalanx stump or suturing of the flexor hallucis longus tendon to the proximal phalanx. Although some procedures do help stabilize the joint, the forces involved in walking tend, over time, to force the remaining portion of the hallux into dorsiflexion and lateral deviation. With

Figure 6-221 Complications after proximal phalangeal osteotomy. A, Radiograph demonstrating delayed union, which usually results because the osteotomy site is in the diaphysis rather than the metaphyseal portion of the bone. B, Sequence of radiographs demonstrating progressive avascular necrosis of the proximal phalanx after revision of the osteotomy site (C) and eventual complete collapse (D).

a fixed deformity, the toe pulp no longer strikes the ground. This creates a significant problem with footwear (Fig. 6-222; see also Figs. 6-195 to 6-199). The incidence of this complication can usually be diminished by adequate stabilization of the hallux with a Steinmann pin (for a period of 4 weeks) after the Keller procedure. Another complication associated with instability of the proximal phalanx is that weight bearing of the great toe is greatly diminished. Weight is transferred to the lateral metatarsals, and either metatarsalgia or a transfer lesion develops (see Fig. 6-197). Correction of instability of the hallux generally requires MTP joint arthrodesis. The authors prefer not to lengthen the toe but to accept some shortening.104,536 The success rate of primary fusion without a bone graft is approximately 95%,104,536 versus about 70% when a bone graft is added (see Fig. 6-202). This salvage type of arthrodesis usually requires internal fixation with two intramedullary threaded Steinmann pins. Deficient bone stock or severe osteopenia in the 293

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proximal phalanx makes plate or screw fixation very difficult. Most patients are satisfied with the results of this salvage procedure.104,536 The fusion increases the functional length of the first metatarsal and creates a lever arm that diminishes the stress placed on the second metatarsal head, which often relieves the metatarsalgia (see Fig. 6-203).

Figure 6-222 Complications after resection of the base of the proximal phalanx (the Keller procedure). A, co*ck-up and claw toe deformity caused by loss of function of the intrinsic muscles inserting into the plantar aspect of the base of the proximal phalanx. B, co*ck-up deformity. C, Hallux varus caused by excessive excision of the medial eminence. D, Recurrent hallux valgus after a Keller arthroplasty. (D, Courtesy E. Greer Richardson, MD.)

Complications Associated with Capsular Tissue of the First Metatarsophalangeal Joint LOSS OF CORRECTION SECONDARY TO FAILURE OF MEDIAL JOINT CAPSULAR TISSUE The etiology of recurrent hallux valgus is multifactorial. One cause is inadequate medial capsulorrhaphy, regardless of the procedure performed. This failure can result from an intrinsic problem within the capsule, such as ganglion formation or degeneration within the substance of the medial capsular tissue, or, with a very severe hallux valgus deformity, it can result from marked attenuation of the medial capsular tissue. When one of these conditions is encountered at surgery, it is preferable to imbricate the capsule rather than excise the medial capsule. A suture anchor can also be placed at the area of the defect to help stabilize the capsular deficiency (see Fig. 6-172). The formation of capsular fibrosis or scar tissue may prevent recurrence of the deformity (Fig. 6-223). When the medial capsular flap is developed, it may be inadvertently detached at its proximal attachment. Using a capsular flap that leaves substantial attachments to both the base of the proximal phalanx and the plantar sesamoid region may reduce the frequency of this complication (see Fig. 6-91D). Anchoring the repair with metaphyseal drill holes may secure the proximal capsule. Postoperative dressings are crucial in this situation, to afford adequate support while healing takes place. Likewise, inadequate postoperative dressings may allow capsular elongation or disruption of the capsular repair. This may necessitate a revision of the capsulorrhaphy, with substantial recurrence of the deformity. FAILURE OF LATERAL JOINT CAPSULAR TISSUE A significant lateral MTP joint contracture develops in most patients with a severe hallux valgus deformity. After lateral capsular release, a large gap is created that can be as long as 1 cm. With a defect of this size, it is uncommon for adequate tissue to re-form across this defect. This places the hallux at increased risk for a postoperative

Figure 6-223 A–C, Recurrent hallux valgus deformity, probably caused by failure of the medial joint capsule to hold alignment of first metatarsophalangeal joint.

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Figure 6-224 Early joint mobilization is very important to avoid restricted range of motion. A and B, Incorrect technique mobilizes the interphalangeal joint. C and D, Correct technique mobilizes the metatarsophalangeal joint.

hallux varus deformity. Mann and Coughlin336 observed that hallux varus occurred most commonly in feet in which a more severe deformity was corrected. To avoid this complication, the lateral joint capsule can be initially perforated with multiple small puncture incisions. Next, with varus pressure on the hallux, the lateral capsule is gradually torn and the capsular tissue is “stretched out.” This can lead to the formation of a large lateral capsular gap. Elevation and suturing of the adductor tendon to the lateral capsule aid in the re-formation of scar tissue in this area. An alternative technique is to detach the capsule proximally and dorsally (L-shaped capsular release), which permits the lateral capsule to be slid distally as an entire unit, rather than incising it. The conjoined adductor tendon can actually be severed 3 cm proximal to its insertion and the stump sutured to the lateral capsule; this technique reinforces the lateral capsulorrhaphy as well.93 Using this technique, Coughlin and Jones100 reduced the incidence of postoperative hallux varus to a negligeable amount. ARTHROFIBROSIS OF THE METATARSOPHALANGEAL JOINT Marked arthrofibrosis of the MTP joint can occur after a hallux valgus reconstruction of any type. Restricted joint motion can be quite disabling if the toe is fixed in marked plantar flexion or dorsiflexion. If excessive stiffness around the joint is detected early during the postoperative period, early joint mobilization is initiated. When seen late, a vigorous course of physical therapy is instituted to mobilize the MTP joint. The arthrofibrosis will usually

diminish in time and permit a functional but not normal range of motion. Joint manipulation may improve motion; however, repeat surgery in these patients rarely results in improved motion (Fig. 6-224). Complications Involving the Sesamoids Repositioning of the sesamoids after hallux valgus surgery is difficult when the crista (which normally divides the plantar surface of the metatarsal head into two distinct articulating surfaces) is attenuated. Constant pressure by gradual migration of the metatarsal head off the sesamoid complex leads to erosion of the metatarsosesamoidal facets and significant osteocartilagenous wear can develop (see Fig. 6-1FG).35,449 Stabilization of the sesamoids is more difficult without a definite crista, and the sesamoids may assume a central rather than a medial position. Mann et al344 were able to relocate the sesamoids from a medial to a normal or central location in 80% of cases; however, in the remaining cases, the sesamoids remained in a lateral position. Mann and Donatto340 found no significant change in the tibial sesamoid position after a chevron osteotomy. Thus a chevron procedure is contraindicated in a patient with preoperative pain attributed to the position of the tibial sesamoid beneath the metatarsal head. Because the sesamoids are connected to the base of the proximal phalanx by the plantar plate, their location is determined in large part by the position and alignment of the proximal phalanx. If the sesamoids are not realigned adequately, more than likely the hallux valgus deformity has been undercorrected. In this situation, early recurrence is possible. Overcorrection of the position of the 295

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medial sesamoid leads to medial subluxation and a hallux varus deformity. If the tibial sesamoid is located directly beneath the metatarsal crista, a plantar callus may develop. Shaving of the plantar half of the sesamoid will usually alleviate the problem (see Chapter 10). UNCORRECTED SESAMOIDS Inadequate correction of the position of the sesamoids generally results from failure to release the lateral MTP joint soft tissue contracture. This contracture is composed of several structures: the lateral joint capsule, the adductor tendon, and the transverse metatarsal ligament. The sesamoids cannot be mobilized and repositioned beneath the metatarsal head if this contracture is not released. The first metatarsal must be sufficiently mobile at the MTC joint to permit reduction of the metatarsal over the sesamoid complex. In the presence of fixed metatarsus primus varus or metatarsus adductus, unsuccessful relocation of the sesamoids requires a proximal osteotomy, or a recurrent hallux valgus deformity will develop. MEDIAL SUBLUXATION OR DISLOCATION OF THE TIBIAL SESAMOID Medial subluxation or complete dislocation of the tibial sesamoid may develop after a distal soft tissue procedure to correct a hallux valgus deformity. It may occur after an overcorrected proximal first metatarsal osteotomy or after lateral sesamoid excision, although it can occur even with the fibular sesamoid intact. When the fibular sesamoid is excised, there is increased mobility of the sesamoid complex. A distal soft tissue realignment creates a situation in which medial displacement of the tibial sesamoid may occur. Subluxation or dislocation of the tibial sesamoid can also occur if the postoperative dressing holds the toe in excessive medial deviation or if a metatarsal osteotomy results in excessive lateral deviation of the metatarsal head. Probably the most frequent cause of medial subluxation of the tibial sesamoid is excessive resection of the medial eminence. Although alignment of the sesamoids may not be too abnormal, absence of the plantar-medial metatarsal articulation allows the tibial sesamoid to displace dorsally along the medial aspect of the metatarsal head. In time, this instability can lead to further medial migration of the sesamoid and a painful hallux varus deformity (Fig. 6-225). Treatment of this complication must be individualized. A certain amount of medial subluxation of the sesamoid is often well tolerated. However, in very active persons, the medial sesamoid may become quite painful, even if a hallux varus deformity has not developed. Excision of the tibial sesamoid can be considered if it causes irritation along the medial aspect of the metatarsal head. Although excision of both sesamoids should be avoided, on occasion, a painful tibial sesamoid is excised. If it has been a year or more since excision of the fibular 296

Figure 6-225 Medial subluxation of the tibial sesamoid. A, Excessive excision of the medial eminence and medial capsular plication resulting in medial subluxation of the sesamoid. B, Excessive excision of the medial eminence resulting in medial dislocation of the sesamoid.

sesamoid, the tibial sesamoid can be removed with only a small risk of a claw toe deformity developing. Medial dislocation of the tibial sesamoid is most commonly associated with a hallux varus deformity. When the hallux varus deformity is corrected, the tibial sesamoid is usually relocated beneath the metatarsal head. With a severe hallux varus deformity, MTP joint arthrodesis is performed with excision of the dislocated tibial sesamoid. co*ck-UP DEFORMITY OF THE FIRST METATARSOPHALANGEAL JOINT Plantar flexion of the first MTP joint is achieved primarily by the flexor hallucis brevis muscle, which inserts into the base of the proximal phalanx. With disruption of this mechanism, a muscle imbalance exists. The MTP joint is pulled into dorsiflexion by the unopposed force of the extensor hallucis brevis and the extensor hallucis longus. The flexor hallucis longus causes flexion of the IP joint. This deformity is often associated with hallux varus. After fibular sesamoid excision, the tibial sesamoid (which is the only connection between the flexor hallucis brevis and the proximal phalanx) is displaced medially. In this medially displaced position, no short flexor function is present at the MTP joint. Over time, soft tissue adhesions develop along with contracture of the abductor hallucis muscle, which leads to a fixed deformity (Fig. 6-226). With previous tibial sesamoid excision, if a hallux valgus correction is performed with excision of the fibular sesamoid, a co*ck-up deformity can develop. Thus, under most circ*mstances, dual sesamoid excision, whether simultaneous or staged, should be avoided. If a co*ck-up deformity of the hallux develops after removal of both sesamoids, treatment is tailored to the

Hallux Valgus ■ Chapter 6

19). After a Keller procedure, a co*ck-up deformity is caused by loss of function of the flexor hallucis brevis muscle. This deformity is best treated by MTP joint arthrodesis rather than attempting to transfer a tendon to this small, unstable segment of the proximal phalanx (see Fig. 6-202).

INTRACTABLE PLANTAR KERATOSIS After correction of a hallux valgus deformity, an intractable plantar keratosis may develop beneath the first metatarsal head. This lesion corresponds to the location of the tibial sesamoid, which at times is located in a central position directly beneath the metatarsal head. With progression of a hallux valgus deformity, the intersesamoidal ridge or crista is eroded by lateral pressure from the medial sesamoid. The crista is a major stabilizer of the sesamoid complex. With a relatively flat plantar metatarsal surface, the tibial sesamoid may be located centrally, which can be a source of pain for the patient. Conservative treatment involves placing a metatarsal pad proximal to the sesamoid to relieve plantar pressure. Periodic trimming of the lesion is helpful. If the callosity continues to be painful, shaving the plantar half of the medial sesamoid usually produces a satisfactory clinical response (see Chapter 10). Excision of the tibial sesamoid should be avoided, especially if the lateral sesamoid has previously been removed. Dual sesamoid excision can result in a co*ck-up deformity of the first MTP joint because it disrupts the remaining short flexor function that stabilizes the first MTP joint. If the fibular sesamoid has not previously been removed, tibial sesamoidectomy is an option. Tibial sesamoid shaving, however, frequently alleviates the symptoms associated with a painful plantar callus in this area and is associated with much less morbidity than excision of the tibial sesamoid bone is. Recurrent Hallux Valgus Deformity

C Figure 6-226 co*ck-up varus deformity of the metatarsophalangeal joint after a McBride-type bunion repair. Clinical (A) and radiographic (B and C) views.

magnitude and rigidity of the deformity. In patients with a flexible MTP joint (with a minimum of 10 degrees of passive plantar flexion), an IP joint arthrodesis is performed. This procedure realigns the fixed flexion deformity of the IP joint and also permits the flexor hallucis longus tendon to function as a plantar flexor of the MTP joint. With a fixed extension contracture of the MTP joint, a “first-toe Jones procedure” is performed. This procedure involves transfer of the extensor hallucis longus tendon to the neck of the metatarsal. Transfer of this tendon provides the metatarsal head with a dorsiflexion force but also releases the dorsal contracture of the first MTP joint. A simultaneous IP joint arthrodesis realigns the IP joint and restores flexion power to the MTP joint (see Chapter

Many factors need to be considered when evaluating a recurrent hallux valgus deformity. The characteristics of the initial deformity must be considered, as well as whether the correct surgical procedure was selected. Review of the postoperative management with the patient may provide information on the reason for failure. The following broad categories need to be considered: ■

Was selection of the surgical procedure appropriate? Were there technical problems during the course of the procedure that made it difficult to bring about complete correction? ■ Was there a soft tissue problem, such as inadequate medial joint capsule secondary to capsular attenuation or ganglion formation within the capsule? ■ Was postoperative care inadequate? ■

These general questions are appropriate for the review of any recurrent hallux valgus deformity. For each general 297

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group of hallux valgus procedures, certain problems arise. They are briefly discussed in the following section. Distal Soft Tissue Procedure For a distal soft tissue procedure to succeed, adequate release of the distal soft tissues must be performed. The lateral capsular structures, including the adductor tendon insertion into the sesamoid and proximal phalanx, must be released along with the lateral joint capsule. The transverse metatarsal ligament must also be released from the sesamoid complex to allow the sesamoids to rotate beneath the metatarsal head. The medial joint capsule must be adequately plicated. If it has deteriorated secondary to cyst formation or a ganglion involving the capsular tissue, it will have insufficient strength to stabilize the joint. The main reason for failure of a distal soft tissue procedure is failure to recognize that significant metatarsus primus varus is present. A distal soft tissue procedure cannot be used to correct a fixed bone deformity (see Fig. 6-93). A “simple bunionectomy” fails to release the lateral joint contracture, and recurrence is common. Chevron Procedure A frequent cause of recurrent hallux valgus after a chevron procedure is when it is selected to correct a deformity that is of greater magnitude than the procedure was intended for. Failure to appreciate joint congruency and a lateral slope of the distal metatarsal articular surface will prevent full correction with the chevron procedure. The DMAA should be measured before a chevron procedure. If it is greater than 15 degrees, a medial closing-wedge chevron or an Akin procedure should be added (see Fig. 6-115). Inadequate capsular plication may also be another cause of recurrence. If the osteotomy is not stabilized with internal fixation, deformation may occur at the osteotomy site, with the capital fragment drifting medially and the toe laterally (see Fig. 6-121 and Fig. 6-227). Proximal Metatarsal Osteotomy Recurrent deformity after a crescentic, closing- or openingwedge, or chevron-shaped proximal metatarsal osteotomy usually results from inadequate bone correction. This may be caused by failure to rotate the osteotomy site adequately or failure to remove enough bone to correct the metatarsus primus varus (Fig. 6-228). Recurrence may also be caused by failure of the associated distal soft tissue procedure. Use of a cirlage suture or wire between the first and second metatarsals may temporaily reduce the 1–2 IM angle but may be at risk for lesser metatarsal stress fracture with time (Fig. 6-229). Akin Procedure Recurrent deformities after an Akin procedure are generally the result of performing the procedure when it is not indicated. If there is incongruence or subluxation of the MTP joint, the Akin procedure rarely will bring about lasting correction of the deformity, and rapid recurrence 298

Figure 6-227 Clinical (A) and radiographic (B) views of recurrent deformity after distal metatarsal osteotomy. In the same patient, clinical (C) and radiographic (D) appearance of severe varus postoperative deformity after distal metatarsal osteotomy.

may result (see Fig. 6-112). Likewise, an increased 1–2 IM angle cannot be corrected with a phalangeal osteotomy and distal soft tissue repair. Scarf Procedure After a scarf osteotomy, recurrence can develop for a number of regions: pushing the procedure beyond its indications in the treatment of a severe deformity— an MTP articulator with a substantial DMAA or slope to the articular surface—or its use in osteopenic bone where fixation is tenuous and displacement or troughing occurs. Keller Procedure After a Keller procedure, instability often develops at the MTP joint because the base of the proximal phalanx has been resected. As a result, the proximal phalanx may drift back into a valgus deformity and result in recurrent hallux valgus (see Fig. 6-222D). Typically, a Keller procedure corrects only about 50% of the angular deformity present with hallux valgus. Preoperative Conditions Certain underlying conditions associated with a hallux valgus deformity may preclude a satisfactory result. It is

Hallux Valgus ■ Chapter 6

Figure 6-228 Recurrent hallux valgus deformity from inadequate medial displacement of the proximal metatarsal fragment at metatarsocuneiform joint after osteotomy. Preoperative radiograph (A) demonstrates lack of correction of the intermetatarsal angle after proximal metatarsal osteotomy (B), and recurrent hallux valgus develops (C).

Figure 6-229 Stress fracture of the second metatarsal. A, Severe hallux valgus deformity. B, After circlage “tight rope” to reduce 1–2 intermetatarsal angle. C, After fracture of the second metatarsal and recurrence of the bunion deformity.

important to recognize these situations so that they can be addressed when performing the bunion procedure. At the very least, a patient should be alerted to the fact that the surgery may not be completely successful. The following conditions, when present, may preclude obtaining a satisfactory result and should be considered in the preoperative planning: ■

Lateral deviation of the distal articular surface will preclude complete correction of the MTP joint with a distal soft tissue realignment. This problem can be corrected with a medial closing-wedge chevron

procedure or a closing-wedge metatarsal or phalangeal osteotomy. ■ An underlying arthritic condition (hallux rigidus, rheumatoid arthritis) may be accompanied by inadequate capsular tissue to support a soft tissue repair. Likewise, articular cartilage degeneration may be present. In this situation, MTP joint arthrodesis should be considered for correction of the hallux valgus deformity. ■ When joint hyperelasticity is present (Ehlers-Danlos syndrome), little can be done to increase stability of the joints other than an MTP joint arthrodesis. 299

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■

With a severely pronated foot, rear foot surgery may be necessary to realign the foot and should be performed before a hallux valgus repair. If not corrected, the deformity may recur. ■ While uncommon, if first-ray hypermobility is present, MTC arthrodesis is performed in conjunction with the repair if the surgeon is convinced the increased mobility occurs at the MTC joint. ■ When a significant equinus deformity at the ankle joint is present in conjunction with a hallux valgus deformity, the foot must be corrected to a plantigrade position before hallux valgus repair is attempted. ■ If spasticity of any cause is present, an MTP joint soft tissue realignment is at high risk for failure, and an MTP joint arthrodesis is the procedure of choice. HALLUX VARUS

Hallux varus is medial deviation of the great toe. Similar to hallux valgus deformities, hallux varus has varying degrees of severity and causes. This condition can occur on a congenital basis, although this is quite uncommon (Fig. 6-230). More frequently, it is a deformity acquired after either a surgical procedure or trauma in which the lateral collateral ligament of the hallux is ruptured. Hallux varus may occur after a distal soft tissue or McBride type of bunionectomy,336,343,369 but it is also observed after the chevron, Mitchell, Keller, and Lapidus procedures (see Fig. 6-227C and D). The classic hallux varus deformity after the McBride procedure, in which excision of the fibular sesamoid is followed by MTP joint hyperextension, IP joint flexion, and medial deviation of the hallux (Video Clip 61).

Anatomically, this deformity results from a muscle imbalance caused by medial dislocation of the tibial sesamoid, although other factors are involved as well (Fig. 6-231A). The MTP joint is flexed by the flexor hallucis brevis muscle primarily through its pull on the sesamoid complex. After fibular sesamoid excision, the MTP joint hyperextends as the metatarsal head “buttonholes” through the soft tissue defect created by the deficiency in the flexor hallucis brevis. The medial deviation is aggravated by the detachment of the adductor tendon when the medial sesamoid is removed and compounded by the unopposed pull of the abductor hallucis muscle. With time, it becomes a fixed deformity that makes it difficult for the patient to obtain comfortable footwear. The IP joint of the great toe becomes flexed because the long extensor tendon can no longer effectively extend the IP joint. Simultaneously, the long flexor tendon is stretched around the metatarsal head, which creates a constant flexion force on the IP joint. In time, this entire deformity becomes rigid. When the metatarsal head does not buttonhole through the soft tissue defect, the hallux varus deformity consists mainly of medial deviation of the proximal phalanx without any significant co*ck-up deformity of the MTP joint or flexion of the IP joint (Fig. 6-231B-D). The following soft tissue factors can contribute to a hallux varus deformity:

Figure 6-230 Congenital hallux varus deformity.

300

Figure 6-231 Hallux varus deformity. A, “Classic” hallux varus deformity with medial deviation and a co*ck-up deformity of the first metatarsophalangeal (MTP) joint after a distal soft tissue procedure. B, Hallux varus deformity with medial deviation of the MTP joint but no co*ck-up deformity of the joint. This type of varus may occur with both sesamoids intact. C, Mild hallux varus deformity. D, Mild varus associated with a mild co*ck-up deformity of the first MTP joint and flexion of the interphalangeal joint.

Hallux Valgus ■ Chapter 6

Figure 6-232 Various causes of hallux varus. A, Varus deformity, probably caused by overplication of the medial capsular structures. B, Medial displacement of the tibial sesamoid resulting in a varus deformity, probably caused by imbalance from lack of adequate lateral joint stability. C, Sesamoid view demonstrating medial displacement of the tibial sesamoid as a result of, or resulting in, a hallux varus deformity. ■

Overplication of the medial capsule (Fig. 6-232A) Medial displacement of the tibial sesamoid (Fig. 6-232B and C) ■ Overpull of the abductor hallucis muscle against an incompetent lateral ligamentous complex (Fig. 6-233A-E) ■ Overcorrection with a postoperative dressing holding the MTP joint in a varus position ■ Excessive resection of the medial eminence (Fig. 6-233 F and G) ■

Hallux varus may occur after a proximal or distal metatarsal osteotomy when the metatarsal head is translated too far laterally, or if too much metatarsal head is resected, the potential exists for MTP joint instability and hallux varus. With a chevron osteotomy, if the capital fragment is excessively displaced lateralward, a hallux varus deformity can develop (Fig. 6-234A). Likewise, with a proximal osteotomy, the distal segment can be translated too far laterally (Fig. 6-234B-G). With a crescentic osteotomy, the authors initially directed the concavity distally toward the great toe. If the metatarsal osteotomy site is translated too far medially, excessive lateral translation of the metatarsal head occurs. Once this problem was recognized, the concavity was reversed so that it faced proximally toward the heel. With this orientation, overtranslation rarely occurs because the distal metatarsal segment is locked into the proximal segment. Less commonly, a lateral closingwedge or proximal chevron osteotomy or Lapidus procedure can be overcorrected. This can create the dual deformity of overcorrection and shortening. A hallux varus deformity must be carefully evaluated to determine which salvage procedure is appropriate. If the varus deformity is caused by overplication of the medial capsule, release of the medial capsule may be sufficient. With a fixed deformity, however, a soft tissue capsular release is rarely effective. Plication of the lateral capsule can be added to the medial capsular release, but

this does not generally produce a lasting result. On occasion, the surgeon may encounter a mild varus deformity, and yet the sesamoids remain well aligned. In this instance, the surgeon may perform a phalangeal osteotomy to realign the hallux. This “reverse Akin” osteotomy may be performed through the prior medially based incision (Fig. 6-235A-C). These more mild and passively correctable varus deformities may also be amenable to a realignment procedure by using suture-button fixation. This minimally invasive technique allows rebalancing of the joint via medial soft tissue release and lateral fixation (Fig. 6-236A-E).403 A tendon allograft may also be used to augment the repair. With medial displacement of the tibial sesamoid after excision of the fibular sesamoid or excessive resection of the medial eminence, a more aggressive surgical repair may be necessary. In the initial determination, the question is whether sufficient articular surface remains to permit adequate joint function after realignment. In the presence of degenerative arthrosis, a soft tissue reconstruction is contraindicated because the MTP joint will only deteriorate further. Arthrodesis is the appropriate salvage procedure, although MTP joint motion is sacrificed. In a hallux varus deformity with reasonable articular surface remaining, the extensor hallucis longus tendon can be used to create a dynamic correction of the deforming forces. Initially, the entire extensor hallucis longus tendon was transferred beneath the transverse metatarsal ligament and inserted into the base of the proximal phalanx of the great toe.247 This was coupled with IP joint arthrodesis. Although this technique can produce a satisfactory result, if the IP joint does not have a fixed deformity (or can be straightened to within 10-15 degrees of full extension), it is not necessary to sacrifice IP joint function. Furthermore, if the extensor hallucis longus transfer fails and MTP joint arthrodesis is necessary, a mobile and functional IP joint is preferable. Therefore the authors modified the original procedure and split the extensor hallucis longus tendon. A portion is transferred 301

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Figure 6-233 A, Immediately postoperatively. B, Progressive varus deformity developing over a period of 8 months after a distal soft tissue procedure. Note that both sesamoids are intact. This varus probably occurred because of lack of adequate lateral ligamentous stability. C, Preoperative radiograph. D, One month postoperatively, a radiograph demonstrates satisfactory alignment of the metatarsophalangeal joint. E, Two years postoperatively, a varus deformity has developed, probably from lack of reestablishment of the lateral ligamentous complex. Preoperative (F) and postoperative (G) radiographs demonstrate hallux varus caused by excessive excision of the medial eminence.

and a portion is left intact to control the IP joint of the hallux. EXTENSOR HALLUCIS LONGUS TRANSFER The surgical technique for correction of hallux varus is divided into the surgical approach and preparation for the tendon transfer, release of the medial joint contracture, and reconstruction of the MTP joint. Surgical Approach and Preparation for Tendon Transfer 1. A dorsal curvilinear incision is made starting just lateral to the insertion of the extensor hallucis longus tendon. The incision is carried laterally toward the first web space and follows the interval between the first and second metatarsals. It is then inclined medially and ends along the lateral aspect of the extensor hallucis longus tendon in the region of the first MTC joint (Fig. 6-237A). 302

2. The extensor hallucis tendon is dissected free of soft tissue attachments, and the lateral two thirds of the tendon is released from its insertion. Starting with the free end, the tendon is carefully “teased out” proximally to the level of the MTC joint (Fig. 6-237B and see Video Clip 61). If when developing the lateral two thirds of the tendon the remaining portion of the tendon is inadvertently ruptured, it can be repaired by suturing the extensor hallucis brevis tendon to it. 3. The transverse metatarsal ligament is identified and a right-angle clamp or Mixner clamp is passed beneath it. Even if the transverse metatarsal ligament had been released at the time of the initial surgery, a sufficient amount of ligament usually re-forms. This remnant of the transverse metatarsal ligament is used as a pulley for the extensor tendon (Fig. 6-237C). A ligature is passed beneath the transverse metatarsal ligament to be used later in the procedure for pulling the extensor hallucis longus tendon beneath it.

Hallux Valgus ■ Chapter 6

Figure 6-234 Hallux varus secondary to metatarsal osteotomies. A, Varus deformity after a chevron osteotomy. B, Varus deformity after a proximal crescentic osteotomy with excessive medial displacement of the base of the osteotomy, leading to lateral translation of the metatarsal head. C, Varus deformity after an oblique metatarsal osteotomy resulting in excessive lateral translation of the metatarsal head. D, Varus deformity after metatarsophalangeal arthrodesis secondary to lateral displacement of the metatarsal head. E, Varus deformity secondary to midshaft metatarsal osteotomy with excessive lateral displacement of the metatarsal head. Preoperative (F) and postoperative (G) radiographs demonstrate a hallux varus deformity after proximal and distal metatarsal osteotomy.

Medial Joint Capsule Release 1. The medial aspect of the MTP joint is approached through a long midline incision, beginning just proximal to the IP joint and ending at the midportion of the metatarsal shaft. Full-thickness dorsal and plantar

skin flaps are developed, with care taken to avoid the cutaneous nerves. Too thin a skin flap can inadvertently result in sloughing of skin. 2. The medial joint capsule is cut obliquely starting at the plantar medial aspect of the base of the proximal 303

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Figure 6-235 A, Anteroposterior (AP) standing radiograph of a patient having a prior bunionectomy and hallux interphalangeal arthrodeses complicated by hallux varus. Sesamoids are well aligned, and the joint is preserved. B, A lateral closing-wedge osteotomy of the proximal phalanx has been performed and secured with crossed Kirschner wires. C, AP radiograph at 1 year postoperatively. Note maintenance of correction.

Figure 6-236 A, Hallux varus after prior bunion correction with proximal metatarsal osteotomy. Note absence of sesamoid displacement or degeneration. B, Clinical appearance of hallux varus. Anteroposterior (C) and lateral (D) radiographs at 6 months postoperative, confirming restoration of hallux alignment with suture-button technique. E, Clinical appearance of the foot at 1 year postoperatively.

phalanx where the abductor hallucis tendon inserts. The capsulotomy proceeds obliquely in a proximal and dorsal direction. This flap is dissected off the metatarsal head to permit the proximal phalanx to be brought out of its fixed varus deformity. A 5- to 7-mm gap is usually created in the capsular tissue. 304

3. The abductor hallucis tendon is identified beneath the cut in the capsule, and a long oblique cut releases the last remaining deforming force. At this point, the proximal phalanx can be brought into a valgus position with no resistance. If resistance is still present, some residual medial structure has not been adequately released.

Hallux Valgus ■ Chapter 6

Medial capsular lengthening

Figure 6-237 Technique of hallux varus correction. A, Initial skin incision. B, Detachment of the lateral two thirds of the extensor hallucis longus tendon and proximal split of the extensor tendon. C, The tendon is passed beneath the transverse metatarsal ligament. The ligature is pulled through and can be used later to pull the extensor tendon beneath the transverse metatarsal ligament. D, The medial joint capsule is released through a longitudinal incision. E, A transverse drill hole is made through the base of the proximal phalanx. F, Diagram demonstrating passage of the lateral two thirds of the extensor hallucis longus tendon beneath the transverse metatarsal ligament and across the proximal phalanx. Note that the medial capsular structures have been lengthened. G, The extensor tendon is pulled through the drill hole in the proximal phalanx as the ankle joint is held in dorsiflexion to gain added length of the tendon and the hallux is held in lateral deviation and slight plantar flexion. H, Preoperative radiograph. I, Postoperative radiograph demonstrating correction of the hallux varus deformity. J, Postoperative clinical appearance.

4. If the tibial sesamoid is displaced medially, the abductor hallucis tendon must be freed from its attachment to it to permit the sesamoid to be placed back beneath the metatarsal head. If too much of the metatarsal head was resected at the initial surgery and the sesamoid cannot be replaced beneath the metatarsal head or if the medial sesamoid is too prominent, excision of the sesamoid should be considered (Fig. 6-237D). 5. If an MTP joint dorsiflexion contracture is present, it is treated by releasing the dorsal capsule, which enables the MTP joint to be brought into approximately 10 degrees of plantar flexion. 6. A transverse drill hole in the base of the proximal phalanx is started in the midline. It is important that the hole be drilled distal enough so that it does not inadvertently penetrate the articular surface of the proximal phalanx (Fig. 6-237E).

2. With the ankle joint in dorsiflexion (which relaxes the extensor hallucis longus), the extensor hallucis longus tendon is passed through the drill hole in the base of the proximal phalanx. It is pulled taut, and the hallux is brought into valgus. The tendon is sutured into the periosteum along the medial aspect of the proximal phalanx. At this point, the toe should be aligned in approximately 10 to 15 degrees of valgus. If the toe still tends to drift into varus, either the soft tissue contracture on the medial side was inadequately released or the extensor hallucis longus tendon was not placed under sufficient tension (Fig. 6-237F and G). 3. The remaining medial third of the extensor hallucis longus tendon is plicated by weaving a suture through it to place it under tension. 4. The skin is closed with interrupted suture in routine manner, and a compression dressing is applied postoperatively (Fig. 6-123H and I).

Reconstruction of the Metatarsophalangeal Joint 1. A ligature is placed on the end of the extensor hallucis longus tendon and is used to pass the tendon beneath the transverse metatarsal ligament.

Alternative Procedures Alternative surgical techniques have been described to correct mild and moderate postoperative varus deformities. Lee et al304 and Choi et al68 have both described a 305

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Figure 6-238 Technique of reverse chevron osteotomy to correct hallux varus deformity. A, Chevron osteotomy with medial displacement. B, After internal fixation. (Modified from Choi KJ, Lee HS, Yoon YS, et al: Distal metatarsal osteotomy for hallux varus following surgery for hallux valgus. J Bone Joint Surg Br 93:1079-1083, 2011.)

distal metatarsal reverse chevron procedure in which the capital fragment is medialized to correct the varus deformity. Choi et al68 reported on 19 patients, of which 17 of 19 had a successful realignment (Fig. 6-238). Leemrijse et al308 have proposed developing a slip of abductor hallucis medially, and then routing in through a phalangeal drill hole and then transferring this fascial slip back through a transverse metatarsal drill hole to create a stout lateral collateral ligament (Fig. 6-239). Postoperative Care The postoperative dressing is removed and replaced with a snug gauze dressing and adhesive tape to hold the toe in a slightly overcorrected valgus position. The patient is permitted to ambulate in a postoperative shoe. The dressings are changed weekly for 8 weeks. A postoperative shoe should be used for another 2 weeks to allow further maturation of the tendon transfer (Fig. 6-240). This procedure will produce a satisfactory clinical result in about 80% of patients. On occasion, slight overcorrection or undercorrection of the MTP joint occurs but is usually well tolerated. Typically, 50% to 60% of MTP joint motion is maintained after this procedure (Fig. 6-241). If little or no motion is present at the MTP joint preoperatively, the patient should be advised that this procedure will not significantly improve range of motion but will improve the overall position of the hallux. On occasion, minor skin slough develops in the skin along the medial side of the MTP joint, or delayed wound healing occurs because of the tension created by pulling the toe into a valgus position from its previous varus position. The authors do not know how to avoid this 306

Figure 6-239 Abductor hallucis technique: technique of repair of hallux varus deformity using strip of abductor hallucis. A, A distally based flap of tendon of the abductor hallucis is created. Two transverse drill holes are created in the based of the proximal phalanx and in the subcapital region of the first metatarsal head. The tendon is transferred through the phalangeal drill hole (B) and then through the metatarsal drill hole (C). D, It is tightened and sewn to the periosteum of the first metatarsal shaft creating a tight lateral soft tissue cuff.308 (Modified with permission from Leemriuse T, Hoang B, Maldague P, et al: A new surgical procedure for iatrogenic hallux varus: reverse transfer of the abductor hallucis tendon: a report of 7 cases. Acta Orthop Belg 74:227-234, 2008.)

problem because the medial incision cannot be placed in another location. If the varus deformity develops after a resection arthroplasty (the Keller procedure), after excessive resection of the medial aspect of the metatarsal head, or in conjunction with MTP joint degenerative arthritis, MTP joint arthrodesis is the treatment of choice (see Figs. 6-202 and 6-203). Salvage with a silicone implant is contraindicated unless the deforming forces that led to the hallux varus deformity can be completely corrected. A joint replacement or silicone implant will maintain satisfactory joint alignment only if the surrounding soft tissues are well balanced. A hallux varus deformity caused by nonunion of a metatarsal osteotomy is best corrected by MTP joint

Hallux Valgus ■ Chapter 6

Figure 6-240 Complications after distal soft tissue repair. A, Hallux varus deformity after the McBride procedure. B, Footwear modified for the deformity. C, Schematic diagram of partial flexor hallucis longus transfer and interphalangeal joint fusion, which can be used to correct a hallux varus deformity. D, Postoperative radiograph after realignment.

arthrodesis rather than an attempt at either tendon transfer or corrective metatarsal osteotomy. Although realignment osteotomy can occasionally be performed, complete balancing of the MTP joint soft tissues is crucial to obtain a successful and long-lasting correction. PAIN AROUND THE FIRST METATARSOPHALANGEAL JOINT AFTER BUNION SURGERY

The most common complaint before bunion surgery is pain over the medial eminence.344 Secondary problems include sesamoid pain, pain over the medial aspect of the great toe, pain from a transfer lesion beneath a lesser metatarsal head, and, at times, pain within the MTP joint. After hallux valgus surgery, regardless of the surgical procedure, most patients are satisfied with the reduction in pain over the medial eminence. Ten percent of patients continue to complain of pain around the first MTP joint area. The causes include nerve entrapment, degenerative

Figure 6-241 A and C, Hallux varus deformity resulting from a distal soft tissue procedure. B and D, Postoperative reconstructive procedure involving transfer of the extensor hallucis longus tendon.

MTP joint disease, sesamoid malalignment, and MTP joint arthrofibrosis. This discomfort is often poorly defined and rarely associated with clearly delineated intraarticular degenerative changes visible on radiographs. Although bone scans can define areas of arthritis, they are generally negative. Patients should be counseled preoperatively that they may have MTP joint discomfort after bunion surgery.482 PROSTHESES

The use of an MTP joint prosthesis in primary bunion surgery is rarely, if ever, indicated (Fig. 6-242). The occasional sedentary patient with advanced MTP joint degenerative arthritis who desires a prosthesis may be a candidate for the procedure. The use of a prosthesis in an active individual, regardless of age, is inadvisable because of the inherent problems of loosening, breakage, osteolysis, and synovitis and the high incidence of transfer metatarsalgia (Figs. 6-243 and 6-244). 307

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E Figure 6-242 Complications of a single-stem prosthesis. A, One year after implantation. B, Five years later, severe reaction to the implant is demonstrated. C, At surgical removal. D, Eroded specimen. E, Severe silicone synovitis associated with a singlestem implant.

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Figure 6-243 Complications of double-stem implants. A, Six months after implantation. B, Three years after surgery there is collapse and reaction surrounding the metatarsophalangeal joint. C, After removal later, the implant had fractured. D, A difficult salvage may involve an interposition bone graft. It is preferable to merely excise the reactive area and permanently remove the prosthesis when a severe reaction occurs.

Figure 6-244 A and B, Lateral radiographs demonstrating settling and synovitis after implantation of a double-stemmed prosthesis. C, Severe osteolysis associated with loosening of components of a prosthetic replacement. D–F, Loosening of the metatarsal and phalangeal components with subluxation of the metatarsophalangeal joint.

The salvage procedure for a painful prosthesis entails removal of the prosthesis, complete joint synovectomy, placement of an intramedullary K-wire to stabilize the joint, and soft tissue capsulorrhaphy. The K-wire is removed 3 weeks after surgery, and range-of-motion

exercises are commenced.278 After this technique, 70% to 80% of prostheses can be removed and the first ray salvaged without performing a simple arthrodesis or a much more extensive procedure entailing arthrodesis with an interposition bone block.189,215 309

Part II ■ Forefoot REFERENCES 1. Adam SP, Choung SC, Gu Y, O’Malley MJ: Outcomes after scarf osteotomy for treatment of adult hallux valgus deformity, Clin Orthop Relat Res 469:854–859, 2011. 2. Akin O: The treatment of hallux valgus: a new operative procedure and its results, Med Sentinel 33:678–679, 1925. 3. Akinbo S, Aiyegusi A, Owoeye O, Ogunsola M: Prevalence of hallux valgus among youth population in Lagos, Nigeria, Nigerian Postgrad Med J 18:51–55, 2011. 4. Albrecht G: The pathology and treatment of hallux valgus, Tussk Vrach 10:14–19, 1911. 5. Amarnek DL, Jacobs AM, Oloff LM: Adolescent hallux valgus: its etiology and surgical management, J Foot Surg 24:54–61, 1985. 6. Amarnek DL, Mollica A, Jacobs AM, Oloff LM: A statistical analysis on the reliability of the proximal articular set angle, J Foot Surg 25:39–43, 1986. 7. Aminian A, Kelikian A, Moen T: Scarf osteotomy for hallux valgus deformity: an intermediate followup of clinical and radiographic outcomes, Foot Ankle Int 27:883–886, 2006. 8. Anderson M, Blais MM, Green WT: Lengths of the growing foot, J Bone Joint Surg Am 38:998–1000, 1956. 9. Anderson R: Hallux valgus: Report of end results, South Med J 91:74–78, 1929. 10. Antrobus JN: The primary deformity in hallux valgus and metatarsus primus varus, Clin Orthop 184:251–255, 1984. 11. Arnold H: Die Korrektur des Hallux Valgus interphalangeus durch Closing-Wedge-Osteotomie nach Akin, Oper Orthop Traumatol 20:477–483, 2008. 12. Austin DW, Leventen EO: A new osteotomy for hallux valgus: a horizontally directed “V” displacement osteotomy of the metatarsal head for hallux valgus and primus varus, Clin Orthop 157:25–30, 1981. 13. Austin DW, Leventen EO: Scientific exhibit: V-osteotomy of the first metatarsal head, Chicago, 1968, American Academy of Orthopaedic Surgery. 14. Bacardi BE, Boysen TJ: Considerations for the Lapidus operation, J Foot Surg 25:133–138, 1986. 15. Badwey TM, Dutkowsky JP, Graves SC, Richardson EG: An anatomical basis for the degree of displacement of the distal chevron osteotomy in the treatment of hallux valgus, Foot Ankle Int 18:213–215, 1997. 16. Bae SY, Schon LC: Surgical strategies: Ludloff first metatarsal osteotomy, Foot Ankle Int 28:137–144, 2007. 17. Bai LB, Lee KB, Seo CY, et al: Distal chevron osteotomy with distal soft tissue procedure for moderate to severe hallux valgus deformity, Foot Ankle Int 31:683–688, 2010. 18. Banks AS, Hsu YS, Mariash S, Zirm R: Juvenile hallux abducto valgus association with metatarsus adductus, J Am Podiatr Med Assoc 84:219–224, 1994. 19. Barca F, Busa R: Austin/chevron osteotomy fixed with bioabsorbable poly-L-lactic acid single screw, J Foot Ankle Surg 36:15– 20; discussion 79–80, 1997. 20. Barnett CH: Valgus deviation of the distal phalanx of the great toe, J Anat 96:171–177, 1962. 21. Barnicot NA, Hardy RH: The position of the hallux in West Africans, J Anat 89:355–361, 1955. 22. Barouk LS: Scarf osteotomy of the first metatarsal in the treatment of hallux valgus, Foot Dis 2:35–48, 1991. 23. Barouk LS: Osteotomie scarf du primier metarsien, Med Surg Pied 10:111–120, 1994. 24. Barouk LS: Scarf osteotomy for hallux valgus correction. Local anatomy, surgical technique, and combination with other forefoot procedures, Foot Ankle Clin 5:525–558, 2000. 25. Barouk LS, Barouk P: Joint-preserving surgery in rheumatoid forefoot: preliminary study with more-than-two-year follow-up, Foot Ankle Clin 12:435–454, vi, 2007.

310

26. Bartolozzi P, Magnan BL: Osteotomia diatale percutanea nella chirurgia dell’alluce valgo. Bologna, Italy, 2000, Timeo, pp 1–71. 27. Beauchamp CG, Kirby T, Rudge SR, et al: Fusion of the first metatarsophalangeal joint in forefoot arthroplasty, Clin Orthop 190:249–253, 1984. 28. Bednarz PA, Manoli A 2nd: Modified Lapidus procedure for the treatment of hypermobile hallux valgus, Foot Ankle Int 21:816– 821, 2000. 29. Beighton PGR, Bird H: Hypermobility of joints, New York, 1983, Springer-Verlag, pp 10–12. 30. Berg RP, Olsthoorn PG, Poll RG: Scarf osteotomy in hallux valgus: a review of 72 cases, Acta Orthop Belg 73:219–223, 2007. 31. Berner A, Sage R, Niemela J: Keller procedure for the treatment of resistant plantar ulceration of the hallux, J Foot Ankle Surg 44:133–136, 2005. 32. Berntsen A: De l’hallux valgus, contribution a son étiologie et a son traitment, Rev Orthop 17:101–111, 1930. 33. Bingold AC: Arthrodesis of the great toe, Proc R Soc Med 51:435–437, 1958. 34. Blum JL: The modified Mitchell osteotomy-bunionectomy: indications and technical considerations, Foot Ankle Int 15:103– 106, 1994. 35. Bock P, Kristen KH, Kroner A, Engel A: Hallux valgus and cartilage degeneration in the first metatarsophalangeal joint, J Bone Joint Surg Br 86:669–673, 2004. 36. Bock P, Lanz U, Kroner A, et al: The Scarf osteotomy: a salvage procedure for recurrent hallux valgus in selected cases, Clin Orthop Relat Res 468:2177–2187, 2010. 37. Bohay D, Johnson K, Manoli A: The traumatic bunion, Foot Anle Int 17:383–387, 1996. 38. Bonney G, Macnab I: Hallux valgus and hallux rigidus; a critical survey of operative results, J Bone Joint Surg Br 34:366–385, 1952. 39. Bordelon L, editor: Surgical and conservative foot care: a unified approach to principles and practice, Thorofare, NJ, 1988, Slack, pp 13–14. 40. Borrelli AH, Weil LS: Modified scarf bunionectomy: our experience in more than one thousand cases, J Foot Surg 30:609–612, 1991. 41. Borton DC, Stephens MM: Basal metatarsal osteotomy for hallux valgus, J Bone Joint Surg Br 76:204–209, 1994. 42. Bosch P, Markowski H, Rannicher V: Technik und erste Ergebnisse der subkutanen distalen Metatarsale-I-Osteotomie, Orthop Praxis 26:51–56, 1990. 43. Bosch P, Wanke S, Legenstein R: Hallux valgus correction by the method of Bosch: a new technique with a seven-to-ten-year follow-up, Foot Ankle Clin 5:485–498, v–vi, 2000. 44. Bouaicha S, Ehrmann C, Moor BK, et al: Radiographic analysis of metatarsus primus elevatus and hallux rigidus, Foot Ankle Int 31:807–814, 2010. 45. Brage ME, Holmes JR, Sangeorzan BJ: The influence of x-ray orientation on the first metatarsocuneiform joint angle, Foot Ankle Int 15:495–497, 1994. 46. Brahm SM: Shape of the first metatarsal head in hallux rigidus and hallux valgus, J Am Podiatr Med Assoc 78:300–304, 1988. 47. Brattwall M, Turan I, Jakobsson J: Pain management after elective hallux valgus surgery: a prospective randomized doubleblind study comparing etoricoxib and tramadol, Anesth Analg 111:544–549, 2010. 48. Breslauer C, Cohen M: Effect of proximal articular set angle correcting osteotomies on the hallucal sesamoid apparatus: a cadaveric and radiographic investigation, J Foot Ankle Surg 40:366–373, 2001. 49. Briggs TW, Smith P, McAuliffe TB: Mitchell’s osteotomy using internal fixation and early mobilisation, J Bone Joint Surg Br 74:137–139, 1992.

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50. Broca P: Des difformities de la partie anterieure du pied produite par faction de la chaussure, Bull Soc Anat 27:60–67, 1852. 51. Brodsky JW, Beischer AD, Robinson AH, et al: Surgery for hallux valgus with proximal crescentic osteotomy causes variable postoperative pressure patterns, Clin Orthop Relat Res 443:280–286, 2006. 52. Bryant A, Tinley P, Singer K: A comparison of radiographic measurements in normal, hallux valgus, and hallux limitus feet, J Foot Ankle Surg 39:39–43, 2000. 53. Budny AM, Masadeh SB, Lyons MC 2nd, Frania SJ: The opening base wedge osteotomy and subsequent lengthening of the first metatarsal: an in vitro study, J Foot Ankle Surg 48:662–667, 2009. 54. Burns AE, Varin J: Poly-L-lactic acid rod fixation results in foot surgery, J Foot Ankle Surg 37:37–41, 1998. 55. Burutaran H: Hallux valgus y cortedad anatomica del primer metatarsano (correction quinrugica), Med Chir Pied 13:261– 266, 1976. 56. Butson AR: A modification of the Lapidus operation for hallux valgus, J Bone Joint Surg Br 62:350–352, 1980. 57. Campbell JT, Schon LC, Parks BG, et al: Mechanical comparison of biplanar proximal closing wedge osteotomy with plantar plate fixation versus crescentic osteotomy with screw fixation for the correction of metatarsus primus varus, Foot Ankle Int 19:293–299, 1998. 58. Canale PB, Aronsson DD, Lamont RL, Manoli A II: The Mitchell procedure for the treatment of adolescent hallux valgus. A longterm study, J Bone Joint Surg Am 75:1610–1618, 1993. 59. Carl A, Ross S, Evanski P, Waugh T: Hypermobility in hallux valgus, Foot Ankle 8:264–270, 1988. 60. Carr CR, Boyd BM: Correctional osteotomy for metatarsus primus varus and hallux valgus, J Bone Joint Surg Am 50:1353– 1367, 1968. 61. Catanzariti AR, Mendicino RW, Lee MS, Gallina MR: The modified Lapidus arthrodesis: a retrospective analysis, J Foot Ankle Surg 38:322–332, 1999. 62. Cathcart E: Physiological aspect: nature of incapacity. The feet of the industrial worker: clinical aspect; relation to footwear, Lancet 2:1480–1482, 1938. 63. Cedell CA, Astrom M: Proximal metatarsal osteotomy in hallux valgus, Acta Orthop Scand 53:1013–1018, 1982. 64. Chana GS, Andrew TA, Cotterill CP: A simple method of arthrodesis of the first metatarsophalangeal joint, J Bone Joint Surg Br 66:703–705, 1984. 65. Chi TD, Davitt J, Younger A, et al: Intra- and inter-observer reliability of the distal metatarsal articular angle in adult hallux valgus, Foot Ankle Int 23:722–726, 2002. 66. Chiodo CP, Schon LC, Myerson MS: Clinical results with the Ludloff osteotomy for correction of adult hallux valgus, Foot Ankle Int 25:532–536, 2004. 67. Cho NH, Kim S, Kwon DJ, Kim HA: The prevalence of hallux valgus and its association with foot pain and function in a rural Korean community, J Bone Surg Br 91:494–498, 2009. 68. Choi KJ, Lee HS, Yoon YS, et al: Distal metatarsal osteotomy for hallux varus following surgery for hallux valgus, J Bone Joint Surg Br 93:1079–1083, 2011. 69. Choi WJ, Yoon HK, Yoon HS, et al: Comparison of the proximal chevron and Ludloff osteotomies for the correction of hallux valgus, Foot Ankle Int 30:1154–1160, 2009. 70. Cholmeley JA: Hallux valgus in adolescents, Proc R Soc Med 51:903–906, 1958. 71. Chou LB, Mann RA, Casillas MM: Biplanar chevron osteotomy, Foot Ankle Int 19:579–584, 1998. 72. Chow FY, Lui TH, Kwok KW, Chow YY: Plate fixation for crescentic metatarsal osteotomy in the treatment of hallux valgus: an eight-year followup study, Foot Ankle Int 29:29–33, 2008.

73. Clark HR, Veith RG, Hansen ST Jr: Adolescent bunions treated by the modified Lapidus procedure, Bull Hosp Jt Dis Orthop Inst 47:109–122, 1987. 74. Cleveland M, Winant EM: An end-result study of the Keller operation, J Bone Joint Surg Am 32:163–175, 1950. 75. Clutton H: The treatment of hallux valgus, St Thomas Hosp Rep 22:1–12, 1894. 76. Coetzee JC: Scarf osteotomy for hallux valgus repair: the dark side, Foot Ankle Int 24:29–33, 2003. 77. Coetzee JC, Resig SG, Kuskowski M, Saleh KJ: The Lapidus procedure as salvage after failed surgical treatment of hallux valgus. Surgical technique, J Bone Joint Surg Am 86(Suppl 1): 30–36, 2004. 78. Coetzee JC, Rippstein P: Surgical strategies: scarf osteotomy for hallux valgus, Foot Ankle Int 28:529–535, 2007. 79. Coetzee JC, Wickum D: The Lapidus procedure: a prospective cohort outcome study, Foot Ankle Int 25:526–531, 2004. 80. Colloff B, Weitz EM: Proximal phalangeal osteotomy in hallux valgus, Clin Orthop 54:105–113, 1967. 81. Cooper AJ, Clifford PD, Parikh VK, et al: Instability of the first metatarsal-cuneiform joint: diagnosis and discussion of an independent pain generator in the foot, Foot Ankle Int 30:928– 932, 2009. 82. Cooper MT, Berlet GC, Shurnas PS, Lee TH: Proximal openingwedge osteotomy of the first metatarsal for correction of hallux valgus, Surg Technol Int 16:215–219, 2007. 83. Corless JR: A modification of the Mitchell procedure, J Bone Joint Surg Br 55/58:138, 1976. 84. Cornwall MW, Fishco WD, McPoil TG, et al: Reliability and validity of clinically assessing first-ray mobility of the foot, J Am Podiatr Med Assoc 94:470–476, 2004. 85. Corte-Real NM, Moreira RM: Modified biplanar chevron osteotomy, Foot Ankle Int 30:1149–1153, 2009. 86. Coughlin MJ: Arthrodesis of the first metatarsophalangeal joint, Orthop Rev 19:177–186, 1990. 87. Coughlin MJ: Arthrodesis of the first metatarsophalangeal joint with mini-fragment plate fixation, Orthopedics 13:1037–1044, 1990. 88. Coughlin MJ: Hallux valgus, J Bone Joint Surg Am 78:932–966, 1996. 89. Coughlin MJ: Hallux valgus. Causes, evaluation, and treatment, Postgrad Med 75:174–178, 183, 186–187, 1984. 90. Coughlin MJ: Hallux valgus in the athlete, J Sports Med Arthrosc Rev 2:326–340, 1994. 91. Coughlin MJ: Hallux valgus in men: effect of the distal metatarsal articular angle on hallux valgus correction, Foot Ankle Int 18:463–470, 1997. 92. Coughlin MJ: President’s Forum: evaluation and treatment of juvenile hallux valgus, Contemp Orthop 21:169–203, 1990. 93. Coughlin MJ: Proximal first metatarsal osteotomy. In Kitaoka H, editor: The foot and ankle, 2nd ed, Philadelphia, 2002, Williams & Wilkins, pp 71–98. 94. Coughlin MJ: Rheumatoid forefoot reconstruction. A long-term follow-up study, J Bone Joint Surg Am 82:322–341, 2000. 95. Coughlin MJ: Roger A. Mann Award. Juvenile hallux valgus: etiology and treatment, Foot Ankle Int 16:682–697, 1995. 96. Coughlin MJ, Abdo RV: Arthrodesis of the first metatarsophalangeal joint with Vitallium plate fixation, Foot Ankle Int 15:18– 28, 1994. 97. Coughlin MJ, Carlson RE: Treatment of hallux valgus with an increased distal metatarsal articular angle: evaluation of double and triple first ray osteotomies, Foot Ankle Int 20:762–770, 1999. 98. Coughlin MJ, Freund E: Roger A. Mann Award. The reliability of angular measurements in hallux valgus deformities, Foot Ankle Int 22:369–379, 2001.

311

Part II ■ Forefoot

99. Coughlin MJ, Grebing BR, Jones CP: Arthrodesis of the metatarsophalangeal joint for idiopathic hallux valgus: Intermediate results, Foot Ankle Int 26:783–792, 2005. 100. Coughlin MJ, Jones CP: Hallux valgus and first ray mobility. A prospective study, J Bone Joint Surg Am 89:1887–1898, 2007. 101. Coughlin MJ, Jones CP: Hallux valgus: demographics, etiology, and radiographic assessment, Foot Ankle Int 28:759–777, 2007. 102. Coughlin MJ, Jones CP, Viladot R, et al: Hallux valgus and first ray mobility: a cadaveric study, Foot Ankle Int 25:537–544, 2004. 103. Coughlin MJ, Kaz A: Correlation of Harris mats, physical exam, pictures, and radiographic measurements in adult flatfoot deformity, Foot Ankle Int 30:604–612, 2009. 104. Coughlin MJ, Mann RA: Arthrodesis of the first metatarsophalangeal joint as salvage for the failed Keller procedure, J Bone Joint Surg Am 69:68–75, 1987. 105. Coughlin MJ, Mann RA: The pathophysiology of the juvenile bunion, Instr Course Lect 36:123–136, 1987. 106. Coughlin MJ, Saltzman CL, Nunley JA 2nd: Angular measurements in the evaluation of hallux valgus deformities: a report of the ad hoc committee of the American Orthopaedic Foot and Ankle Society on angular measurements, Foot Ankle Int 23:68–74, 2002. 107. Coughlin MJ, Shurnas PS: Hallux rigidus, J Bone Joint Surg Am 86(Suppl 1):119–130, 2004. 108. Coughlin MJ, Shurnas PS: Hallux rigidus: demographics, etiology, and radiographic assessment, Foot Ankle Int 24:731–743, 2003. 109. Coughlin MJ, Shurnas PS: Hallux rigidus. Grading and long term results of operative treatment, J Bone Joint Surg Am 85: 2072–2088, 2003. 110. Coughlin MJ, Shurnas PS: Hallux valgus in men. Part II: first ray mobility after bunionectomy and factors associated with hallux valgus deformity, Foot Ankle Int 24:73–78, 2003. 111. Coughlin, MJ, Smith BW: Hallux valgus and first ray mobility. Surgical technique, J Bone Joint Surg Am 90(Suppl 2 Pt 2):153– 170, 2008. 112. Coughlin MJ, Thompson FM: The high price of high-fashion footwear, Instr Course Lect 44:371–377, 1995. 113. Craigmile DA: Incidence, origin, and prevention of certain foot defects, BMJ 4839:749–752, 1953. 114. Creer WS: The feet of the industrial worker: clinical aspect; relation to footwear, Lancet 2:1482–1483, 1938. 115. Crevoisier X, Mouhsine E, Ortolano V, et al: The scarf osteotomy for the treatment of hallux valgus deformity: a review of 84 cases, Foot Ankle Int 22:970–976, 2001. 116. Cronin JJ, Limbers JP, Kutt S, Stephens MM: Intermetatarsal angle after first metatarsophalangeal joint arthrodesis for hallux valgus, Foot Ankle Int 27:104–109, 2006. 117. Daniels SE, Baum DR, Clark F, et al: Diclofenac potassium liquid-filled soft gelatin capsules for the treatment of postbunionectomy pain, Curr Med Res Opin 26:2375–2384, 2010. 118. Das De S, Hamblen DL: Distal metatarsal osteotomy for hallux valgus in the middle-aged patient, Clin Orthop 218:239–246, 1987. 119. Davids JR, McBrayer D, Blackhurst DW: Juvenile hallux valgus deformity: surgical management by lateral hemiepiphyseodesis of the great toe metatarsal, J Pediatr Orthop 27:826– 830, 2007. 120. Davies-Colley N: Contraction of the metatarsophalangeal joint of the great toe (hallux flexus), BMJ 1:728, 1887. 121. Day MR, White SL, DeJesus JM: The “Z” osteotomy versus the Kalish osteotomy for the correction of hallux abducto valgus deformities: a retrospective analysis, J Foot Ankle Surg 36:44–50; discussion 80, 1997.

312

122. Day T, Charlton TP, Thordarson DB: First metatarsal length change after basilar closing wedge osteotomy for hallux valgus, Foot Ankle Int 32:S513–S518, 2011. 123. De Lavigne C, Rasmont Q, Hoang B: Percutaneous double metatarsal osteotomy for correction of severe hallux valgus deformity, Acta Orthop Belg 77:516–521, 2011. 124. De Vil JJ, Van Seymortier P, Bongaerts W, et al: Scarf osteotomy for hallux valgus deformity: a prospective study with 8 years of clinical and radiologic follow-up, J Am Podiatr Med Assoc 100:35–40, 2010. 125. Deenik A, van Mameren H, de Visser E, et al: Equivalent correction in scarf and chevron osteotomy in moderate and severe hallux valgus: a randomized controlled trial, Foot Ankle Int 29:1209–1215, 2008. 126. Deenik AR, Pilot P, Brand SE, et al: Scarf versus chevron osteotomy in hallux valgus: a randomized controlled trial in 96 patients, Foot Ankle Int 28:537–541, 2007. 127. Dennis NZ, Das De S: Modified Mitchell’s osteotomy for moderate to severe hallux valgus: an outcome study, J Foot Ankle Surg 50:50–54, 2011. 128. DeOrio J: Technique tip: dorsal wedge resection (uniplanar) in the chevron osteotomy for high distal metatarsal articular angle bunions, Foot Ankle Int 28:642–644, 2007. 129. Deorio JK, Ware AW: Single absorbable polydioxanone pin fixation for distal chevron bunion osteotomies, Foot Ankle Int 22:832–835, 2001. 130. Dereymaeker G: Scarf osteotomy for correction of hallux valgus. Surgical technique and results as compared to distal chevron osteotomy, Foot Ankle Clin 5:513–524, 2000. 131. Dermon A, Tilkeridis C, Lyras D, et al: Long-term results of Mitchell’s procedure for hallux valgus deformity: a 5- to 20-year followup in 204 cases, Foot Ankle Int 30:16–20, 2009. 132. Devos Bevernage B, Deleu PA, Leemrijse T: The translating Weil osteotomy in the treatment of an overriding second toe: a report of 25 cases, Foot Ankle Surg 16:153–158, 2010. 133. Dhukaram V, Hullin MG, Senthil Kumar C: The Mitchell and Scarf osteotomies for hallux valgus correction: a retrospective, comparative analysis using plantar pressures, J Foot Ankle Surg 45:400–409, 2006. 134. DiGiovanni CW, Kuo R, Tejwani N, et al: Isolated gastrocnemius tightness, J Bone Joint Surg Am 84:962–970, 2002. 135. Donley BG, Vaughn RA, Stephenson KA, Richardson EG: Keller resection arthroplasty for treatment of hallux valgus deformity: increased correction with fibular sesamoidectomy, Foot Ankle Int 23:699–703, 2002. 136. Dreeben S, Mann RA: Advanced hallux valgus deformity: long-term results utilizing the distal soft tissue procedure and proximal metatarsal osteotomy, Foot Ankle Int 17:142–144, 1996. 137. du Plessis M, Zipfel B, Brantingham JW, et al: Manual and manipulative therapy compared to night splint for symptomatic hallux abducto valgus: an exploratory randomised clinical trial, Foot (Edinb) 21:71–78, 2011. 138. Durman DC: Metatarsus primus varus and hallux valgus, AMA Arch Surg 74:128–135, 1957. 139. DuVries H, editor: Surgery of the foot, St Louis, 1959, CV Mosby, pp 346–442. 140. Easley ME, Kiebzak GM, Davis WH, Anderson RB: Prospective, randomized comparison of proximal crescentic and proximal chevron osteotomies for correction of hallux valgus deformity, Foot Ankle Int 17:307–316, 1996. 141. Easley ME, Trnka HJ: Current concepts review: hallux valgus part 1: pathomechanics, clinical assessment, and nonoperative management, Foot Ankle Int 28:654–659, 2007. 142. Easley ME, Trnka HJ: Current concepts review: hallux valgus part II: operative treatment, Foot Ankle Int 28:748–758, 2007.

Hallux Valgus ■ Chapter 6

143. Ellington JK, Jones CP, Cohen BE, et al: Review of 107 hallux MTP joint arthrodesis using dome-shaped reamers and a stainless-steel dorsal plate, Foot Ankle Int 31:385–390, 2010. 144. Ellington JK, Myerson MS, Coetzee JC, Stone RM: The use of the Lapidus procedure for recurrent hallux valgus, Foot Ankle Int 32:674–680, 2011. 145. Ellis VH: A method of correcting metatarsus primus varus; preliminary report, J Bone Joint Surg Br 33:415–417, 1951. 146. ElSaid AG, Tisdel C, Donley B, et al: First metatarsal bone: an anatomic study, Foot Ankle Int 27:1041–1048, 2006. 147. Engel E, Erlick N, Krems I: A simplified metatarsus adductus angle, J Am Podiatr Assoc 73:620–628, 1983. 148. Engle ET, Morton DJ: Notes on foot disorders among natives of the Belgian Congo, J Bone Joint Surg 13:311, 1931. 149. Espinosa N, Wirth SH: Tarsometatarsal arthrodesis for management of unstable first ray and failed bunion surgery, Foot Ankle Clin 16:21–34, 2011. 150. Ewald P: Die Actiologie des Hallux valgus, Dtsch Ztschr Chir 114:90–103, 1912. 151. Fabeck L, Zekhnini C, Farrokh D, Descamps P, Delince P: Traumatic hallux valgus following rupture of the medial collateral ligament of the first metatarsalphalangeal joint: a case report, J Foot Ankle Surg 41:1258, 2002. 152. Faber FW, Kleinrensink GJ, Verhoog MW, et al: Mobility of the first tarsometatarsal joint in relation to hallux valgus deformity: anatomical and biomechanical aspects, Foot Ankle Int 20:651– 656, 1999. 153. Fadel GE, Hussain SM, Sripada S, Jain AS: Fixation of first metatarsal basal osteotomy using Acutrak screw, Foot Ankle Surg 14:21–25, 2008. 154. Fadel GE, Rowley DI, Jain AS: Compression screw fixation for first metatarsal basal osteotomy, Foot Ankle Int 23:253–254, 2002. 155. Ferrari J, Malone-Lee J: The shape of the metatarsal head as a cause of hallux abductovalgus, Foot Ankle Int 23:236–242, 2002. 156. Ferrari J, Malone-Lee J: A radiographic study of the relationship between metatarsus adductus and hallux valgus, J Foot Ankle Surg 42:9–14, 2003. 157. Fitzgerald JA: A review of long-term results of arthrodesis of the first metatarso-phalangeal joint, J Bone Joint Surg Br 51:488– 493, 1969. 158. Fokter SK, Podobnik J, Vengust V: Late results of modified Mitchell procedure for the treatment of hallux valgus, Foot Ankle Int 20:296–300, 1999. 159. Fox IM, Smith SD: Juvenile bunion correction by epiphysiodesis of the first metatarsal, J Am Podiatr Assoc 73:448–455, 1983. 160. Frey C, Zamora J: The effects of obesity on orthopaedic foot and ankle pathology, Foot Ankle Int 28:996–999, 2007. 161. Fridman R, Cain JD, Weil L Jr, Weil LS Sr, Ray TB: Unilateral versus bilateral first ray surgery: a prospective study of 186 consecutive cases–patient satisfaction, cost to society, and complications, Foot Ankle Spec 2:123–129, 2009. 162. Fritz GR, Prieskorn D: First metatarsocuneiform motion: a radiographic and statistical analysis, Foot Ankle Int 16:117–123, 1995. 163. Fuhrmann RA, Zollinger-Kies H, Kundert HP: Mid-term results of Scarf osteotomy in hallux valgus, Int Orthop 34:981–989, 2010. 164. Funk FJ Jr, Wells RE: Bunionectomy—with distal osteotomy, Clin Orthop 85:71–74, 1972. 165. Galland W, Jordan H: Hallux valgus, Surg Gynecol Obstet 66:95, 1938. 166. Gallardo J, Lagos L, Bastias C, et al: Continuous popliteaal block for postoperative analgesia in total ankle arthroplasty, Foot Ankle Int 33:208–212, 2112.

167. Gallentine JW, Deorio JK, Deorio MJ: Bunion surgery using locking-plate fixation of proximal metatarsal chevron osteotomies, Foot Ankle Int 28:361–368, 2007. 168. Garcia-Bordes L, Jimenez-Potrero M, Vega-Garcia J, Yunta-Gallo A: Opening first metatarsal osteotomy and resection arthroplasty of the first MPJ in the treatment of first ray insufficiency associated with degenerative hallux valgus, Foot Ankle Surg 16:132–136, 2010. 169. Garrido IM, Rubio ER, Bosch MN, et al: Scarf and Akin osteotomies for moderate and severe hallux valgus: clinical and radiographic results, Foot Ankle Surg 14:194–203, 2008. 170. Geissele AE, Stanton RP: Surgical treatment of adolescent hallux valgus, J Pediatr Orthop 10:642–648, 1990. 171. Gerbert J: The indications and techniques for utilizing pre operative templates in podiatric surgery, J Am Podiatr Assoc 69:139–148, 1979. 172. Giannestras N: The Giannestras modification of the Lapidus operation. In Giannestras NJ, editor: Foot disorders: medical and surgical management, Philadelphia, 1973, Lea & Febiger. 173. Gill LH, Martin DF, Coumas JM, Kiebzak GM: Fixation with bioabsorbable pins in chevron bunionectomy, J Bone Joint Surg Am 79:1510–1518, 1997. 174. Gimple K, Anspacher J, Kopta J: Metatarsophalangeal joint fusion of the great toe, Orthopedics 1:462–467, 1978. 175. Ginsburg AI: Arthrodesis of the first metatarsophalangeal joint: a practical procedure, J Am Podiatr Assoc 69:367–369, 1979. 176. Glasoe WM, Allen MK, Saltzman CL: First ray dorsal mobility in relation to hallux valgus deformity and first intermetatarsal angle, Foot Ankle Int 22:98–101, 2001. 177. Glasoe WM, Allen MK, Saltzman CL, et al: Comparison of two methods used to assess first-ray mobility, Foot Ankle Int 23:248– 252, 2002. 178. Glasoe WM, Allen MK, Yack HJ: Measurement of dorsal mobility in the first ray: elimination of fat pad compression as a variable, Foot Ankle Int 19:542–546, 1998. 179. Glasoe WM, Grebing B, Beck S, et al: A comparison of device measures of dorsal first ray mobility, Foot Ankle Int 26:957–961, 2005. 180. Glasoe WM, Yack HJ, Saltzman CL: Measuring first ray mobility with a new device, Arch Phys Med Rehabil 80:122–124, 1999. 181. Glasoe WM, Yack HJ, Saltzman CL: The reliability and validity of a first ray measurement device, Foot Ankle Int 21:240–246, 2000. 182. Glover JP, Hyer CF, Berlet GC, et al: A comparison of crescentic and Mau osteotomies for correction of hallux valgus, J Foot Ankle Surg 47:103–111, 2008. 183. Glover JP, Hyer CF, Berlet GC, Lee TH: Early results of the Mau osteotomy for correction of moderate to severe hallux valgus: a review of 24 cases, J Foot Ankle Surg 47:237–242, 2008. 184. Glynn MK, Dunlop JB, Fitzpatrick D: The Mitchell distal metatarsal osteotomy for hallux valgus, J Bone Joint Surg Br 62:188– 191, 1980. 185. Goldberg I, Bahar A, Yosipovitch Z: Late results after correction of hallux valgus deformity by basilar phalangeal osteotomy, J Bone Joint Surg Am 69:64–67, 1987. 186. Goldner JL, Gaines RW: Adult and juvenile hallux valgus: analysis and treatment, Orthop Clin North Am 7:863–887, 1976. 187. Goucher NR, Coughlin MJ: Hallux metatarsophalangeal joint arthrodesis using dome-shaped reamers and dorsal plate fixation: a prospective study, Foot Ankle Int 27:869–876, 2006. 188. Grace D, Hughes J, Klenerman L: A comparison of Wilson and Hohmann osteotomies in the treatment of hallux valgus, J Bone Joint Surg Br 70:236–241, 1988. 189. Granberry WM, Noble PC, Bishop, JO, Tullos HS: Use of a hinged silicone prosthesis for replacement arthroplasty of the

313

Part II ■ Forefoot

first metatarsophalangeal joint, J Bone Joint Surg Am 73:1453– 1459, 1991. 190. Grebing BR, Coughlin MJ: The effect of ankle position on the exam for first ray mobility, Foot Ankle Int 25:467–475, 2004. 191. Grebing BR, Coughlin MJ: Evaluation of the Esmark bandage as a tourniquet for forefoot surgery, Foot Ankle Int 25:397–405, 2004. 192. Grebing BR, Coughlin MJ: Evaluation of Morton’s theory of second metatarsal hypertrophy, J Bone Joint Surg Am 86:1375– 1386, 2004. 193. Green MA, Dorris MF, Baessler TP, et al: Avascular necrosis following distal chevron osteotomy of the first metatarsal, J Foot Ankle Surg 32:617–622, 1993. 194. Griffiths TA, Palladino SJ: Metatarsus adductus and selected radiographic measurements of the first ray in normal feet, J Am Podiatr Med Assoc 82:616–622, 1992. 195. Grill F, Hetherington V, Steinbock G, Altenhuber J: Experiences with the chevron (V-) osteotomy on adolescent hallux valgus, Arch Orthop Trauma Surg 106:47–51, 1986. 196. Grimes JS, Coughlin MJ: First metatarsophalangeal joint arthrodesis as a treatment for failed hallux valgus surgery, Foot Ankle Int 27:887–893, 2006. 197. Groiso JA: Juvenile hallux valgus. A conservative approach to treatment, J Bone Joint Surg Am 74:1367–1374, 1992. 198. Gupta S, Fazal MA, Williams L: Minifragment screw fixation of the Scarf osteotomy, Foot Ankle Int 29:385–389, 2008. 199. Haas Z, Hamilton G, Sundstrom D, Ford L: Maintenance of correction of first metatarsal closing base wedge osteotomies versus modified Lapidus arthrodesis for moderate to severe hallux valgus deformity, J Foot Ankle Surg 46:358–365, 2007. 200. Haines RW, McDougall AM: The anatomy of hallux valgus, J Bone Joint Surg Br 36:272–293, 1954. 201. Halebian JD, Gaines SS: Juvenile hallux valgus, J Foot Surg 22:290–293, 1983. 202. Hamilton GA, Mullins S, Schuberth JM, Rush SM, Ford L: Revision lapidus arthrodesis: rate of union in 17 cases, J Foot Ankle Surg 46:447–450, 2007. 203. Hammel E, Abi Chala ML, Wagner T: [Complications of first ray osteotomies: a consecutive series of 475 feet with first metatarsal Scarf osteotomy and first phalanx osteotomy], Rev Chir Orthop Reparatrice Appar Mot 93:710–719, 2007. 204. Hansen ST: Functional reconstruction of the foot and ankle, Philadelphia, 2000, Lippincott Williams & Wilkins, p 221. 205. Hansen ST Jr: Hallux valgus surgery. Morton and Lapidus were right! Clin Podiatr Med Surg 13:347–354, 1996. 206. Hara B, Beck JC, Woo RA: First cuneiform closing abductory osteotomy for reduction of metatarsus primus adductus, J Foot Surg 31:434–439, 1992. 207. Hardy RH, Clapham JC: Observations on hallux valgus; based on a controlled series, J Bone Joint Surg Br 33:376–391, 1951. 208. Hardy RH, Clapham JC: Hallux valgus; predisposing anatomical causes, Lancet 1:1180–1183, 1952. 209. Harper MC: Correction of metatarsus primus varus with the chevron metatarsal osteotomy. An analysis of corrective factors, Clin Orthop 243:180–183, 1989. 210. Harris R, Beath T: Hypermobile flat-foot with short tendo Achilles, J Bone Joint Surg Am 30:116–138, 1948. 211. Harris R, Beath T: The short first metatarsal: Its incidence and clinical significance, J Bone Joint Surg Am 31:553–565, 1949. 212. Harrison M, Harvey F: Arthrodesis of the first metatarsophalangeal joint for hallux valgus and rigidus, J Bone Joint Surg Am 45:471–480, 1963. 213. Hattrup SJ, Johnson KA: Chevron osteotomy: analysis of factors in patients’ dissatisfaction, Foot Ankle 5:327–332, 1985.

314

214. Hawkins F, Mitchell C, Hedrick D: Correction of hallux valgus by metatarsal osteotomy, J Bone Joint Surg Am 37:387–394, 1945. 215. Hecht PJ, Gibbons MJ, Wapner KL, et al: Arthrodesis of the first metatarsophalangeal joint to salvage failed silicone implant arthroplasty, Foot Ankle Int 18:383–390, 1997. 216. Helal B: Surgery for adolescent hallux valgus, Clin Orthop 157:50–63, 1981. 217. Helal B, Gupta SK, Gojaseni P: Surgery for adolescent hallux valgus, Acta Orthop Scand 45:271–295, 1974. 218. Henry AP, Waugh W, Wood H: The use of footprints in assessing the results of operations for hallux valgus. A comparison of Keller’s operation and arthrodesis, J Bone Joint Surg Br 57:478– 481, 1975. 219. Hernandez A, Hernandez PA, Hernandez WA: Lapidus: when and why? Clin Podiatr Med Surg 6:197–208, 1989. 220. Hetherington VJ, Steinbock G, LaPorta D, Gardner C: The Austin bunionectomy: a follow-up study, J Foot Ankle Surg 32:162–166, 1993. 221. Hewitt D, Stewart AM, Webb JW: The prevalence of foot defects among wartime recruits, BMJ 4839:745–749, 1953. 222. Hirvensalo E, Bostman O, Tormala P, et al: Chevron osteotomy fixed with absorbable polyglycolide pins, Foot Ankle 11:212– 218, 1991. 223. Hiss J: Hallux valgus: its causes and simplified treatment, Am J Surg 11:50–57, 1931. 224. Hodor L, Hess T: Shortening Z-osteotomy for the proximal phalanx of the hallux using axial guides, J Am Podiatr Med Assoc 85:249–254, 1995. 225. Hohmann G: Der Hallux valgus und die uebrigen Zchenverkruemmungen, Egerb Chir Orthop 18:308–348, 1925. 226. Hope M, Savva N, Whitehouse S, Elliot R, Saxby TS: Is it necessary to re-fuse a non-union of a Hallux metatarsophalangeal joint arthrodesis? Foot Ankle Int 31:662–669, 2010. 227. Horne G, Tanze T, Ford M: Chevron osteotomy for the treatment of hallux valgus, Clin Orthop 183:32–36, 1984. 228. Houghton GR, Dickson RA: Hallux valgus in the younger patient: the structural abnormality, J Bone Joint Surg Br 61:176– 177, 1979. 229. Huang PJ, Lin YC, Fu YC, et al: Radiographic evaluation of minimally invasive distal metatarsal osteotomy for hallux valgus, Foot Ankle Int 32:S503–S507, 2011. 230. Hueter C: Klinik der Gelenkkrankheiten mit Einschluss der Orthopadie, Leipzig, Germany, 1870–1871, Vogel. 231. Humbert JL, Bourbonniere C, Laurin CA: Metatarsophalangeal fusion for hallux valgus: indications and effect on the first metatarsal ray, Can Med Assoc J 120:937–941, 956, 1979. 232. Hurst JM, Nunley JA 2nd: Distraction osteogenesis for the shortened metatarsal after hallux valgus surgery, Foot Ankle Int 28:194–198, 2007. 233. Hyer CF, Glover JP, Berlet GC, et al: A comparison of the crescentic and Mau osteotomies for correction of hallux valgus, J Foot Ankle Surg 47:103–111, 2008. 234. Hyer CF, Philbin TM, Berlet GC, Lee TH: The incidence of the intermetatarsal facet of the first metatarsal and its relationship to metatarsus primus varus: a cadaveric study, J Foot Ankle Surg 44:200–202, 2005. 235. Inman VT: Hallux valgus: a review of etiologic factors, Orthop Clin North Am 5:59–66, 1974. 236. Ito H, Shimizu A, Miyamoto T, et al: Clinical significance of increased mobility in the sagittal plane in patients with hallux valgus, Foot Ankle Int 20:29–32, 1999. 237. Jahss MH: LeLeivre bunion operation, Instr Course Lect 21:295– 309, 1972. 238. Jahss MH: Hallux valgus: Further considerations—the first metatarsal head, Foot Ankle 2:1–4, 1981.

Hallux Valgus ■ Chapter 6

239. James C: Footprints and feet of natives of Soloman Islands, Lancet 2:1390, 1939. 240. Jawish R, Assoum H, Saliba E: Opening wedge osteotomy of the first cuneiform for the treatment of hallux valgus, Int Orthop 34:361–368, 2010. 241. Johal S, Sawalha S, Pasapula C: Post-traumatic acute hallux valgus: a case report, Foot (Edinb) 20:87–89, 2010. 242. Johansson JE, Barrington TW: Cone arthrodesis of the first metatarsophalangeal joint, Foot Ankle 4:244–248, 1984. 243. John S, Weil L Jr, Weil LS Sr, Chase K: Scarf osteotomy for the correction of adolescent hallux valgus, Foot Ankle Spec 3:10–14, 2010. 244. Johnson JE, Clanton TO, Baxter DE, Gottlieb MS: Comparison of Chevron osteotomy and modified McBride bunionectomy for correction of mild to moderate hallux valgus deformity, Foot Ankle 12:61–68, 1991. 245. Johnson KA, Cofield RH, Morrey BF: Chevron osteotomy for hallux valgus, Clin Orthop 142:44–47, 1979. 246. Johnson KA, Kile TA: Hallux valgus due to cuneiform-metatarsal instability, J South Orthop Assoc 3:273–282, 1994. 247. Johnson KA, Spiegl PV: Extensor hallucis longus transfer for hallux varus deformity, J Bone Joint Surg Am 66:681–686, 1984. 248. Johnston O: Further studies of the inheritance of hand and foot anomalies, Clin Orthop 8:146–160, 1956. 249. Jones A: Hallux valgus in the adolescent, Proc R Soc Med 41:392–393, 1948. 250. Jones C, Coughlin M, Pierce-Villadot R, Galano P: Proximal crescentic metatarsal osteotomy: the effect of saw blade orientation on first ray elevation, Foot Ankle Int 26:152–157, 2005. 251. Jones CP, Coughlin MJ, Grebing BR, et al: First metatarsophalangeal joint motion after hallux valgus correction: a cadaver study, Foot Ankle Int 26:614–619, 2005. 252. Jones CP, Coughlin MJ, Pierce-Villadot R, et al: The validity and reliability of the Klaue device, Foot Ankle Int 26:951–956, 2005. 253. Jones S, Al Hussainy HA, Ali F, et al: Scarf osteotomy for hallux valgus. A prospective clinical and pedobarographic study, J Bone Joint Surg Br 86:830–836, 2004. 254. Joplin RJ: Sling procedure for correction of splay-foot metatarsus primus varus, and hallux valgus, J Bone Joint Surg Am 32:779–785, 1950. 255. Jordan HH, Bordsky AE: Keller operation for hallux valgus and hallux rigidus. An end-result study, AMA Arch Surg 62:586–596, 1951. 256. Joseph J: Range of movement of the great toe in men, J Bone Joint Surg Br 36:450–457, 1954. 257. Kadakia AR, Smerek JP, Myerson MS: Radiographic results after percutaneous distal metatarsal osteotomy for correction of hallux valgus deformity, Foot Ankle Int 28:355–360, 2007. 258. Kalen V, Brecher A: Relationship between adolescent bunions and flatfeet, Foot Ankle 8:331–336, 1988. 259. Kato T, Watanabe S: The etiology of hallux valgus in Japan, Clin Orthop 157:78–81, 1981. 260. Kayali C, Ozturk H, Agus H, et al: The effectiveness of distal soft tissue procedures in hallux valgus, J Orthop Traumatol 9:117–121, 2008. 261. Kayiaros S, Blankenhorn BD, Dehaven J, et al: Correction of metatarsus primus varus associated with hallux valgus deformity using the arthrex mini tightrope: a report of 44 cases, Foot Ankle Spec 4:212–217, 2011. 262. Kazzaz S, Singh D: Postoperative cast necessity after a lapidus arthrodesis, Foot Ankle Int 30:746–751, 2009. 263. Kelikian H: Hallux valgus, allied deformities of the forefoot and metatarsalgia, Philadelphia, 1965, WB Saunders, pp 136–235. 264. Keller W: Further observations on the surgical treatment of hallux valgus and bunions, N Y Med J 95:696, 1912.

265. Kemp TJ, Hirose CB, Coughlin MJ: Fracture of the second metatarsal following suture button fixation device in the correction of hallux valgus, Foot Ankle Int 31:712–716, 2010. 266. Keogh P, Nagaria J, Stephens M: Cheilectomy for hallux rigidus, Ir J Med Sci 161:681–683, 1992. 267. Kerr HL, Jackson R, Kothari P: Scarf-Akin osteotomy correction for hallux valgus: short-term results from a district general hospital, J Foot Ankle Surg 49:16–19, 2010. 268. Kilmartin TE, Barrington RL, Wallace WA: Metatarsus primus varus. A statistical study, J Bone Joint Surg Br 73:937–940, 1991. 269. Kilmartin TE, Barrington RL, Wallace WA: A controlled prospective trial of a foot orthosis for juvenile hallux valgus, J Bone Joint Surg Br 76:210–214, 1994. 270. Kilmartin TE, Flintham C: Hallux valgus surgery: a simple method for evaluating the first-second intermetatarsal angle in the presence of metatarsus adductus, J Foot Ankle Surg 42:165– 166, 2003. 271. Kilmartin TE, O’Kane C: Combined rotation scarf and Akin osteotomies for hallux valgus: a patient focussed 9 year follow up of 50 patients, J Foot Ankle Res 3:2, 2010. 272. Kilmartin TE, Wallace WA: The significance of pes planus in juvenile hallux valgus, Foot Ankle 13:53–56, 1992. 273. Kim B, Shim D, Lee J, et al: Comparision of multi-drug injection versus placebo after hallux valgus surgery, Foot Ankle Int 32:856–860, 2011. 274. Kim JY, Park JS, Hwang SK, et al: Mobility changes of the first ray after hallux valgus surgery: clinical results after proximal metatarsal chevron osteotomy and distal soft tissue procedure, Foot Ankle Int 29:468–472, 2008. 275. King DM, Toolan BC: Associated deformities and hypermobility in hallux valgus: an investigation with weightbearing radiographs, Foot Ankle Int 25:251–255, 2004. 276. Kinnard P, Gordon D: A comparison between chevron and Mitchell osteotomies for hallux valgus, Foot Ankle 4:241–243, 1984. 277. Kitaoka HB, Franco MG, Weaver AL, Ilstrup DM: Simple bunionectomy with medial capsulorrhaphy, Foot Ankle 12:86–91, 1991. 278. Kitaoka HB, Holiday AD Jr, Chao EY, Cahalan TD: Salvage of failed first metatarsophalangeal joint implant arthroplasty by implant removal and synovectomy: clinical and biomechanical evaluation, Foot Ankle 13:243–250, 1992. 279. Klaue K, Hansen ST, Masquelet AC: Clinical, quantitative assessment of first tarsometatarsal mobility in the sagittal plane and its relation to hallux valgus deformity, Foot Ankle Int 15:9– 13, 1994. 280. Kleinberg S: Operative cure of hallux valgus and bunions, Am J Surg 15:75–81, 1932. 281. Klosok JK, Pring DJ, Jessop JH, Maffulli N: Chevron or Wilson metatarsal osteotomy for hallux valgus. A prospective randomised trial, J Bone Joint Surg Br 75:825–829, 1993. 282. Kose O, Celiktas M, Kisin, B, et al: Is there a relationship between forefoot alignment and ingrown toenal? A casecontrol study, Foot Ankle Spec 4:14–17, 2011. 283. Kramer J: Die Kramer-Osteotomie zur Behandlung des Hallux valgus und des Digitus quintus varus, Operat Orthop Traumatol 2:29–38, 1990. 284. Kramer J, Barry LD, Helfman DN, et al: The modified Scarf bunionectomy, J Foot Surg 31:360–367, 1992. 285. Krannitz KW, Fong HW, Fallat LM, Kish J: The effect of cigarette smoking on radiographic bone healing after elective foot surgery, J Foot Ankle Surg 48:525–527, 2009. 286. Kristen KH, Berger C, Stelzig S, et al: The SCARF osteotomy for the correction of hallux valgus deformities, Foot Ankle Int 23:221–229, 2002.

315

Part II ■ Forefoot

287. Kuhn MA, Lippert FG 3rd, Phipps MJ, Williams C: Blood flow to the metatarsal head after chevron bunionectomy, Foot Ankle Int 26:526–529, 2005. 288. Kumar S, Pradhan R, Rosenfeld PF: First metatarsophalangeal arthrodesis using a dorsal plate and a compression screw, Foot Ankle Int 31:797–801, 2010. 289. Kundert HP, Fuhrmann R: Personal communication, April 21, 2005. 290. Kuo CH, Huang PJ, Cheng YM, et al: Modified Mitchell osteotomy for hallux valgus, Foot Ankle Int 19:585–589, 1998. 291. Lagaay PM, Hamilton GA, Ford LA, et al: Rates of revision surgery using Chevron-Austin osteotomy, Lapidus arthrodesis, and closing base wedge osteotomy for correction of hallux valgus deformity, J Foot Ankle Surg 47:267–272, 2008. 292. Lampropulos M, Puigdevall M, Zapozko D, Malvarez H: Treatment of first metatarsal longitudinal epiphyseal bracket by excision before closure, J Foot Ankle Surg 46:297–301, 2007. 293. Lane W: The causation, pathology, and physiology of several of the deformities which develop during young life, Guy’s Hosp Rep 44:241, 1887. 294. Lapidus PW: Operative correction of metatarsus varus primus in hallux valgus, Surg Gynecol Obstet 58:183–191, 1934. 295. Lapidus PW: A quarter of a century of experience with the operative correction of the metatarsus varus primus in hallux valgus, Bull Hosp Jt Dis 17:404–421, 1956. 296. Lapidus PW: The author’s bunion operation from 1931 to 1959, Clin Orthop 16:119–135, 1960. 297. La Reaux RL, Lee BR: Metatarsus adductus and hallux abducto valgus: their correlation, J Foot Surg 26:304–308, 1987. 298. Larholt J, Kilmartin TE: Rotational scarf and akin osteotomy for correction of hallux valgus associated with metatarsus adductus, Foot Ankle Int 31:220–228, 2010. 299. Lau JT, Daniels TR: Effect of increasing distal medial closing wedge metatarsal osteotomies on the distal metatarsal articular angle, Foot Ankle Int 20:771–776, 1999. 300. Leaseburg JT, DeOrio JK, Shapiro SA: Radiographic correlation of hallux MP fusion position and plate angle, Foot Ankle Int 30:873–876, 2009. 301. Lee HJ, Chung JW, Chu IT, Kim YC: Comparison of distal chevron osteotomy with and without lateral soft tissue release for the treatment of hallux valgus, Foot Ankle Int 31:291–295, 2010. 302. Lee KB, Hur CI, Chung J, Jung S: Outcome of unilateral versus siutaneous correction for hallux valgus, Foot Ankle Int 30:120– 123, 2009. 303. Lee KB, Seo CY, Hur CI, et al: Outcome of proximal chevron osteotomy for hallux valgus with and without transverse Kirschner wire fixation, Foot Ankle Int 29:1101–1106, 2008. 304. Lee KT, Park YU, Young KW, et al: Reverse distal chevron osteotomy to treat iatrogenic hallux varus after overcorrection of the intermetatarsal 1-2 angle: technique tip, Foot Ankle Int 32:89–91, 2011. 305. Lee KT, Young K: Measurement of first-ray mobility in normal vs. hallux valgus patients, Foot Ankle Int 22:960–964, 2001. 306. Lee WC, Kim YM: Correction of hallux valgus using lateral soft-tissue release and proximal Chevron osteotomy through a medial incision, J Bone Joint Surg Am 89(Suppl 3):82–89, 2007. 307. Lee WC, Kim YM: Technique tip: lateral soft-tissue release for correction of hallux valgus through a medial incision using a dorsal flap over the first metatarsal, Foot Ankle Int 28:949–951, 2007. 308. Leemrijse T, Hoang B, Maldague P, et al: A new surgical procedure for iatrogenic hallux varus: reverse transfer of the abductor hallucis tendon: a report of 7 cases, Acta Orthop Belg 74:227– 234, 2008.

316

309. Leventen EO: The chevron procedure, Orthopedics 13:973–976, 1990. 310. Lewis RJ, Feffer HL: Modified chevron osteotomy of the first metatarsal, Clin Orthop 157:105–109, 1981. 311. Lian GJ, Markolf K, Cracchiolo A 3rd: Strength of fixation constructs for basilar osteotomies of the first metatarsal, Foot Ankle 13:509–514, 1992. 312. Limbird TJ, DaSilva RM, Green NE: Osteotomy of the first metatarsal base for metatarsus primus varus, Foot Ankle 9:158– 162, 1989. 313. Lippert FG 3rd, McDermott JE: Crescentic osteotomy for hallux valgus: a biomechanical study of variables affecting the final position of the first metatarsal, Foot Ankle 11:204–207, 1991. 314. Lipscomb PR: Arthrodesis of the first metatarsophalangeal joint for severe bunions and hallux rigidus, Clin Orthop 142:48–54, 1979. 315. Lipscombe S, Molloy A, Sirikonda S, Hennessy MS: Scarf osteotomy for the correction of hallux valgus: midterm clinical outcome, J Foot Ankle Surg 47:273–277, 2008. 316. Lombardi CM, Silhanek AD, Connolly FG, et al: First metatarsocuneiform arthrodesis and Reverdin-Laird osteotomy for treatment of hallux valgus: an intermediate-term retrospective outcomes study, J Foot Ankle Surg 42:77–85, 2003. 317. Loretz L, DeValentine S, Yamaguchi K: The first metatarsal bicorrectional head osteotomy (distal “L”/Reverdin-Laird procedure) for correction of hallux abducto valgus: a retrospective study, J Foot Ankle Surg 32:554–568, 1993. 318. Love TR, Whynot AS, Farine I, et al: Keller arthroplasty: a prospective review, Foot Ankle 8:46–54, 1987. 319. Luba R, Rosman M: Bunions in children: treatment with a modified Mitchell osteotomy, J Pediatr Orthop 4:44–47, 1984. 320. Ludloff K: Die Beseitigung des Hallux valgus durch die schrage planta dorsale Osteotomie des Metatarsus, Arch Klin Chir 110:364–387, 1918. 321. Lui TH: First metatarsophalangeal joint arthroscopy in patients with hallux valgus, Arthroscopy 24:1122–1129, 2008. 322. Maclennan R: Prevalence of hallux valgus in a Neolithic New Guinea population, Lancet 1:1398–1400, 1966. 323. Mader DW, Han NM: Bilateral second metatarsal stress fractures after hallux valgus correction with the use of a tension wire and button fixation system, J Foot Ankle Surg 49:488. e415– e489, 2010. 324. Maffulli N, Longo UG, Oliva F, et al: Bosch osteotomy and scarf osteotomy for hallux valgus correction, Orthop Clin North Am 40:515–524, ix–x, 2009. 325. Maguire WB: The Lapidus procedure for hallux valgus [abstract], J Bone Joint Surg Br 55:221, 1973. 326. Mahan KT, Jacko J: Juvenile hallux valgus with compensated metatarsus adductus. Case report, J Am Podiatr Med Assoc 81: 525–530, 1991. 327. Majkowski RS, Galloway S: Excision arthroplasty for hallux valgus in the elderly: a comparison between the Keller and modified Mayo operations, Foot Ankle 13:317–320, 1992. 328. Malal JJ, Shaw-Dunn J, Kumar CS: Blood supply to the first metatarsal head and vessels at risk with a chevron osteotomy, J Bone Joint Surg Am 89:2018–2022, 2007. 329. Mancuso JE, Abramow SP, Landsman MJ, et al: The zero-plus first metatarsal and its relationship to bunion deformity, J Foot Ankle Surg 42:319–326, 2003. 330. Magnan B, Pezze L, Rossi N, Bartolozzi P: Percutaneous distal metatarsal osteotomy for correction of hallux valgus, J Bone Joint Surg Am 87:1191–1199, 2005. 331. Magnan B, Fieschi S, Bragantini A, et al: Trattamento chircurgico dell’alluce del primo metatarsale, G Ital Ortop Traumatol 24:473–487, 1998.

Hallux Valgus ■ Chapter 6

332. Mankey M, Mann RA: Arthrodesis of the first metatarsophalangeal joint utilizing a dorsal plate. Paper presented at the Summer Meeting of American Orthopaedic Foot and Ankle Society, Boston, July 1991. 333. Mann RA: Complications associated with the Chevron osteotomy, Foot Ankle 3:125–129, 1982. 334. Mann RA: Decision-making in bunion surgery, Instr Course Lect 39:3–13, 1990. 335. Mann RA: Hallux valgus, Instr Course Lect 35:339–353, 1986. 336. Mann RA, Coughlin MJ: Hallux valgus—etiology, anatomy, treatment and surgical considerations, Clin Orthop 157:31–41, 1981. 337. Mann RA, Coughlin MJ: Hallux valgus and complications of hallux valgus. In Mann RA, editor: Surgery of the foot, St Louis, 1986, CV Mosby, pp 167–296. 338. Mann RA, Coughlin MJ: The great toe. In Mann RA, Coughlin MJ, editors: Video textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions, pp 146–184. 339. Mann RA, Coughlin MJ: Adult hallux valgus. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, 7th ed, St Louis, 1999, Mosby—–Year Book, pp 150–269. 340. Mann RA, Donatto KC: The chevron osteotomy: a clinical and radiographic analysis, Foot Ankle Int 18:255–261, 1997. 341. Mann RA, Katcherian DA: Relationship of metatarsophalangeal joint fusion on the intermetatarsal angle, Foot Ankle 10:8–11, 1989. 342. Mann RA, Oates JC: Arthrodesis of the first metatarsophalangeal joint, Foot Ankle 1:159–166, 1980. 343. Mann RA, Pfeffinger L: Hallux valgus repair. DuVries modified McBride procedure, Clin Orthop 272:213–218, 1991. 344. Mann RA, Rudicel S, Graves SC: Repair of hallux valgus with a distal soft-tissue procedure and proximal metatarsal osteotomy. A long-term follow-up, J Bone Joint Surg Am 74:124–129, 1992. 345. Mann RA, Schakel ME 2nd: Surgical correction of rheumatoid forefoot deformities, Foot Ankle Int 16:1–6, 1995. 346. Mann RA, Thompson FM: Arthrodesis of the first metatarsophalangeal joint for hallux valgus in rheumatoid arthritis, J Bone Joint Surg Am 66:687–692, 1984. 347. Marin GA: Arthrodesis of the metatarsophalangeal joint of the big toe for hallux valgus and hallux rigidus. A new method, Int Surg 50:175–180, 1968. 348. Markbreiter LA, Thompson FM: Proximal metatarsal osteotomy in hallux valgus correction: a comparison of crescentic and chevron procedures, Foot Ankle Int 18:71–76, 1997. 349. Martinelli N, Marinozzi A, Cancilleri F, Denaro V: Hallux valgus correction in a patient with metatarsus adductus with multiple distal oblique osteotomies, J Am Podiatr Med Assoc 100:204– 208, 2010. 350. Marwil T, Brantingham C: Foot problems of women’s reserve, Hosp Corp Q 16:98, 1943. 351. Mattila K, Kontinen VK, Kalso E, Hynynen MJ: Dexamethasone decreases oxycodone consumption following osteotomy of the first metatarsal bone: a randomized controlled trial in day surgery, Acta Anaesthesiol Scand 54:268–276, 2010. 352. Mauldin DM, Sanders M, Whitmer WW: Correction of hallux valgus with metatarsocuneiform stabilization, Foot Ankle 11:59–66, 1990. 353. Mayo C: The surgical treatment of bunions, Ann Surg 48:300, 1908. 354. Mayo C: The surgical treatment of bunions, Minn Med J 3:326– 331, 1920. 355. McBride ED: A conservative operation for bunions, J Bone Joint Surg 10:735–739, 1928. 356. McBride ED: The conservative operation for “bunions”: end results and refinements of technic, JAMA 105:1164–1168, 1935.

357. McBride E: Hallux valgus, bunion deformity; its treatment in mild, moderate and severe stages, J Int Coll Surg 21:99–105, 1954. 358. McBride ED: The McBride bunion hallux valgus operation, J Bone Joint Surg Am 49:1675–1683, 1967. 359. McCluney JG, Tinley P: Radiographic measurements of patients with juvenile hallux valgus compared with age-matched controls: a cohort investigation, J Foot Ankle Surg 45:161–167, 2006. 360. McCluskey LC, Johnson JE, Wynarsky GT, Harris GF: Comparison of stability of proximal crescentic metatarsal osteotomy and proximal horizontal “V” osteotomy, Foot Ankle Int 15:263– 270, 1994. 361. McHale K, McKay D: Bunions in a child: conservative versus surgical management, J Musculoskel Med 3:56–62, 1986. 362. McInnes BD, Bouche RT: Critical evaluation of the modified Lapidus procedure, J Foot Ankle Surg 40:71–90, 2001. 363. McKeever DC: Arthrodesis of the first metatarsophalangeal joint for hallux valgus, hallux rigidus, and metatarsus primus varus, J Bone Joint Surg Am 34:129–134, 1952. 364. Meehan PL: Adolescent bunion, Instr Course Lect 31:262–264, 1982. 365. Meier PJ, Kenzora JE: The risks and benefits of distal first metatarsal osteotomies, Foot Ankle 6:7–17, 1985. 366. Merkel KD, Katoh Y, Johnson EW Jr, Chao EY: Mitchell osteotomy for hallux valgus: long-term follow-up and gait analysis, Foot Ankle 3:189–196, 1983. 367. Meyer JM, Hoffmeyer P, Borst F: The treatment of hallux valgus in runners using a modified McBride procedure, Int Orthop 11:197–200, 1987. 368. Miller JM, Ferdowsian,VN, Collman DR: Inverted Z-scarf osteotomy for hallux valgus deformity correction: intermediateterm results in 55 patients, J Foot Ankle Surg 50:55–61, 2011. 369. Miller JW: Acquired hallux varus: a preventable and correctable disorder, J Bone Joint Surg Am 57:183–188, 1975. 370. Mitchell CL, Fleming JL, Allen R, et al: Osteotomy-bunionectomy for hallux valgus, J Bone Joint Surg Am 40:41–58; discussion 59–60, 1958. 371. Mitchell LA, Baxter DE: A chevron-Akin double osteotomy for correction of hallux valgus, Foot Ankle 12:7–14, 1991. 372. Mittal D, Anjum SN, Raja S, Raut V: The spike osteotomy for hallux valgus: a clinical and radiological evaluation, J Foot Ankle Surg 45:261–265, 2006. 373. Mittal D, Raja S, Geary NP: The modified McBride procedure: clinical, radiological, and pedobarographic evaluations, J Foot Ankle Surg 45:235–239, 2006. 374. Mizuno K, Hashimura M, Kimura M, Hirohata K: Treatment of hallux valgus by oblique osteotomy of the first metatarsal, Foot Ankle 13:447–452, 1992. 375. Morandi A, Dupplicato P, Sansone V: Results of distal metatarsal osteotomy using absorbable pin fixation, Foot Ankle Int 30:34–38, 2009. 376. Morton DJ: Hypermobility of the first metatarsal bone: the interlinking factor between metatarsalgia and longitudinal arch strains, J Bone Joint Surg 10:187–196, 1928. 377. Morton DJ: The human foot, New York, 1935, Columbia University Press. 378. Mote GA, Yarmel D, Treaster A: First metatarsal-cuneiform arthrodesis for the treatment of first ray pathology: a technical guide, J Foot Ankle Surg 48:593–601, 2009. 379. Moynihan FJ: Arthrodesis of the metatarso-phalangeal joint of the great toe, J Bone Joint Surg Br 49:544–551, 1967. 380. Munuera PV, Polo J, Rebollo J: Length of the first metatarsal and hallux in hallux valgus in the initial stage, Int Orthop 32:489–495, 2008.

317

Part II ■ Forefoot

381. Murawski CD, Egan CJ, Kennedy JG: A rotational scarf osteotomy decreases troughing when treating hallux valgus, Clin Orthop Relat Res 469:847–853, 2011. 382. Murawski DE, Beskin JL: Increased displacement maximizes the utility of the distal chevron osteotomy for hallux valgus deformity correction, Foot Ankle Int 29:155–163, 2008. 383. Myerson MS: Metatarsocuneiform arthrodesis for treatment of hallux valgus and metatarsus primus varus, Orthopedics 13:1025–1031, 1990. 384. Myerson MS: Hallux valgus. In Myerson MS, editor: Foot and ankle disorders, Philadelphia, 2000, WB Saunders, pp 213–289. 385. Myerson M, Allon S, McGarvey W: Metatarsocuneiform arthrodesis for management of hallux valgus and metatarsus primus varus, Foot Ankle 13:107–115, 1992. 386. Myerson MS, Badekas A: Hypermobility of the first ray, Foot Ankle Clin 5:469–484, 2000. 387. Nedopil A, Rudert M, Gradinger R, et al: Closed wedge osteotomy in 66 patients for the treatment of moderate to severe hallux valgus, Foot Ankle Surg 16:9–14, 2010. 388. Neese DJ, Zelent, ME: The modified Mau-Reverdin double osteotomy for correction of hallux valgus: a retrospective study, J Foot Ankle Surg 48:22–29, 2009. 389. Neven E, Vandeputte G: Technical tip: fixation of the scarf metatarsal osteotomy with a proximal buttress and a standard distal screw, Foot Ankle Int 30:1235–1236, 2009. 390. Newman AS, Negrine JP, Zecovic M, et al: A biomechanical comparison of the Z step-cut and basilar crescentic osteotomies of the first metatarsal, Foot Ankle Int 21:584–587, 2000. 391. Nicklas BJ, McEneaney PA, Lichniak JE, et al: Surgical repair of abductor hallucis muscle herniation: a case report, J Foot Ankle Surg 49:488.e485–e489, 2010. 392. O’Donnell T, Hogan N, Solan M, Stephens MM: Correction of severe hallux valgus using a basal chevron osteotomy and distal soft tissue release, Foot Ankle Surg 16:126–131, 2010. 393. Oh IS, Choi SW, Kim MK, et al: Clinical and radiological results after modified distal metatarsal osteotomy for hallux valgus, Foot Ankle Int 29:473–477, 2008. 394. Okuda R, Kinosh*ta M, Yasuda T, et al: The shape of the lateral edge of the first metatarsal head as a risk factor for recurrence of hallux valgus, J Bone Joint Surg Am 89:2163–2172, 2007. 395. Okuda R, Kinosh*ta M, Yasuda T, et al: Proximal metatarsal osteotomy for hallux valgus: comparison of outcome for moderate and severe deformities, Foot Ankle Int 29:664–670, 2008. 396. Opsomer G, Deleu PA, Bevernage BD, Leemrijse T: Cortical thickness of the second metatarsal after correction of hallux valgus, Foot Ankle Int 31:770–776, 2010. 397. Orzechowski W, Dragan S, Romaszkiewicz P, et al: Evaluation of follow-up results of McBride operative treatment for hallux valgus deformity, Ortop Traumatol Rehabil 10:261–273, 2008. 398. Owoeye BA, Akinbo SR, Aiyegbusi AL, Ogunsola MO: Prevalence of hallux valgus among youth population in Lagos, Nigeria, Nigerian Postgrade Med J 18:51–55, 2011. 399. Ozan F, Bora OA, Filiz MA, Kement Z: Interposition arthroplasty in the treatment of hallux rigidus, Acta Orthopaedica Traumatol Turc 44:143–151, 2010. 400. Ozkurt B, Aktekin CN, Altay M, et al: Range of motion of the first metatarsophalangeal joint after chevron procedure reinforced by a modified capsuloperiosteal flap, Foot Ankle Int 29:903–909, 2008. 401. Oznur A: Technical Tip: mini-fixator assisted correction of DMAA in hallux valgus surgery, Foot Ankle Int 27:849–850, 2006. 402. Panchbhavi VK: Technique tip: buttress Kirschner wire fixation for distal chevron osteotomy, Foot Ankle Int 28:133–134, 2007.

318

403. Pappas A, Anderson R: Management of acquired hallux varus with an endobutton, Tech Foot Ankle Surg 7:134–138, 2008. 404. Park J, Jung H, Kim T, Kang M: Intraoperative incidence of hallux valgus interphalangeus following basilar first metatarsal osteotomy and distal soft tissue realignment, Foot Ankle Int 32:962–967, 2011. 405. Patel S, Ford LA, Etcheverry J, et al: Modified Lapidus arthrodesis: rate of nonunion in 227 cases, J Foot Ankle Surg 43:37–42, 2004. 406. Pavlovich R Jr, Caminear D: Granuloma formation after chevron osteotomy fixation with absorbable copolymer pin: a case report, J Foot Ankle Surg 42:226–229, 2003. 407. Peabody D: Surgical care of hallux valgus, J Bone Joint Surg 13:273–282, 1931. 408. Pearce CJ, Sexton SA, Sakellariou A: The triplanar chevron osteotomy, Foot Ankle Surg 14:158–160, 2008. 409. Pearson SW, Kitaoka HB, Cracchiolo A, Leventen EO: Results and complications following a proximal curved osteotomy of the hallux metatarsal, Contemp Orthop 23:127–132, 1991. 410. Peterson DA, Zilberfarb JL, Greene MA, Colgrove RC: Avascular necrosis of the first metatarsal head: incidence in distal osteotomy combined with lateral soft tissue release, Foot Ankle Int 15:59–63, 1994. 411. Peterson HA, Newman SR: Adolescent bunion deformity treated with double osteotomy and longitudinal pin fixation of the first ray, J Pediatr Orthop 13:80–84, 1993. 412. Petratos DV, Anastasopoulos JN, Plakogiannis CV, Matsinos GS: Correction of adolescent hallux valgus by proximal crescentic osteotomy of the first metatarsal, Acta Orthop Belg 74:496–502, 2008 413. Phisitkul P, Sripongsai R, Chaichankul C, Femino JE: Anatomy of the plantarmedial hallucal nerve in relation to the medial approach of the first metatarsophalangeal joint, Foot Ankle Int 30:558–561, 2009. 414. Piggott H: The natural history of hallux valgus in adolescence and early adult life, J Bone Joint Surg Br 42:749–760, 1960. 415. Pinney S, Song K, Chou L: Surgical treatment of mild hallux valgus deformity: the state of practice among academic foot and ankle surgeons, Foot Ankle Int 27:970–973, 2006. 416. Pinney SJ, Song KR, Chou LB: Surgical treatment of severe hallux valgus: the state of practice among academic foot and ankle surgeons, Foot Ankle Int 27:1024–1029, 2006. 417. Pique-Vidal C: The first metatarsophalangeal arc circumference: correlation with angular measurements, Foot Ankle Int 28:186– 193, 2007. 418. Pique-Vidal C, Maled-Garcia I, Arabi-Moreno J, Vila J: Radiographic angles in hallux valgus: differences between measurements made manually and with a computerized program, Foot Ankle Int 27:175–180, 2006. 419. Pique-Vidal C, Sole MT, Antich J: Hallux valgus inheritance: pedigree research in 350 patients with bunion deformity, J Foot Ankle Surg 46:149–154, 2007. 420. Plattner PF, Van Manen JW: Results of Akin type proximal phalangeal osteotomy for correction of hallux valgus deformity, Orthopedics 13:989–996, 1990. 421. Pochatko DJ, Schlehr FJ, Murphey MD, Hamilton JJ: Distal chevron osteotomy with lateral release for treatment of hallux valgus deformity, Foot Ankle Int 15:457–461, 1994. 422. Ponnapula P, Wittock R: Application of an interosseous suture and button device for hallux valgus correction: a review of outcomes in a small series, J Foot Ankle Surg 49:159.e121–e156, 2010. 423. Pontious J, Mahan KT, Carter S: Characteristics of adolescent hallux abducto valgus. A retrospective review, J Am Podiatr Med Assoc 84:208–218, 1994.

Hallux Valgus ■ Chapter 6

424. Popoff I, Negrine JP, Zecovic M, et al: The effect of screw type on the biomechanical properties of SCARF and crescentic osteotomies of the first metatarsal, J Foot Ankle Surg 42:161–164, 2003. 425. Portaluri M: Hallux valgus correction by the method of Bosch: a clinical evaluation, Foot Ankle Clin 5:499–511, vi, 2000. 426. Potenza V, Caterini R, Farsetti P, et al: Chevron osteotomy with lateral release and adductor tenotomy for hallux valgus, Foot Ankle Int 30:512–516, 2009. 427. Pouliart N, Haentjens P, Opdecam P: Clinical and radiographic evaluation of Wilson osteotomy for hallux valgus, Foot Ankle Int 17:388–394, 1996. 428. Price GF: Metatarsus primus varus: Including various clinicoradiologic features of the female foot, Clin Orthop 145:217–223, 1979. 429. Prieskorn DW, Mann RA, Fritz G: Radiographic assessment of the second metatarsal: measure of first ray hypermobility, Foot Ankle Int 17:331–333, 1996. 430. Pring DJ, Coombes RRH, Closok JK: Chevron or Wilson osteotomy: a comparison and follow-up [abstract], J Bone Joint Surg Am 67:671–672, 1985. 431. Radovic PA, Shah E: Nonsurgical treatment for hallux abducto valgus with botulinum toxin A, J Am Podiatr Med Assoc 98:61– 65, 2008. 432. Rambani R, Elnaggar M, Sturdee S: Syndactyly with hallux valgus: a case report, Foot Ankle Int 32:641–643, 2011. 433. Randhawa S, Pepper D: Radiographic evaluation of hallux valgus treated with opening wedge osteotomy, Foot Ankle Int 30:427–431, 2009. 434. Raymakers R, Waugh W: The treatment of metatarsalgia with hallux valgus, J Bone Joint Surg Br 53:684–687, 1971. 435. Resch S, Stenstrom A, Egund N: Proximal closing wedge osteotomy and adductor tenotomy for treatment of hallux valgus, Foot Ankle 9:272–280, 1989. 436. Reverdin J: De la deviation en dehors du gros orteil et de son traitement chirurgical, Trans Int Med Congr 2:408–412, 1881. 437. Richardson EG: Keller resection arthroplasty, Orthopedics 13:1049–1053, 1990. 438. Richardson EG, Graves SC, McClure JT, Boone RT: First metatarsal head-shaft angle: a method of determination, Foot Ankle 14:181–185, 1993. 439. Riedel HL: Zur operativen Behandlung des Hallux valgus, Zentralbl Chir 44:573–580, 1886. 440. Riggs SA Jr, Johnson EW Jr: McKeever arthrodesis for the painful hallux, Foot Ankle 3:248–253, 1983. 441. Rink-Brune O: Lapidus arthrodesis for management of hallux valgus—a retrospective review of 106 cases, J Foot Ankle Surg 43:290–295, 2004. 442. Robinson AH, Cullen NP, Chhaya NC, et al: Variation of the distal metatarsal articular angle with axial rotation and inclination of the first metatarsal, Foot Ankle Int 27:1036–1040, 2006. 443. Robinson AH, Limbers JP: Modern concepts in the treatment of hallux valgus, J Bone Joint Surg Br 87:1038–1045, 2005. 444. Rogers WA, Joplin RJ: Hallux valgus, weak foot and the Keller operations: an end-result study, Surg Clin North Am 27:1295– 1302, 1947. 445. Rosenberg GA, Donley BG: Plate augmentation of screw fixation of proximal crescentic osteotomy of the first metatarsal, Foot Ankle Int 24:570–571, 2003. 446. Ross SD: Technical tip: the crescentic shelf: a modified Ludoff osteotomy, Foot Ankle Int 32:452–454, 2011. 447. Roukis TS: Hallux proximal phalanx Akin-scarf osteotomy, J Am Podiatr Med Assoc 94:70–72, 2004. 448. Roukis TS, Landsman AS: Hypermobility of the first ray: a critical review of the literature, J Foot Ankle Surg 42:377–390, 2003.

449. Roukis TS, Weil L, Weil L, Landsman A: Predicting cartilage erosion in hallux valgus: clinical, radiographic analysis, J Foot Ankle Surg 44:13–21, 2005. 450. Rush SM, Christensen JC, Johnson CH: Biomechanics of the first ray. Part II: metatarsus primus varus as a cause of hypermobility. A three-dimensional kinematic analysis in a cadaver model, J Foot Ankle Surg 39:68–77, 2000. 451. Salvi AE, Mondanelli N: The Reverdin hallux valgus correction: back to the future, J Foot Ankle Surg 50:267–268, 2011. 452. Sammarco GJ, Brainard BJ, Sammarco VJ: Bunion correction using proximal chevron osteotomy, Foot Ankle 14:8–14, 1993. 453. Sammarco GJ, Idusuyi OB: Complications after surgery of the hallux, Clin Orthop 391:59–71, 2001. 454. Sammarco GJ, Russo-Alesi FG: Bunion correction using proximal chevron osteotomy: a single-incision technique, Foot Ankle Int 19:430–437, 1998. 455. Sammarco VJ: Surgical strategies: Mau osteotomy for correction of moderate and severe hallux valgus deformity, Foot Ankle Int 28:857–864, 2007. 456. Sangeorzan BJ, Hansen ST Jr: Modified Lapidus procedure for hallux valgus, Foot Ankle 9:262–266, 1989. 457. Sanhudo JA: Correction of moderate to severe hallux valgus deformity by a modified chevron shaft osteotomy, Foot Ankle Int 27:581–585, 2006. 458. Saragas NP: Proximal opening-wedge osteotomy of the first metatarsal for hallux valgus using a low profile plate, Foot Ankle Int 30:976–980, 2009. 459. Saragas NP, Becker PJ: Comparative radiographic analysis of parameters in feet with and without hallux valgus, Foot Ankle Int 16:139–143, 1995. 460. Sarrafian S: Anatomy of the foot and ankle, Philadelphia, 1983, JB Lippincott, pp 81–86. 461. Saro C, Andren B, Wildemyr Z, Fellander-Tsai L: Outcome after distal metatarsal osteotomy for hallux valgus: a prospective randomized controlled trial of two methods, Foot Ankle Int 28:778–787, 2007. 462. Schede F: Hallux valgus, Hallux flexus und Fussenkung, Z Orthop Chir 48:564–571, 1927. 463. Schemitsch E, Horne G: Wilson’s osteotomy for the treatment of hallux valgus, Clin Orthop 240:221–225, 1989. 464. Schneider W, Knahr K: Keller procedure and chevron osteotomy in hallux valgus: five-year results of different surgical philosophies in comparable collectives, Foot Ankle Int 23:321–329, 2002. 465. Schoen NS, Zygmunt K, Gudas C: Z-bunionectomy: retrospective long-term study, J Foot Ankle Surg 35:312–317, 1996. 466. Schoenhaus HD, Cohen RS: Etiology of the bunion, J Foot Surg 31:25–29, 1992. 467. Schuh R, Hofstaetter SG, Adams SB Jr, et al: Rehabilitation after hallux valgus surgery: importance of physical therapy to restore weight bearing of the first ray during the stance phase, Phys Ther 89:934–945, 2009. 468. Schwartz N, Hurley JP: Derotational Akin osteotomy: further modification, J Foot Surg 26:419–421, 1987. 469. Schweitzer ME, Maheshwari S, Shabshin N: Hallux valgus and hallux rigidus: MRI findings, Clin Imaging 23:397–402, 1999. 470. Scranton PE, Coetzee JC, Carreira D: Arthrodesis of the first metatarsocuneiform joint: a comparative study of fixation methods, Foot Ankle Int 30:341–345, 2009. 471. Scranton PE Jr: Adolescent bunions: Diagnosis and management, Pediatr Ann 11:518–520, 1982. 472. Scranton PE Jr, Zuckerman JD: Bunion surgery in adolescents: results of surgical treatment, J Pediatr Orthop 4:39–43, 1984. 473. Seelenfreund M, Fried A, Tikva P: Correction of hallux valgus deformity by basal phalanx osteotomy of the big toe, J Bone Joint Surg Am 55:1411–1415, 1973.

319

Part II ■ Forefoot

474. Seiberg M, Green R, Green D: Epiphysiodesis in juvenile hallux abducto valgus. A preliminary retrospective study, J Am Podiatr Med Assoc 84:225–236, 1994. 475. Selner AJ, Selner MD, Tucker RA, Eirich G: Tricorrectional bunionectomy for surgical repair of juvenile hallux valgus, J Am Podiatr Med Assoc 82:21–24, 1992. 476. Shannak O, Sehat K, Dhar S: Analysis of the proximal phalanx size as a guide for an Akin closing wedge osteotomy, Foot Ankle Int 32:419–421, 2011. 477. Shariff R, Attar F, Osarumwene D, et al: The risk of avascular necrosis following chevron osteotomy: a prospective study using bone scintigraphy, Acta Orthop Belg 75:234–238, 2009. 478. Shereff MJ, Yang QM, Kummer FJ: Extraosseous and intraosseous arterial supply to the first metatarsal and metatarsophalangeal joint, Foot Ankle 8:81–93, 1987. 479. Sheridan LE: Correction of juvenile hallux valgus deformity associated with metatarsus primus adductus using epiphysiodesis technique, Clin Podiatr Med Surg 4:63–74, 1987. 480. Sherman KP, Douglas DL, Benson MK: Keller’s arthroplasty: is distraction useful? A prospective trial, J Bone Joint Surg Br 66:765–769, 1984. 481. Shima H, Okuda R, Yasuda T, et al: Radiographic measurements in patients with hallux valgus before and after proximal crescentic osteotomy, J Bone Joint Surg Am 91:1369–1376, 2009. 482. Shurnas PS, Coughlin MJ: Recall of the risks of forefoot surgery after informed consent, Foot Ankle Int 24:904–908, 2003. 483. Shurnas PS, Watson TS, Crislip TW: Proximal first metatarsal opening wedge osteotomy with a low profile plate, Foot Ankle Int 30:865–872, 2009. 484. Siclari A, Decantis V: Arthroscopic lateral release and percutaneous distal osteotomy for hallux valgus: a preliminary report, Foot Ankle Int 30:675–679, 2009. 485. Silberman FS: Proximal phalangeal osteotomy for the correction of hallux valgus, Clin Orthop 85:98–100, 1972. 486. Silver D: The operative treatment of hallux valgus, J Bone Joint Surg 5:225–232, 1923. 487. Sim-f*ck L, Hodgson AR: A comparison of foot forms among the non-shoe and shoe-wearing Chinese population, J Bone Joint Surg Am 40:1058–1062, 1958. 488. Simmonds F, Menelaus M: Hallux valgus in adolescents, J Bone Joint Surg Br 42:761–768, 1960. 489. Simon W: Der Hallux valgus und seine chirurgische Behandlung mit besonderer Berucksichtigung der Ludlof schen Operation, Beitrage Klin Chir 3:467–537, 1918. 490. Singh B, Draeger R, Del Gaizo DJ, Parekh SG: Changes in length of the first ray with two different first MTP fusion techniques: a cadaveric study, Foot Ankle Int 29:722–725, 2008. 491. Smith AM, Alwan T, Davies MS: Perioperative complications of the scarf osteotomy, Foot Ankle Int 24:222–227, 2003. 492. Smith BW, Coughlin MJ: The first metatarsocuneiform joint, hypermobility, and hallux valgus: what does it all mean? Foot Ankle Surg 14:138–141, 2008. 493. Smith NR: Hallux valgus and rigidus treated by arthrodesis of the metatarsophalangeal joint, BMJ 2:1385–1387, 1952. 494. Smith RW, Joanis TL, Maxwell PD: Great toe metatarsophalangeal joint arthrodesis: a user-friendly technique, Foot Ankle 13:367–377, 1992. 495. Smith RW, Reynolds JC, Stewart MJ: Hallux valgus assessment: report of research committee of American Orthopaedic Foot and Ankle Society, Foot Ankle 5:92–103, 1984. 496. Smith SE, Landorf KB, Gilheany MF, Menz HB: Development and reliability of an intraoperative first metatarsophalangeal joint cartilage evaluation tool for use in hallux valgus surgery, J Foot Ankle Surg 50:31–36, 2011. 497. Smith WB, Hyer CF, DeCarbo WT, et al: Opening wedge osteotomies for correction of hallux valgus: a review of wedge plate fixation, Foot Ankle Spec 2:277–282, 2009.

320

498. Sorto LA Jr, Balding MG, Weil LS, Smith SD: Hallux abductus interphalangeus: etiology, x-ray evaluation and treatment, J Am Podiatr Assoc 66:384–396, 1976. 499. Sorto LA Jr, Balding MG, Weil LS, Smith SD: Hallux abductus interphalangeus. Etiology, x-ray evaluation and treatment. 1975, J Am Podiatr Med Assoc 82:85–97, 1992. 500. Staheli LT: Lower positional deformity in infants and children: a review, J Pediatr Orthop 10:559–563, 1990. 501. Stamatis ED, Chatzikomninos IE, Karaoglanis GC: Mini locking plate as “medial buttress’ ’ for oblique osteotomy for hallux valgus, Foot Ankle Int 31:920–922, 2010. 502. Steel MW 3rd, Johnson KA, DeWitz MA, Ilstrup DM: Radiographic measurements of the normal adult foot, Foot Ankle 1:151–158, 1980. 503. Stein HC: Hallux valgus, Surg Gynecol Obstet 66:889–898, 1938. 504. Stephens MM: Does shortening of the first ray in the treatment of adolescent hallux valgus prejudice the outcome? J Bone Joint Surg 88:858–859, 2006. 505. Stienstra JJ, Lee JA, Nakadate DT: Large displacement distal chevron osteotomy for the correction of hallux valgus deformity, J Foot Ankle Surg 41:213–220, 2002. 506. Sung W, Kluesner AJ, Irrgang J, et al: Radiographic outcomes following primary arthrodesis of the first metatarsophalangeal joint in hallux abductovalgus deformity, J Foot Ankle Surg 49:446–451, 2010. 507. Szaboky GT, Raghaven VC: Modification of Mitchell’s lateral displacement angulation osteotomy, J Bone Joint Surg Am 51: 1430–1431, 1969. 508. Takao M, Komatsu F, Oae K, et al: Proximal oblique-domed osteotomy of the first metatarsal for the treatment of hallux valgus associate with flat foot: effect to the correction of the longitudinal arch of the foot, Arch Orthop Trauma Surg 127:685– 690, 2007. 509. Tanaka Y, Takakura Y, Kumai T, et al: Radiographic analysis of hallux valgus. A two-dimensional coordinate system, J Bone Joint Surg Am 77:205–213, 1995. 510. Tanaka Y,Takakura Y, Kumai T, et al: Proximal spherical metatarsal osteotomy for the foot with severe hallux valgus, Foot Ankle Int 29:1025–1030, 2008. 511. Thomas RL, Espinosa FJ, Richardson EG: Radiographic changes in the first metatarsal head after distal chevron osteotomy combined with lateral release through a plantar approach, Foot Ankle Int 15:285–292, 1994. 512. Thompson F, McElveney R: Arthrodesis of the first metatarsophalangeal joint, J Bone Joint Surg 22:555–558, 1940. 513. Thompson FM, Coughlin MJ: The high price of high fashion footwear, J Bone Joint Surg Am 76:1586–1593, 1994. 514. Thompson GH: Bunions and deformities of the toes in children and adolescents, Instr Course Lect 45:355–367, 1996. 515. Thordarson DB, Krewer P: Medial eminence thickness with and without hallux valgus, Foot Ankle Int 23:48–50, 2002. 516. Thordarson DB, Leventen EO: Hallux valgus correction with proximal metatarsal osteotomy: Two-year follow-up, Foot Ankle 13:321–326, 1992. 517. Tonbul M, Adas M, Keris I, Zengin S: Distal first metatarsal dome (crescentic) osteotomy for repair of mild to moderate hallux valgus deformity, J Foot Ankle Surg 47:259–262, 2008. 518. Tonbul M, Baca E, Adas M, et al: Crescentic distal metatarsal osteotomy for the treatment of hallux valgus: a prospective, randomized, controlled studyof two different fixation methods, Acta Orthop Traumatol Turc 43:497–503, 2009. 519. Toth K, Huszanyik I, Boda K, et al: The influence of the length of the first metatarsal on transfer metatarsalgia after Wu’s osteotomy, Foot Ankle Int 29:396–399, 2008. 520. Toth K, Kellermann P, Wellinger K: Fixation of Akin osteotomy for hallux abductus with absorbable suture, Arch Orthop Trauma Surg 130:1257–1261, 2010.

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521. Tourne Y, Saragaglia D, Zattara A, et al: Hallux valgus in the elderly: metatarsophalangeal arthrodesis of the first ray, Foot Ankle Int 18:195–198, 1997. 522. Trnka HJ, Hofstaetter SG, Hofstaetter JG, et al: Intermediateterm results of the Ludloff osteotomy in one hundred and eleven feet, J Bone Joint Surg Am 90:531–539, 2008. 523. Trnka HJ, Zembsch A, Easley ME, et al: The chevron osteotomy for correction of hallux valgus. Comparison of findings after two and five years of follow-up, J Bone Joint Surg Am 82:1373– 1378, 2000. 524. Trnka HJ, Zembsch A, Wiesauer H, et al: Modified Austin procedure for correction of hallux valgus, Foot Ankle Int 18:119– 127, 1997. 525. Trnka HJ, Zettl R, Hungerford M, et al: Acquired hallux varus and clinical tolerability, Foot Ankle Int 18:593–597, 1997. 526. Trott A: Hallux valgus in adolescent, Instr Course Lect 21:262– 268, 1972. 527. Truslow W: Metatarsus primus varus or hallux valgus? J Bone Joint Surg 7:98–108, 1925. 528. Tupman S: Arthrodesis of the first metatarsophalangeal joint, J Bone Joint Surg Br 40:826, 1958. 529. Turan I, Lindgren U: Compression-screw arthrodesis of the first metatarsophalangeal joint of the foot, Clin Orthop 221:292– 295, 1987. 530. Turnbull T, Grange W: A comparison of Keller’s arthroplasty and distal metatarsal osteotomy in the treatment of adult hallux valgus, J Bone Joint Surg Br 68:132–137, 1986. 531. Vallier GT, Petersen SA, LaGrone MO: The Keller resection arthroplasty: a 13-year experience, Foot Ankle 11:187–194, 1991. 532. Varner KE, Matt V, Alexander JW, et al: Screw versus plate fixation of proximal first metatarsal crescentic osteotomy, Foot Ankle Int 30:142–149, 2009. 533. Venn A, LaValette D, Harris NJ: Re: technique tip. Plate augmentation of screw fixation of proximal crescentic osteotomy of the first metatarsal, (Rosenbery GA, Donley BG: Foot Ankle Int 24:570–571, 2003.) Foot Ankle Int 25:605–606; author reply 606, 2004. 534. Verbrugge J: Pathogenie et traitement de l’hallux valgus, Mem Bull Soc Delge Orthop 3:40, 1933. 535. Veri JP, Pirani SP, Claridge R: Crescentic proximal metatarsal osteotomy for moderate to severe hallux valgus: a mean 12.2 year follow-up study, Foot Ankle Int 22:817–822, 2001. 536. Vienne P, Sukthankar A, Favre P, et al: Metatarsophalangeal joint arthrodesis after failed Keller-Brandes procedure, Foot Ankle Int 27:894–901, 2006. 537. Viladot A: Metatarsalgia due to biomechanical alterations of the forefoot, Orthop Clin North Am 4:165–178, 1973. 538. Villas C, Del Rio J, Valenti A, Alfonso M: Symptomatic medial exostosis of the great toe distal phalanx: a complication due to over-correction following akin osteotomy for hallux valgus repair, J Foot Ankle Surg 48:47–51, 2009. 539. Voellmicke KV, Deland JT: Manual examination technique to assess dorsal instability of the first ray, Foot Ankle Int 23:1040– 1041, 2002. 540. Volkmann A: Ueber die sogennante Exostose der grossen Zehe, Virchows Arch Patgol Anat 10:297, 1856. 541. von Salis-Soglio G, Thomas W: Arthrodesis of the metatarsophalangeal joint of the great toe, Arch Orthop Trauma Surg 95:7–12, 1979. 542. Wagner FW Jr: Technique and rationale: Bunion surgery, Contemp Orthop 3:1040–1053, 1981. 543. Wanivenhaus AH, Feldner-Busztin H: Basal osteotomy of the first metatarsal for the correction of metatarsus primus varus associated with hallux valgus, Foot Ankle 8:337–343, 1988. 544. Wanivenhaus A, Pretterklieber M: First tarsometatarsal joint: anatomical biomechanical study, Foot Ankle 9:153–157, 1989.

545. Weil L Jr: Mastering the Scarf procedure for hallux valgus correction, Foot Ankle Spec 2:151–155, 2009. 546. Weil LS: Scarf osteotomy for correction of hallux valgus. Historical perspective, surgical technique, and results, Foot Ankle Clin 5:559–580, 2000. 547. Wells LH: The foot of the South African native, Am J Phys Anthropol 15:185, 1931. 548. West BC: Mini TightRope system for hallux abducto valgus deformity: a discussion and case report, J Am Podiatr Med Assoc 100:291–295, 2010. 549. Westbrook AP, Subramanian KN, Monk J, Calthorpe D: Best foot forward. Proceeding of the British Orthopaedic Foot Surgery Society, J Bone Joint Surg Br 85(Suppl 3):249, 2003. 550. White LE, Lucas G, Richards A, Purves D: Cerebral asymmetry and handedness, Nature 368:197–198, 1994. 551. White P, Issioui T, Skrivanek G, et al: The use of continuous popliteral sciatic nerve block after surgery involving the foot and ankle: does it improve the quality of recovery, Anesth Analg 97:1303–1309, 2003. 552. Wilkins EH: Feet with particular reference to school children, Med Officer 66:5, 13, 21, 29, 1941. 553. Wilkinson J: Cone arthrodesis of the first metatarsophalangeal joint, Acta Orthop Scand 49:627–630, 1978. 554. Wilkinson SV, Jones RO, Sisk LE, et al: Austin bunionectomy: postoperative MRI evaluation for avascular necrosis, J Foot Surg 31:469–477, 1992. 555. Williams WW, Barrett DS, Copeland SA: Avascular necrosis following chevron distal metatarsal osteotomy: a significant risk? J Foot Surg 28:414–416, 1989. 556. Wilson DW: Treatment of hallux valgus and bunions, Br J Hosp Med 24:548–549, 1980. 557. Wilson JD, Baines J, Siddique MS, Fleck R: The effect of sesamoid position on outcome following scarf osteotomy for hallux abducto valgus, Foot Ankle Surg 15:65–68, 2009. 558. Wilson JN: Oblique displacement osteotomy for hallux valgus, J Bone Joint Surg Br 45:552–556, 1963. 559. Wilson JN: Cone arthrodesis of the first metatarso-phalangeal joint, J Bone Joint Surg Br 49:98–101, 1967. 560. Wu DY: Syndesmosis procedure: a non-osteotomy approach to metatarsus primus varus correction, Foot Ankle Int 28:1000– 1006, 2007. 561. Wu K: Mitchell’s bunionectomy and Wu’s bunionectomy: a comparison of 100 cases of each procedure, Orthopedics 13:1001–1007, 1990. 562. Wu KK: Wu’s bunionectomy: a clinical analysis of 150 personal cases, J Foot Surg 31:288–297, 1992. 563. Wukich DK, Roussel AJ, Dial DM: Correction of metatarsus primus varus with an opening wedge plate: a review of 18 procedures, J Foot Ankle Surg 48:420–426, 2009. 564. Wynne-Davis R: Family studies and the causes of congenital clubfoot talipes equinovarus, talipes calcaneovalgus, and metatarsus varus, J Bone Joint Surg Am 46:445, 1967. 565. Young J: A new operation for adolescent hallux valgus, Univ Penn Med Bull 23:459, 1910. 566. Young KW, Lee KT, Kwak JJ, et al: Mass-induced unilateral hallux valgus, Orthopedics 33:927, 2010. 567. Yucel I, Tenekecioglu Y, Ogut T, Kesmezacar H: Treatment of hallux valgus by modified McBride procedure: a 6-year follow-up, J Orthop Traumatol 11:89–97, 2010. 568. Zadik FR: Arthrodesis of the great toe, BMJ 5212:1573–1574, 1960. 569. Zimmer TJ, Johnson KA, Klassen RA: Treatment of hallux valgus in adolescents by the chevron osteotomy, Foot Ankle 9:190– 193, 1989. 570. Zygmunt KH, Gudas CJ, Laros GS: Z-bunionectomy with internal screw fixation, J Am Podiatr Med Assoc 79:322–329, 1989.

321

Chapter

Lesser Toe Deformities Michael J. Coughlin

CHAPTER CONTENTS LESSER TOE DEFORMITIES Etiology Mallet Toe Hammer Toe Claw Toe Anatomy and Pathophysiology Extensor Digitorum Longus Muscle and Tendon Interosseous Tendons Plantar Plate and Collateral Ligaments Pathophysiology Preoperative Evaluation Physical Examination Radiographic Examination FIXED HAMMER TOE DEFORMITY (Video Clip 75, 76) Preoperative Planning Indications Contraindications FLEXIBLE HAMMER TOE DEFORMITY (Video Clip 77) Preoperative Planning Indications Contraindications MALLET TOE DEFORMITY (Video Clip 74) Preoperative Planning Indications Contraindications CLAW TOE DEFORMITIES (Video Clip 75) Preoperative Planning Indications Contraindications SUBLUXATION AND DISLOCATION OF THE LESSER METATARSOPHALANGEAL JOINT Etiology Anatomy of Lesser Metatarsophalangeal Joint Subluxation History and Demographics Physical Examination Radiographic Examination

322

322 325 325 326 327 328 328 330 330 331 332 332 333 333 333 338 338 351 353 353 353 357 358 358 358 361 361 362 362 366 366 368 369 372 374

Treatment Conservative Treatment Surgical Treatment (Video Clips 70-72, 86) SALVAGE PROCEDURES Indications Contraindications FIFTH TOE DEFORMITIES Etiology Anatomy Preoperative Evaluation Physical Examination Conservative Treatment MILD OVERLAPPING FIFTH TOE DEFORMITIES SEVERE OVERLAPPING FIFTH TOE DEFORMITIES (Video Clip 73) UNDERLAPPING FIFTH TOE Surgical Treatment co*ck-UP FIFTH TOE DEFORMITY Surgical Treatment KERATOTIC DEFORMITIES OF LESSER TOES Etiology Preoperative Evaluation Physical Examination Radiographic Evaluation Treatment Conservative Treatment Surgical Treatment (Video Clips 78-80)

375 375 377 400 400 400 403 403 403 403 403 404 404 406 410 410 410 411 413 413 414 414 415 415 415 415

LESSER TOE DEFORMITIES

Lesser toe deformities can be static or dynamic. They can occur as isolated entities or be associated with deformities of the hallux, midfoot, or hindfoot. Poor footwear is the most commonly attributed cause of lesser toe deformities, but they also can be due to heritable causes or can result from congenital and neuromuscular conditions.32,35,40,45,46,204 The terms hammer toe, mallet toe, and claw toe have been used interchangeably by various authors in describing deformities of the toes, and their definitions have been confusing. The nomenclature adopted for this book is simple, and to a certain extent, it follows that used to

Lesser Toe Deformities ■ Chapter 7

Figure 7-1 A, Mallet toe deformity involving distal phalangeal joint. B, Radiograph demonstrating mallet toe deformity.

B Figure 7-2 A, Simple hammer toe deformity with plantar flexion contracture of the proximal interphalangeal (PIP) joint. B, Complex hammer toe with hyperextension deformity of the metatarsophalangeal joint and plantar flexion contracture of the PIP joint. Although this is similar to a claw toe, it typically involves only one digit. (A, From Coughlin MJ: Lesser toe abnormalities, Instr Course Lect 52:421–444, 2003.)

describe deformities of the fingers. A mallet toe involves the distal interphalangeal (DIP) joint; the distal phalanx is flexed on the middle phalanx (Fig. 7-1). A simple hammer toe involves the proximal interphalangeal (PIP) joint; the middle and distal phalanges are flexed on the

B Figure 7-3 A, Complex hammer toe deformity involving metatarsophalangeal and proximal interphalangeal (PIP) joints. B, Lateral radiograph demonstrating severe flexion deformity of PIP joint.

proximal phalanx (Fig. 7-2A). A complex hammer toe typically involves one toe and consists of a flexion deformity of the PIP joint and hyperextension deformity of the metatarsophalangeal (MTP) joint (Figs. 7-2B and 7-3). A claw toe involves a hammer toe deformity of the 323

Part II ■ Forefoot

A A

Figure 7-4 Photograph (A) and radiograph (B) of claw toe deformities involving hammer toe deformity associated with dorsiflexion of metatarsophalangeal joint.

phalanges and dorsiflexion (extension) deformity at the MTP joint (Fig. 7-4).212 To some extent, there is an overlap in the definitions of complex hammer toes and claw toes; however, claw toes usually involve all of the lesser toes and often have an underlying neuromuscular cause. With regard to the great toe, a hammer toe can involve the interphalangeal joint. No mallet toe deformity exists in the hallux (Fig. 7-5). A claw toe deformity, which is essentially synonymous with a co*ck-up deformity of the great toe, occurs when there is also hyperextension of the MTP joint. These deformities of the lesser toes range in severity from a mild and easily correctable flexible deformity to a rigid and fixed contracture. In most cases, these deformities are acquired. Both the mallet toe and the hammer toe deformities can occur in one or several toes of the same foot35,40,45; a claw toe deformity often involves multiple toes but can occur as an isolated entity.39 These deformities occur with varying frequency among different populations, but they are much more common in shoe-wearing societies. The literature dealing with deformities of the forefoot in populations that rarely wear shoes rarely mentions the mallet toe, hammer toe, or claw toe deformities.5,71,111,233 In various surveys regarding the incidence of these deformities among industrial workers54,128 and military male recruits,102,105 the incidence of hammer toe and claw toe deformities ranged from 2% to 20%. All of these 324

Figure 7-5 A, Hammered great toe. Note articulation of distal phalanx with plantar surface of the head of the proximal phalanx. B, Hammer toe deformity of hallux.

250

224 220

Legend: Total Women Men

200

228 202

188

150

Cases

148

184

133

100 67 50 23

14 0

32 15 40

Age (years)

57 52

5 50

Figure 7-6 Hammer toe deformities peak during the fifth, sixth, and seventh decades in the female population. In the male population, there is no increase in the frequency of hammer toe deformities with increasing age. (From Coughlin MJ, Thompson FM: The high price of high-fashion footwear, Instr Course Lect 44:371–377, 1995.)

studies seem to indicate that the deformities develop slowly and insidiously and that their incidence increases almost linearly with age, peaking in the sixth and seventh decades.* These deformities occur much more commonly in women than in men (4 to 5 : 1).26,40,45,46,51 A hammer toe deformity rarely is seen in infants (Fig. 7-6).104 The incidence of forefoot surgery is unknown, but in studies of specific regional populations, Shirzad et al210 suggested *References 26, 37, 51, 141, and 201.

Lesser Toe Deformities ■ Chapter 7

these deformities constitute between 28% and 48% of all forefoot surgery. Etiology Footwear is generally considered to play an important role in the etiology of hammer toe and mallet toe deformities.32,40,45 Placing the forefoot into the constricted confines of a pointed shoe no doubt plays a major role in the onset of these deformities. The toes, to conform to a small toe box, must of necessity buckle (Fig. 7-7). This fact explains why acquired mallet toes and hammer toes are among the most common deformities of the forefoot in shoe-wearing societies (Fig. 7-8). DuVries66 thought that shoes restrict the normal movement of the joints and impedes the actions of the intrinsic muscles of the foot. It must be kept in mind, however, that anatomic predisposing factors vary extensively, and a large number of shoe wearers do escape deformities of the forefoot. Mallet Toe Other than its general relationship to pressure of the toe against the shoe, the specific cause of a mallet toe is

Figure 7-7 A, Phalanx extended to normal length. B, Buckling of the phalanx is caused by restriction of the toe box. The interphalangeal joints and metatarsophalangeal joints become subluxed. Over time, dislocation can occur.

unknown. Although most often idiopathic in nature, it can develop after a hammer toe repair or trauma,40,130 or it can be associated with inflammatory arthritis.40,41 A mallet toe can also develop after a hammer toe repair, possibly because of scarring on contracture of the long flexor tendon. The high incidence of mallet toe in the female population has led to speculation that a constricting toe box is a causative factor.34,39,40 Female subjects constituted 84% of the patient population in one reported series,42 the gender difference being highly significant. Brahms21 stated that a mallet toe is often limited to one toe, although Mann and Coughlin140 noted that the deformity can occur in more than one toe. Coughlin40 noted in his report (60 patients, 86 toes) that although 65% of patients had single toe involvement, 18% of patients had multiple toe involvement, with three to five toes affected. A mallet toe occurs with equal frequency in the second, third, and fourth toes,40 but most often the involved toe is longer than the adjacent toes (Fig. 7-9). Because of pressure against the end of the shoe, the toe becomes plantar flexed at the DIP joint. Tightness of the flexor digitorum longus tendon in patients with a mallet toe deformity can be demonstrated, but whether this tightness is a primary cause or a secondary change is not known. In young children, a tight flexor tendon can result in a flexion deformity of the PIP and DIP joint. This pediatric deformity has been termed a curly toe* and may also be associated with a delta-shaped phalanx.58 The major symptoms leading to surgical repair in the adult population include discomfort because of pressure on the tip of the toe, with callus formation or dorsal pain over the DIP joint.† *References 12, 98, 108, 179, 192, 210, and 214. † References 20, 21, 24, 39, 40, 158, and 191.

Figure 7-8 A, Clinical appearance of foot and pointed toe box of high-fashion shoe. B, Radiograph of foot without shoes showing width measuring 4 inches. C, Within high-fashion shoe, the forefoot width is compressed to 3 inches. Note constriction of toe box and lateral deviation of hallux.

325

Part II ■ Forefoot

Figure 7-9 The mallet toe and hammer toe occur most often the second toe, especially when it is significantly longer than the adjacent toes.

Figure 7-10 Types of mallet toe deformities. A, Plantar flexion and lateral deviation lead to overlapping of the third toe. B, Mallet toe deformity of the third toe leads to underlapping of the second toe. C, Curvature of the third toe impinges against the adjacent digit in the interspace. D, Multiple mallet toe deformities. E, Plantar flexion contracture of classic mallet toe. F, Callus formation on the dorsal aspect of the distal interphalangeal joint. (D, From Coughlin MJ: Lesser toe abnormalities, Instr Course Lect 52:421–444, 2003.)

Preoperative nail deformities occurred in 7% of mallet toes in Coughlin’s series, and 93% were noted to have dorsal pain or pain at the tip of the toe, with callus formation (Figs. 7-10B and F and 7-11C and D). Hammer Toe The causes of a hammer toe appear to be multifactorial. The high incidence of hammer toes in the female 326

population has led some to suggest that a constricting toe box is also a causative factor of this deformity.17,37,51,201 Coughlin45 reported that 62% of the patients in his series considered ill-fitting shoes to be a cause of their hammer toe deformity. The high incidence of female involvement has been previously reported26,51,188,196,201; females constituted 85% of the patient population in a large series,45 the gender difference being highly significant. The

Lesser Toe Deformities ■ Chapter 7

Figure 7-11 A, Molding of the toe after mallet toe repair. B, Lateral deviation after repair. C and D, Toenail deformity that preceded mallet toe repair does not improve after surgery. E, Callus at tip of toe usually resolves with time after surgical realignment.

Figure 7-12 On physical examination, a patient with severe claw toe deformities is noted to have a hairy patch over the lumbosacral spine, a condition often associated with diastematomyelia.

A hammer toe deformity may be caused by a muscle imbalance in association with neuromuscular diseases, such as Charcot-Marie-Tooth disease, Friedreich ataxia, cerebral palsy, myelodysplasia, multiple sclerosis, and degenerative disk disease. The deformity also is seen in patients with an insensate foot associated with diabetes mellitus and Hansen disease.43 Patients with rheumatoid arthritis, psoriatic arthritis, and other types of inflammatory arthritis also can develop a hammer toe deformity.37,39,43 Associated hallux valgus deformities have also been implicated as a cause of hammer toe formation.22,43,202,203 Occasionally, after fractures of the tibia or other trauma,74,203 a progressive hammer toe deformity is observed and is likely the result of nerve or muscle injury from elevated compartment pressures in the involved leg or foot.137

incidence of hammer toes is reported to increase with increasing age,26,51,201 with the peak incidence in the fifth through seventh decades. Coughlin45 noted in his report (67 patients, 118 toes) that 30% had only single toe involvement, and 40% had three or more toes involved. Although Reece,188 Coughlin,45 and others202,203,228 have reported the second toe to be the most commonly involved, Ohm170 reported an equal frequency of occurrence in the second, third, and fourth toes. Coughlin45 noted that increased length in comparison to adjacent digits might be a factor in hammer toe development, although this was not a factor in almost one half of cases.

Claw Toe The cause of a claw toe deformity often is unclear, but it may be associated with the same neuromuscular diseases, arthritic deformities, and metabolic diseases that cause hammer toe deformities (Fig. 7-12). In many patients with a severe claw toe deformity, no cause can be identified. A claw toe is a result of muscle imbalance between the intrinsic and extrinsic musculature.157,203 Simultaneous contracture of the long flexors and extensors of the toe, without the modifying action of the intrinsic muscles of the foot, causes the typical deformity seen in this condition (Figs. 7-13 and 7-14).201 Taylor,216 however, found no abnormality of the intrinsic muscles in a series of 68 327

Part II ■ Forefoot

C C

D Figure 7-13 Action of muscles in claw toe deformity (from a fresh cadaver foot). A, At rest. B, Tension on the extensor digitorum longus alone. Note extension of the metatarsophalangeal joints and minimal extension of the interphalangeal joints. C, Tension on the flexor digitorum longus alone. Note that maximal flexion occurs at the interphalangeal joints. D, Tension simultaneously on the extensor digitorum longus and flexor digitorum longus. Note the resulting deformities in all but the great toe.

patients who had claw toes and in whom the muscles were examined by gross inspection, stimulation, and histologic analysis. A claw toe deformity usually involves multiple toes and often both feet (Fig. 7-15).35 The deformity may be either rigid or flexible. It is often associated with a cavus foot, with or without a contracted Achilles tendon. Claw toes are often made worse because the patient cannot find adequate shoes, and a painful bursa develops over the PIP joint. As the claw toe deformity becomes more rigid, the toes strike the top of the shoe and the metatarsal heads are forced plantarward. As the toes subluxate dorsally, the plantar fat pad is pulled distally, and the metatarsal heads become more prominent on the plantar aspect of the foot. This deformity can result in the development of painful plantar callosities, which can ulcerate in severe cases, particularly if sensation of the foot is impaired. Anatomy and Pathophysiology An understanding of the anatomy and pathophysiology is helpful in selecting a treatment regimen. The most common deformity is the hammer toe, and this is used 328

D Figure 7-14 Action of muscles in a claw toe deformity of the hallux (from a fresh cadaver foot). A, At rest. B, Tension on the extensor hallucis longus alone. Note the extension of the metatarsophalangeal and interphalangeal joints. C, Tension on the flexor hallucis longus alone. Note the maximal flexion of the interphalangeal joints. D, Simultaneous tension on the extensor hallucis longus and flexor hallucis longus, with a resulting claw toe deformity.

as the prototype in discussing the pathophysiology of all three deformities. Extensor Digitorum Longus Muscle and Tendon The central dorsal structure of the toe is formed by the tendon of the extensor digitorum longus, which divides into three slips over the proximal phalanx; the middle slip inserts into the base of the middle phalanx, and the two lateral slips extend over the dorsolateral aspect of the middle phalanx and converge to form the terminal tendon, which inserts into the base of the distal phalanx (Fig. 7-16).198,199 The tendon is held in a central position dorsally by a fibroaponeurotic sling that anchors the long extensor to the plantar aspect of the MTP joint and to the base of the proximal phalanx. It is surprising that there is no dorsal insertion of the extensor digitorum longus into the proximal phalanx; rather, the phalanx is virtually suspended by the extensor digitorum longus tendon and its extensor sling (Fig. 7-17). The main function of the extensor digitorum longus is to dorsiflex the proximal phalanx (Fig. 7-18). Only when the proximal phalanx is held in flexion or in a neutral position at the MTP joint can this tendon become an extensor of the PIP joint. This concept is important

Lesser Toe Deformities ■ Chapter 7

Figure 7-15 A, Lateral view of foot with claw toe deformities with diagnosis of Charcot-Marie-Tooth disease. B, Lateral view of another patient’s foot; in equinus, the deformity is not obvious. The patient had a previous compartment syndrome of calf. C, Frontal view of both feet demonstrates claw toe deformity of right foot and normal left foot. D, With dorsiflexion of the ankle, the deformity substantially increases. Note scar from the previous compartment release laterally. E, Radiograph of claw toe deformity. Note articulation of base of lesser phalanges with dorsal aspect of metatarsal heads. Also note the plantar-flexed first metatarsal resulting from contracted extensor hallucis longus tendon.

Ext. longus

Interossei

Ext. digitorum longus

Extensor sling

Ext. digitorum brevis

Extensor hood Ext. brevis

Interossei

Transverse metatarsal ligament

Figure 7-16 Diagram of dorsal view of the extensor mechanism of toes. (Modified from Sarrafian SK, Topouzian LK: Anatomy and physiology of the extensor apparatus of the toes, J Bone Joint Surg Am 51:669–679, 1969.)

Ext. digitorum longus

Extensor sling

Ext. digitorum brevis

Figure 7-17 Lateral view of extensor mechanism of the lesser toe. Note that the extensor digitorum longus inserts only into the distal phalanx and secondarily suspends the metatarsophalangeal joint through the extensor sling mechanism.

Figure 7-18 Lateral view of the extensor mechanism demonstrates the main function of the extensor digitorum longus, which is to dorsiflex the proximal phalanx.

because, with a hammer toe deformity, the long extensor tendon function on the PIP joint may be neutralized by extension of the proximal phalanx.201 The flexor digitorum longus tendon inserts into the distal phalanx and flexes the DIP joint, whereas the flexor digitorum brevis inserts into the middle phalanx, flexing the PIP joint. There is no insertion into the proximal phalanx, so the long flexor tendon influence on the proximal phalanx is minimal (Fig. 7-19A). Resistance to flexion at the MTP joint is maintained in the normal toe by the long extensor. Another important factor is the reactive force of the foot against the ground, which pushes the MTP joint into extension. As a result, with the proximal phalanx in an extended position, there are no major 329

Part II ■ Forefoot

Toe from bottom Flexor digitorum brevis

Flexor digitorum longus

A Extensor tendons MTP capsule

Metatarsal head

Extensor hood and aponeurosis

Interosseous tendon

Plantar pad Transverse metatarsal Lumbrical ligament tendon

Flexor tendons

B Figure 7-19 A, Plantar view of flexor tendon insertion. B, Cross section through the metatarsal head of the lesser toe demonstrates structures that pass through this region. Note that the interossei tendons are dorsal to the transverse metatarsal ligament, whereas the lumbrical is plantar to it. MTP, metatarsophalangeal.

Ext. tendon

Lumbrical

Ext. hood

Flexor tendon

Figure 7-20 Lateral view of a lesser toe demonstrates that both tendons of the intrinsic muscles pass plantar to the axis of motion of the metatarsophalangeal joint, thereby flexing it. They pass dorsal to the axis of motion of the proximal and distal interphalangeal joints, thereby extending them. The lumbrical does not insert into the phalanx but into the extensor hood, and it is thus is a strong extensor of the interphalangeal joints.

motor antagonists to the long and short flexors; thus the toe buckles, resulting in flexion of the DIP joint and the PIP joint. Over a long period of time, if this position becomes fixed, a hammer toe deformity occurs. Interosseous Tendons The interosseous tendons are located dorsal to the transverse metatarsal ligament, and the lumbricals are located plantar to this ligament (Fig. 7-19B). Both tendons of the intrinsic muscles, however, pass plantar to the axis of motion of the MTP joint, flexing the MTP joint (Fig. 7-20), and pass dorsal to the axis of the PIP joint and DIP joint, extending these joints. This is an important concept to understand when performing a Weil osteotomy of the 330

Osteotomy

Interosseous tendon

Transverse metatarsal ligament

Interossei

C Figure 7-21 Axis of the metatarsophalangeal joint before and after Weil osteotomy. A, Lesser metatarsal before ostotomy; note intrinsics are plantar to the axis. B, Osteotomy is above the center of the metatarsal head. C, After the osteotomy and proximal translation of the capital fragment, the intrinsics course dorsal to the axis of rotation. This can lead to metatarsophalangeal joint dorsiflexion.

distal metatarsal; the center of MTP joint rotation is shifted plantarward, effectively making the intrinsic musculature MTP joint dorsiflex, which can lead to the development of a hyperextension deformity of the MTP joint (Fig. 7-21).224,231,232 The plantar and dorsal interossei have only a few fibers that reach the extensor sling and therefore are weak extensors of the interphalangeal joints. The lumbrical, with all of its fibers terminating in the extensor sling, is a stronger extensor of these joints. The interossei flex the proximal phalanx by their direct attachment to the base of the proximal phalanx, whereas the lumbrical achieves flexion by placing tension on the extensor sling (Fig. 7-22). With marked dorsiflexion at the MTP joint, the lumbrical flexion power is quite limited because it is pulling at a 90-degree angle. Plantar Plate and Collateral Ligaments The most significant stabilizing factor of the MTP joint is the plantar plate, a combination of the plantar aponeurosis and plantar capsule.* During the walking cycle, varying degrees of dorsiflexion occur at the MTP joint. The static resistance of the plantar capsule combines with the dynamic force of the intrinsic flexors to pull the proximal phalanx back into a neutral position at the MTP joint (Fig. 7-23A). With chronic hyperextension forces on the *References 43, 47, 50, 182, and 201.

Lesser Toe Deformities ■ Chapter 7

Interossei

Ext. tendon

Flexor tendon Lumbrical

A A

Figure 7-22 A, Lateral aspect of a lesser toe with portion of the extensor hood removed to demonstrate insertion of the interossei into the base of the proximal phalanx. This insertion permits the interossei to plantar flex the proximal phalanx on the metatarsal head. B, Anatomic dissection demonstrating extensor hood and intrinsics. A, central axis of metatarsophalangeal joint; B, lumbrical; C, interossei.

proximal phalanx, the plantar plate can become stretched or attenuated and rendered less efficient (Fig. 7-23B). The lesser MTP joint is stabilized by both the collateral ligaments and the plantar plate.8,61,62 (Fig. 7-23C and D). The plantar plate inserts on the base of the proximal phalanx, but it is attached to the metatarsal head by only a thin layer of synovial tissue that inserts just proximal to the articular surface.61 The distal attachment of the plantar plate is composed of a medial and a lateral bundle. Proximally, the plantar plate forms the major attachment of the plantar aponeurosis. The plantar plate is the central stabilizing structure that determines the position of the flexor digitorum longus. The collateral ligaments are composed of two major structures: the phalangeal collateral ligament (PCL), which inserts onto the base of the proximal phalanx, and the accessory collateral ligament (ACL), which inserts onto the plantar plate (Fig. 7-23E).61 The transverse metatarsal ligament attaches to the adjacent medial and lateral borders of the plantar plate.115 Pathophysiology Fortin and Myerson78 reported that the collateral ligaments were the primary stabilizers of the lesser MTP joint. When the collateral ligaments were sectioned in vitro, 48% less force was required to dislocate the lesser MTP joint. When the researchers did an isolated release of the plantar plate, 29% less force was required to dislocate the MTP joint. The position of the proximal phalanx at the MTP joint is subject to the actions of the strong extensor digitorum

Plantar plate and capsule

PCL

Elongated or rupture of plantar plate and capsule

ACL

1. Zone of rupture

Figure 7-23 A, Diagram demonstrates the plantar plate and the capsule of the metatarsophalangeal (MTP) joint, which is sufficiently resilient to bring the MTP joint back into a neutral position after the joint has been dorsiflexed at lift-off. B, Lateral view diagram illustrates the effects of the elongated plantar plate and capsule and area of rupture. As a result of certain disease states, the capsular structures no longer are sufficient to restore the joint to its normal position after lift-off. C, Dorsal view with removal lesser metatarsal head; a tear or rupture off of the base of the proximal phalanx may occur. Note 1, which is the potential zone of plantar plate rupture, and 2, which is the proximal loose synovial attachment at proximal extent of metatarsal articular surface, where a rupture rupture rarely occurs. D, Clinical photograph of partial plantar plate rupture (arrow points to grade I rupture of lateral plantar plate). E, Diagram of collateral ligaments of the lesser MTP joint. The PCL inserts on the plantar tubercles of the proximal phalanx, and the ACL inserts in a broad expansion into the edge of the plantar plate. ACL, accessory collateral ligament; PCL, phalangeal collateral ligament.

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longus through its sling mechanism, in opposition to the decidedly weaker antagonistic intrinsic muscles and the more static capsule and plantar aponeurosis complex. The positions of the middle and distal phalanges, on the other hand, are subject to the forces of the long and short flexors, which are directly opposed by the weaker intrinsic muscles. At each of these joints, an obvious mismatch can occur, and in each case, the extrinsic muscle overpowers the intrinsic muscle (Fig. 7-24). The extensor digitorum longus helps extend the interphalangeal joints if the proximal phalanx is not hyperextended, and the flexor digitorum longus helps to flex the MTP joint if the proximal phalanx is not hyperextended. The hyperextended proximal phalanx, then, is definitely the key to the production of most hammer toe deformities. With a chronic hyperextended position of the proximal phalanx, maintained throughout the entire walking cycle (by wearing high-heeled shoes), the plantar structures gradually become stretched and inefficient, and thus the proximal phalanx remains in a chronically

EDL

Intrinsics

Flexors Intrinsics Figure 7-24 Diagram demonstrates the relationship of the intrinsic and extrinsic muscles about a lesser toe. The smaller intrinsics are overpowered by the extrinsics, leading to a hammer toe deformity. EDL, extensor digitorum longus.

dorsiflexed position. Therefore, with chronic extension of the proximal phalanx, the extensor digitorum longus tendon loses its tenodesing effect on the interphalangeal joints, allowing the distal phalanges to migrate into flexion. As the proximal phalanx extends, the extrinsic flexors are under greater tension, further increasing the flexion deformity at the PIP joint. The only counteracting forces to this flexion deformity are the lumbricals and the interossei, which are easily overpowered by the long flexor tendons. Preoperative Evaluation Physical Examination When examining a foot with a lesser toe deformity, it is important to assess the circulatory status of the lower extremity. Although some surgical procedures require limited exposure, other procedures require extensive dissection at the MTP joint, at the interphalangeal joints, and even along both the medial and lateral aspects of the phalanges. Whether an individual digit can withstand multiple procedures and extensive surgical exposure depends on the vascular status of the digit. Preoperative evaluation is necessary to assess not only the feasibility of an individual procedure but also whether multiple procedures can be performed if necessary. The sensory status of a foot must be evaluated as well. An impaired sensory status can indicate a systemic disease, such as diabetes, a peripheral neuropathy, or lumbar disk disease. Careful physical examination is necessary to differentiate MTP joint pain from an interdigital neuroma of the adjacent interrmetatarsal space (Fig. 7-25).48,49 Preoperative documentation of sensation is important because a surgical dissection can diminish postoperative sensation. The plantar aspect of the foot is examined for development of intractable plantar keratoses. Callosities can develop in association with contractures of the lesser toes,

Figure 7-25 The diagnosis of combined metatarsophalangeal instability and an adjacent interdigital neuroma is uncommon and difficult to make. A, Medial deviation of the second toe with exposure of enlarged symptomatic interdigital neuroma. B, After Weil osteotomy to realign the second toe and excision of the interdigital neuroma.

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Figure 7-26 A, With a hammer toe deformity, a callus has developed at the tip of the second toe. B, A toe cradle. C, The cradle is used to decrease pressure beneath the tip of the lesser toe. (C, From Coughlin MJ: Lesser toe abnormalities, Instr Course Lect 52:421–444, 2003.)

the result of a buckling effect of the toes. A patient typically complains of pain caused by a callus over the distal aspect of the PIP joint but also can develop pain beneath the tip of the toe or a lesser metatarsal head (Fig. 7-26).45,135 Realignment of the MTP joint and interphalangeal joints can decrease plantar pressure and help relieve symptomatic calluses. The individual digits are examined for callosities on the medial and lateral aspects, as well as over the interphalangeal joint and at the tip of the toe. With a fixed hammer toe deformity, callosities can develop over the contracted PIP joint as well as at the tip of the toe. Toenail deformities can develop as well. The alignment of the MTP joint must be evaluated.201 Medial or lateral deviation of the toe should be noted, as well as an MTP joint hyperextension deformity. The stability of the digit is assessed by the drawer test. The digit is grasped between the thumb and index finger of the examiner, and with the digit slightly dorsiflexed, dorsal pressure is placed on the digit in an attempt to subluxate the MTP joint (Fig. 7-27). Even if the toe is not subluxed, the eliciting of pain with this maneuver is indicative of an intraarticular or periarticular abnormality. (See further discussion under subluxation second MTP joint.) Although the evaluation of a hammer toe deformity may be seen as relatively simple, certain factors must be carefully considered to fully appreciate the nature of the deformity. These include the rigidity of the toe contractures (Fig. 7-28), the position of the MTP joint (Fig. 7-29A), and Achilles tendon tightness with the patient both sitting and standing. Tightness of the flexor digitorum longus tendon must be assessed along with examination of all of the lesser toes. Also, it is important to determine whether there is sufficient space for the involved toe when it is reduced to a normal position. The presence of prior surgical scars can influence the planned surgical exposure.

Radiographic Examination Although a physical examination is necessary to define the extent of a lesser toe deformity, radiographic examination is necessary to evaluate the magnitude of the bone deformity (Fig. 7-29B). On an anteroposterior (AP) projection, a severe hammer toe deformity can have the appearance of a gun barrel deformity (Fig. 7-29C) when the proximal phalanx is seen end on. Assessment of the interphalangeal joints is difficult on this projection. Diminution of the MTP joint space can indicate subluxation, and overlap of the base of the proximal phalanx in relation to the metatarsal head can indicate dislocation of the MTP joint (Fig. 7-30). Medial or lateral deviation of the MTP joint can be determined as well. Subchondral erosion, flattening of the articular surfaces, or a Freiberg infraction can indicate the need for further radiographic or laboratory evaluation. A lateral radiograph may be helpful to assess the magnitude of contracture of the interphalangeal joints (see Fig. 7-29B). Stress radiographs can help to determine subluxability of the MTP joint (see Fig. 7-27). Bone scans, computed tomography (CT), and magnetic resonance imaging (MRI) evaluation may also be used to increase information of both osseous and soft tissue abnormalties (Fig. 7-31). FIXED HAMMER TOE DEFORMITY

Preoperative Planning A hammer toe deformity may be flexible, semiflexible, or rigid.* If the deformity is flexible, the toe may be passively corrected to a neutral position. However, if the deformity is rigid, joint contractures preclude passive correction. The rigidity of the deformity determines *References 2, 32, 35, 45, 140-142, 210, and 212.

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Figure 7-27 Drawer test for metatarsophalangeal (MTP) joint instability. A, The toe is grasped between the thumb and second finger. B, With dorsal force, an attempt is made to subluxate the MTP joint. With instability of the MTP joint, pain is elicited with stress on the plantar structures. C, Lateral radiograph of unstable second MTP joint before drawer test. D, Lateral radiograph after drawer test with the base of the proximal phalanx subluxed dorsally. E, Before dorsal subluxation of metatarsophalangeal joint with drawer test. F, Position of the base of the toe after dorsal subluxation.

Figure 7-28 A hammer toe deformity is inspected to determine its flexibility. A, Fixed deformity. B, Flexible deformity.

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Figure 7-29 A, Hammer toe deformity demonstrates severe hyperextension. B, Lateral radiograph demonstrates hyperextension deformity of the proximal phalanx. C, Anteroposterior radiograph demonstrates the gun barrel sign. The proximal phalanx is seen end on, superimposed over the condyle. This conformation is pathognomonic of hyperextension deformity of the proximal phalanx.

Figure 7-30 A, A 52-year-old man with pain at the second metatarsophalangeal (MTP) joint and a slight hallux valgus deformity. B, Six-month follow-up demonstrates narrowing of the joint space, pathognomonic of a hyperextension deformity. Often subluxation can occur insidiously. C, At 15-month follow-up, the second MTP joint has dislocated.

Figure 7-31 Patient with ill-defined forefoot pain. A, Clinical location of pain. Technetium-99m (99mTc) bone scan, anteroposterior (B) and lateral (C) views, can demonstrate pathologic changes before radiographic changes. Note the increased uptake in the area of the second metatarsophalangeal joint.

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Figure 7-32 An isolated hammer toe repair or a flexor tenotomy can lead to hyperextension deformity of the involved toe.

whether conservative or surgical treatment is indicated, as well as the specific surgical procedure that should be performed. The position of the MTP joint when the patient is standing must be carefully evaluated. If a hyperextension deformity is present, correction of only the hammer toe deformity will result in the toe sticking up in an extended position (Fig. 7-32), making shoe wearing difficult. If the MTP joint is subluxated or dislocated, this deformity should be corrected simultaneously with the hammer toe correction.43,72,133,141,179 Tightness of the flexor digitorum longus tendon should be carefully observed with the patient in a standing position. If the flexor digitorum longus tendon appears to be tight in the toe adjacent to the involved toe, the involved toe probably also has a contracture of the flexor digitorum longus tendon. In this case, the tendon should be released in the deformed toe at surgery or the deformity will probably recur over time (Fig. 7-33). Another consideration in the treatment of a hammer toe is that there must be sufficient space for the corrected toe to occupy (Fig. 7-34A). If a patient has a concomitant hallux valgus deformity that has diminished the interval between the first and third toes and forced the second toe into dorsiflexion, adequate space must be obtained for the corrected lesser toe or the deformity can recur.140 An Akin phalangeal osteotomy may be used to create room for a second toe when a hammer toe correction is performed.179 A hallux valgus repair may be necessary to obtain sufficient space between the first and third toes to realign the second toe successfully. At times, the adjacent lesser toes can drift into medial or lateral deviation, again diminishing the interval that the corrected toe should occupy. These toes may need to be corrected to afford the corrected hammer toe adequate space. A young patient with a flexible deformity is a candidate for conservative treatment. Likewise, an older patient with multiple medical problems may be a poor surgical candidate as well. The most important conservative measure 336

B Figure 7-33 With a tight flexor tendon in an adjacent toe, a flexor tenotomy should be performed at the time of hammer toe repair. A, Contracture of just the second toe indicates a flexor tenotomy is possibly not necessary. B, A contracture is noted in all of the lesser toes. (B, From Chapman M, editor: Operative orthopaedics, Philadelphia, JB Lippincott, 1988, pp 1765–1776.)

is for the patient to acquire roomy, well-fitted shoes.51,212 The preferable characteristics of such shoes include a high and wide toe box and a soft sole with a soft upper portion of the toe box. This helps to prevent direct pressure against a hammer toe and subsequent development of painful callosities. Local treatment can consist of a doughnut-shaped cushion, foam toe cap (Fig. 7-34B), foam tube-gauze, or viscoelastic toe sleeves placed over the PIP joint (Fig. 7-34C-F).2,210,212 Shoes with a stiff insole or a rocker-type outer sole may relieve pressure on the forefoot and diminish metatarsalgia (Fig. 7-35). The shoe itself might need to be modified if the patient has pain beneath the metatarsal head. Such a modification can consist of a soft metatarsal support, a metatarsal bar, or a comfortable orthosis that relieves pressure beneath the involved metatarsal head. At times, patients modify their shoes to reduce pressure on a symptomatic hammer toe (see Fig. 7-34G and H). A toe cradle can elevate the involved digit and reduce pressure on the tip of the toe (see Fig. 7-26B and C). In more advanced cases and with multiple toe involvement, an extra-depth shoe with a polyethylene foam (Plastazote) insole can help to distribute pressure more uniformly on the plantar aspect of the foot. A program with daily manipulation of the toes should be started to try to keep the toes flexible.

Lesser Toe Deformities ■ Chapter 7

Figure 7-34 A, A hallux valgus deformity can reduce the space available for the second toe once the hammer toe has been corrected. B, A toe cap may be used to decrease pressure on the distal tip of the hammer toe. C and D, Various types of tube gauze may be used to pad a lesser toe deformity. E and F, Tube gauze is slid over the symptomatic toe to relieve pressure. G, Patient has modified footwear to make room for the prominent second toe. H, A shoe may be modified as in this case by a patient with a bunion, bunionette, and hammer toe deformity.

Figure 7-35 A and B, Examples of roomy shoes. Rocker sole with stiff insole may provide increased depth to the toe box and a stiff insole to diminish lesser toe joint excursion.

A traumatic boutonnière deformity can develop with a hammer toe deformity (Fig. 7-36). Rau and Manoli187 initially reported on this rare deformity, which is caused by a rupture of the central extensor slip. As the lateral bands displace, they become flexors of the PIP joint. A flexion deformity of the PIP joint occurs and is associated with a hyperextension deformity of the DIP joint. The authors recommended a direct repair of the central slip and recentralization of the lateral bands. Quebedeaux et al185 reported on two cases of traumatic boutonnière deformity; one developed in association with chronic rheumatoid arthritis and was treated conservatively, and the other one developed after trauma. A delayed repair and PIP arthroplasty were performed. If a deformity of the MTP joint exists along with a hammer toe deformity (a complex hammer toe

deformity), surgical correction of this deformity also must be considered. In cases of a mild deformity, an extensor tenotomy or lengthening may be sufficient to achieve correction. In cases of a moderate hyper extension deformity of the MTP joint, an extensor tenotomy and MTP capsule release may be necessary.64 Kirschner wire fixation also may be necessary to stabilize the arthroplasty site as well as the MTP joint. A flexor tendon transfer also may be necessary to achieve stability of the MTP joint. Where subluxation has progressed to frank dislocation of the MTP joint, the soft tissue procedures described are inadequate to achieve reduction, and a metatarsal osteotomy is necessary. (A complete discussion of the evaluation and treatment of MTP joint subluxation and dislocation is presented later in the chapter.) 337

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Figure 7-36 A, Traumatic boutonnière deformity of the second toe. B, A traumatic swan-neck deformity has occurred with development of a mallet toe as well as hyperextension of the proximal interphalangeal joint.

With time, and even with appropriate conservative management, most of these deformities become fixed and often require surgical correction.* The algorithm presented in Figure 7-37 is a useful guide to treatment of the hammer toe deformity. If surgery is required, it is important that the procedure be carefully selected, depending on the specific cause and type of the deformity. Indications The DuVries arthroplasty is recommended for reduction of a fixed hammer toe deformity involving the middle three toes. This procedure does not necessarily achieve a joint fusion; it can achieve a fibrous union that usually allows approximately 15 degrees of motion. The arthroplasty may be performed under a digital anesthetic block if there is no MTP joint involvement. If there is an MTP joint deformity, more extensive anesthesia is necessary.

Flexible

Fixed

Flexor tendon transfer

Condylectomy, proximal phalanx

Hyperextended proximal phalanx (MTP joint stable)

Contraindications Contraindications include acute or chronic infection, vascular insufficiency, and flexible deformities for which a resection arthroplasty is not necessary. Relative contraindications include more severe deformities involving the MTP joint, for which more extensive surgery must be combined with the DuVries arthroplasty to realign the digit completely. DUVRIES ARTHROPLASTY PROCEDURE Surgical Technique 1. The patient is placed in a supine position on the operating room table. The foot is cleansed and draped in the usual fashion. The use of a 1 4 -inch Penrose drain as a tourniquet is optional. If MTP joint surgery is *References 2, 34-37, 45, 169, 210, and 212.

338

Kirschner wire fixation

Realigned toe

Metatarsophalangeal soft tissue release • Dorsal capsular release • Medial or lateral capsular release • Extensor tendon lengthening

Kirschner wire fixation

Figure 7-37 Algorithm for treatment of hammer toe deformity.

Lesser Toe Deformities ■ Chapter 7

Figure 7-38 Technique for repair of a hammer toe deformity. A, Elliptic incision over the proximal interphalangeal (PIP) joint excises callus, if present, along with the extensor tendon and joint capsule. B, Removal of extensor tendon and joint capsule along lines of incision. C, When a knife blade is placed flat against the condyles, the collateral ligaments are cut, thereby delivering the head of the proximal phalanx into the wound. D, Excision of the head of the proximal phalanx proximal to the flare of the condyles. E, Condyles have been removed. At this time, a decision is made as to whether to perform a flexor tenotomy. If a flexor tenotomy is done, the plantar capsule is incised, and the long flexor tendon is incised in the depths of the wound. F, A 0.045-inch Kirschner wire is introduced at the PIP joint and driven distally, exiting the tip of the toe. The PIP joint is reduced, and the pin then is driven retrograde, stabilizing the repair. G, Alternative means of stabilization. Insertion of vertical mattress suture of 3-0 nylon. The deep portion of the suture approximates the extensor tendon, and the superficial portion of the suture coapts skin edges. The Telfa bolster is used to gain leverage to hold the toe in satisfactory alignment. H, The toe is held in satisfactory alignment after placement of sutures and bolsters.

performed, an Esmarch bandage can be used to exsanguinate the extremity and as an ankle tourniquet.91 A digital block or regional anesthesia is used for anesthesia, depending upon the need for additional surgical procedures at the same time. 2. An elliptic or longitudinal incision210 is centered over the dorsal aspect of the PIP joint, excising the callus, extensor tendon, and joint capsule, thereby exposing the PIP joint (Figs. 7-38A and 7-39A and Video Clip 75). 3. The collateral ligaments on the medial and lateral aspects of the proximal phalanx are severed to allow the condyles of the proximal phalanx to be delivered into the wound (see Figs. 7-38B and C and 7-39B and C). Care is taken to protect the adjacent neurovascular bundles. 4. The head of the proximal phalanx is resected just proximal to the flare of the condyles, and any prominent edges are smoothed with a rongeur (see Figs. 7-38D and 7-39D). 5. At this point, the toe should be brought into corrected alignment. If there still appears to be tension at the PIP joint, so that it is difficult to adequately correct the deformity, more bone should be resected. Also, consideration should be given to release of the flexor digitorum longus through this wound (see Figs. 7-38E and 7-33).

6. If a flexor tenotomy is performed, the plantar capsule of the PIP joint is carefully incised, and the long flexor tendon is identified in the flexor tendon sheath. The tendon is transected and allowed to retract. 7. The articular surface of the base of the middle phalanx may be resected with a rongeur.221 This is optional.35,45 8. A 0.045-inch Kirschner wire is introduced at the PIP joint and driven distally, exiting the tip of the toe. With the toe held in proper alignment, the pin is driven in a retrograde fashion to stabilize and align the toe. The wire is then bent at the tip of the toe and the excess pin removed (see Figs. 7-38F and 7-39E). The Kirschner wire has enough flexibility that it can be bent at the operative site to alter the alignment when necessary.68 9. The wound is closed with vertical interrupted mattress sutures of 3-0 nylon (see Fig. 7-38F). Alternative Fixation and Joint Preparation A vertical mattress-type suture using 3-0 nylon and incorporating two Telfa bolsters is inserted. As the suture is tightened, a certain degree of leverage is placed on the toe to bring it into satisfactory alignment (Fig. 7-40, see Fig. 7-38G and H). This technique is much less commonly used. On the other hand, in an effort to secure permanent fixation without the use of Kirschner wires, several reports 339

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Figure 7-39 Hammer toe deformity of the second toe. A, After a longitudinal skin excision, the dorsal capsule and extensor tendon are exposed. B, Removal of extensor tendon and joint capsule along the lines of the incision. C, The collateral ligaments and plantar capsule are released. D, Exposing the condyles of the proximal phalanx, which are excised. (After excision of the head of the proximal phalanx, a flexor tenotomy may be performed; also, the articular surface of the base of the middle phalanx may be resected.) E, Kirschner wire fixation. F, After completion of repair.

have described the use of intramedullary fixation for hammer toe correction. Absorbable implants,125,180 screw fixation27,131,227 (Figs. 7-41 and 7-42), wire loops,99 and other permanent intramedullary devices2,69,193 (Fig. 7-43) have all been reported. Weil230 described the use of conical reamers for preparation of the joint surfaces to aid in achieving proper alignment and coaptation of the surfaces. No series have been published on this technique. HAMMER TOE REPAIR WITH INTERMEDULLARY IMPLANT (NITINOL, SMART TOE IMPLANT)2,193 Surgical Technique 1. The patient is placed in a supine position on the operating room table. The foot is cleansed and draped in the usual fashion. The use of a 1 4 -inch Penrose drain as a tourniquet is optional. If MTP joint surgery is performed, an Esmarch bandage can be used to exsanguinate the extremity and as an ankle 340

tourniquet.91 A digital block or regional anesthesia is used for anesthesia, depending upon the need for additional surgical procedures at the same time. 2. A longitudinal incision is centered over the dorsal aspect of the PIP joint. A daper elliptical incision excises the callus, extensor tendon, and joint capsule, thereby exposing the PIP joint (Fig. 7-44A and B and Video Clip 76). 3. The collateral ligaments on the medial and lateral aspects of the proximal phalanx are severed to allow the condyles of the proximal phalanx to be delivered into the wound (Fig. 7-44C). Care is taken to protect the adjacent neurovascular bundles. 4. The head of the proximal phalanx is resected at the metaphyseal–diaphyseal junction, and any prominent edges are smoothed with a rongeur (Fig. 7-44D and E). 5. If a flexor tenotomy is performed, the plantar capsule of the PIP joint is carefully incised, and the long flexor

Lesser Toe Deformities ■ Chapter 7

digit in the first few weeks after surgery can lead to recurrent deformity and must be avoided. Results and Complications

C Figure 7-40 A, Proposed area of bone resection. B, After bone resection, stabilization with intramedullary Kirschner wire. C, Stabilization with sutures and Telfa bolsters.

tendon is identified in the flexor tendon sheath. The tendon is transected and allowed to retract. 6. The articular surface of the base of the middle phalanx may be resected with a rongeur.193 7. A 2-mm drill is introduced at the PIP joint and driven both proximally and distally (Figure 7-44F). 8. A broach enlarges each canal (Fig. 7-44G), and then the temperature-sensitive implant is removed from the refrgierated storage area and immediately inserted into the prepared intramedullary canal (Fig. 7-44H and I). 9. The middle phalanx is then positioned adjacent to the prepared surface of the proximal phalanx and held securely while the implant expands and stabilizes the digit. The position of the implant is verified under fluoroscopy (Fig. 7-44J). 10. The wound is closed with vertical interrupted mattress sutures of 3-0 nylon. Postoperative Care A small compression dressing is placed around the toe, and the patient is allowed to ambulate in a postoperative wooden shoe. If Telfa bolsters have been used, the suture and bolsters are removed 1 week after surgery. The bolsters should not be left in place for more than 1 week because of the possibility of skin necrosis developing beneath them. If a Kirschner wire has been used, the sutures and Kirschner wire are removed 3 weeks after surgery. In either case, it is important to support the toe with tape for the next 4 to 6 weeks after internal or external fixation has been removed. Localized trauma to the

Ohm et al170 reported on 25 patients (62 hammer toe repairs); hammer toes were corrected with a digital fusion technique. An equal number of corrections were performed on the second, third, and fourth toes. At shortterm follow-up, a 100% fusion rate was reported. Newman and Fitton169 reported on results in 19 patients treated with a similar technique and surprisingly noted only 40% satisfactory results. Coughlin et al45 reported on the results of a DuVries condylectomy in one of the largest studies (67 patients, 118 toes). Patients were evaluated at an average of 5 years after proximal phalangeal condylectomy, middle phalangeal articular resection, and intramedullary Kirschner wire fixation. Fusion of the PIP joint occurred in 81% of cases, and subjective satisfactory results were observed in 84% of cases. Pain relief in 92% of patients was no different in those with a fibrous or a bony union, although many reports suggest that a fibrous union is consistent with a successful outcome.* O’Kane et al171 reported their results with excisional arthroplasty in 75 patients (100 toes). They used suture fixation as opposed to intramedullary Kirschner wires and reported a high complication rate (31%). Although they did not report angular measurements, malalignment was a common occurrence (rotation, extension, axial plane malalignment), probably because of their lack of internal fixation. This lack of fixation allowed a higher rate of “toe-touch” with plantar flexion (mild recurrence) at the operative site. Suprisingly, patients were allowed, even with a lack of internal fixation, to return to regular shoes 2 weeks after surgery. Higgs104 stated that a fibrous union placed the digit at risk for recurrent deformity. This notion was not confirmed by Coughlin’s series.45 Although a PIP fusion is not necessarily the ultimate objective, increased stiffness or fusion of the PIP joint appears to help maintain alignment. Kelikian121 observed that resection of both articular surfaces leads to a satisfactory result if it is followed by stiffness of the joint. The goal of surgery is to correct the deformity and maintain the correction. Although some authors advocate attempted arthrodesis,1,213,221,237 others have stated that a PIP joint resection suffices as treatment by achieving adequate alignment of the toe.45,53,88,198 A fusion of the PIP joint or an arthrofibrosis succeeds by converting the pull of the flexor digitorum longus to flex the MTP joint. A fusion also gives triplanar stability to the toe. The rate of pseudoarthrosis in attempted PIP joint fusions approaches 50% in some series, although some surgeons have obtained a high fusion rate (>90%) with a peg-and-dowel technique.1,135,202 Pichney et al and others155,179 have used a V-type arthro desis technique for correcting a hammer toe deformity *References 53, 104, 122, 169, 170, 203, 206, and 228.

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Figure 7-41 Examples on intramedullary screws for hammer toe fixation. A, Placement of intramedullary Kirschner wire and cannulated screw from the tip of the toe. B, Cannulated screw fixation. C, Preoperative radiograph demonstrating subluxation of second and third metatarsophalangeal (MTP) joints and hammer toes of second and third toes. D, After intramedullary hammer toe fixation and distal osteotomies of second and third metatarsals. E, Intramedullary Herbert-type screws placed from the tips of the toes for treatment of hammer toe deformities. Note marked lesser MTP joint subluxation. (A and B, From Lane G: Lesser digital fusion with a cannulated screw, J Foot Ankle Surg 44:172–173, 2005. Used with permission. C and D, Courtesy George Lane, DPM.)

with good success. Lehman and Smith135 reported on PIP arthrodesis, noting a 50% satisfaction rate with a pegand-dowel technique. Major reasons for postoperative dissatisfaction were toe angulation and incomplete relief of pain. Because of the straight nature of the fusion, toe tip elevation (a “floating toe”) was noted in 14% of cases. Transverse plane angulation was observed in 11%. Forty-four percent of patients developed flexion at the DIP joint, a finding also noted by Schlefman et al202 in their series. Ohm et al170 and Schlefman et al202 noted that more bone resection was necessary for a peg-and-dowel technique. Shortening, however, is a common complaint after this technique of hammer toe repair. Any attempt at arthrodesis may place the digit in “too straight” a position. Although intrameduallary devices 342

may increase the incidence of successful fusion, they may be predisposed to a straight toe that does not necessarily touch the ground and may be a source of dissatisfaction. On the other hand, the development of transverse plane deformities, which can occur with inadequate hammer toe fixation, are equally unpopular. Attempts at more permanent fixation have been reported. Lane,131 Caterini et al,27 and Vitek227 have reported the use of either a distally introduced intra meduallary screw27,131 or an oblique screw fixation227 (see Figs. 7-41 to 7-43). Vitek227 reported a 93% fusion rate. Caternini et al27 reported a similar fusion rate; however, this technique sacrifices the DIP joint with fixation that crosses both interphalangeal joints. Konkel et al125 reported the use of an absorbable intramedullary pin for

Lesser Toe Deformities ■ Chapter 7

Figure-7-42 Example of screw fixation with hammer toe repair. A, Clinical preoperative photograph and, B, radiograph of hammer toe deformities of second and third toes. C, Postoperative clinical photograph and, D, radiograph after placement of oblique proximal interphalangeal joint screw fixation. (Courtesy M. Vitek, DPM.)

Figure 7-43 Examples of intramedullary fixation for hammer toe repairs. A, Stayfuse (Tornier, Minneapolis, Minn.), with correction of deformity. B, Ipp-On (Integra, Plainsboro, N.J.), with correction of deformity. C, Pro-Toe (Wright Medical, Memphis Tenn.), preoperative anteroposterior (AP) view. D, After implant placement in lateral four toes, with hallux interphalangeal (IP) joint arthrodesis. E, Smart Toe (Stryker, Kalamazoo, Mich.), with extra Kirschner wire fixation. (A, From Ellington JK, Anderson RB, Davis WH, et al: Radiographic analysis of proximal interphalangeal joint arthrodesis with an intramedullary fusion device for lesser toe deformities, Foot Ankle Int 31:372–376, 2010. Used with permission. C, Courtesy C. Hirose, MD. D, Courtesy T.J. Kemp, MD.)

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Figure 7-44 Hammer toe repair with Nitinol implant. A, Dorsal longitudinal incision. B, Excision of dorsal capsule. C, Release of collateral ligaments. D, Resection of condyles of proximal phalanx. E, Flat surfaces are created on both middle and proximal phalangeal surfaces. F, 2-mm drill hole is placed in each of the phalanges. G, The canals are broached. H, The implant is removed from refrigerated source. I, The implant is placed in the proximal phalanx and then placed in the middle phalanx. J, Postoperative fluoroscopy showing implant and additional Kirschner wire.

fixation of a hammer toe repair. A 73% union rate was noted. Three mallet toes and eight transverse plane deformities were reported, as well as a similar rate of “floating toes.” Others have used an intramedullary implant placed at the operative site that does not traverse the DIP joint: the Smart Toe (Stryker, Kalamazoo, Mich.),18,193 the Stayfuse (Tornier, Minneapolis, Minn.),69 the Ipp-On (Integra, Plainsboro, N.J.), and the Pro-Toe (Wright Medical, Memphis, Tenn.). Ellington et al69 reported a 60% union rate in 38 toes, and sagittal or coronal plane malalignment in 18% of cases (Fig. 7-45). Only three patients had revision surgery; the authors felt the implant assisted in maintaining alignment despite a union rate very similar to Kirschner wire fixation. Roukis193 reported his results with the Smart Toe in 30 toes. The fusion rate was 93%; malunion occurred in 7%. No reports on the Pro-Toe have been published. The advent of intrameduallary fixation may reduce recurrence rate,* although these changes in technique and fixation will have to be weighed against the increased cost of the implants. Malalignment is often a major reason for dissatisfaction.45,68,125 Malalignment can occur in any one of three *References 2, 27, 69, 125, 131, 180, 193, and 227.

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planes–medial–lateral, dorsal–plantar, or rotational. Also, a hammer toe can develop in an adjacent nonoperated toe. A patient should be warned that there is a possibility of developing deformities in other toes. The development of a mallet toe deformity after a hammer toe repair is uncommon but can occur as well.125,193 The results of hammer toe repairs are in general most gratifying, and few, if any, complications are routinely reported. Swelling of the toe can persist for 1 to 6 months after the procedure.135,170,182 Almost invariably, however, the swelling subsides if given sufficient time (Fig. 7-46). Coughlin45 noted that no patient had digital swelling at long-term follow-up. Alternative treatments for hammer toe deformities include either a diaphysectomy or partial proximal phalangectomy (Fig. 7-47). McConnell148,149 reported on a large series of patients treated with diaphysectomy of the proximal phalanx to correct a hammer toe deformity (Fig. 7-48). Satisfactory results were reported with this procedure. McConnell stated that “most cases heal by bony union.” The actual alignment of the toe, complications, and rate of nonunion were not described in the report. A diaphysectomy is a useful procedure to treat a hammer toe and obtain shortening of a toe that is significantly longer than adjacent toes.

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Partial proximal phalangectomy has been recommended by Johnson114 and others25,28,55,73 (Figs. 7-49 and 7-50) as a treatment for a hammer toe deformity in association with MTP joint deformity. Cahill and Connor25 reported on 78 patients (84 toes). They noted poor objective results in 50% of patients and concluded that partial proximal phalangectomy relieved symptoms but left a cosmetically poor end result (Fig. 7-51). Conklin and Smith30 noted a 29% postoperative dissatisfaction rate; major complaints were shortening of the ray, floppiness of the toes, metatarsalgia, weakness, and stiffness.

Figure 7-45 Broken implant with recurrent deformity. (From Ellington JK, Anderson RB, Davis WH, et al: Radiographic analysis of proximal interphalangeal joint arthrodesis with an intramedullary fusion device for lesser toe deformities, Foot Ankle Int 31:372–376, 2010. Used with permission.)

A limited syndactylization may be combined with a partial proximal phalangectomy of adjoining phalanges. Daly and Johnson55 reported 75% patient satisfaction with this procedure; however, 43% of patients had moderate footwear restrictions, 27% reported residual pain, 28% noted moderate or severe cosmetic problems, and 18% reported a recurrent co*ck-up deformity. In general, the treatment of a hammer toe deformity by creating another deformity with a partial proximal phalangectomy and syndactylization should be discouraged except in a salvage situation. Ely70 believed a hallux valgus deformity would not progress after amputation of a second toe. Vander Wilde and Campbell226 reported on 16 patients (22 feet) who underwent a second toe amputation. They observed mild progressive drift of the hallux but thought that it was usually not significant. Despite these reports, it is generally accepted that removal of the second toe can place the patient at risk for a progressive hallux valgus deformity in time. Amputation of the second toe may be an expeditious treatment for severe deformity in an elderly patient, but it is ill-advised in a younger patient because a hallux valgus deformity can progress (Fig. 7-52A, C, and D). Arthrodesis of the hallux MTP joint may be combined with a second toe amputation to ensure that a hallux valgus deformity will not progress with time (see Fig. 7-52E and F). Gallentine and DeOrio82 reported on 17 amputations in patients averaging 78 years of age; 14 of 17 had a severe hallux valgus deformity, and absence of the toe was not an issue for them. They reported this to be a simple procedure with a predictable healing and recovery (Fig. 7-53). Implants in the lesser toes have been reported by a number of authors. Shaw and Alvarez209 reported on 672 implants placed over an 11-year period for hammer toe deformities. Several implants were removed for pain, infection, or implant failure. The authors* noted that the only true function of an implant in the lesser toe was to act as a spacer, and they found no difference between *References 52, 79, 84, 151, 207-209, and 211.

Figure 7-46 A, Postoperative swelling is common. B, With time, edema of the toe usually subsides. (From Coughlin MJ, Dorris J, Polk E: Operative repair of the hammertoe deformity, Foot Ankle Int 21:94–104, 2000. Copyright 2000 by the American Orthopaedic Foot and Ankle Society [AOFAS]; originally published in Foot Ankle Int 21:94–104, 2000. Used with permission.)

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Figure 7-47 Excessively long second toe treated with diaphysectomy. Preoperative clinical (A) and radiographic (B) appearance. C, Dorsal phalangeal exposure with proposed excision. D, Sagittal saw is used for careful resection. E, Removal of 5-mm diaphyseal segment. F, Kirschner wire fixation. G, After skin closure. H, Postoperative radiograph demonstrating shortening of digit. I and J, Evaluation of postoperative vascularity is important. Capillary filling may be slow and should be monitored.

implants left in permanently and those removed at least 6 weeks after surgery. Reports of hinged silicone joint replacement for hammer toe deformities have also been reported by Gerbert and Benedetti84 and others.207-209,211 Although these series reported a high level of satisfactory results, it is doubtful that the long-term results of PIP joint implants are significantly different from results of excisional arthroplasty. The risk of implant placement in this relatively subcutaneous area and the cost of the implant and surgical procedure make its use questionable when similar results are obtainable with excisional arthroplasty. Cracchiolo et al52 and others79,151,208,211 have reported on the use of silicone implant arthroplasty in the lesser MTP joints (Fig. 7-54). Sgarlato208 proposed silicone arthroplasty of the lesser MTP joints for a dislocated MTP joint, arthritis, a Freiberg infraction, congenitally shortened toes, bunionette deformity, and failed resection 346

arthroplasty. Cracchiolo et al52 reported on lesser MTP replacement arthroplasty in 31 feet (28 patients), noting acceptable results in 63%. Transfer metatarsalgia was the most common postoperative complication, but other complications included lesser metatarsal stress fracture, soft tissue infection, and implant failure. Cracchiolo et al52 concluded that the implant aided in maintaining the joint in a reduced position but that there were strict limitations in the indications for silicone replacement arthroplasty. Fox and Pro79 reported on a similar success rate (70%) with lesser MTP implant arthroplasty. Silicone replacement arthroplasty of the lesser MTP joints or lesser toes is rarely indicated and should be reserved for the occasional salvage procedure when other more standard techniques either are contraindicated or have been unsuccessful. Recurrence of a hammer toe deformity is one of the most frustrating complications after surgery. Although

Lesser Toe Deformities ■ Chapter 7

Figure 7-48 Preoperative clinical (A) and radiographic (B) views of patient with hammer toe symptoms and an unusually long second ray. C, Long-term radiographic follow-up.

excessive resection of bone should be avoided because it leads to a floppy and unstable toe (Fig. 7-55A and B), adequate bone resection is necessary to decompress the toe to obtain an adequate correction. In the face of recurrence, a flexor tenotomy may be necessary to achieve adequate correction. If sufficient bone has been excised and the flexor digitorum longus has been released when indicated, recurrent deformity rarely occurs. Placing two pins for fixation and leaving Kirchner wires for 4 to 5 weeks can help to successfully stabilize a toe after redo surgery. After excessive bone resection, development of a flail toe is a most difficult complication to salvage.* Mahan138,139 described a technique of bone graft stabilization of an iatrogenic flail second toe after unsuccessful hammer toe repair; however, this is an extensive reconstruction to perform on a lesser toe and should be reserved for a patient with significant symptoms (Fig. 7-55C to I). Friend81 described a soft tissue repair using a V-Y skinplasty, soft tissue release, and partial metatarsal head resection to reconstruct an unstable flail lesser toe (Fig. 7-56). The toe often assumes the shape of adjacent toes, a process termed molding (Fig. 7-57). Preoperative patient counseling about the possibility of molding usually alleviates postoperative concern on the part of the patient. If the great toe has an element of hallux valgus interphalangeus, the second toe will also probably have a slight *References 81, 129, 138, 150, 163, and 179.

Figure 7-49 With a partial proximal phalangectomy, the base of the proximal phalanx is excised. Often, adjacent partial proximal phalangectomies are performed in combination with syndactylization. A and B, An intramedullary web space incision is made to approach the adjacent metatarsophalangeal joints. C, The bases of the proximal phalanges of the second and third toes have been excised. D-F, Closure of deep and superficial tissue. (Courtesy K. Johnson, MD.)

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Figure 7-50 A, Painful degenerative arthritis of the second metatarsophalangeal joint. Radiograph demonstrates complete loss of the remaining joint space. B, After excision of the base of the proximal phalanx of the second toe, an intramedullary Kirschner wire is used to stabilize the repair until adequate healing is achieved. C, Intraoperative photograph after partial proximal phalangectomy. D, After removal of Kirschner wire.

B C

Figure 7-51 A and B, Intraoperative photographs after Kirschner wire fixation and syndactylization after partial proximal phalangectomy of the second toe deformity. C, Radiograph immediately after surgery. D, A radiograph 5 years postoperatively demonstrates severe shortening of the proximal phalanx with a varus deformity of the third toe. E, Cosmetically unacceptable syndactylization after partial proximal phalangectomy of only the second toe. (E, From Coughlin MJ: Lesser toe abnormalities, Instr Course Lect 52:421–444, 2003.)

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Figure 7-52 A, After amputation of second toe. B and C, Progressive hallux valgus after amputation of second toe. D, Preoperative radiograph with hallux valgus and dislocated second metatarsophalangeal (MTP) joint. E, After MTP fusion and second toe amputation.

Figure 7-53 A, After multiple procedures to the second toe, soft tissue atrophy and chronic pain were associated with minimal metatarsophalangeal joint motion. B, A 3-year follow-up after second metatarsophalangeal joint disarticulation for chronic pain.

lateral curvature. It is not possible for a repaired hammer toe to remain straight when a deforming force is applied by the great toe or an adjacent toe (Fig. 7-58). Kirschner wire fixation of hammer toe repairs was introduced by Taylor in 1940215 to stabilize the correction. This remains the most popular technique of digital stabilization because of the ease of placement and removal, the maintenance of alignment,189 and the increased stability after correction. Although complications such as pin tract infection (Fig. 7-59),* migration,206,240,193 and breakage† have been observed (see Figs. 7-58G and H and Fig. 7-21), Zingas et al240 reported a 2.5% failure rate when using 0.045-inch Kirschner wires for fixation of lesser toe deformities; however, they routinely left their Kirschner wires implanted for 6 weeks. A shorter period of implantation may in fact diminish the incidence of Kirschner wire failure. They noted the area of wire fracture *References 1, 101, 170, 176, 177, 179, 188, 193, and 209. † References 1, 43, 125, 170, 193, 202, and 240.

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Figure 7-54 Second metatarsophalangeal (MTP) joint silicone implant arthroplasty. A, Mild hallux valgus deformity with painful second MTP joint. B, After first metatarsal osteotomy and placement of second MTP joint double-stem silicone implant. (The implant went on to failure, with eventual salvage with a second toe amputation.) C, At long-term follow-up, the lateral lesser toes have migrated medially.

Figure 7-55 A and B, Excessive resection of bone can destabilize the lesser toes. C and D, Unstable second toe after excessive bone resection. E, Operative exposure of area of prior resection arthroplasty. F, Calcaneal exposure to obtain graft. G, Cylindric donor graft. H, Placement of graft. I, Final clinical appearance after interposition graft. Note adequate vascularity of digit. (C-I, Courtesy M.K. Mahan, DPM.)

Lesser Toe Deformities ■ Chapter 7

60 o

Figure 7-56 Soft tissue V-Y plasty for contracted lesser toe. A, Proposed V-shaped skin incision. B, Operative incision. C, Closure in Y fashion to lengthen the lesser toe. D and E, Z-plasty to correct contracted lesser toes.

Figure 7-57 Molding of adjacent toes. Preoperative clinical examination (A) and radiograph (B) demonstrate molding of second toe. C, Molding of the second and third toes often occurs immediately after surgery but resolves with diminution of swelling. D and E, Molding of second toe after hammer toe repair. (E, From Coughlin MJ: Lesser toe abnormalities, Instr Course Lect 52:421–444, 2003.)

occurred a few millimeters proximal to the metatarsal head but was rarely symptomatic. Wires can be bent at the operative site after placement to improve digital alignment.68 An 18% infection rate was reported by Reece188 when Kirschner wires were left in place 6 weeks or more. In Coughlin’s series,45 only 3 of 118 toes developed a pin tract infection, and all resolved after pin removal. Kirschner wires were removed routinely 3 weeks after surgery. Herstik et al,101 in a large review of lesser toes stabilized with Kirschner wires, reported an even lower infection rate (90%) in patients in 355

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Figure 7-63 Fracture of the proximal phalanx after flexor tendon transfer A, After flexor tendon transfer but before phalangeal fracture. B, After fracture of the proximal phalanx. (From Fishco W, Roth B: Digital fracture after a flexor tendon transfer for hammertoe repair: a case report, J Foot Ankle Surg 49:179–181, 2010. Used with permission.)

their series after flexor tendon transfer. Barbari and Brevig3 reported three cases where a fixed contracture of the interphalangeal joint developed postoperatively. Complications experienced after this procedure are uncommon. Occasionally, swelling of varying degrees persists for a time, but it usually subsides. Transient numbness probably caused by stretching or contusion of the adjacent neurovascular bundles can occur, but this usually improves with time. Hyperextension of the DIP joint has been noted in a few patients with concomitant spasticity and is usually associated with recurrence of flexion at the PIP joint. This may be a result of concomitant tightness of the flexor digitorum brevis. After a flexor tendon transfer, the ability to curl the toe is sacrificed. Often, at longterm follow-up after a flexor tendon transfer, stiffness develops in the PIP joint. Boyer and DeOrio19 estimate a 50% loss of MTP and IP joint motion after a flexor tendon transfer. Myerson and Jung165 reported that 19 of 59 patients reported serious reservations about this procedure, much of the dissatisfaction stemming from the postoperative digital stiffness. A patient should be counseled preoperatively that there will be an absence of dynamic function of the involved toe and often the other lesser toes after a flexor tendon transfer. This does not tend to cause disability, but it can be annoying to the patient. They should be alerted to the trade-off of sacrificing flexor digitorum longus function for stability and realignment of the malaligned digit. Occasionally, the patient with a dynamic hammer toe also has an element of clawing. A release of the extensor digitorum longus tendon and simultaneous MTP capsulotomies may be performed at the same time as a flexor tendon transfer. 356

If a Kirschner wire has been placed across the MTP joint, the pin can break (see Fig. 7-58H).188,240 Often, the pin fractures just proximal to the articular surface of the metatarsal head, and in this case, the distal fragment is removed and the proximal fragment is left within the metatarsal. If the distal aspect of the remaining pin penetrates the MTP joint, or if it migrates, it may be surgically removed through an MTP joint arthrotomy. Fishco76 has reported isolated fracture of the proximal phalanx after a flexor tendon transfer procedure (Fig. 7-63). Postoperative vascular insufficiency of a digit can require removal of the Kirschner wire. (If the Kirschner wire has been driven across the MTP joint, sometimes just withdrawing it below this joint may improve vascularity.) Other alternatives, when there is slow capillary filling after surgery, are avoiding ice or elevation, removing and rewrapping the dressing, and temporarily dropping the extremity over the side of the bed. When these methods are unsuccessful, topical nitroglycerin ointment (Nitropaste) along the borders of the involved digit can increase the capillary filling of the digit.19 Postoperative observation is important with this complication. Achievement of adequate alignment intraoperatively without the use of a Kirschner wire is important should the removal of internal fixation be necessary in the immediate postoperative period. Thus the Kirschner wire is used to protect a flexor tendon transfer but not to achieve further realignment of the toe. A curly toe deformity is often associated with a mallet toe. Typically, a curly toe occurs in a younger patient, is characterized by a flexion deformity of the PIP joint and DIP joint, and is caused by a contracture of the flexor

Lesser Toe Deformities ■ Chapter 7

Figure 7-64 Repair of curly toe deformity. A, Preoperative dorsal view demonstrating curly toe or contracture of the second toe. B, Preoperative frontal view demonstrating contracture of the third toe of another patient. C, Open lengthening of long flexor tendon of third toe. D, Postoperative taping of third digit for 6 weeks. E, Final result with correction of third toe curly toe deformity (preoperative from photograph A). (E, Courtesy G. Vandeputte, MD.)

digitorum longus tendon to a specific toe (Fig. 7-64A).167 Radiographs often demonstrate a deviation of the toe (Fig. 7-64B). Although some advocate stretching and taping to correct the deformity, Sweetnam214 concluded that conservative treatment is rarely successful in straightening the toe. He found that there was a similar level of improvement in patients who were treated conservatively and in those who had no treatment, concluding that there was no progression or correction of deformity in either group. A flexor tenotomy often enables complete correction of the deformity. Ross and Menelaus192 have noted no significant weakness of the involved toe at almost 10-year follow-up after flexor tenotomy. They reported 95% successful results after flexor tenotomy. Although a flexor tendon transfer may be performed, Hamer et al98 examined patients who had either a flexor tenotomy or flexor tendon transfer for a curly toe deformity and noted no significant postoperative difference. Thus a simple flexor tenotomy appears to be sufficient treatment. Jacobs and Vandeputte108 reported on 11 children in whom they performed a Z-lengthening of the flexor digitorum longus

(FDL) for hammer toes and a tenotomy for mallet toes as a treatment of curly toes. A total of 15 toes (5 second, 3 third, 6 forth, and 1 fifth toes were involved). They reported excellent results in 70% of the cases (see Fig. 7-64). Boc and Martone12 treated an adduction deformity of the distal digit with a laterally based elliptic arthroplasty. This procedure may indeed be necessary to correct a fixed bony deformity, but in most cases, a flexor tenotomy is adequate treatment for the flexible curly toe deformity in the younger child. MALLET TOE DEFORMITY39,40

A mallet toe usually is a fixed deformity, but occasionally, in a young patient, it is flexible. Symptoms develop when the tip of the toe strikes the ground. This results in development of a callosity on the tip of the involved toe. This can be treated conservatively with a small felt pad placed beneath the toe to prevent the tip of the toe from striking the ground. A shoe with an adequate toe box must be worn to accommodate the toe with a felt pad beneath it.39 357

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Figure 7-65 Mallet toe deformity. A, Dorsal view. B, View end on. C, Plantar view of another patient with severe mallet toe deformity.

A mallet toe occurs much less often than a hammer toe (ratio, 1 : 9).40 It occurs in the longer toe in 75% of cases but with equal frequency in the second, third, and fourth toes (see Fig. 7-10).40 Although excess length has been implicated as a cause of mallet toe, trauma may lead to this deformity with disruption of the extensor insertion onto the dorsal base of the proximal phalanx.130

Mallet toe

Preoperative Planning When the deformity is flexible, release of the flexor digitorum longus tendon percutaneously may be sufficient.98,192 When the deformity is fixed (Fig. 7-65), which is more often the case, surgical intervention may be required. Bone decompression of the DIP joint, with resection of the head of the middle phalanx and release of the flexor digitorum longus tendon, results in satisfactory correction. An algorithm, presented in Figure 7-66, describes the decision-making process for the treatment of mallet toe. Indications The main indication for a surgical repair is a symptomatic mallet toe. Lateral or medial deviation of the digit at the DIP joint may be corrected with a mallet toe repair as well.

Flexible

Fixed

Condylectomy, middle phalanx

Flexor digitorum longus tenotomy

Kirschner wire fixation

Contraindications In the presence of a combined mallet toe and hammer toe, a decision must be made as to which deformity is more severe. A combined procedure for hammer toe and mallet toe is rarely, if ever, performed.173 When merely a flexor tenotomy is sufficient, a formal mallet toe repair can be avoided. MALLET TOE REPAIR34,35,40 Surgical Technique 1. The patient is placed in a supine position on the operating room table. If MTP joint surgery is performed, an 358

Realigned toe Figure 7-66 Algorithm for treatment of mallet toe.

Esmarch bandage may be used to exsanguinate the extremity and may also be used as an ankle tourniquet.91 A digital block or ankle block is administered, depending upon the necessity for additional surgical procedures.

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Figure 7-67 Technique for correction of mallet toe deformity. A, Elliptic skin incision centered over the distal interphalangeal joint. B, Excision of skin, extensor tendon, and capsule, exposing condyles of middle phalanx. C, The collateral ligaments are severed, exposing the condyles of the middle phalanx. D, Generous excision of the distal portion of the middle phalanx. E, After resection of the condyle. F, The articular surface of the distal phalanx is removed with a rongeur. The flexor digitorum longus tendon is identified in the base of the wound and is released. G, Stabilization with intramedullary Kirschner wire. Vertical mattress sutures are used to coapt the skin.

2. The foot is cleansed and draped in the usual fashion. A 1 4 -inch Penrose drain may be used as a tourniquet (Fig. 7-67A and Video Clip 74). 3. An elliptic incision is centered over the dorsal aspect of the interphalangeal joint. The dissection is carried down through the extensor tendon and joint capsule. The distal portion of the ellipse should be sufficiently proximal to avoid injuring the nail matrix (Figs. 7-67B and 7-68A). 4. The collateral ligaments are released on the medial and lateral aspects of the DIP joint. Care is taken to protect the adjacent neurovascular bundles (see Fig. 7-67C). 5. The condyles of the middle phalanx are delivered into the wound. The bone is transected in the supracondylar region, and the distal fragment is excised (see Fig. 7-67D and E). 6. The plantar capsule is incised in the depths of the wound, and the flexor digitorum longus is identified and released under direct vision (see Fig. 7-68B). The toe is brought into satisfactory alignment without tension. If the toe cannot be completely aligned, more bone is resected from the middle phalanx. 7. The articular cartilage is removed from the base of the distal fragment (optional) (see Figs. 7-67F and 7-68C). 8. A 0.045-inch Kirschner wire is introduced at the DIP joint and driven distally, exiting the tip of the toe (see Figs. 7-67G and 7-68D). The toe is then aligned properly, and the Kirschner wire is driven in a retrograde fashion into the middle phalanx. The pin is bent at the tip of the toe, and the remaining pin is removed (see

Fig. 7-68E-G). Often, a second pin is placed to add rotational control to the fixation construct. 9. A gauze-and-tape compression dressing is applied at surgery and changed on a weekly basis until drainage has subsided. Alternative Fixation Interrupted vertical mattress sutures of 3-0 nylon are used to incorporate two Telfa bolsters (Fig. 7-69). They are inserted in a similar fashion for fixation of a hammer toe. As tension is applied to the suture, leverage is created to bring the toe into satisfactory alignment. This is used quite uncommonly at this point (see technique in hammer toe section). Postoperative Care The patient is allowed to ambulate in a wooden-soled postoperative shoe. If bolsters have been placed, they are removed 1 week after surgery. If the bolsters are left longer than 1 week, there is risk of skin necrosis. If a Kirschner wire has been placed, the pin is removed 3 weeks after surgery. Sutures are removed at this time as well. After removal of the pin or bolsters, the toe is held in a corrected position with a piece of tape for 6 weeks to ensure soft tissue healing. Results and Complications The expected results after this procedure have been routinely satisfactory. Using this procedure, with resection of the condyles of the middle phalanx and the corresponding articular surface of the distal phalanx, Coughlin40 359

Figure 7-68 Mallet toe repair. A, Dorsal elliptic incision. B, After condyles of the middle phalanx are resected, a flexor tenotomy is performed. C, The articular surface of the distal phalanx is removed (optional). D, Insertion of Kirschner wire. E and F, After Kirschner wire insertion and closure. G, Radiograph with stable and painless fibrous union of corrected mallet toe deformity of the second toe.

Figure 7-69 Alternative means of fixation for mallet toe repair. A and B, Placement of Telfa bolsters beneath 3-0 nylon vertical mattress suture.

Figure 7-70 A, Stable fibrous union of second toe distal interphalangeal joint after mallet toe repair (distal interphalangeal [DIP]) joint after mallet toe repair. B, Fibrous union of DIP joint of the second toe after mallet toe repair with significant soft tissue distraction (asymptomatic).

Lesser Toe Deformities ■ Chapter 7

reported successful fusion in 72% of cases (Fig. 7-70A). The satisfaction rate was only slightly higher in the group with a successful arthrodesis. Some 75% of those with a fibrous union were satisfied, although slightly less so than those with a successful DIP arthrodesis (Fig. 7-70B). Pain relief was noted by 97% and correction of the deformity by 91%. Although not performed in all cases, a flexor tenotomy appeared to be associated with a slightly higher rate of satisfaction and maintenance of the corrected position. Usually, correct alignment is maintained and complications are uncommon. Oliver et al173 reported on a series of 20 patients (63 toes) in which a double resection arthroplasty was performed for a dual correction of deformities at both the DIP and PIP joint (hammer toe + mallet toe). A 10% recurrence rate was noted. They used both a longitudinal incision for the proximal interphalangeal joint and a transverse incision for the DIP joint. No internal fixation was used. The few problems that have been observed postoperatively include the following: Swelling often persists for several months after the procedure, but it invariably resolves with time. At longterm follow-up, no patients were noted to have swelling.40 Molding resulting from extrinsic pressure from adjacent toes can cause angulation or malalignment (see Fig. 7-11A and B). n Occasionally, recurrence of a mallet toe deformity is noted. This is usually because the flexor digitorum longus tendon was not released. n Injury to an adjacent digital nerve can leave an area of numbness along either the medial or lateral border of the toe, although this is rarely a significant complaint. n When a preoperative toenail deformity is associated with a mallet toe, this usually does not resolve after correction of the mallet toe (see Fig. 7-11C-E). The patient should be warned that although the toe can be realigned, the toenail deformity will not be corrected.

hammer toe may or may not be associated with hyperextension of the proximal phalanx, but a claw toe classically has a hyperextension deformity at the MTP joint.80,103 In a claw toe, the DIP joint may be extended or flexed. The chronic hyperextended posture of the MTP joint forces the metatarsal heads plantarward and displaces the plantar fat pad, often resulting in symptomatic metatarsalgia over time. In patients with an insensate foot, ulcers can develop beneath the metatarsal heads. Preoperative Planning To successfully correct a claw toe deformity, the MTP joint must be brought into a neutral position so that the extensor tendon can function to extend the PIP joint and the intrinsic tendons can function as flexors of the MTP joint. Treatment of a claw toe depends on the underlying condition. Figure 7-71 presents an algorithm for treatment of claw toe. If a significant pes cavus deformity is present, attention should be directed first to the midfoot and hindfoot deformities.29,34,37,140,141 With a pes cavus

CLAW TOE DEFORMITIES

A claw toe often develops in association with neurologic conditions in which a muscle imbalance occurs203 with weakness or loss of intrinsic muscle function.157 It can also occur in arthritic conditions, such as rheumatoid arthritis and other collagen deficiency syndromes. At times, a claw toe deformity is associated with a cavus foot deformity.106 It may also be associated with the sequelae of compartment syndromes after lower-extremity trauma.74,181 In evaluating a claw toe deformity, every effort should be made to determine the specific diagnosis.39 However, many of these cases are idiopathic. What differentiates a claw toe from a hammer toe is the hyperextension deformity of the MTP joint.167 A

Flexible

Fixed

Flexor tendon transfer

Metatarsophalangeal soft tissue release • Dorsal capsular release • Medial and lateral capsular release • Extensor tendon lengthening

Reduced

Not reduced

Weil osteotomy

Realigned toe

Fixed hammer toe repair

Figure 7-71 Algorithm for treatment of claw toe.

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deformity, the metatarsal heads are depressed as a result of the anatomic alignment of the foot, and the toes are extended by the contracted long extensors, creating the claw toe deformity (see Fig. 7-15A).103,104 When there is dynamic clawing without a significant cavus deformity, attention should be directed to the forefoot itself. If there is no clawing of the toes when the ankle is held in plantar flexion, and if clawing occurs with dorsiflexion of the ankle joint, a flexible claw toe deformity is present (see Fig. 7-15B-E). This may be treated with a flexor tendon transfer.3,184,215,216 This is the same type of procedure that is used to correct a flexible or dynamic hammer toe (see Figs. 7-60 and 7-61); however, release of the MTP joints (extensor tenotomies or MTP joint capsulotomies, or both) also may be necessary.3 Feeney et al,74 in treating patients with the sequelae of compartment syndromes after tibia fractures, have advocated selective proximal lengthenings of the flexor hallucis longus and flexor digitorum longus to relieve lesser toe contractures. In the presence of a fixed contracture, a DuVries arthroplasty of the PIP joint is carried out with concomitant release of the contracted structures at the MTP joint (Fig. 7-72). In patients with severe contractures of the MTP and interphalangeal joints, release of both flexor tendons should be carried out at the time of the surgery. In patients with severe contractures, longitudinally placed Kirschner wires may be used to stabilize both the interphalangeal and MTP joints in satisfactory alignment. Indications In the presence of a fixed claw toe deformity, a condylectomy of the base of the proximal phalanx is performed. Release of the extensor tendon and contracted capsule at the MTP joint depends on whether a fixed contracture is present. A fixed contracture at the interphalangeal joint of the hallux is treated with an interphalangeal joint fusion. With a contracture of the extensor hallucis longus tendon, a Jones tendon transfer is performed. An extensor

tendon transfer to the distal metatarsal80,103 (Jones transfer) and the midfoot147 also has been advocated for treatment of claw toe deformity. A distal metatarsal osteotomy may also be an alternative in the treatment regimen of a severe claw toe deformity (discussed under Weil osteotomy). Contraindications In the presence of a flexible claw toe deformity, a flexor tendon transfer is performed identical to that for a flexible hammer toe deformity. Transfer of a flexor tendon as sole treatment of a fixed deformity is rarely successful. DUVRIES ARTHROPLASTY PROCEDURE Surgical Technique 1. The patient is placed in a supine position on the operating room table. A peripheral nerve block is typically used for anesthesia. The foot is cleansed and draped in the usual fashion. The foot is exsanguinated with an Esmarch bandage, which may be used as a tourniquet above the level of the ankle. 2. A longitudinal incision is centered over the PIP joint. The skin, extensor tendon, and capsule are exposed and excised (Fig. 7-73A and B). 3. The toe is flexed and the collateral ligaments released on the medial and lateral borders of the condyle. The plantar capsule also is released (Fig. 7-73C and Video Clip 75). 4. The condyles of the proximal phalanx are resected with a bone-cutting forceps (Fig. 7-73D). 5. If an arthrodesis is desired, a rongeur is used to remove the base of the middle phalanx (Fig. 7-73E). 6. The toe is stabilized with a 0.045-inch Kirschner wire introduced at the interphalangeal joint and driven distally (Fig. 7-73F). A release of the flexor tendons may be necessary and may be performed in the depths of the wound from a dorsal approach. 7. With the toe aligned properly, the Kirschner wire is driven proximally, stabilizing the proximal phalanx.

Figure 7-72 Soft tissue release and realignment. A, Lateral view of a cadaver dissection demonstrating a fixed hammer toe deformity and a fixed contracture of the metatarsophalangeal joint. Note the lumbrical pulling at a right angle. Also note the thickness of the lateral capsule. B, An extensor tenotomy and dorsal capsule release have been performed. This is an inadequate release to reduce the toe, as can be seen in this dissection. Note that a more extensive capsule release must be performed on the medial and lateral aspect to reduce the toe. C, Intraoperative photograph demonstrating inadequate release. D, An adequate capsule release has been performed. E, After metatarsophalangeal joint release, often intermedullary Kirschner wire fixation is used to stabilize the repair.

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Figure 7-73 Repair of claw toe deformity. Longitudinal incision is centered over the proximal interphalangeal joint (A), exposing the skin, extensor tendon, and capsule (B), which is excised. C, The toe is flexed and the plantar capsule is released. The collateral ligaments are released from the medial and lateral border of condyles. D, The condyles of the proximal phalanx are removed with a bone-cutting forceps. E, If an arthrodesis is desired, the articular surface of the base of the middle phalanx is removed. F, A 0.045-inch Kirschner wire is introduced at the arthroplasty site and driven distally. G, With the toe reduced, the Kirschner wire is driven in a retrograde fashion, stabilizing the proximal phalanx. After skin closure, the toe is adequately aligned.

B Figure 7-74 A, Claw toe deformity. B, After proximal interphalangeal joint arthroplasty, metatarsophalangeal soft tissue release, and intramedullary Kirschner wire fixation.

Surgical Technique 1. A 1.5-cm incision is centered over the MTP joint. 2. The dissection is deepened to the extensor tendon, which is released. 3. With retractors exposing the MTP joint capsule, the dorsal, medial, and lateral capsules and collateral ligaments are released. (This release must be carried down approximately 1 cm plantarward to allow reduction of the MTP joint.) If adhesions of the plantar plate are present, a release of the plantar capsule with a McGlamry elevator may allow reduction of the dorsiflexion contracture of the MTP joint. 4. A 0.045-inch Kirschner wire is driven retrograde across the MTP joint, stabilizing the joint. 5. The pin is bent at the tip of the toe and the remainder of the pin is cut and removed. 6. A gauze-and-tape compression dressing is applied and is changed weekly until drainage has subsided.

If an MTP joint capsule release is performed, the Kirschner wire may be driven across the MTP joint (Fig. 7-73G). 8. The skin is approximated with interrupted vertical mattress sutures.

HALLUX/INTERPHALANGEAL JOINT ARTHRODESIS With a fixed contracture of the interphalangeal joint of the hallux, an interphalangeal joint arthrodesis is performed.

CONTRACTURE RELEASE In the presence of a hyperextension deformity of the MTP joint, a release of the contracted tissue and a tenotomy of the extensor tendon is performed (Fig. 7-74).

Surgical Technique 1. The foot is cleansed and draped in the usual fashion. 2. An elliptic incision is centered over the dorsal aspect of the interphalangeal joint. The skin, extensor tendon, 363

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and capsule are resected. The medial and lateral collateral ligaments and plantar capsule are released (Fig. 7-75A-C). 3. A power saw is used to resect the articular surface of the condyles of the proximal phalanx (Fig. 7-75D). 4. The articular surface of the distal phalanx is also resected with the power saw (Fig. 7-75E). 5. A puncture wound is created in the skin (Fig. 7-75F). A 3.5-mm gliding hole is drilled through the distal phalanx. The drill is introduced at the interphalangeal joint and driven distally through the tip of the toe. 6. A 2.5-mm fixation hole is drilled in the proximal phalanx (Fig. 7-75G). 7. A lag screw is used to stabilize the fusion. Care must be taken not to place an excessively long screw that can penetrate the MTP joint (Fig. 7-75H). A 0.062-inch Kirschner wire may be added as additional internal fixation to prevent rotation at the arthrodesis site. 8. A gauze-and-tape dressing is applied (Fig. 7-75I-K).

Postoperative Care The patient is allowed to ambulate in a postoperative shoe. Sutures and Kirschner wires are removed 3 weeks after surgical repair of a fixed claw toe. The compression screw placed in the hallux to fuse the interphalangeal joint may be left in permanently, or if it causes discomfort, it may be removed after administration of local anesthetic. Results and Complications Taylor216 performed both soft tissue release and transfer of the long and short flexor tendons to the extensor hood. He reported that the operation restores “useful function to the toe at the cost of their prehensile action.” In 68 patients (112 feet), 72% good results were reported. No resection arthroplasties were performed in this series. Pyper184 transferred both the long and short flexors to the extensor hood and reported 51% excellent and good results and 49% fair and poor results with this procedure.

Figure 7-75 A, Repair of hammered great toe. After elliptical skin incision excises skin, extensor tendon, and capsule (B), the collateral ligaments are released (C). D, A power saw is used to remove the articular surface of the condyles of the proximal phalanx. E, The articular surface of the distal phalanx is removed with a power saw. F, A gliding hole is created through the distal phalanx. G, A fixation hole is created in the proximal phalanx. H, A lag screw is placed to stabilize the repair. I, Result after repair of all five toes.

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Suboptimal results were thought to result from uncorrected fixed flexion contractures of the lesser toes. Parrish175 transferred the flexor digitorum longus to the extensor hood in 23 patients. Transfer of the short flexor tendon was abandoned because of technical difficulties. Eighty-nine percent good and excellent results were reported. Cyphers and Feiwell54 reported their experience with flexor tendon transfer in patients with meningomyelocele and noted 60% good results. Barbari and Brevig3 reported on flexor tendon transfer for correction of a claw toe deformity. Satisfactory results were reported in 90% of cases, although one third of patients complained of metatarsalgia postoperatively. MTP motion was greater than 50 degrees in 33% of patients and less than 50 degrees in 6 patients. Twelve patients had no interphalangeal joint motion, 15 had reduced motion, and 12 had the same amount of motion at the interphalangeal joints. Continuing complaints were noted by patients who had a fixed claw toe deformity that might have been better treated with a resection arthroplasty. With refinement of this procedure and the use of just the flexor digitorum longus tendon, improved results have been noted, although Thompson and Deland218 observed that only 54% of patients in their series achieved complete realignment of the MTP joint after flexor tendon transfer. Heyman103 advocated soft tissue release of the contracted capsular structures at the MTP and interphalangeal joints. No “excellent” results were noted, although no long-term evaluation was reported.

Lapidus134 performed a dorsal capsule reefing at the interphalangeal joints coupled with a plantar capsulotomy and extensor tenotomy and reported uniformly good results. Frank and Johnson80 and McCluskey et al147 advocated PIP joint arthroplasty to decompress the claw toe deformity and realign the toe. Complications associated with repair of a claw toe deformity usually are related to recurrent deformity. In the presence of a flexible claw toe deformity, a flexor tendon transfer can adequately realign the deformed toes. Where a fixed contracture is present, a capital oblique osteotomy of the metatarsal may be necessary to achieve adequate realignment. (See the discussion of the Weil osteotomy later.) MTP joint capsule releases and an extensor tenotomy or lengthening may be combined to correct a significant hyperextension deformity. Lui et al,137 in a cadaver study, tenodesed the plantar plate to the extensor tendons. Basically, they achieved correction with both extensor and plantar releases of soft tissue contractures. They then followed up with the treatment of 23 patients with claw toe deformities using this procedure and reported satisfactory realignment. Further long-term follow-up will be necessary to assess the efficacy of this procedure. Metatarsalgia may continue to be a complaint despite realignment of the lesser toes.72 An algorithm is helpful in the approach to differentiating forefoot problems (Fig. 7-76). Attention to midfoot and hindfoot deformities may be necessary to relieve symptoms of metatarsalgia. Treatment of the underlying problem leading to a claw

Metatarsalgia (forefoot pain)

No plantar callosity

Neuritic symptoms

Interdigital neuroma

Plantar callosity

No neuritic symptoms

Instability MTP joint

No instability MTP joint

MTP instability

MTP capsulitis

Plantar metatarsal callosity

Plantar/lateral 5th metatarsal callosity

Metatarsal stress fracture

Without hammer toe

Bunionette

IPK

Dorsal callosity over toe

Web space callosity

Mallet toe Hammer toe Lateral 5th toe corn

Interdigital corn

With hammer toe

Claw toe

Figure 7-76 Algorithm for treatment of metatarsalgia. IPK, intractable plantar keratosis; MTP, metatarsophalangeal. (From Coughlin MJ: Common causes of pain in the forefoot in adults, J Bone Joint Surg Br 82:781–790, 2000.)

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toe deformity should be considered before lesser toe realignment. With extensive surgery, which can include an MTP joint release, a condylectomy of the proximal phalanx, and even a flexor tendon transfer, the vascular status of the toe or toes may be compromised. The patient must be monitored closely postoperatively, because it may be necessary to remove internal fixation (e.g., Kirschner wire) in the presence of vascular compromise. SUBLUXATION AND DISLOCATION OF THE LESSER METATARSOPHALANGEAL JOINT

Subluxation and dislocation of the lesser MTP joints can occur with relative frequency.22,43,65 Since Coughlin33 introduced the term crossover toe in 1987, several etiologies have been proposed. Certainly, a lesser MTP joint can be dislocated acutely after an injury with disruption of the plantar capsule and MTP collateral ligaments. Chronic capsular insufficiency, however, can develop in association with systemic arthritides (such as rheumatoid arthritis) and other connective tissue disorders as well as nonspecific synovitis.143,144 Chronic synovitis eventually can lead to deterioration of the plantar plate and collateral ligaments with subsequent instability of the MTP joint.110,144 The use of high-heel shoes is also thought to cause repetitive hyperextension forces on the lesser MTP joints, which in time may lead to attenuation or rupture of the plantar plate, and in time this can lead to subluxation or dislocation of the lesser MTP joints (Fig. 7-77).33,120,229 Etiology A traumatic episode can lead to dislocation of the MTP joints (Fig. 7-78). Occasionally, after a dorsiflexion injury

to the MTP joint, the joint is irreducibly dislocated.162,186 The typical injury mechanism occurs with forced hyperextension and axial loading of the involved toe. The postinjury radiograph often demonstrates an increased MTP joint space, and an interposed plantar plate is often identified at surgery. Brunet and Tubin23 reported on 27 injuries (17 patients) to the lesser MTP joint associated with sporting activities, motor vehicle accidents, and trauma. Invariably, the plantar plate and capsule were torn from the metatarsal head and become interposed, preventing successful reduction. Occasionally, the transverse metatarsal ligament had to be sectioned to allow joint reduction. Boussouga et al16 reported a similar finding with an irreducible dislocation of the fifth MTP joint (Fig. 7-79). Dislocation of lesser MTP joints is often associated with inflammatory arthropathy,143 and although these often

Figure 7-77 Unstable second metatarsophalangeal (MTP) joint that has developed into fully dislocated MTP joint with degenerative changes as well.

Figure 7-78 Traumatic dislocation of second metatarsophalangeal (MTP) joint after skydiving accident. A, Dislocated second MTP joint. B, After open reduction and internal fixation. C, Follow-up shows adequately realigned second MTP joint.

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Figure 7-79 Irreducible dislocation of the fifth metatarsophalangeal (MTP) joint. A, Radiograph demonstrating isolated fifth MTP joint. B, Clinical appearance of fifth MTP joint. C, Intraoperative photograph demonstrating interposed plantar plate (arrow). D, After open reduction and fixation with Kirschner wire. E, Final result after Kirschner wire removal. (From Boussouga M, Boukhriss J, Jaafar A, Lazrak K: Irreducible dorsal metatarsophalangeal joint dislocation of the fifth toe: a case report, J Foot Ankle Surg 48:298 e217–220, 2010. Used with permission.)

present as multiple lesser MTP dislocations, they can develop initially as an isolated subluxtion of dislocation (Fig. 7-80). One reason for a dislocation of the second MTP joint is that the second ray (consisting of the second metatarsal and phalanges) is usually the longest in the foot.33-37,160 Because of the pressure of the end of the toe against the toe box, the toe buckles and the proximal phalanx have a tendency to ride up onto the dorsal aspect of the second metatarsal head. Subluxation can eventually occur, and if untreated, it can progress to dislocation. The longer period of time that the dislocation is present, the greater the degree of change noted in the surrounding soft tissue and bone. The soft tissue contractures can include shortening of the extensor tendons and contracture of the dorsal, medial, and lateral capsule. Associated with this may be a complete rupture or an attenuation of the plantar capsule. Although initially MTP joint instability was attributed to lateral collateral ligament insufficiency,33,42-44 we now think this collateral ligament insufficiency is more commonly a later development after plantar plate deterioration.47,50,168 Anatomic dissections of the second MTP joint suggests to us that the plantar plate is the key stabilizing structure of the joint.8,50,120 Bhatia et al8 and others77 used cadaveric models to determine the anatomic restraints to dislocation of the second MTP joint and demonstrated that sectioning of the plantar plate created an unstable joint.8 Dislocation of any of the lesser MTP joints may be caused by degeneration or

rupture of the plantar plate, which then permits the MTP joint to subluxate dorsally.35,50,61,62 During walking, all of the forces across the MTP joint tend to hyperextend or dorsiflex the joint. Therefore any imbalance about the MTP joint (i.e., capsular or tendinous) can result in progressive dorsal subluxation. In long-standing dislocations, an accessory facet can develop on the dorsal aspect of the metatarsal head. With a marked hallux valgus deformity (Fig. 7-81A-C; see also Fig. 7-34A), it is not uncommon to see a subluxed or dislocated second MTP joint that deviates laterally (because of pressure from the hallux) or dorsally (with the hallux crossing under the second toe). Often, however, the second toe actually deviates medially, leaving a gap between the second and third toes174; this deformity is termed a crossover toe deformity.33 This can occur with or without a hallux valgus deformity. The toe may or may not be subluxed dorsally. Over time, erosion of the plantar plate, fibular collateral ligament of the second MTP joint, and deterioration of the lateral joint capsule allow the toe to drift in a dorsomedial direction. Less commonly, a third or fourth toe also dislocates (Fig. 7-81D and E; see Fig. 7-80). Although most prior series have reported on only instability of the second MTP joint, Nery et al168 also reported the treatment of third and fourth MTP joint instability, although the second MTP joint was by far the most frequently involved (63%). Hatch and Burns100 suggested that an accessory medial head of the extensor digitorum brevis was associated with 367

Part II ■ Forefoot

Figure 7-80 Isolated dislocation of fourth metatarsophalangeal (MTP) joint. A, A 62-year-old female with low-grade inflammatory arthritis, prior proximal phalanx fracture, and bunionette repair, with prodromal pain in lateral forefoot. B, One month later, radiographs demonstrate an isolated fourth MTP dislocation (the third MTP joint has degenerative arthritis). C, After open reduction internal fixation of the fourth MTP joint.

Figure 7-81 Hallux valgus deformity. Clinical (A) and radiographic (B) appearance of dislocation of second metatarsophalangeal (MTP) joint. The hallux has caused sufficient pressure against the second toe, which led to dislocation of the second MTP joint. C, With hallux valgus or hallux valgus interphalangeus, there is insufficient room for the adjacent second toe, necessitating realignment of the great toe. D, Isolated dislocation of the third MTP joint due to synovitis. E, Radiographic appearance of dislocated third toe in a different patient.

a crossover toe deformity and noted its presence in four of seven cadaver specimens. They speculated that the action of the extensor digitorum brevis to dorsiflex and adduct the second toe could be an underlying cause of a crossover second toe. Anatomy of Lesser Metatarsophalangeal Joint Subluxation The lesser MTP joints are stabilized by a combination of the static resistance provided by the collateral ligaments and plantar plate as well as the dynamic pull of the intrinsic flexors.8,38 It is, however, mainly the plantar plate that provides this major stabilizing force.50 The plantar plate is rectangular to trapezoidal in shape, forming a cradle 368

beneath the metatarsal head. It originates on the metatarsal head with a thin weak synovial attachment, just proximal to the metatarsal articular surface and inserts with a stout attachment onto the plantar base of the proximal phalanx.* It also has a number of important structures that attach to it, including the distal fibers of the plantar fascia, the collateral ligaments, the transverse metatarsal ligaments, the interosseus tendons, and the fibrous sheath of the flexor tendons.63 The overall thickness of the plantar plate can range from 2 to 5 mm. The length can range from 16 to 23 mm, and the width can range from 8 to 13 mm, depending upon the size of the metatarsal.115 The peripheral borders of the plantar plate have been noted *References 47, 50, 60, 61, 115, 168.

Lesser Toe Deformities ■ Chapter 7

to be thicker than in the central region.115 Johnson et al,115 in a biochemical analysis of the plantar plate, observed type 1 collagen to be the most common collagen type (75%), while type 2 collagen was next most common (21%). Deland61 also reported an analysis of the plantar plate in five normal feet and discerned that the plate was composed mainly of type 1 collagen. This collagenous composition may be a factor that affects the poor healing capability of the plantar plate tear.77 The same healing problem has been reported to occur in the meniscus of the knee, where there is also a high level of type 1 collagen. In the plantar plate, these collagen fibers run mostly in a longitudinal fashion, with some oblique bundles interspersed at somewhat regular intervals.115 Biomechanically, the plantar plate functions to resist tensile loads in the longitudinal direction (particularly with dorsiflexion of the joint) as well as in an axial plane (with varus/valgus stress); it functions as well to cushion the joint and support forefoot weight-bearing forces.61,63,115 With the application of long-term, chronic, hyperextension forces to the MTP joint, the plantar plate and the capsule may tear, stretch, or become attenuated, with eventual loss of stabilizing control of the MTP joint.31,33,38 Recent reports have suggested a relationship between lesser MTP joint instability and the loss of plantar plate integrity.* Haddad et al97 observed that the weakest area of the plantar capsule is the thin synovial attachment of the plantar plate to the metatarsal neck and suggested that this tissue either lengthens or ruptures, leading to sagittal and axial deformity. It now appears, based on anatomic and surgical observation, that the initial deficiency occurs distally at the insertion of the plantar plate or in the midportion of the plantar plate.† Deland and Sung63 demonstrated a rupture of the lateral collateral ligament and attenuation of the lateral plantar plate in the dissection of a single specimen of a crossover second toe. Associated with this deformity was a medial subluxation of the plantar plate. As tension was applied on the medially subluxated long flexor tendon, the proximal phalanx deviated medially. The stout attachment of the plantar plate to the proximal phalanx was observed to be intact. Coughlin et al50 reported on the anatomic dissection of 16 cadaveric specimens with second MTP joint instability and observed distal transverse plantar plate tears in all specimens, but in only 6 (38%) was disruption of a collateral ligament noted (Fig. 7-82). In a study of cadaveric specimens, Coughlin50 reported a grading scheme to further quantify the magnitude and direction of plantar plate tears (Table 7-1). The grading of the anatomic findings (grades 0-IV) gives a means to evaluate the pathology, as well as to assist in the planning of an appropriate surgical approach, and then later to assess the results of surgical reconstruction in light of the varying magnitudes of plantar plate tears. *References 14, 15, 23, 33, 42, 47, 50, 61, 168, and 229. † References 10, 11, 15, 31, 47, 50, 83, 92-95, 168, 229, and 236.

Table 7-1 Anatomic Grading of Plantar Plate Tear47,50,168 Grade

Description

Plantar plate or capsular attenuation, and/or discoloration (see Fig. 7-83A) Transverse distal tear (adjacent to insertion into proximal phalanx [ 75%

≈Serum ≈Serum 10 degrees).188 It is contraindicated if the bony procedures have not corrected 50% of the original subluxation at the talonavicular joint (Fig. 25-23). If such failure of bony correction is occurring, a triple arthrodesis is performed. For spring ligament reconstruction, there needs to be flexible deformity as described above and correction of 50% of deformity at the talonavicular joint by the bony procedures, such as lateral column lengthening and medial slide calcaneal osteotomies. If the correction by bony procedures is less than this, there may not be enough secondary ligamentous support to enable the success of a spring ligament reconstruction. Preoperative Planning Major planning is not required for spring ligament repair or reconstruction. Reconstruction along with the other procedures makes for a long procedure. There is the option of using allograft tendon or the peroneus longus tendon. A series of reconstructions with the allograft 1327

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

Figure 25-23 Preoperative anteroposterior (A) and lateral (B) views of a patient with severe fixed deformity. In the operating room, even after lateral capsular release, the patient’s talonavicular joint could not be brought into inversion and therefore a triple arthrodesis was performed. C and D, Postoperative views showing correction. The plate for the Cotton osteotomy is too long but was asymptomatic. Plates for Cotton osteotomies are not recommended as they are far too prominent and not necessary (use simple screw fixation).

tendon has not been published, and therefore confirmation of the efficacy of allograft reconstruction has not been done. However, use of allograft Achilles tendon is currently under trial. A set of cannulated reamers that include sizes from 7 to 9 mm is very helpful when doing this procedure. Preoperative standing AP and lateral radiographs of the foot should be studied to determine if the deformity is a primarily abduction, primarily plantar flexion, or, most commonly, combined. Surgical Technique for Spring Ligament Repair 1. The medial incision used for FDL tendon transfer is used for plication of the ligament. 2. The easiest and strongest method to repair the spring ligament is through a transverse incision, without excising redundant tissue 3. Closure is done through a pants-over-vest suture. The foot is held in position with the talonavicular joint reduced, and markings are made on the ligament, outlining the overlap of the redundant ligament. 4. Nonabsorbable suture is then placed from the distal segment to the proximal mark. A second set of 1328

nonabsorbable sutures is placed from the proximal segment to the distal mark. 5. These sutures are not tied until after the flexor digitorum longus tendon is brought through the hole drilled into the navicular but before the tendon transfer is tied down. This prevents undue tension on the spring ligament repair. In fact, the appropriate tension to be applied to the FDL tendon transfer should be done before tying the spring ligament sutures (i.e., the FDL tendon must be marked at the appropriate tension as well so that the tendon is under moderate tension with the foot in slight inversion). Once the FDL tendon is brought through the drill hole, the ligament sutures are tied. The FDL tendon is then secured to the stump of the posterior tibial tendon, during which time the assistant continues to hold the talonavicular joint in reduction. 6. This method has value in that it is a reinforced approach to repairing the ligament. Simply excising the redundant segment and repairing the ligament end to end has a potentially higher rate of failure because of the compromised tissue.

Pes Planus ■ Chapter 25

Figure 25-24 Preoperative anteroposterior (A) and lateral (B) radiographs of a patient with combined abduction and plantarflexion deformity. C and D, Patient was treated with an Evans lateral column lengthening, posterior first metatarsal fusion, and spring ligament reconstruction.

Surgical Technique for Spring Ligament Reconstruction (Figs. 25-24 to 25-29) 1. The navicular tunnel for the tendon transfer must be centrally placed in the navicular in the proximal-todistal plane, with an adequate bone bridge so that widening the tunnel to 7 or 8 mm will not result in navicular fracture when the graft is placed. Place a K-wire in the navicular with a good surrounding bone bridge, and check AP and lateral fluoroscopic views for proper position. Once good position is confirmed, put the guidewire in the K-wire hole and sequentially enlarge the hole to reach 7 or 8 mm, stopping before the bone bridge becomes thin. 2. In the case of a combined or primarily abduction deformity, a tibial bone tunnel is then made (Fig. 25-27). A K-wire is placed in between the colliculi at the medial malleolus and positioned to exit directly dorsally at the medial tibial metaphysis. Using fluoroscopy, check the wire position on AP ankle view to confirm that enlarging the hole will not violate the medial gutter. 3. Pass a suture attached to a snap at the dorsal end of the navicular tunnel through the navicular to the medial malleolus and up through the tibial tunnel. Pull on the free end of the suture to confirm that this path will reduce the deformity. If it does not, consider using the alternative technique described in step 8. If correction is confirmed, measure the length of the suture from the dorsal navicular to the proximal end of the tibial tunnel with the foot in neutral and add 1 cm to avoid too short a graft. 4. If the deformity is primarily the talar head sag type, the same navicular tunnel is used but not the tibial

tunnel. A calcaneal tunnel from just underneath the sustentaculum tali to the lateral calcaneus is made; exiting just above the osteotomy site (Fig. 25-28). Expose the sustentaculum tali and retract the FHL medially and plantarly. Place a trial K-wire and then replace with a guide pin from underneath the sustentaculum to the lateral calcaneus. Using the guide pin, drill the calcaneal hole, usually 8 mm in diameter. Place a suture and measure the length of this graft, again adding 1 cm. 5. The tendon graft is then prepared. Use a cylinder sizer to confirm that the tendon graft (allograft or peroneal longus) is not too large to pass through the tunnels. Two No. 2 nonabsorbable sutures are woven at the end of the graft for a strong hold. 6. If a peroneus longus autograft is used, care is taken to confirm by direct inspection that the brevis is of adequate quality because it will be the remaining evertor for the foot. If the brevis is in poor condition, an allograft is definitely used for reconstruction instead of the longus. If used, the peroneus longus is harvested proximally just distal to its musculotendinous junction. The proximal stump is tenodesed to the brevis. The longus is brought through the cubital tunnel, after releasing its attachments to the lateral aspect of the foot. It is then passed through the navicular from dorsal to plantar and into the tibial tunnel. If an Achilles tendon allograft is used, a small bone block with the calcaneal insertion is kept, ending up in the navicular tunnel. Two No. 2 nonabsorbable sutures are woven into each end of the graft. The allograft (nonbone end first) is passed through the navicular from dorsal to plantar, fixed at the navicular tunnel, 1329

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

Figure 25-25 A and B, Patient with a primarily plantar-flexion deformity. C and D, The patient was treated with a lateral column lengthening, first metatarsal–tarsal fusion, and spring ligament reconstruction. The plantar flexion did not correct with the lateral column lengthening, and therefore a spring ligament reconstruction was done. The patient achieved good radiographic correction. However, correction was not just based on radiographic parameters but leaving near-normal eversion motion.

and finally passed into the tibial tunnel. The bone end of the graft is fixed at the navicular tunnel by sutures from the graft tied to a dorsal screw as a post. 7. Having fixed the graft at the navicular tunnel, pull on graft/sutures at the exit of the tibial tunnel, confirming reduction of the deformity and good tension on the graft. Tie down the No. 2 sutures to screw as a post on the medial tibia and place bone graft in the tunnels. 8. If the abduction or combined deformity does not reduce with the trial suture or tendon graft, an alternative technique can be used which is under clinical trial (Fig. 25-29). A drill hole is made in the navicular and two drill holes are made in the calcaneus at the inferior aspect of the sustentaculum tali. The first calcaneal drill hole is at the distal aspect of the sustentaculum tali, and the second more posteriorly. The calcaneal drill holes exit laterally above the level of a calcaneal 1330

osteotomy. Confirm that the graft is sized to easily slide through the navicular and calcaneal bone tunnels. The graft is first placed through the navicular drill hole and then each limb is placed through the calcaneal drill hole under tension as depicted in Figure 25-29. The graft can be fixed by interference screws in the calcaneal tunnels once the talonavicular joint is reduced and temporarily pinned in the corrected position. The grafts can also be sewn to one another at the lateral calcaneus. Results and Complications No study has proven that spring ligament repair (not reconstruction) adds to the correction or the clinical result. Although it is difficult to confirm the efficacy of spring ligament repair when other procedures are done at the same time, the authors of this chapter think it may still be reasonable to repair the spring ligament if there

Pes Planus ■ Chapter 25

Sutures to screw post (behind bone)

B Sutures to screw post (behind bone)

Figure 25-26 A and B, Preoperative severe deformity at the talonavicular joint, which was reducible into an inverted position of the joint. C and D, Postoperative radiographs showing good correction from the spring ligament reconstruction, which was added after the bony correction had not adequately reduced the deformity.

is adequate tissue and clear laxity present. In a biomechanical study, Choi18 found that the peroneus longus tendon graft functioned best when the entire reconstruction was performed (i.e., a combined repair with both the superomedial and inferior portions done). A better clinical result from combined repair has not yet been reported in the literature. The spring ligament reconstruction results so far show correction with either a navicular to tibial or navicular to calcaneal technique in properly selected patients.188 A combined repair using both the navicular to tibial and navicular to calcaneal techniques (or the other combined technique described in step 6, using the talar neck) could result in more supporting tissue. Because of the risk of navicular fracture and the difficulty of a combined procedure, particular care should be taken if two grafts are placed in the navicular tunnel. It is for this reason that the technique in step 8 is under clinical trial. It should be remembered that the dorsal aspect of the superomedial spring ligament inserts at the dorsal navicular and interlaces with the superficial deltoid. Therefore it is not illogical that a medial attachment point on the tibia (or talus) should be used. Although potentially a stronger repair, the efficacy of the combined techniques awaits clinical follow-up. Also, whether allograft tissue results in a reconstruction more likely to stretch out has not been determined. Follow-up from the peroneus longus study, good correction was noted in the AP talonavicular coverage angle but was not statistically significant for the other angle measurements.188 Most patients kept good, but not full,

Figure 25-27 Spring ligament reconstruction. Drill holes for combined abduction and plantar-flexion deformity are shown. Also used for primarily abduction deformity. Graft goes from navicular to talus.

1 Sutures to screw behind bone

Figure 25-28 Spring ligament reconstruction showing drill holes for a primarily plantar-flexion deformity, where graft goes from navicular to calcaneus.

triple joint motion. For the 14 feet treated, 10 were capable of a single-stance heel rise and inversion of the heel, with 2 being unable invert the heel. However, it should be remembered that spring ligament reconstruction was done in feet that did not get adequate correction with the use of a medial heel slide and lateral column lengthening, and the procedure was performed as an alternative to a triple arthrodesis. No patient had to be converted to a triple arthrodesis. Care was taken that reconstruction was done only when lateral column lengthening and a medial heel slide gave 50% correction or more of the abduction deformity but clearly left too much deformity without 1331

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Figure 25-29 Spring ligament reconstruction with combined technique simultaneously replacing superomedial and inferior spring ligament. Technique is presently under clinical trial.

reconstruction. Spring ligament reconstruction is a reasonable alternative to arthrodesis in patients who have partial but incomplete correction with osteotomies. PLANATAR-FLEXION OPENING-WEDGE (COTTON) OSTEOTOMY OF THE MEDIAL CUNEIFORM In the patient with a symptomatic flatfoot, elevation of the first ray or forefoot varus is a concern. After flatfoot reconstruction, collapse of the arch distal to the talonavicular joint as well as at that joint is an undesirable outcome. It is therefore attractive to bring the first ray down and correct significant forefoot varus when present. However, there are no precise guidelines as to when this is necessary, and studies proving symptomatic benefit from this procedure have not been done. Numbers that have been suggested as describing significant forefoot varus have been greater than 10 to 15 degrees. Although leaving such forefoot varus can result in excessive lateral weight bearing after triple arthrodesis, the results after a flatfoot correction without a fusion of the talonavicular joint in the setting of forefoot varus have not been studied. It is nevertheless reasonable to maintain the tripod of the foot with good plantar alignment of the first and fifth metatarsal heads in a flatfoot reconstruction. In the setting of moderate deformity at the naviculocuneiform joint, a Cotton osteotomy can be used as an alternative to naviculocuneiform fusion if the first metatarsal–tarsal joint is stable. A dorsal opening-wedge osteotomy of the medial cuneiform, described by Cotton,25 can bring the first ray down. The relative efficacy of this procedure versus a first metatarsal–tarsal fusion, to correct elevation of the first ray, has also not been well studied. It is true that both procedures can bring the first ray down. If the Cotton osteotomy does this as well as the first metatarsal–tarsal fusion, the osteotomy has the advantage of being faster and easier to perform and probably has a higher union rate. Because it is being performed adjacent to intact Lisfranc and 1332

intercuneiform ligaments, there is likely to be a limitation in the amount of correction possible because of tensioning the ligaments with an opening-wedge osteotomy. Certainly, release of these ligaments is not a good option. In Dr. Jonathan Deland’s personal experience there is a limitation to how much a Cotton osteotomy can bring down the first ray. Until data is available, the Cotton osteotomy may therefore be best used to correct moderate elevation of the first ray. In cases of severe elevation or considerable instability at the first metatarsal–tarsal joint, a first metatarsocuneiform fusion may be the more reliable choice because the limitation from ligament tension is less likely to be a factor. The surgeon should be aware that some shortening of the first ray occurs with this fusion, and plantar flexion and shortening of the first metatarsal can dorsiflex the first metatarsophalangeal joint. Excessive shortening or plantar flexion of the first ray should be minimized. Indications The osteotomy is indicated with significant forefoot varus (greater than 10 degrees) and a stable first metatarsal– tarsal joint. It can produce a better-appearing arch, but whether it achieves a better outcome is a different question. It is not known whether this procedure clinically decreases excessive lateral weight bearing from a lateral column lengthening because the lateral weight bearing may be at least in part from the postlengthening stiffness along the lateral column as well as elevation of the first ray. It is better to ensure maintenance of both adequate flexibility (eversion) along the lateral column as well as normal eversion of the foot, rather than bring the first ray down. The surgeon should not correct the elevation of the first ray as an antidote for excessive stiffness along the lateral column. Bringing the first ray down and leaving the lateral column stiff still results in symptoms from a stiff lateral column. Contraindications This procedure is contraindicated in patients with osteoarthritis of the first metatarsal–cuneiform joint. These patients are better served with an arthrodesis with careful plantar resection to bring the first ray down in good alignment with the second metatarsal head. Patients with gapping at the plantar first metatarsal–tarsal joint, or considerable instability of that joint, are likely to be better served with arthrodesis. Preoperative Evaluation Patients are examined in both a seated and standing position to evaluate the forefoot varus. Correction of the subtalar joint to neutral reveals elevation of the first ray in patients with forefoot varus. Palpation of the plantar metatarsal heads while correcting the hindfoot to neutral shows the magnitude of this elevation. Adequate vascularity must be present in the distal foot to support healing of the bone graft. Thus noninvasive Doppler studies with toe pressures are helpful in this evaluation.

Pes Planus ■ Chapter 25 Preoperative Planning Care should be given to incision placement. The incision for this osteotomy is dorsally based. The surgeon should either not carry the medial incision too distally for the FDL transferred, to avoid an insufficient skin bridge, or make the medial incision for the transfer more plantar to the medial cuneiform to maximize the skin bridge. Also, if the alternative of a first metatarsal–tarsal fusion is chosen, the incision for that should be over the lateral edge of the first metatarsal rather than directly over the first metatarsal– tarsal joint, to avoid too small a skin bridge. There is the choice of allograft or autograft for the bone graft. Both are quite acceptable. There is minimal chance of allograft or autograph collapse as long as there is a good bicortical strut in the graft perpendicular to the osteotomy line. SURGICAL TECHNIQUE FOR COTTON OSTEOTOMY 1. The patient is in a supine position, with the foot vertical (not internally or externally rotated). 2. A dorsal incision is made overlying the medial cuneiform (Fig. 25-30C). 3. The extensor hallucis longus is retracted medially, and dissection proceeds to the medial cuneiform. Care is taken to avoid the superficial and deep peroneal nerves and the dorsalis pedis artery, which lie just

lateral to the osteotomy. The branch of the superficial peroneal nerve is most at risk. 4. Fluoroscopic imaging is used to locate the middle of the medial cuneiform, the location of the osteotomy. 5. A transverse osteotomy is made with a microsagittal saw from dorsal to plantar, with retractors protecting the lateral structures mentioned above and the extensor hallucis longus (EHL) medially. The osteotomy should not violate the deep plantar cortex but stop about 5 mm short of it. Measuring the depth of the bone with K-wires, on either side of the osteotomy and appropriately marking the depth on the saw blade, is helpful. 6. A straight osteotome placed dorsal to plantar is used to lever the medial cuneiform open at the osteotomy site. The same K-wires used in the last step can be used to open the osteotomy with a laminar spreader–type device. 7. The width of the dorsal base of the graft can be determined by either of two methods. The assistant wedges the dorsal cuneiform open with an osteotome until the surgeon feels a precise balance to the metatarsal heads, and the dorsal gap is measured. It is important to measure the depth of the graft as well, to create an interference fit. The second method involves wedging the medial cuneiform open, while using a lateral

Figure 25-30 A and B, Preoperative radiographs of a flatfoot patient. C and D, postoperative radiographs following posterior calcaneal osteotomy, stepcut osteotomy and Cotton osteotomy. Note the single screw fixation of the Cotton osteotomy. This deformity is flexible and remained painful with orthotic management.

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fluoroscopic image and looking for appropriate declination of the first metatarsal. This latter method is susceptible to difficulty in judging the position of the first ray because of not obtaining a perfect lateral view. Once a good position is confirmed, the dorsal gap is measured. 8. The bone graft is harvested in a standard fashion, or the allograft is used after soaking in an antibiotic solution. 9. After interposition of the appropriate graft size, lateral fluoroscopic radiographs may be used to ensure excellent fit and the appropriate talus–first metatarsal angle. If the fit is not precise, the surgeon can improve the fit by inserting the saw blade from the microsagittal saw into the osteotomy site (proximally and distally), with the graft in place, and creating a perfect fit by dorsal-to-plantar cutting with the blade. This technique is very helpful, but it must be done carefully to prevent shortening the graft or altering the shape of the wedge. 10. This graft is stable and thus does not require fixation. However, the surgeon can use a cannulated screw from dorsal-proximal to plantar-distal. 11. The wound is closed in layers.

populations were studied: adult and pediatric. The average time to union was 7 weeks in the pediatric population and 12 weeks in the adult population. The authors noted a statistically significant improvement in the lateral first talometatarsal angle, the calcaneal pitch, and the plantar medial cuneiform–to-floor height. They also noted the power of this procedure to correct forefoot varus with an adjustment in wedge width and taper. Complications include painful hardware because of the lack of fat cushioning between the skin and hardware; neuromas of the superficial peroneal nerve, deep peroneal nerve, or saphenous nerve; and also nonunion. A small proximal dorsal-to-plantar distal screw can help avoid prominent hardware, and the neuromas can be avoided by careful dissection and retraction. Nonunion with good apposition and fixation is uncommon (Fig. 25-31). The Cotton osteotomy is useful if the first metatarsal–tarsal joint is stable and the surgeon wishes to bring the first ray down in the setting of the moderate deformity. It is best used to make the plantar first and fifth metatarsal heads approximately equal in alignment in the setting of significant elevation, but not use it to counteract a lateral column lengthening that has created too much supination or to offset a triple arthrodesis set in supination.

Results and Complications The only study in the literature looking specifically at this osteotomy, used in conjunction with an adult-acquired flatfoot deformity and pediatric congenital flatfoot, comes from Hirose and Johnson.77 Using the above-mentioned technique, the authors reviewed 16 feet.77 Two separate

LATERAL COLUMN LENGTHENING Although originally thought to be a procedure that might not stand the test of time, lateral column lengthening has grown in use in patients with PTTD. It has allowed patients with more severe deformity to gain adequate correction of the triple joint complex (talonavicular,

Figure 25-31 Patient with hindfoot (A) and midfoot (B) deformity as well as elevation of the first ray and first metaphalangeal (MP) arthritis. The preoperative radiographs did not reflect the extent of the deformity at the talonavicular joint (patient did not let arch collapse for the radiograph, deformity was demonstrated fluoroscopically in the operating room). The deformity was corrected with a medial heal side (C) and Evans-type lateral (D) column lengthening, leaving good eversion motion remaining. The first MP arthritis was treated with a first MP fusion, and the elevation of the first ray was corrected with a Cotton osteotomy fixed with a single screw at the medial cuneiform.

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subtalar, and calcaneocuboid joints) but avoid fusion of at least two of those joints: the talonavicular and subtalar joints.* These latter joints are important joints for motion and if fused can eventually promote arthritis of the ankle. Specifically, lateral column lengthening is for patients with severe flexible deformity whose triple joint complex subluxation cannot be adequately addressed by a medial slide osteotomy and who would otherwise need to be addressed by fusion in the triple joint complex, The deformity includes abduction/plantar sag at the talonavicular joint and subluxation at the subtalar joint resulting in a pronated valgus hindfoot. A severe pronation deformity ultimately results in lateral impingement. The lateral impingement has been found to be at the angle of Gissane in the sinus tarsi and, in the most severe cases, at subfibular area with calcaneal abutment against the fibula.47,114 One solution for this impingement is to fuse one or more of the joints of the triple joint complex in a corrected position. Another solution is to lengthen the lateral column, as long as it adequately corrects deformity. It most commonly adequately corrects deformity as well as stiffens the hindfoot. If properly used, it should stiffen it to a much lesser degree than an arthrodesis. If done properly, it leaves good motion in the triple joint complex. So far lateral column lengthening, although it may increase pressure in the calcaneocuboid joint, has not led to a high incidence of adjacent joint arthritis.25,136 Although it is well-known that lateral column lengthening can lead to lateral discomfort or pain,47,49 why lateral column lengthening has the potential to cause lateral symptoms is not completely understood. Dumontier et al,43 in a cadaveric study of lateral column lengthening, showed that the talonavicular joint rotates not as a perfect sphere but takes a path around the ellipsoid talar head. The authors hypothesized that the long plantar ligament and other soft tissue structures may have a role in the correction gained by lengthening the lateral column. The spring ligament complex, whatever part of it is still functioning, probably acts as a ligamentous fulcrum for correction during lateral column lengthening. Therefore correction occurs around the ellipsoid talar head and is dependent on the remaining ligaments mentioned above. Whatever the mechanism, if adequate ligaments remain, the foot becomes increasingly supinated with lateral column lengthening with potential of overstiffening of the lateral hindfoot. In effect, the correction can be so powerful that not only does it eliminate the excessive eversion and abduction motion of the deformity but reduces normal subtalar motion. If too much motion is lost, the foot will become too stiff, with limited eversion resulting in excessive lateral weight bearing. It is a powerful corrector of deformity, with just a 2 to 3 extra millimeters of extra lengthening often having a significant effect on position as well as stiffness. Therefore it has been helpful to gauge correction not just by radiographic correction but by eversion motion intraoperatively. Thus the

Varus of the heel or failure to maintain normal eversion/abduction motion will risk stiffness and lateral weight bearing. Slight stiffness is acceptable; considerable stiffness results in unacceptable symptoms. Progressive arthritis of the calcaneocuboid joint, originally thought to be a possible frequent complication of lateral column lengthening, is uncommon, and when it occurs, is usually minimally symptomatic.134 Two procedures, the Evans lateral column lengthening and a lateral column lengthening stepcut osteotomy (a modification of the Vander Griend osteotomy), are highlighted below.66,153 The Evans procedure, developed for the treatment of painful adolescent flatfoot, is the more frequently used at present and has been well studied clinically.153 However, the stepcut osteotomy, with its longitudinal arm, provides an area of healing that is not dependent upon interpositional bone graft and minimizes the chance of elevation of the distal fragment or graft collapse.32,66 Although the Vander Griend, or stepcut, osteotomies can potentially still fail to heal, loss of correction is less likely because of the longitudinal arm. Also, the osteotomy has the potential to be displaced in a primarily rotatory fashion, as described by Vander Griend.66 The modification of the Vander Griend osteotomy uses a stepcut, which is the same type of cut as in the Vander Griend but with a trapezoidal graft, rather than the rotatory correction with some lengthening that Vander Griend described. The term lateral column lengthening stepcut osteotomy, or LCL stepcut osteotomy, will be used in the remainder of this chapter because the technique involves trapezoidal wedges. It therefore creates more distraction at the osteotomy site and is likely to gain more correction. The correction of a Vander Griend osteotomy versus an

*References 6, 19, 33, 52, 70, 134, 145, and 179.

*References 9, 32, 38, 68, 76, 178, and 189.

goal is to remove the excessive eversion/abduction motion but retain normal or near-normal eversion motion and thereby minimize lateral stiffness and overload. Although both radiographic correction of deformity and motion are important, the primary determinant of correction becomes the elimination of excessive eversion motion but retaining near-normal eversion/abduction motion to achieve the most comfortable foot. Some surgeons use lateral column lengthening by itself, without a medial slide osteotomy, and others in combination with it.* If used with a medial slide osteotomy, careful attention must be given to the combined effect of the two osteotomies, with each temporarily fixed so that the surgeon can assess the foot for proper position of the heel and midfoot as well as the remaining eversion/ adduction motion. The goals are 1. Central position of the heel, no varus 2. Near-normal eversion motion remaining with mild restriction of eversion at the subtalar joint 3. Radiographic correction of the talonavicular joint minimizing remaining abduction or plantar flexion

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LCL stepcut osteotomy needs to be studied, but it is likely that the probable greater correction of the stepcut can lead to lateral overload. Any lateral column lengthening can be combined or not combined with a medial slide osteotomy, if the medial slide osteotomy is necessary to correct remaining excessive valgus of the heel. Indications Indications for lateral column lengthening include (1) lateral impingement or (2) abduction or combined abduction/plantar-flexion deformity at the talonavicular joint that is not likely to be addressed by a medial slide osteotomy. A medial slide osteotomy does not commonly give a large amount of correction to abduction or plantarflexion deformity. Although this second indication of abduction/eversion deformity is not precise, it can be tested by temporarily fixing the medial slide in the operating room and looking at correction of the talonavicular joint fluoroscopically and assessing eversion motion before a lateral column lengthening is done. Preoperative radiographs are helpful, but surgeons must remember that they are limited by how much the patient lets his or her arch collapse while the radiograph is taken, and the radiograph should be compared with an observation of the patient standing and letting the arch collapse. Uncoverage of the talar head on a standing AP of the foot of more than 30%, and certainly at 40% in a symptomatic flatfoot, suggests the need for lateral column lengthening. Also, because suggestive, excessive passive eversion motion of the hindfoot should be examined. The talonavicular coverage angle or the incongruency angle may be a more precise measurement than the percentage uncovered, but the former measurements have not been as frequently used in the literature.50 The AP radiograph must be taken with the patient fully weight bearing on the foot and with the patient letting the arch pronate. The x-ray beam should be centered as much as possible directly dorsal to the talonavicular joint. Confirmation of the uncoverage can be done under fluoroscopy in the operating room. Contraindications Patients with stage III disease (fixed hindfoot deformity in the triple joint complex) are not candidates for lateral column lengthening. The deformity must be passively correctible with the talonavicular joint being able to be manipulated past neutral into inversion or adduction. There are cases of severe deformity in which the talonavicular joint cannot be adducted in the office, but after release of the lateral talonavicular joint capsule, the joint can be brought into adduction. Also, patients with symptomatic or severe arthritis in the triple joint complex are not good candidates for lateral column lengthening. Preoperative Evaluation Flexibility of the hindfoot joints, allowing good correction of the foot, must be confirmed preoperatively. Specifically, correction of the position of the heel and the to 1336

bring the talonavicular joint into inversion with reduction of the subtalar joint should be confirmed by physical examination. If necessary, a stress AP radiograph of the foot with the foot placed into inversion can be used to demonstrate the ability to bring the talonavicular joint into adduction. Standing AP and lateral radiographs of the foot and a standing AP radiograph of the ankle should be assessed for the amount of deformity (Fig. 25-32). Care should be taken to check for valgus deformity of the ankle on a standing AP ankle radiograph because that can be missed if the ankle radiograph is not done. Also, a patient can appear clinically to have severe deformity in the foot, yet the radiograph evaluation is not impressive. This most commonly occurs because the patient is not fully weight bearing when the radiographs are taken or the patient is leaning back. If the radiographs are unimpressive compared with the physical examination, they should be repeated with the patient letting the arch completely collapse with full weight bearing. A Saltzman (hindfoot alignment view) is also a very helpful radiograph (Fig. 25-34) and should be considered a routine radiographic view for this condition. It is very helpful in visualizing and measuring the amount of hindfoot valgus. An equation has been developed to predict the amount of correction needed in the operating room.14 This equation needs to be applied to a large group of patients for confirmation of its usefulness and accuracy. However, there is benefit

Figure 25-32 This hindfoot alignment view, as described by Saltzman,158 is used to measure the hindfoot moment arm. This view and measurement accurately depicts the hindfoot deformity and can be used to estimate the amount of correction needed. In this example, this patient with bilateral flat feet needs a large medial slide on the left but not on the right. The hindfoot alignment view is best taken as a single view for each side.

Pes Planus ■ Chapter 25

to visualizing the amount of hindfoot valgus and measuring it so the result can be used as an estimate of how much to slide the heel, minimizing the chance of over- or undercorrection. A lateral column lengthening also affects the position of the heel, although it is likely that it will not correct heel valgus to the same degree as a medializing calcaneal osteotomy. When using that osteotomy with a lateral column lengthening, it is important to realize that there will be some correction of the heel from the lengthening procedure. Both osteotomies should be temporarily fixed and the position of the heel assessed in the operating room by looking at the position of the heel from an end-on view (Fig. 25-33), as well as palpating the heel to make sure that the heel is not in varus but centrally placed. Care should be taken not to perform a lateral column lengthening in the setting of minimal deformity because this can result in an adducted, stiff, uncomfortable foot. It is important to achieve adequate correction of deformity and eliminate excessive eversion while retaining adequate (near-normal) eversion of the hindfoot. Thus performing a lateral column lengthening when there is not excessive eversion will overstiffen the foot. Surgical Technique for Evans Procedure (Fig. 25-34) A lateral column lengthening requires good access to the lateral hindfoot with the patient in the lateral decubitus position or in the supine position with the leg internally rotated to gain access to the lateral hindfoot. Fluoroscopic imaging to obtain an AP and lateral view of the foot is essential. The leg should be able to be rotated to a position to allow eversion of the foot and simulate loading of the foot to judge correction and subtalar motion.

Figure 25-33 Clinical photograph demonstrating a useful position to assess heel alignment in the operating room. Heel should be centrally placed in relation to the ankle and calf, without varus but neutral to slight valgus.

1. This procedure can be performed with or without a medial slide osteotomy. By the end of the foot reconstruction, the patient should have central position to a central slight valgus of the heel. The medial calcaneal osteotomy can be performed first in a patient with severe heel valgus but should not be permanently fixed until after the lateral column lengthening has been set. Failure to check the position of the heel and adjust as necessary after the lateral column lengthening can result in improper position of the heel, most commonly varus. The lateral column lengthening does change the position of the posterior heel but does not as much as a medial slide osteotomy. 2. Under thigh tourniquet, an incision is made longitudinally along the sinus tarsi just above its floor, ending at the calcaneocuboid joint. In general, the dissection should remain well above the level of the floor of the sinus tarsi and the peroneal tendons to avoid possible injury to the sural nerve. Once on the floor of the sinus tarsi, dissection is made subperiosteally over the anterolateral calcaneus, mobilizing and retracting the peroneal tendons away from the lateral calcaneus. The very dorsal aspect of the calcaneocuboid joint is also exposed to confirm the calcaneocuboid joint line. 3. A K-wire is placed as a guide for the osteotomy cut. To avoid too small a distal fragment, place the pin 1.5 cm proximal to the calcaneocuboid joint, aiming 10 to 15 degrees posteriorly from a direct perpendicular to the lateral calcaneus. This should place the pin just anterior to the middle facet or at the junction of the anterior and middle facets. A blunt elevator or Freer elevator can be used to locate the middle facet. It is preferable to stay distal to the medial facet with the bone cut. 4. Check pin placement on AP and lateral views of the foot. Note that the saw cut will be made on the distal side of the pin, with retractors in place to protect the peroneal tendons. 5. Make the cut, taking care not to plunge through the medial cortex. The medial cortex can be weakened by

Figure 25-34 Diagram of lateral column lengthening stepcut osteotomy. Note that the longitudinal arm of the osteotomy gives an area of primary bone healing and graft is placed at the vertical arms at either end of the osteotomy. The vertical arms are shorter than those described by Vander Griend, to minimize the chance of fracturing through the intact bone.

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small motions of the saw to preserve medial periosteum and soft tissue. Irrigation is helpful to avoid thermal necrosis. 6. Open the osteotomy site laterally. (Distraction will usually occur on the medial side, but it is best not to overdistract the medial side.) 7. With the use of trial wedges or a laminar spreader, try different amounts of lengthening to gain correction yet not overstiffen the midfoot and hindfoot. The authors prefer using trial wedges because, with wedges in place, easy manipulation of the foot is allowed, to judge both the amount of correction at the talonavicular joint and the eversion motion of the triple joint complex. Two millimeters of correction can make a very significant difference to the patient in terms of stiffness or over-/undercorrection. Fluoroscopy with the foot everted should be used to check the position of the talonavicular joint on the AP and lateral views. Correction of the joint should occur, but the amount of correction should not be judged purely radiographically. Eversion/abduction motion must also be checked to confirm that normal or nearnormal motion remains with manipulation of the calcaneus and hindfoot. This latter motion must remain for the patient to have the least risk of lateral discomfort or pain from stiffness. However, leaving excessive eversion motion (with residual abduction of the talonavicular joint or excessive valgus of the heel) can lead to recurrence of lateral impingement. 8. Once good position and motion is confirmed, the trial wedge or space determined by the laminar spreader is used to fashion the tricortical bone graft.

9. The surgeon has the option of either using allograft or iliac crest autograft. Good results have been reported with both, although there may be less chance of graft collapse with autograft. 10. Using a laminar spreader, the tricortical graft is placed in the osteotomy site. No space should be seen either dorsally or laterally at the interfaces of the graft and host bone. AP and lateral fluoroscopy is also used to confirm good fit of the graft. If space is present, carefully shave the appropriate location on the graft or host bone so that excellent contact is achieved. If at the correct size, take care not to shorten the graft laterally because this will change the correction. 11. Pin the osteotomy site with two longitudinal K-wires from the distal fragment to the proximal fragment. Place a long lag screw from the distal fragment across the graft and into the proximal calcaneus. A 3.5-mm lag screw is used; a smaller screw or larger screw is preferred by some surgeons. Most important, good fixation as well as compression and apposition should be achieved. Compression fixation using a thin lateral plate or a compression staple device can be very helpful in addition to the screw. 12. After fixation is placed, check that the graft is stable and good apposition is present. Surgical Technique for LCL Stepcut Osteotomy (Fig. 25-35A-D) 1. Incision is the same as for the Evans, except that is extended 1 to 2 cm more proximally, to the distal tip of the fibula (Video Clip 119). 2. Similar dissection is made laterally over the anterior calcaneus. However, this dissection is carried proximal

Figure 25-35 A and B, Patient with advanced abduction and plantar-flexion deformity in the hindfoot and midfoot, showing combined plantar flexion and abduction at the talonavicular joint. C and D, Correction with lateral column lengthening stepcut osteotomy for lateral column lengthening as well as medial slide calcaneal osteotomy and metatarsal–tarsal fusion.

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and plantar to the peroneal tubercle. The peroneus longus is held against the lateral calcaneus by a sheath attached to the peroneal tubercle. Open this sheath and make sure both peroneal tendons are mobilized away from the lateral calcaneus proximally as well as dorsally. A pin is placed, retracting the peroneal tendons inferiorly and proximally, giving maximal exposure of the lateral calcaneus. The proximal bone cut, in particular, risks injuring the peroneal tendons. A pin can be placed proximally and plantarly pushing the peroneal tendons out of the way. 3. Pins are placed to mark the elbows of the stepcut osteotomy. The first pin is placed just over 1 cm proximal to the calcaneocuboid joint at the junction of the dorsal one third and plantar two thirds of the bone. The second pin is placed 2 cm proximal to this at the junction of the dorsal two thirds and plantar one third of the bone. These placements of the pins help minimize the risk of fracturing at the proximal and distal arms of the osteotomy. These vertical arms are shorter than as described by Vander Griend; the shorter arms, which minimize risk of saw cuts straying vertically in the wrong direction, are depicted in Figure 25-35A. 4. Cut the longitudinal 2-cm arm, being careful to retract the peroneal tendons. After cutting the lateral cortex, carefully cut the medial cortex so as not to plunge. 5. Cut the distal dorsal arm, but do not to stray inferiorly and weaken the distal fragment. Be sure to cut the elbow junctures well because this can help avoid difficulty in mobilizing the osteotomy later. 6. Cut the dorsal aspect of the proximal plantar cut, being careful to protect the peroneal tendons. If the plantar portion of the proximal plantar cut is too difficult to make because of the peroneal tendons, dissect around the peroneal tendons and sural nerve and retract them dorsally to gain access to the plantar area for the cut. Protect the tendons and soft tissue with wide retractors when performing these cuts. 7. Mobilize the osteotomy site with an osteotome, but do not hinge aggressively on the dorsal distal or proximal plantar limbs. If the osteotomy does not move easily, check with the saw that the cuts are complete medially, especially at the elbows. 8. Place a pin in the distal more plantar aspect of the calcaneus adjacent the calcaneocuboid joint but away from the elbow of the cut. Place another pin in the more dorsal proximal aspect beyond the osteotomy so that the osteotomy can be distracted with a laminar spreader or pin distractor device. With the device, spread the osteotomy open, making sure that the longitudinal cut remains apposed. 9. Use the laminar spreader to hold the correction, or better, use a trial wedge/spacer of appropriate size in the dorsal arm to judge the amount of correction. The criteria for correction are the same as with the Evans procedure described above.

10. Place tricortical autograft or allograft at the dorsal arm of the osteotomy site keeping the longitudinal arm well opposed. This graft can be gently wedged into the distal arm. The osteotomy should be manually compressed to confirm excellent apposition and a snug stable fit of the graft as described for step 10 of the Evans procedure. 11. Drill a longitudinal K-wire from distal to proximal, from the dorsal aspect of the calcaneus across the graft and into the posterior calcaneus. Start a second K-wire just distal and lateral to the posterior facet and drill it dorsal to plantar for both temporary fixation and the path for a second screw. 12. Replace the proximal-to-distal K-wire with a 3.5-mm lag screw and place a second screw along the path of the dorsal-to-plantar K-wire hole. 13. Wedge a carefully sized tricortical graft into the plantar arm for a snug fit. Trim away any prominent tricortical wedge bone at the distal dorsal arm of the osteotomy to avoid impingement against the talus and smooth any sharp edges along the lateral calcaneus. 14. Check for impingement in the sinus tarsi with eversion range of motion. If necessary, shave away prominent bone on the anterior aspect of the lateral talar process at the posterior facet joint, to avoid bony impingement at the angle of Gissane. TREATMENT OF DELTOID INSUFFICIENCY Deltoid ligament insufficiency or disruption occurs late in the course of PTT insufficiency and has been quantified as stage 4 disorder. Although there are components of the deltoid ligament that merge with the spring ligament, for purposes of this discussion, only the failure of the strongest bands will be considered: the tibiocalcaneal (superficial) and posterior (deep) tibiotalar ligaments.11 The integrity of the deltoid ligament has been shown to be critically important in the maintenance of normal biomechanics of the ankle joint. Sectioning of the deltoid ligament has been shown to decrease the tibiotalar contact area by 43%.46 Thus, in advanced PTT insufficiency with a valgus deforming force already present, if the disrupted deltoid is left unchecked, the increases in peak pressures leads to the eventual development of osteoarthritic changes within the ankle joint. Indications Deltoid ligament reconstruction is indicated if rupture is visible or laxity is noted upon direct inspection intraoperatively. Valgus and/or external rotation stress testing showing increased talar tilt or rotation suggests the necessity of ligament reconstruction. Note that restoration of the medial column of the foot is not sufficient to take the strain and subsequent deforming force upon the ankle.167 Significant increase in strain upon the deltoid, if present with heel rise even after said reconstructions, allows degenerative wear upon the ankle joint because of improper biomechanics. Finally, similar to other soft tissue procedures mentioned in this chapter, isolated 1339

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reconstruction of the deltoid ligament is rarely performed and is almost exclusively done in combination with other realignment procedures. Contraindications The only relative contraindication to deltoid ligament reconstruction is advanced degenerative disease that may require ankle arthrodesis. With advancement in ankle replacement technology, it is clear that reconstruction under these circ*mstances remains a relative contraindication. If the patient has potential to undergo total ankle arthroplasty to correct advanced degenerative disease, then reconstruction of the deltoid ligament becomes an indicated component to advanced flatfoot reconstruction. Preoperative Evaluation If available, MRI is a useful adjunct to planning deltoid ligament repair because of both its sensitivity and specificity. The location and the poor quality of the tissue can be mapped, allowing the surgeon to decide if any residual deltoid tissue will have value in assisting the reconstruction. Plain radiographs document a tibiotalar tilt, even if subtle, on weight-bearing ankle views. The surgeon must look carefully for this tilt because its presence dictates deltoid instability. Finally, stressing the ankle in both eversion and external rotation tests the rigidity of the deltoid ligament, creating pain that must be discerned from PTT pain based on location. Of note, the deep deltoid component is directly inferior to the posterior tibial tendon, and thus direct palpation of that ligament has less value in confirming ligament disruption because the diseased tendon is generally in this same location. Preoperative Planning Planning for deltoid reconstruction primarily involves determination of incision placement commensurate with the additional surgical procedures planned in flatfoot reconstruction. The incision for deltoid reconstruction through tendon transfer requires exposure of the superficial deltoid ligament insertion, which is at the sustentaculum tali of the calcaneus. This incision is virtually vertical, which does not have the same curvilinear slope of the flexor digitorum longus tendon transfer incision directed toward the navicular. As such, the surgeon must plan compromise of both incisions to achieve both goals. Similar to spring ligament reconstruction, patient positioning does matter, as external rotation of the extremity will help to gain access to the medial ankle. Surgical Technique for Deltoid Reconstruction There are a variety of procedures in the literature developed to reconstruct the deficient deltoid ligament.8,34,69 All involve tendon transfers on some level because repair of the chronically insufficient deltoid ligament more often than not results in failure resulting from poorquality tissue under significant tension. Unlike lateral ligament reconstruction, deltoid reconstruction requires significant tension to prevent recurrent valgus deformity. 1340

HADDAD TECHNIQUE69 1. A thigh tourniquet is used for this procedure but must be deflated before closure to ensure adequate hemostasis and prevent postoperative hematoma. 2. A semitendinosus allograft is soaked in antibiotic solution to allow thawing. Graft length should approach 300 mm. The graft is tubularized to facilitate passage. Tension is placed on the graft to minimize late creep of the tendon (Fig. 25-36A). 3. Medial exposure is critical, and thus external rotation of the involved extremity is helped by placing a bump beneath the opposite hip. Note, however, that at certain points in the procedure the surgeon will require access to the lateral hindfoot, and thus the bump is normally removed after deep medial exposure is complete (Fig. 25-36B). 4. As noted above, exposure involves an incision over the intercollicular groove of the medial malleolus, extending distally over the sustentaculum tali. This incision is nearly vertical. Note that to address both the PTT and the deltoid ligament the surgeon may need to alter this incision by beginning just posterior to the medial malleolus and extending toward the navicular. However, this modification should incorporate a larger curvature to incorporate the sustentaculum tali. 5. The PTT is exposed and retracted to expose the deep deltoid insertion, and the flexor hallucis longus is traced to expose the sustentaculum tali. Structures at risk are the tibial nerve, primarily at the inferior portion of the incision near the sustentaculum tali (Fig. 25-36C-E). 6. Drill holes will be placed beginning medially at the insertion of both the superficial and deep deltoid ligaments. These drill holes are through and through the calcaneus and talus, respectively (Fig. 25-36F). To position the drill holes without violation of offending bone structures, the drill holes are placed over guidewires. The guidewires serve a secondary purpose of allowing exact measurement of the length of the drill holes, which is critical in establishing appropriate graft length. The direction of the talus guidewire is from the insertion point of the deep deltoid, 1 cm posterior and inferior to the intercollicular groove, and exiting anterior to the fibula. The central portion of the sustentaculum tali is the starting point for the guidewire, given the small size of this projection and the subsequent potential for the drill to fracture this portion of bone. The wire is directed both inferiorly and anteriorly, exiting 1 cm proximal to the calcaneocuboid joint, and at the inferior margin of the calcaneus (Fig. 25-36G). This direction allows the wire (and drill hole) to avoid the sinus tarsi. Both guidewire lengths within the bone are measured. In general, the talar length is 45 mm, and the calcaneal length is 55 mm. 7. A third guidewire begins at the intercollicular groove of the medial malleolus, directed in the central medial malleolus both anterior and lateral. This wire exits in the central metaphyseal tibia. This length is also mea-

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PTT Superficial deltoid insertion FHL FDL

Deep deltoid insertion

Figure 25-36 A, Isolated anterior tibial tendon graft after tubularization and with No. 2 Ethibond suture, undergoing Krakow suture weave on both ends. B, Standard medial approach to the ankle, with the posterior tibial tendon retracted posteriorly. This approach allows excellent visualization of the deltoid ligament complex. C-E, Visualization of the deltoid ligament complex deep to the posterior tibial tendon. The fibers of the deep deltoid (a) and superficial deltoid (d) are easily recognizable by their footprint and orientation. After defining both the deep and superficial deltoid ligaments, they are sectioned (e). F and G, Medial ankle visualization (F), with tendons identified (FDL, flexor digitorum longus tendon; FHL, flexor hallucis longus tendon; PTT, posterior tibial tendon). Guidewire insertion points are labeled for both the superficial and deep deltoid ligaments, based on their footprints and anatomic locations. Anterior view of the ankle (G) showing orientation of guidewires and exit points inferior and anterior to fibula. H, Actual patient with orientation of three guidewires visualized in the operating room. Note the orientation of the tibial guidewire from the intercollicular groove, exiting at the anterior tibia. I-K, Graft preparation was performed by first attaching the suture buttons to each end of the sutured tendon graft (I). This graft is then pretensioned to minimize creep (J). The graft is then sized for absolute width and doubled width (K) to determine appropriate tunnel size. L-O, Graft passage first required the use of cannulated reamers set to the appropriate tunnel depth, leaving a 1-cm “bone bridge” laterally to maintain the holding power of the suture button (L). The sutures that facilitate suture button passage are placed through the respective holes within the medial guidewires (M), allowing each end to be passed through a separate cannulated drill hole (one end in the talus and the other in the calcaneus). Continued

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

S X-Y slide (above)

Axial loading (z-axis)

Leg holder

Inversion/ eversion [motor II]

Plantar/ dorsiflexion [motor I]

Internal/external rotation [motor III] (underneath the foot)

Figure 25-36, cont’d The looped end of the graft is then pulled through the tibial tunnel (N) with the assistance of a suture through the loop. Note the power of maximal tension pulling the foot into varus. Fixation is then achieved with a spiked ligament washer over a 6.5-mm cancellous screw post (O). P and Q, Final radiographs demonstrating graft passage in as a white line. Note that in the lateral radiograph (P) the suture buttons are secure against the drill holes, both being placed anterior and inferior to the fibula to facilitate passage. The anteroposterior radiograph (Q) again demonstrates the security of the suture button passage, and the lack of violation of the medial articular surface of the ankle joint. R and S, Final construct demonstrates lack of bulk associated with this tendon transfer medially (R). In fact, the posterior tibial tendon and flexor digitorum longus tendons sit appropriately within the medial malleolar groove (S) without the tendency for dislocation. T and U, The custom multiaxis ankle testing apparatus with active driving in plantar/dorsiflexion, inversion/eversion, and internal/ external rotation by motors I, II, and III, respectively (R and S). The tibia was loaded axially through the vertical Z slide and was free to move mediolaterally and anteroposteriorly along the X and Y slides.

Pes Planus ■ Chapter 25

sured and is doubled to measure the looped component of the tendon transfer (Fig. 25-36H). 8. Summation is now done for graft length—talus length + calcaneal length + (tibial length × 2) + distance between origin and insertion point of deep and superficial deltoid ligaments − distance between suture button and allograft tendon (the latter is usually 1 cm per button). 9. The allograft is then cut to size, with strong Krakow weave stitches placed at either end. 10. A metallic button is secured with a 1-cm distance between the tendon graft and buttons. Multiple ties are placed to secure this button. 11. The talus and calcaneus drill diameters are normally 5 mm, although the graft diameter needs to be sized (Fig. 25-36L). 12. The metallic buttons are passed through the talus and calcaneus, respectively, and flipped to provide secure lateral fixation of each tendon end (Fig. 25-36M). This leaves a loop medially. The graft is pulled upon to ensure the buttons are engaging the lateral cortex. 13. A drill hole is now made in the medial malleolus, following the third guidewire. The diameter of this drill hole is normally 7.5 mm. Again, the graft diameter is sized as a looped construct. An incision is made at the exit point of this guidewire, usually medial to the anterior tibial tendon to avoid the neurovascular complex deep. 14. The graft is now passed through the medial malleolus drill hole by passing a looped suture through the anterior tibial cortex, exiting at the medial malleolus. This suture is used to pull the graft through the tibia, exiting the anterior tibial cortex (Fig. 25-36N). 15. The graft is maximally tensioned, secured over a screw and post construct, with a spiked ligament washer placed over the post (screw) (Fig. 25-36O). Again, this graft is placed at maximal tension (Fig. 25-36P-S). DELAND TECHNIQUE34 1. The technique begins with a 16- to 18-cm incision in the lateral midcalf. Allograft tendon can be used instead of peroneus longus autograft. With allograft tendon the sinus tarsi end of the incision is necessary but not an incision above the tip of the fibula. 2. Peroneus longus tendon is transected proximally at the junction of the proximal two thirds and distal one third of the calf, just distal to where the peroneus longus tendon is well formed. This allows for a long graft that is still attached distally, easily long enough to make it through the described talar and tibial bone tunnels below. Incise the longus tendon proximally enough for adequate length. Bone tunnels can be drilled and measured first so proper length of graft can be checked. 3. Side-to-side tenodesis of the peroneus longus to peroneus brevis tendon is done proximally. Weave two No. 2 permanent sutures into the free end of the graft for a strong hold. 4. Similar to the approach above, the deltoid is exposed through a near-vertical incision along its anterior border. A second surgical approach is through the sinus tarsi.

5. A bone tunnel of sufficient diameter to accommodate the peroneus longus tendon is drilled from the lateral neck of the talus (visualized through the sinus tarsi approach) exiting the medial talar body directly inferior to the medial malleolus. This is the insertion point of the deep deltoid, at the center of rotation of the talus. This tunnel is nearly parallel to the dome of the talus and exits medially inferior to the intercollicular notch of the distal medial malleolus. Confirmation of a good isometric point on the talus during ankle range of motion can be confirmed by placing a small K-wire at the proposed medial talar exit point and dorsiflex and plantar flex the ankle. 6. Once the position for the medial talar exit hole is confirmed, drill a K-wire hole from medial to lateral, exiting in the sinus tarsi dorsally but staying in the middle of the talar neck to minimize chance of subsequent stresss fracture. A lateral fluoroscopic view with the K-wire in place can be taken to confirm position of the pin. The pin is then replaced with the guide pin for use with the cannulated drill. 7. Drill the talar hole of sufficient size for the graft, often an 8- to 9-mm drill hole. 8. The peroneus longus tendon is passed from lateral to medial through this tunnel. 9. A second tunnel is made from the tip of the medial malleolus, exiting at the medial tibial metaphysis as described in step 6 of the Haddad technique. 10. The graft is tensioned at the talar exit point, followed by secondary tensioning at the medial tibial exit point at the medial tibial metaphysis. Simulated weightbearing intraoperative radiographs confirm the talus is reduced to neutral in the mortise. 11. Under tension, the graft is secured with No. 2 permanent sutures already woven into the end of the graft and tied under tension with the ankle reduced (ankle pinned if desired) to a screw on the medial tibia. Do not drill for this screw until the graft is tensioned, so that good screw placement is confirmed. Myerson Technique8,87 1. This technique uses medial allograft tendon for the reconstruction. To allow appropriate reduction, it is used only in stage IVA PTT insufficiency patients because a flexible deformity is the “A” group. 2. The graft is first passed in the medial distal tibia (straight medial) and approximately 2 cm proximal to the tibial plafond and anchored securely in the tunnel with an interference screw. 3. The graft is then passed through a subcutaneous tunnel overlying the medial malleolus and split for transfer into the talus and calcaneus. 4. Krakow suture weave technique is performed on both limbs of the split graft. 5. The talar tunnel is created first through a drill hole at the medial center or tibiotalar rotation, exiting at the lateral junction of the talar dome and neck. 1343

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

6. One limb of the split graft is placed through this tunnel and anchored under tension with an interference screw. 7. A calcaneal tunnel is then created from the sustentaculum tali exiting 1  cm superior to the peroneal tubercle laterally. The other graft limb is placed through this tunnel and anchored with an interference screw. 8. The superior limb of the tendon graft is sutured to the patient’s natural deltoid ligament at the apex of the medial malleolus, to add additional stability and prevent the graft from shifting too much. Postoperative Care Patients are generally in a cast for 6 weeks, with inversion applied to the cast to minimize risk of tendon rupture. In addition, if these techniques involve an osteotomy or arthrodesis, ultimate weight bearing will depend on the strength of the fusion or osteotomy. Progressive weight bearing begins first in a walking boot, followed by a shoe with a stirrup splint. In general, patients are back into a shoe without protective ankle devices by 3 months postsurgery; although, if there is any tendency toward medial column collapse of the foot, a medial posted orthosis is placed in the shoe. Results and Complications This Haddad technique has undergone biomechanical testing to ensure anatomic strength (Fig. 25-36T and U). External rotation and eversion laxity, calculated as angular displacement at 2-Nm level torque, was significantly greater in the sectioned group compared with the deltoid reconstruction group, with P = .006 and P = .017, respectively. There was no statistical difference in laxity in external rotation and eversion (tested at 2 Nm of torque) between the deltoid intact and reconstructed group, with P = .865 and P = .470, respectively. Loading the specimens at 2 Nm of torque revealed the deltoid ligament reconstruction was 98.1% ± 22.2% and able to withstand angular displacement when compared with the intact ligament in external rotation (Fig. 25-37A). Although, the laxity of the reconstruction was significantly reduced compared with the sectioned state in internal rotation (P = .034), the reconstruction was only able to withstand 52.3 ± 7.0% angular displacement in internal rotation compared with the intact ligament (Fig. 25-37B). At 2-Nm torque in eversion, the deltoid ligament reconstruction was able to withstand 92.4 ± 37.4% of the angular displacement compared with the intact ligament (Fig. 25-37C). Sectioning of the deltoid ligament increased inversion laxity by only 44.1 ± 41.4% compared with the deltoid intact condition. There was no significant difference in inversion laxity between the intact and reconstruction groups (P = .986) (Fig. 25-37C). Angular displacement was not statistically significant in plantar flexion between groups. Dorsiflexion laxity did show a statistically significant difference between reconstruction and sectioned groups (P = .014), but the magnitude of this difference 1344

was small, with only a 25.6 ± 21.3% increase in dorsiflexion laxity in the sectioned state. Stiffness was statistically significant in eversion but not inversion between the reconstructed and sectioned groups (P = .022 and P = .202, respectively). The stiffness of the reconstruction was 89.8 ± 54.3% compared with the intact ligament (Fig. 25-37E). Stiffness was statistically significant in external but not internal rotation between the reconstructed and sectioned groups (P = .001 and P = .161 respectively) (Fig. 25-37F). The stiffness of the reconstruction was 136.4 ± 40.2% compared with the intact ligament. Stiffness data was not statistically insignificant in both plantar flexion and dorsiflexion between the reconstructed and sectioned groups (P = .050 and P = .126, respectively). Mode of failure was then analyzed for the six specimens in the reconstruction group. Three of the six specimens failed at the knot over the suture button in the tibiocalcaneal bundle, with the tibiotalar bundle intact. In one specimen, the knot over the suture button failed at both tunnels. The medial malleolus fractured, with both bundles intact in one specimen. The final specimen failed by fracture of the roof of the tibiocalcaneal bone tunnel. The Deland technique has undergone recent clinical follow-up at an average of 8.9 years after the index operation.48 The authors revisited the five patients on whom they performed this technique in the original 2004 study. Both residual valgus talar tilt (via weight-bearing radiographs) and ankle range of motion (with standing hindfoot alignment) were used in combination with clinical assessment tools. Valgus tilt improved from 7.7 degrees preoperative to 2.1 degrees postoperative, and ankle range of motion averaged 47 degrees (no preoperative assessment quantified). In addition, clinical hindfoot alignment averaged 4 degrees of valgus. Confounding the quantification of correction was concomitant surgical procedures (bone work) done for realignment. Finally, there is no known “acceptable” level of valgus correction in patients with valgus deformity secondary to deltoid ligament insufficiency. The authors assume angular measurements within 5 degrees are within an acceptable range, but there is no validation of this figure. The Myerson technique has also undergone clinical follow-up for eight patients at an average of 3 years.87 Again, concomitant procedures were performed, including triple arthrodesis. Using more stringent criteria—3 degrees or less of valgus at final follow-up being considered successful—the authors found that 5 patients reached radiographic success (this patient population averaged 2 degrees of valgus tilt). Based on these results, the authors felt that the upper limit of corrective power of their technique in valgus talar tilt was 10 degrees. Complications revolve around violation of the structures near the site of surgery. As noted above, the tibial nerve may sustain injury at the site of the sustentaculum tali. In addition, the sustentaculum tali itself might sustain fracture with drilling, especially if a

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External 16.00

Intact Reconstruction Cutting

25.00

12.00

Rotation angle [deg]

14.00

Internal 30.00

10.00 8.00 6.00 4.00

0.00

16.00 Rotation angle [deg]

14.00

15.00 10.00

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Intact Reconstruction Cutting

12.00 Rotation angle [deg]

18.00

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0.7 0.6 0.5 0.4

0.25 0.20 0.15 0.10 0.05

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Inversion

0.35

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0.9

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External

Figure 25-37 A and B, Average and standard deviation of angular displacements in external (A) and internal (B) rotation. Note the strength of the repair in external rotation when compared with the intact native ligament. C, Average and standard deviation of angular displacements in eversion. Note the strength of the repair in eversion when compared with the intact native ligament. D, Average and standard deviation of angular displacements in inversion. Note the strength of the repair in inversion when compared with the intact native ligament. E, The stiffness of the reconstruction in eversion was 89.8 ± 54.3% compared with the intact ligament. F, The stiffness of the reconstruction in external rotation was 136.4 ± 40.2% compared with the intact ligament.

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Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

subtalar fusion is done commensurate with the deltoid reconstruction and the middle facet is prepared for fusion. Screw placement for fusion can shear the graft within the body of the talus if the graft is passed before screw placement. The author, Dr. Steven Haddad, prefers to place guidewires for fixation of the subtalar joint and then place the guidewire for the talus tunnel to avoid screw placement for subtalar arthrodesis. This then prevents graft violation with screw placement. The allograft and autograft can sustain creep, and thus appropriate tensioning before graft insertion is important. Also, large diameter, nonabsorbable suture should be used to secure the graft ends to the metal buttons to prevent failure at this weakest point in the construct. SUBTALAR ARTHRODESIS TO TREAT POSTERIOR TIBIAL TENDON DYSFUNCTION Subtalar arthrodesis has been described for the treatment of deformity for the adult acquired flatfoot.21 With the use of lateral column lengthening procedures for flexible deformity, it appears to be used less commonly but still has a role in the treatment of this condition. Deformity correction is noted with this procedure, naturally at the talocalcaneal joint and to some extent at transverse tarsal joint. It is appropriate for fixed or considerable symptomatic deformity at the subtalar joint not corrected by osteotomies or when symptomatic degenerative changes are present. In particular, lateral subluxation at the subtalar joint, if present, is not corrected by a lateral column lengthening. This subluxation can be appreciated on weight-bearing coronal CT imaging or simulated weight-bearing if available. Care should be taken not to put the subtalar joint in varus because this can easily lead to symptomatic lateral weight bearing. In a large series of subtalar fusions, symptomatic varus deformity did occur (although not commonly) as well as leaving too much valgus at the joint. As with other reconstruction procedures for flatfeet, care should be taken to carefully reduce subluxation of the foot and, if excessive heel valgus is still present, perform a medial slide calcaneal osteotomy as well. For forefoot varus not based in deformity of the talonavicular joint or severe naviculocuneiform joint subluxation, a Cotton procedure or metatarsal–tarsal fusion can achieve better positioning of the first metatarsal head and better appearance of the arch. Do not malposition the subtalar joint into varus or just fuse it “in situ” in an everted position. It should be fused in neutral. Surgical Technique for Subtalar Arthrodesis (Video Clips 26 and 27) 1. Prepare the joint surface as described in Chapter 20 (Treatment of Hindfoot and Midfoot Arthritis). 2. A laminar spreader can be used to reduce the subtalar joint. A spreader is placed in the sinus tarsi between the lateral talar tuberosity and the anterior calcaneus, to help reduce the deformity. Care is taken to position 1346

the subtalar joint into neutral and to maintain good apposition of the posterior facet for fusion. 3. Before pinning the joint, apply compression across the joint and confirm good bony apposition. Also confirm neutral and not supinated or pronated position of the joint. 4. Fixation is done with 2 cannulated 6.5, 7.0, or 7.3 mm compression screws or a compression screw and lateral compression staple. SINGLE AND DOUBLE ARTHRODESIS (Video Clips 28 and 29) Single arthrodesis of the talonavicular joint has been used in the adult acquired flatfoot, although not commonly. Because it is a key joint for alignment of the triple joint complex, it is logical that fusion of this joint can correct deformity. However, in stage III, it is common for significant deformity to be present at the subtalar joint, with the most common operation for stage 3 being a triple arthrodesis. In late-stage 2b, talonavicular (TN) fusion can be used when lateral column lengthening does not adequately address deformity and spring ligament reconstruction is not being done. Confirmation should be made that significant deformity or pain is not present at the subtalar joint, which would require a subtalar fusion as well. A calcaneocuboid (CC) fusion can be added to a TN fusion because it does not add significant loss of motion. Deformity at the subtalar joint is not to be likely addressed by a TN/CC double arthrodesis. Therefore, although uncommonly indicated, if the primary deformity is at the TN joint and there is minimal subtalar joint deformity or pain, a TN or a TN and CC fusion is an option. Another double arthrodesis, TN and a subtalar fusion, has been described because patients can have their deformity adequately corrected using this combination.159 Finally, a CC distraction arthrodesis with a tricortical graft should be mentioned. This is essentially a type of lateral column lengthening. Originally, this was thought to be advantageous because of the potential for lateral column lengthening to cause significant CC arthritis. Symptomatic CC arthritis is uncommon both in the short and intermediate term.6,134,145 Arthritic changes, although present in some patients at this joint, do not commonly cause significant symptoms. The distraction CC arthrodesis does have a higher incidence of nonunion than other lateral column lengthenings, (Evans or LCL stepcut techniques). From this perspective and possible additional loss of motion, it is not attractive to use a distraction CC arthrodesis. Nevertheless, a lengthening CC arthrodesis does correct deformity as does a lateral column lengthening. TRIPLE ARTHRODESIS Triple arthrodesis is indicated for fixed deformity in the subtalar and talonavicular joints. The joints can neither be passively manipulated into inversion and adduction, nor can they be rendered stable in a good position by procedures other than fusions. The key to this procedure is properly positioning the triple joint complex and

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obtaining good alignment of the foot. It is important to reduce both the talonavicular and subtalar joints (Fig. 25-38). It is equally important to achieve an even plantar tripod: heel plus first and fifth metatarsal heads. Adjunct procedures to a triple arthrodesis are a posterior medial slide calcaneal osteotomy to correct residual excessive heel valgus and a Cotton osteotomy or first metatarsal– tarsal arthrodesis to correct forefoot varus. When performing a triple arthrodesis for the adult acquired flatfoot, undercorrection is more common than overcorrection, although both are possible. Within the triple joint complex, the main reduction occurs at the talonavicular joint. Care needs to be taken to reduce the subtalar joint, without placing it in varus. Lateral wound problems are a risk in severe valgus deformities. A single medial incision technique for severe valgus deformities has been described. One series of 17 patients has been presented.88 Access to the calcaneocuboid joint is difficult by using one medial incision. Two calcanealcuboid nonunions occurred in this series but were well tolerated. Although no other clinical series has been presented, this approach is a consideration in the setting of severe valgus deformity. Below is a technique description using the standard incisions, highlighting how to achieve a plantigrade well-aligned foot. Technique Triple Arthrodesis 1. Incisions are made along the sinus tarsi and anteromedial talonavicular joint (Video Clip 30). 2. Standard preparation of the joint surfaces to keep the curvilinear shape of the talonavicular and subtalar joints is done with removal of all cartilage, perforating the subchondral bone with multiple K-wire holes, light burring with irrigation, and fish scaling the sclerotic surfaces. The calcaneocuboid joint preparation is performed with minimal lateral bone resection so that the lateral column is not shortened. 3. Position the joints using fluoroscopy to confirm good position and apposition. Commonly, the talonavicular joint will need to be brought out of an abducted and plantar sagged position. Push on the talar head medially to eliminate the abduction, and bring the navicular and medial column down, out of its dorsiflexed and abducted position. If a lateral gap is present at that CC joint, a small amount of additional curvilinear resection can be done at the talonavicular joint to allow good apposition of both joints. Check that there is no prominent bone at the medial CC joint or medial talonavicular joint causing the talonavicular joint to gap laterally. Also, check that the cuboid can be elevated so that, with final positioning of the foot, the cuboid is not prominent plantarly. 4. Once the subtalar and talonavicular joints are in place, they are compressed and temporarily pinned. It is important to place both joints in a good position and compress them for the temporary fixation. An assistant can be useful to pin the joints while the surgeon positions and compresses the joints. Reduction of both

joints must be confirmed clinically and with AP and lateral fluoroscopy. 5. Examine the tripod, if excessive heel valgus remains, through a standard posterior lateral incision. Then perform a medial slide calcaneal osteotomy to correct remaining excessive valgus. 6. If the first ray is elevated in comparison to the second, by assessing the plantar position of the first and second metatarsal heads (residual forefoot varus), bring the first metatarsal down by a Cotton osteotomy or first metatarsal tarsal fusion, the latter being done when there is considerable instability or a plantar gap. The forefoot varus should have been at least partially addressed by setting the position of the talonavicular joint out of dorsiflexion. After these procedures, the plane of the metatarsal heads should not be in forefoot varus or valgus by more than 10 degrees. If elevation of the first ray is primarily from deformity at the naviculocuneiform joint, that may need to be addressed with fusion at that location. This is only done for severe dorsiflexion deformity at the naviculocuneiform joints because these joints have a significant nonunion rate. Some residual dorsiflexion of the naviculocuneiform joints is rarely a problem. 7. A final check of the alignment of the hindfoot, midfoot, and forefoot is then done. With good alignment set, final fixation is placed, usually in the following order: (1) subtalar joint (with medial slide calcaneal osteotomy, if performed); (2) first metatarsal–tarsal fusion or Cotton osteotomy, if performed; (3) talonavicular joint; and finally, (4) the calcaneaocuboid joint. If a gap is present at the CC joint, bone graft is used with tricortical graft being an option but not commonly necessary. The CC joint is fixed with compression screws and/or staples. For the medial calcaneal osteotomy and subtalar fusion, one or two compression screws are used from the heel to the talar body. The talonavicular joint is fixed with compression screws or a compression screw and compression staple. Fluoroscopy is used to confirm good apposition at the joints. If apposition is not good laterally at the TN joint, a separate incision over the lateral talonavicular joint can be made and a screw placed under compression from the navicular into the talus. 8. The foot and ankle is then dorsiflexed to check that it can be brought to neutral. If neutral cannot be achieved with the knee straight but can be with the knee bent, a gastrocnemius lengthening is performed at that time or may have been performed at the beginning of the procedure. The gastrocnemius lengthening (Strayer procedure) can be done at the beginning of the procedure, with the contracture having been demonstrated with the foot manipulated into the corrected position and neutral (not plantar-flexed) position confirmed with the knee bent to 90 degrees. If the hindfoot and ankle remain plantar flexed with the knee flexed, a tricut Achilles lengthening is necessary. 1347

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Figure 25-38 A, Preoperative radiograph of severe forefoot abduction in rigid stage 3 flatfoot deformity. B, Preoperative lateral radiograph in rigid deformity noting plantar flexion of talus and subtalar arthritis. C, Preoperative anteroposterior (AP) ankle radiograph demonstrating no valgus tilt or ankle arthritis despite long-standing valgus deformity. D, Preoperative clinical photograph of heels showing severe valgus and medial column collapse. E, Preoperative clinical AP photograph of feet demonstrating resting forefoot abduction without attempts at correcting foot alignment. F, Preoperative clinical photograph of lower limb documenting uncorrected medial column collapse, with rotation evident as callus at medial intraphalangeal joint of great toe. G, One and half years postcorrection, with standing lower limb foot position, confirmed with alignment of knees at neutral. H, One and a half years postcorrection AP clinical photograph of feet, with knees in neutral. I, One and a half years postcorrection with hindfoot alignment restored. Note required Strayer procedure to assist with postoperative motion. J, One and a half years postcorrection AP radiograph of foot. Note that a simultaneous lateral column lengthening was performed through the calcaneocuboid joint to achieve forefoot abduction correction. K, One and a half years postcorrection lateral radiograph of foot with elevation of the talus. Note autocorrection of sagging medial column through rigid hindfoot correction. This is not possible with joint-preserving operations. L, One and a half years postcorrection AP view of ankle without arthritic changes and elimination of subfibular impingement.

RIGID FLATFOOT ASSOCIATED WITH ADULT TARSAL COALITION

Incidence The majority of the world’s literature pertaining to tarsal coalition involves the adolescent patient. Tarsal coalition results from failure of differentiation of the primitive mesenchyme with the resultant lack of joint formation. This concept was first proposed by Leboucq in 1890.110 The overall incidence is less than 1%.104 However, a number of studies debate this point, stating that tarsal coalition goes unrecognized in asymptomatic persons and in nonosseous variants. Solomon et al166 suggest that the incidence of talocalcaneal coalition may be as high as 12.7%. The incidence of bilaterality varies in the literature, ranging from 20% to 60% in talocalcaneal coalitions and 40% to 68% in calcaneonavicular coalitions. A review of the literature by Stormont and Peterson171 noted that the incidence of talocalcaneal coalitions was 48.1%, calcaneonavicular was 43.6%, talonavicular was 1.3%, and other coalitions were 5.7%. Although most patients with this entity present between the ages of 8 and 16 years,72 symptomatic coalitions do occur in the adult population. Presentation is most often associated with a traumatic event, such as a severe ankle sprain sustained through sports activity or an incidental injury during activities of daily living. It is rare for such a patient to have prior problems with the involved foot. According to Varner and Michelson,182 the lack of prior symptoms may be due to the neutral alignment of most adults with tarsal coalition and lack of spasm about the peroneal tendons. Only 7 of 32 adults (22%) presenting with tarsal coalition had a valgus deformity of their hindfeet. In fact, their cohort included 11 asymptomatic tarsal coalitions, and only one of these patients had a valgus hindfoot. Physical Examination Physical examination often reveals a flatfoot deformity of variable rigidity. Patients with a talocalcaneal coalition

demonstrate no inversion of the calcaneus upon singlelimb heel rise, and those with a calcaneonavicular coalition might demonstrate a percentage of inversion when compared with the unaffected side. Preservation of up to 70% of subtalar motion may be found in patients with a calcaneonavicular coalition. Transverse tarsal motion is preserved in patients with a talocalcaneal coalition, but it is severely restricted in patients with a calcaneonavicular bar. Pain may be elicited medially directly over the anterior middle facets and inferior to the medial malleolus in patients with a talocalcaneal coalition. Often, the clinical appearance of a medial bony prominence is noted in patients with a talocalcaneal bar. Pain to palpation might also be noted in the anterior portion of the sinus tarsi and around the lateral and dorsolateral portion of the talonavicular joint. Stressing the coalition by manipulating the subtalar and transverse tarsal joints can elicit pain directly at the site of the coalition. Paresthesias or frank numbness may be present in the distribution of the deep or superficial peroneal nerve in patients with significant talar beaking. Tarsal tunnel syndrome has been reported in conjunction with a talocalcaneal coalition111 because of impingement on the medial plantar nerve from a bony prominence at the sustentaculum tali. Peroneal spastic flatfoot is a misnomer. Patients might demonstrate periodic spasm of the peroneal tendons because of attempted inversion against relatively shortened peroneal tendons. The shortening occurs from chronic and rigid valgus of the hindfoot. The peroneal tendons elicit a protective mechanism of contracting to minimize pain specifically at the rigid subtalar joint, and thus they might go into spasm because of the length deficit. Radiographic Studies Plain radiography has value in the form of weight-bearing AP, oblique, and lateral images. These routine images are inspected for distortion in the normal bone architecture suggesting union (fibrous or bony) between the involved 1349

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bones. In addition, the lateral radiograph can demonstrate beaking of the talus. This traction spur at the dorsum of the talus is a secondary sign of tarsal coalition and is believed to occur through an aberrant hingelike motion of the navicular upon the talus with dorsiflexion. Subtalar joint rigidity prevents the normal forward subluxation of the calcaneus upon the talus with dorsiflexion, creating a rigid hinge motion of the navicular upon the talus rather than the normal gliding motion. This hinging creates periosteal disturbance upon the head of the talus, which manifests a traction spur at that specific location. Primary signs may be visualized on the 45-degree lateral oblique radiograph, where the calcaneonavicular coalition becomes evident as either complete osseous union or extension of the anterior neck of the calcaneus to the navicular (the anteater nose sign). The talocalcaneal coalition can also be visualized on plain radiography as narrowing of the posterior subtalar joint, failure to see the middle facet, rounding of the lateral process of the talus (on ankle radiographs), or flattening or concavity of the undersurface of the talar neck. The C sign, described by Brown et al,13 is a bean-shaped density noted on the lateral radiograph and was initially thought to be diagnostic for talocalcaneal coalition. This sign relies on a prominent inferior outline of the sustentaculum tali to create an overlap or hyperdense region in combination with the medial outline of the talar dome and a bony bridge between the talar dome and sustentaculum tali. Brown found that although the sign is specific (not sensitive) for flatfoot in general, it is neither specific nor sensitive for talocalcaneal coalition. Clearly, the ability of the technologist to obtain a true lateral radiograph of the foot is pivotal in appropriately interpreting that radiograph for tarsal coalition. A true lateral radiograph should allow visualization of the middle and posterior facets, which are parallel. Any rotation of the hindfoot, or nonperpendicular beam positioning, will erroneously lead the interpreter to suggest tarsal coalition because the facets are not visible. An important primary sign of talocalcaneal coalition may be detected through the Harris axial view73 and requires the patient to stand on the radiographic cassette while dorsiflexing the ankle 10 degrees. The beam is projected downward from posterior to plantar at 45 degrees from vertical. Additional views are taken at 40 degrees and 50 degrees to capture the parallel nature of the posterior and middle facets. Assistance in determining the appropriate orientation of the beam comes from assessing the angle of the posterior and middle facets with reference to the vertical on the true lateral radiograph. Irregularity of the joint contour suggests a fibrous coalition, and complete obliteration of the joint is pathognomonic for bony coalition. Despite the advanced diagnostic modalities mentioned below, unenhanced radiography has value in assessment for tarsal coalition. Crim and Kjeldsberg30 performed a two-phase study in patients with a mean age of 29 years. 1350

The first phase involved retrospectively reviewing radiographs in patients with known tarsal coalitions (confirmed by CT, MRI, or surgery), intermixed with known controls, and assessing diagnostic accuracy. Radiographs provided to the examiners were only AP and lateral foot views, to provide consistency with routine screening radiographs obtained in an office setting. The second phase was prospective—reviewing 150 radiographs in patients with nontraumatic foot and ankle pain and following up suspected coalitions with CT. The authors found that in the first phase, talocalcaneal diagnosis through plain radiographs was sensitive 100% of the time and specific 88% of the time. Calcaneonavicular coalitions ranged from 80% to 100% sensitive and 97% to 98% specific. Observers in this study were a junior musculoskeletal radiologist, a junior radiology resident, and a junior orthopaedics resident, all provided with a 30-minute tutorial before reviewing radiographs. In the second phase of the study, all expected coalitions were confirmed by CT scan, with no false positives noted. CT has superseded plain radiography in diagnostic accuracy for tarsal coalition. The coronal view may be obtained by having the patient supine with the hips and knees flexed and the feet plantar flexed 20 degrees at the ankle. The image provided is perpendicular to the posterior and middle facets and will confirm an osseous talocalcaneal coalition. In addition, the coronal view will demonstrate the nature and cross-sectional area of the coalition. CT has the added benefit of detecting early degenerative joint disease at adjacent surfaces, which can influence treatment options. In the past, the ability of CT to evaluate calcaneonavicular coalitions was questioned. Hochman and Reed78 investigated the ability of CT to make this diagnosis. The authors found that axial CT images provided the best assessment of calcaneonavicular coalition. They also noted, however, that coronal images provide assistance through two features: lateral bridging (an abnormal bone mass lateral to the head of the talus) and abnormal rounding of the head of the talus. In particular, lateral bridging was a definitive finding in all patients studied with a confirmed calcaneonavicular coalition. Thus the authors suggest that while reviewing the coronal CT scan for a potential talocalcaneal coalition, the examiner must focus attention on the additional signs mentioned earlier, to avoid overlooking a calcaneonavicular coalition. If coalition is suspected, the axial images should be reviewed for absence of the normal triangle of soft tissue seen anterolateral to the calcaneus. If a coalition is present, this triangle is replaced by bony protrusions from the calcaneus and the navicular. The limitations of CT stem from fibrous coalitions, where its accuracy may be compromised.146,185 Fibrous or cartilaginous coalition is suggested indirectly by an abnormal angulation of the facet, joint space irregularity, subchondral sclerosis, or articular narrowing. However, the actual fibrous tissue is not well visualized. MRI becomes the better modality to assess this particular component.

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In particular, the T1-weighted images reveal intermediateto-low signal bridging the gap in the suspected fibrous coalitions. In addition, osseous coalitions are confirmed by continuity of the bone marrow across the proposed site. More recently, an ill-defined hyperintense pattern was detected on short T1 inversion recovery (STIR) or T2 images in the subchondral bone adjacent to the coalition.164 It is suspected that this pattern is due to abnormal stresses across the rigid coalition, creating microfractures and edema within the bone. The value of MRI over CT in fibrous tarsal coalitions remains in question. Emery et al51 reviewed 40 MRI and CT scans taken on 20 patients with symptoms suggesting tarsal coalition. The authors found 15 feet in 9 patients demonstrated tarsal coalition by both MRI and CT scans. Ten coalitions were confirmed through surgical exploration. In this study, 71% of the subjects were patients with a fibrous coalition. Sensitivity and specificity were compared, revealing that CT scanning was 94% sensitive and 100% specific, whereas MRI was 88% sensitive and 100% specific. The authors found a 97.5% agreement between CT and MRI in rendering diagnosis of tarsal coalition, despite the large percentage of fibrous coalitions. Thus the choice of study depends on the physician’s expected findings in a particular case; cost-effectiveness currently favors a CT scan in patients with isolated tarsal coalitions, but if additional soft tissue disorder (PTT disorder) is sought, MRI is the better diagnostic modality. COMBINED FLATFOOT CORRECTION AND COALITION TREATMENT It has been noted that failure to correct a moderate-tosevere flatfoot deformity can lead to a poor result in a patient who is having a coalition resection. In fact, the resection of the coalition without surgical treatment of the symptomatic flatfoot deformity has been reported to result in increased deformity and failure of the clinical result.35 Symptoms from the flatfoot deformity can be present and be misinterpreted as being purely from the coalition on initial evaluation. This misinterpretation leads to just resection of the coalition alone without correction of the symptomatic flatfoot. There is scant literature on simultaneous surgical correction of a flatfoot and resection of the coalition. The present author has found this combination to be effective and not to the detriment of the coalition resection. Retaining maximum motion from a coalition resection has been a concern in these patients. Mosca132 in a recent study found simultaneous resection of coalition and correction of the flatfoot gave a good result. Mosca, in his recent article, documented results of correcting the flatfoot with a calcaneal lengthening osteotomy (not a medial slide osteotomy) in patients with talocalcaneal coalitions.132 His largest group of patients were treated with correction of the flatfoot alone and not resection of the coalition. These patients did well. The patients with resection of the coalition and correction of the flatfoot deformity also did well, although the numbers

in this study are small. The patients who did not do well were those with deformity or arthritis who had resection of coalitions previously without correction of the flatfoot deformity. Cain14 reported a series of patients who underwent a medial slide osteotomy for correction of the flatfoot. The medial slide osteotomy was done from a medial approach with resection of bone medially to give more correction. These patients did not get good correction of their pes planus, although good pain relief was reported. Overall, it is likely that the same rules apply to correction of flatfoot deformity that has been described in this chapter to the patients with symptomatic flatfoot and coalitions, whether they be talocalcaneal or calcaneonavicular. It is important to remember that a mild flatfoot is likely to be an asymptomatic flatfoot and coalition resection alone is reasonable, while a severe flatfoot is commonly symptomatic from the flatfoot itself. In the adult with moderate flatfoot deformity, it is still probably best to correct the flatfoot. If the coalition is asymptomatic and the restriction of motion does not interfere with gaining good alignment, the coalition can be left alone. If the restriction of motion must be taken down to achieve good alignment, then take it down for the correction and leave it resected or fuse the joint, fusion being more likely to be necessary in the case of an extensive talocalcaneal coalition. Treatment Most tarsal coalitions are asymptomatic. If a coalition is detected radiographically when evaluating for a separate problem, the patient should be informed about the condition, but no treatment beyond simple observation is necessary. Pain in conjunction with the adult tarsal coalition is often in associated with a traumatic event, most often an ankle sprain. Thus it is important to maintain clinical suspicion when examining a patient with an ankle sprain, evaluating for rigidity in subtalar motion. Patients who present late after sustaining an ankle sprain must be carefully evaluated for tarsal coalition. Conservative Treatment Conservative management for tarsal coalition begins with antiinflammatory medication, icing, and modifying activity. Persistent pain mandates cast immobilization. The clinician must decide the weight-bearing status in the cast based on consultation with the patient. One may certainly use a short-leg walking cast for 6 weeks, but if the patient remains symptomatic after cast removal, a second casting (with a non–weight-bearing cast) will be required. Thus this protocol might extend the casting for a second interval, which can be avoided by making the first cast non–weight bearing. Regardless, it is Dr. Steven Haddad’s experience that 60% to 70% of patients respond to immobilization if they have had no prior symptoms from the coalition. This experience is not supported in the 1351

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literature, where only one third of patients were found to respond to conservative measures.26,106 Many clinicians recommend that when the patient fails attempts at casting, surgical intervention is appropriate. Longer-term conservative management can incorporate a medial heel wedge, Thomas heel, or medial longitudinal arch support.26 In general, in rigid flatfoot, use of a rigid device that attempts to correct the collapsed arch actually increases the patient’s symptoms and limits compliance with the device. Thus accommodative orthotics made of Plastizote, or semirigid devices that accommodate rather than correct the arch, have higher satisfaction. A UCBL orthosis or a lace-up ankle brace may be required for continued sports participation to minimize stress across the coalition. In patients who do not participate in sports, a polypropylene AFO may be required. Cowell and Elener27 found that patients with a fixed hindfoot valgus deformity and a talocalcaneal coalition fared poorly with conservative care when compared with a hindfoot in neutral. Surgical Treatment CALCANEONAVICULAR COALITION Surgical treatment of the calcaneonavicular coalition in an adult with minimal or no secondary changes (arthrosis) consists of resection of the coalition (Fig. 25-39). The goal is to eliminate painful motion at the coalition site while potentially increasing hindfoot motion. The suspected location of pain arising from the coalition appears

to be the site around the coalition rather than the actual coalition itself. In particular, the hyperintense ill-defined areas noted on MRI of tarsal coalition164 can represent bone contusion or edema that creates coalition pain. It is clear that the hyperintensity is present in the subchondral bone and not within the coalition itself. Thus a generous resection of the coalition invariably removes the diseased segment of bone, providing pain relief for the patient. Indications Indications for resection of a calcaneonavicular coalition are pain refractory to conservative care, and limited function from extreme rigidity. Contraindications Improvement with conservative care is a contraindication to surgery. If the patient is asymptomatic, resection of the coalition is not indicated. In addition, if the adjacent joints are arthritic, resection of the coalition is not sufficient, and a double or triple arthrodesis becomes the best alternative. Preoperative Evaluation Patients are evaluated radiographically for coalition. Plain radiographs include the 45-degree oblique view, which demonstrates the coalition. CT scanning reveals the extent of the coalition and whether it is osseous or fibrous. More important, the CT scan assists in evaluating adjacent joint surfaces for arthritic wear. For example, posttraumatic

Figure 25-39 A, Medial exposure for sustentacular coalition. B, The tendons of the flexor hallucis longus and flexor digitorum longus are retracted. C, The coalition is seen deep to the tendons. D, Resection of the coalition. E, The joint is distracted with a lamina spreader to ensure lysis of any remaining fibrous adhesions.

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arthritis of the cuboid or subtalar joint can mimic symptoms of a tarsal coalition. Such arthritis warrants fusion rather than resection. The severity of the planovalgus foot deformity is assessed clinically. The literature does not address correction of the flatfoot deformity in conjunction with coalition resection. However, it must remain a consideration, especially in patients with subfibular impingement (separate from pain at the site of the coalition) or pain medially underlying the talar head. Such patients become candidates for simultaneous medial slide calcaneal osteotomies, lateral column lengthenings, or medial cuneiform opening-wedge osteotomies. Preoperative Planning Radiographs and three-dimensional imaging studies are reviewed to determine the extent and location of the coalition. Surgical Technique 1. Equipment required includes a sharp beveled chisel or a set of sharp straight osteotomes, a rongeur or large pituitary rongeur, and bone wax to cover the exposed bone surfaces (Video Clip 89). 2. The patient is positioned supine with adequate support placed under the ipsilateral hip. Elevation of the lateral hip allows internal rotation of the extremity, facilitating exposure of the coalition. 3. It is helpful to incorporate a popliteal block when considering anesthetic, and if an indwelling popliteal catheter may be used, the patient will experience outstanding pain relief for at least 3 days after the procedure. In fact, the entire procedure can be performed with this block, with the use of a calf tourniquet. If a general anesthetic or spinal anesthetic is chosen, a thigh tourniquet may be used to facilitate hemostasis. 4. The incision begins 1 cm distal to the tip of the fibula and is carried obliquely to the base of the third metatarsal. 5. Two nerves that are subcutaneous at the portion of the foot are at risk. The intermediate dorsal cutaneous branch of the superficial peroneal nerve crosses the surgical path and should be identified and protected with a vessel loop. The anterior branch of the sural nerve can also be found at the proximal portion of the incision. 6. The origin of the extensor digitorum brevis muscle is detached from the lateral surface of the talus and reflected distally. 7. The anterior process of the calcaneus is identified and traced toward the navicular. The coalition is identified as a broad surface of bone (or a surface interrupted by fibrous tissue) connecting the anteromedial aspect of the calcaneus to the plantar-lateral portion of the navicular. 8. The parameters of the coalition are carefully identified. This is critical, to avoid violation of the articular

surface of the navicular or the calcaneocuboid joint. For confirmation, the surgeon can use intraoperative fluoroscopy. 9. The ligaments between the talus and navicular and the calcaneus and cuboid are preserved. Damage to the talonavicular ligaments will allow the navicular to sublux upon the talus. Similarly, damage to the calcaneocuboid ligament will allow the cuboid to shift upon the calcaneus. 10. With a straight osteotome or sharp chisel, the navicular portion of the coalition is resected with an oblique angle, ensuring that the plantar-lateral portion is resected. The calcaneal portion is resected with a parallel cut beginning at the superior-medial articular surface of the calcaneocuboid joint. 11. The block of bone and fibrous tissue removed may be as large as 2 cm by using these resection margins. After removing the coalition, the surgeon looks for additional bone fragments impinging upon the talonavicular or calcaneocuboid joint. All such fragments are removed at this time. 12. Manipulation of the transverse tarsal joint assists in evaluating for impingement along the lateral aspect of the calcaneocuboid joint. On occasion, an abnormally shaped calcaneocuboid joint is detected that can block abduction of the foot. This abnormally shaped bone arises from the calcaneus and must be removed to facilitate abduction of the cuboid. Under normal circ*mstances, the amount of bone removed at this location is small. 13. Bone wax is applied to all cut bone surfaces. 14. The origin of the extensor digitorum brevis may now be interposed into the defect. Keith needles threaded with absorbable suture are placed into the tendinous origin of the muscle. These needles are passed plantarward and may be tied on either side of the plantar fascia through a small separate incision. With this technique, a button may be avoided. 15. The tourniquet is deflated before closure to minimize the risk of hematoma and subsequent scar formation. Hemostasis is very important at this stage, and if drainage is persistent, a suction drain is placed deep in the area of the coalition. 16. The extensor fascia is approximated, as is the subcutaneous tissue and skin. 17. A plaster splint limiting inversion and eversion, or a short-leg fiberglass cast, is applied intraoperatively. Postoperative Care If it was not done before the procedure, the popliteal block with an indwelling catheter can be performed in the recovery room to facilitate pain control. Sutures are removed at 10 days after surgery, unless significant swelling suggests an incisional wound complication. In this instance, sutures are left in place for 3 weeks. The patient is given a walker boot, and ambulation is encouraged. Physical therapy may be instituted simultaneously to encourage aggressive passive range of motion 1353

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of the transverse tarsal and subtalar joints. Gains achieved intraoperatively will be maintained or enhanced through this activity. A compression stocking, or a more formal lymphedema clinic, should be used to minimize soft tissue edema. Swelling compromises motion at this critical juncture. The CAM walker boot should be discontinued by 4 weeks postoperatively, which will further encourage range of motion of the hindfoot. TALOCALCANEAL COALITION Similar to the calcaneonavicular coalition, surgical treatment of the talocalcaneal coalition in an adult with minimal or no secondary changes (arthrosis) consists of resection of the coalition. Again, the goal is to eliminate painful motion at the coalition site while potentially increasing hindfoot motion. Indications Surgical resection of a talocalcaneal coalition is indicated after failure of two trials of conservative care (casting). Pain is the primary indication because recovery of subtalar motion might not be significant enough as an isolated indication. Contraindications Previously, it was thought that a coalition that occupied more than 50% of the total articular surface of the subtalar would have a poor result.163 Scranton163 chose this value based on CT data, and using this arbitrary figure, the author evaluated his own results, finding good results in 13 of 14 patients. He has been misquoted in many orthopaedic texts over the years, leading to the misconception that he found poor results in patients with coalitions occupying greater than 50% of the middle facet as an isolated entity. It has been shown by Comfort and Johnson22 that 77% of patients undergoing resection of a talocalcaneal coalition involving less than one third of the total joint surface (anterior, middle, and posterior facets) experience good or excellent results. This study evaluated 20 patients by using CT to map the surface area of the posterior, anterior, and middle facets. The authors used these data to determine the location and extent of the talocalcaneal coalition as a percentage of the surface area of the entire joint construct. All patients in the study group had the coalition resected for symptoms. On average, these coalitions involved 66.5% of the anterior and middle facets (these facets are contiguous 67% of the time161) and 29.8% of the total joint surface area. With outcome based on level of activity, pain, and subtalar motion, 60% of the results were rated good or excellent. A strong correlation was found between the size of the coalition and the clinical outcome, noting that fair or poor results were found in 75% of the patients sustaining coalitions occupying more than one third of the total joint surface. Age was not correlated with surgical outcome. It has been suggested that increased age correlates with more poor results because 1354

resection allows increased motion across degenerative joint surfaces. This study places that contraindication in question. Finally, the authors compared their results with Scranton’s guidelines and found that if they had followed his initial guidelines for resection, their entire group would be candidates for resection because no coalition involved more than 50% of the total joint surface. In that case, they would have had a much greater percentage of fair or poor results than those illustrated by Scranton. Thus this study, based on Wilde’s criteria for measuring surface area of the subtalar joint,187 suggests that surgery is contraindicated in talocalcaneal coalitions occupying greater than one third of the total articular surface of all three facets of the subtalar joint. Preoperative Evaluation Patients are evaluated for coalition radiographically. Plain radiographs include the Harris axial view, which demonstrates the coalition. CT scanning reveals the extent of the coalition and whether it is osseous or fibrous. More important, the CT scan assists in evaluating adjacent joint surfaces for arthritic wear. For example, posttraumatic arthritis of the subtalar joint can mimic symptoms of a tarsal coalition, and if arthritis is present, it warrants fusion over resection. Clinically, severity of the planovalgus foot deformity is assessed. The literature does not address correction of the flatfoot deformity in conjunction with coalition resection. However, it must remain a consideration, especially in patients with subfibular impingement (separate from pain at the site of the coalition) or pain medially underlying the talar head. Such patients become candidates for simultaneous medial slide calcaneal osteotomies, lateral column lengthenings, and/or medial cuneiform openingwedge osteotomies. Correction of the symptomatic flaftoot is at least as important as resection of the coalition, as documented by Mosca139 in a recent study. Preoperative Planning Radiographs are reviewed to determine the extent and location of the coalition. Whereas the resection of a calcaneonavicular coalition is relatively simple, the resection of a talocalcaneal coalition is technically demanding and requires adequate exposure, careful orientation, and cautious dissection. Surgical Technique 1. Equipment required includes a sharp beveled chisel or a set of sharp straight osteotomes, a rongeur or large pituitary rongeur, and bone wax to cover the exposed bone surfaces (Video Clip 90). 2. It is helpful to incorporate a popliteal block when considering anesthetic, and if an indwelling popliteal catheter can be used, the patient will experience outstanding pain relief for at least 3 days after the procedure. In fact, the entire procedure can be performed with this block, with the use of a calf tourniquet. If a

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general anesthetic or spinal anesthetic is chosen, a thigh tourniquet may be used to facilitate hemostasis. 3. The patient is positioned supine, with adequate support placed under the contralateral hip to facilitate external rotation of the operative extremity. 4. The incision is made along the inferior aspect of the PTT sheath, beginning 1 cm distal to the tip of the medial malleolus and extending distal to the talonavicular joint. 5. The incision is deepened through the subcutaneous tissue and fat to expose the PTT sheath. The inferior aspect of the sheath is opened and the tendon is retracted superiorly. 6. Deep to this, the sheath for the flexor digitorum longus is encountered. This sheath passes along the medial surface of the talus, superior to the sustentaculum tali and thus the location of the coalition. 7. The flexor digitorum longus is retracted superiorly to expose the inferior edge of its tendon sheath. This inferior edge should be exposed from the medial malleolus to the talonavicular joint. Plantar to the flexor digitorum longus tendon is the neurovascular bundle, which should be identified and protected. 8. The area of the coalition can be identified by locating the posterior facet of the subtalar joint proximally and the inferior aspect of the talonavicular joint distally. The coalition lies between these two landmarks. 9. Using an osteotome or a chisel, a wedge of bone is removed to excise the coalition. The apex of the wedge is lateral. It may be easiest to start at the proximal point of the coalition, at the medial aspect of the posterior facet, and proceed distally. The surgeon must excise sufficient bone to visualize the joint surfaces. Once a sufficient amount of bone has been removed from the middle facet, the tarsal canal is visualized. The sustentaculum tali is not removed in its entirety. In addition, although sufficient bone must be resected to regain a portion of subtalar motion, the surgeon must take care to avoid removing excessive bone because the subtalar joint will become destabilized, accelerating arthritic wear. 10. Subtalar motion is checked and is often less than 50% of that detected on the opposite, normal side. 11. Bone wax is placed over the exposed bone surfaces. 12. The tourniquet is deflated, and meticulous hemostasis is performed. Limiting hematoma will limit subsequent scar tissue and enhance motion. 13. The tendon sheaths are approximated, restoring the tendons to their normal anatomic position. 14. The subcutaneous tissue and skin are sutured. 15. A plaster splint limiting subtalar motion, or a shortleg fiberglass cast, is applied. Postoperative Care If not done before the procedure, the popliteal block with an indwelling catheter can be performed in the recovery room to facilitate pain control.

Sutures are removed 10 days postoperatively, unless significant swelling suggests an incisional wound complication. In this instance, sutures are left in place for 3 weeks. The patient is then placed into a walker boot, and ambulation is encouraged. Physical therapy may be instituted simultaneously to encourage aggressive and passive range of motion of the transverse tarsal and subtalar joints. Gains achieved intraoperatively will be maintained or enhanced through this activity. A compressive stocking, or a more formal lymphedema clinic, should be used to minimize soft tissue edema. Swelling compromises motion at this critical juncture. The walker boot should be discontinued by 4 weeks postoperatively, which will further encourage range of motion of the hindfoot. Results and Complications Results of both talocalcaneal and calcaneonavicular coalitions are reviewed. Swiontkowski et al176 performed a follow-up study of 40 patients who underwent 57 procedures for tarsal coalition. In total, 44 calcaneonavicular coalitions and 13 talocalcaneal coalitions were reviewed. Thirty-nine of the 44 calcaneonavicular coalitions underwent resection, whereas 5 underwent triple arthrodesis. At an average follow-up of 4.6 years, 29 (66%) were asymptomatic and 7 (16%) had symptoms with strenuous activity. In all, 90% improved considerably through surgical intervention. In the talocalcaneal group, 5 patients underwent resection and 9 had an arthrodesis (both triple and subtalar). At a mean follow-up of 3.1 years, four of five resections were asymptomatic. Of those undergoing arthrodesis, 78% were symptom-free. In both series, talar beaking had no influence on outcome and is not a contraindication. The authors experienced no complications in any of their procedures, other than some coalition resections requiring arthrodesis for persistent pain. Mann et al120 evaluated 10 patients with a talocalcaneal coalition undergoing subtalar arthrodesis. This adult population (average age, 26 years) was followed for an average 7.5 years. None were candidates for resection of the coalition. Preoperative pain index improved from 3.5 (out of 4) to 1, and postoperative function improved from 3.2 (out of 4) to 0.7. The final modified AOFAS score was 93. Sixty percent (6 out of 10) demonstrated radiographic evidence of mild talonavicular arthrosis, which was not present preoperatively, but none were symptomatic. The authors prefer subtalar arthrodesis for severe flatfoot associated with talocalcaneal coalition over triple arthrodesis, to preserve some of the motion at the Chopart joint. Such limitations clinically amounted to a 40% decrease in transverse tarsal motion, dorsiflexion decrease by 30%, and plantar-flexion decrease of 9%. Gonzalez and Kumar63 evaluated 48 patients who underwent resection of a calcaneonavicular coalition in 75 feet. They divided their population into two groups. Group A (32 feet) patients were directly evaluated by the authors in follow-up. Group B (43 feet) patients were 1355

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evaluated retrospectively. The authors found that 84% of the patients in group A achieved a good or excellent result. Those with a fair result did not warrant conversion to arthrodesis. Group B patients demonstrated 72% good or excellent results, with 7% overall requiring revision to a triple arthrodesis. Combining both groups yielded 77% good or excellent results from resection of a calcaneonavicular coalition. Again, talar beaking did not preclude a good outcome clinically. The result did not deteriorate over time, and some patients followed for more than 20 years maintained a good or excellent result. Cohen et al20 evaluated 13 feet undergoing resection for calcaneonavicular coalition. This cohort consisted of adult patients (average age, 33 years), with 77% demonstrating preexisting degenerative arthritis radiographically. With an average 3-year follow-up, 85% (11 of 13) had subjective relief of preoperative symptoms, and 2 of 13 underwent secondary arthrodesis (one subtalar, one triple). Subtalar motion improved an average of 10 degrees. Preoperative degenerative arthritic changes were noted in the naviculocuneiform joint (23%), the subtalar joint (23%), and the talonavicular joint (46%). Preexisting arthritis was mild or minimal in 12 of 13 patients, and the one patient with moderate osteoarthritis (multiple peripheral osteophytes in the absence of significant joint space narrowing) later required a subtalar arthrodesis. Complications stemmed from the initial use of the extensor digitorum brevis muscle as an interposition graft with a pull-out suture placed medially. This technique resulted in a 50% lateral wound-dehiscence rate. Using bone wax before restoring the extensor digitorum brevis to its anatomic position eliminated this complication. REFERENCES 1. Abosala A, Tumia N, Anderson D: Tibialis posterior tendon rupture in children, Injury 34:866–867, 2003. 2. Alexander IJ, Johnson KA, Berquist TH: Magnetic resonance imaging in the diagnosis of disruption of the posterior tibial tendon, Foot Ankle 8:144–147, 1987. 3. Augustin JF, Lin SS, Berberian WS, Johnson JE: Nonoperative treatment of adult acquired flat foot with the Arizona brace, Foot Ankle Clin 8:491–502, 2003. 4. Balen PF, Helms CA: Association of posterior tibial tendon injury with spring ligament injury, sinus tarsi abnormality, and plantar fasciitis on MR imaging, AJR Am J Roentgenol 176:1137– 1143, 2001. 5. Kulig K, Lederhaus ES, Reischl S, et al: Effect of eccentric exercise program for early tibialis posterior tendinopathy, Foot Ankle Int 30:877–885, 2009. doi:10.3113/FAI.2009.0877. 6. Beals TC, Pomeroy GC, Manoli A 2nd: Posterior tibial tendon insufficiency: diagnosis and treatment, J Am Acad Orthop Surg 7:112–118, 1999. 7. Blake RL, Anderson K, Ferguson H: Posterior tibial tendinitis. A literature review with case reports, J Am Podiatr Med Assoc 84:141–149, 1994. 8. Blumen E, Myerson M: Stage IV posterior tibial tendon rupture, Foot Ankle Clin 12:341–362, 2007. 9. Bolt PM, Coy S, Toolan BC: A comparison of lateral column lengthening and medial translational osteotomy of the calcaneus for the reconstruction of adult acquired flatfoot, Foot Ankle Int 28:1115–1123, 2007.

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10. Bordelon RL: Correction of hypermobile flatfoot in children by molded insert, Foot Ankle 1:143–150, 1980 11. Boss PA, Hintermann B: Anatomical study of the medial ankle ligament complex, Foot Ankle Int 23:547–553, 2002. 12. Brahms MA: The posterior tibial tendon, J Am Podiatry Assoc 56:502–503, 1966. 13. Brown RR, Rosenberg ZS, Thornhill BA: The C sign: more specific for flatfoot deformity than subtalar coalition, Skeletal Radiol 30:84–87, 2001. 14. Cain TJ, Hyman S: Peroneal spastic flat foot: its treament by osteotomy of the os calcis, J Bone Joint Surg Br 60:527–529, 1978. 15. Chan JY, Williams BR, Nair P, et al: The contribution of medializing calcaneal osteotomy on hindfoot alignment in the reconstruction of the stage II adult acquired flatfoot deformity, Foot Ankle Int 34:159–166, 2013. doi:10.1177/1071100712460225. 16. Chao W, Wapner KL, Lee TH, et al: Nonoperative management of posterior tibial tendon dysfunction, Foot Ankle Int 17:736– 741, 1996. 17. Chen YJ, Liang SC: Diagnostic efficacy of ultrasonography in stage I posterior tibial tendon dysfunction: sonographic– surgical correlation, J Ultrasound Med 16:417–423, 1997. 18. Choi K, Lee S, Otis JC, Deland JT: Anatomical reconstruction of the spring ligament using peroneus longus tendon graft, Foot Ankle Int 24:430–436, 2003. 19. Coetzee JC, Hansen ST: Surgical management of severe deformity resulting from posterior tibial tendon dysfunction, Foot Ankle Int 22:944–949, 2001. 20. Cohen BE, Davis WH, Anderson RB: Success of calcaneonavicular coalition resection in the adult population, Foot Ankle Int 17:569–572, 1996. 21. Cohen BE, Johnson JE: Subtalar arthrodesis for treatment of posterior tibial tendon insufficiency, Foot Ankle Clin 6:121–128, 2001. 22. Comfort TK, Johnson LO: Resection for symptomatic talocalcaneal coalition, J Pediatr Orthop 18:283–288, 1998. 23. Conti SF: Posterior tibial tendon problems in athletes, Orthop Clin North Am 25:109–121, 1994. 24. Conti S, Michelson J, Jahss M: Clinical significance of magnetic resonance imaging in preoperative planning for reconstruction of posterior tibial tendon ruptures, Foot Ankle 13:208–214, 1992. 25. Cotton FJ: Foot statics and surgery, N Engl J Med 214:353–362, 1936. 26. Cowell HR: Talocalcaneal coalition and new causes of peroneal spastic flatfoot, Clin Orthop Relat Res 85:16–22, 1972. 27. Cowell HR, Elener V: Rigid painful flatfoot secondary to tarsal coalition, Clin Orthop Relat Res 177:54–60, 1983. 28. Cozen L: Posterior tibial tenosynovitis secondary to foot strain, Clin Orthop Relat Res 42:101–102, 1965. 29. Crates JM, Richardson EG: Treatment of stage I posterior tibial tendon dysfunction with medial soft tissue procedures, Clin Orthop Relat Res 365:46–49, 1999. 30. Crim JR, Kjeldsberg KM: Radiographic diagnosis of tarsal coalition, AJR Am J Roentgenol 182:323–328, 2004. 31. Danko AM, Allen B Jr, Pugh L, Stasikelis P: Early graft failure in lateral column lengthening, J Pediatr Orthop 24:716–720, 2004. 32. Deland JT: Adult-acquired flatfoot deformity, J Am Acad Orthop Surg 16:399–406, 2008. 33. Deland JT, Arnoczky SP, Thompson FM: Adult acquired flatfoot deformity at the talonavicular joint: reconstruction of the spring ligament in an in vitro model, Foot Ankle 13:327–332, 1992. 34. Deland JT, de Asla RJ, Segal A: Reconstruction of the chronically failed deltoid ligament: a new technique, Foot Ankle Int 25:795– 799, 2004.

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35. Deland JT, de Asla RJ, Sung IH, et al: Posterior tibial tendon insufficiency: which ligaments are involved? Foot Ankle Int 26:427–435, 2005. 36. Deland JT, Hamilton WG: Posterior tibial tendon tears in dancers, Clin Sports Med 27:289–294, 2008. doi:10.1016/j. csm.2007.12.001. 37. Deland JT, Otis JC, Lee KT, Kenneally SM: Lateral column lengthening with calcaneocuboid fusion: Range of motion in the triple joint complex, Foot Ankle Int 16:729–733, 1995. 38. Deland JT, Page A, Sung IH, et al: Posterior tibial tendon insufficiency results at different stages, HSS J 2(2):157–160, 2006. doi: 10.1007/s11420-006-9017-0. 39. De Zwart DF, Davidson JS: Rupture of the posterior tibial tendon associated with fractures of the ankle. A report of two cases, J Bone Joint Surg Am 65:260–262, 1983. 40. Donovan A, Rosenberg ZS: Extraarticular lateral hindfoot impingement with posterior tibial tendon tear: MRI correlation, AJR Am J Roentgenol 193:672–678, 2009. doi: 10.2214/ AJR.08.2215. 41. Downey DJ, Simkin PA, Mack LA, et al: Tibialis posterior tendon rupture: a cause of rheumatoid flat foot, Arthritis Rheum 31:441–446, 1988. 42. duch*ene GG: Physiology of motion, Philadelphia, 1949, JB Lippincott, pp 303–369. 43. Dumontier TA, Falicov A, Mosca V, Sangeorzan B: Calcaneal lengthening: investigation of deformity correction in a cadaver flatfoot model, Foot Ankle Int 26:166–170, 2005. 44. Dwyer FC: Osteotomy of the calcaneum for pes cavus, J Bone Joint Surg Br 41:80–86, 1959. 45. Dyal CM, Feder J, Deland JT, Thompson FM: Pes planus in patients with posterior tibial tendon insufficiency: asymptomatic versus symptomatic foot, Foot Ankle Int 18:85–88, 1997. 46. Earll M, Wayne J, Brodrick C, et al: Contribution of the deltoid ligament to the ankle joint contact characteristics: a cadaver study, Foot Ankle Int 17:317–324, 1996. 47. Ellis SJ, Deyer T, Williams BR, et al: Assessment of lateral hindfoot pain in acquired flatfoot deformity using weightbearing multiplanar imaging, Foot Ankle Int 31:361–371, 2010. 48. Ellis SJ, Williams BR, Deland JT, et al: Deltoid ligament reconstruction with peroneus longus autograft in flatfoot, Foot Ankle Int 31:781–789, 2010. doi:10.3113/FAI.2010.0781. 49. Ellis SJ, Williams BR, Garg R, et al: Incidence of plantar lateral foot pain before and after the use of trial metal wedges in lateral column lengthening, Foot Ankle Int 32:665–673, 2011. 50. Ellis SJ, Yu JC, Williams BR, et al: New radiographic parameters assessing forefoot abduction in the adult acquired flatfoot deformity, Foot Ankle Int 30:1168–1176, 2009. 51. Emery KH, Bisset GS 3rd, Johnson ND, Nunan PJ: Tarsal coalition: a blinded comparison of MRI and CT, Pediatr Radiol 28:612–616, 1998. 52. Evans, D: Calcaneo-valgus deformity, J Bone Joint Surg Br 57: 270–278, 1975. 53. Fayazi AH, Nguyen HV, Juliano PJ: Intermediate term follow-up of calcaneal osteotomy and flexor digitorum longus transfer for treatment of posterior tibial tendon dysfunction, Foot Ankle Int 23:1107–1111, 2002. 54. Frey C, Shereff M, Greenidge N: Vascularity of the posterior tibial tendon, J Bone Joint Surg Am 72:884–888, 1990. 55. Funk DA, Cass JR, Johnson KA: Acquired adult flat foot secondary to posterior tibial-tendon pathology, J Bone Joint Surg Am 68:95–102, 1986. 56. Gazdag AR, Cracchiolo A 3rd: Rupture of the posterior tibial tendon. Evaluation of injury of the spring ligament and clinical assessment of tendon transfer and ligament repair, J Bone Joint Surg Am 79:675–681, 1997. 57. Gerling MC, Pfirrmann CW, Farooki S, et al: Posterior tibialis tendon tears: comparison of the diagnostic efficacy of magnetic

resonance imaging and ultrasonography for the detection of surgically created longitudinal tears in cadavers, Invest Radiol 38:51–56, 2003. 58. Giblin MM: Ruptured tibialis posterior tendon associated with a closed medial malleolar fracture, Aust N Z J Surg 50:59–60, 1980. 59. Gleich A: Beitrag zur operativen Plattfussbehandlung. Arch Klin Chir 46:358–362, 1893. 60. Goldner JL: Tendon transfers in rheumatoid arthritis, Orthop Clin North Am 5:425–444, 1974. 61. Goldner JL, Keats PK, Bassett FH 3rd, Clippinger FW: Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibial tendon and medial plantar ligaments, Orthop Clin North Am 5:39–51, 1974. 62. Goncalves-Neto J, Witzel SS, Teodoro WR, et al: Changes in collagen matrix composition in human posterior tibial tendon dysfunction, Joint Bone Spine 69:189–194, 2002. 63. Gonzalez P, Kumar SJ: Calcaneonavicular coalition treated by resection and interposition of the extensor digitorum brevis muscle, J Bone Joint Surg Am 72:71–77, 1990. 64. Gould N: Graphing the adult foot and ankle, Foot Ankle 2:213– 219, 1982. 65. Greene DL, Thompson MC, Gesink DS, Graves SC: Anatomic study of the medial neurovascular structures in relation to calcaneal osteotomy, Foot Ankle Int 22:569–571, 2001. 66. Vander Griend RA: “Z” osteotomy of the calcaneus, Tech Foot Ankle Surg 7:257–263, 2008. 67. Griffiths JC: Tendon injuries around the ankle, J Bone Joint Surg Br 47:686–689, 1965. 68. Guyton GP, Jeng C, Krieger LE, Mann RA: Flexor digitorum longus transfer and medial displacement calcaneal osteotomy for posterior tibial tendon dysfunction: a middle-term clinical follow-up, Foot Ankle Int 22:627–632, 2001. 69. Haddad SL, Dedhia S, Ren Y, et al: Deltoid ligament reconstruction: a novel technique with biomechanical analysis, Foot Ankle Int 31:639–651, 2010. doi:10.3113/FAI.2010.0639. 70. Haddad SL, Myerson MS, Younger A, et al: Symposium: adult acquired flatfoot deformity, Foot Ankle Int 32:95–111, 2011. 71. Hadfield M, Snyder J, Liacouras P, et al: The effects of a medializing calcaneal osteotomy with and without superior translation on Achilles tendon elongation and plantar foot pressures, Foot Ankle Int 26:365–370, 2005. 72. Harris RI: Rigid valgus foot due to talocalcaneal bridge, J Bone Joint Surg Am 37:169–183, 1955. 73. Harris RJ, Beath T: Etiology of peroneal spastic flatfoot, J Bone Joint Surg Br 30:624–634, 1948. 74. Helal B: Tibialis posterior tendon synovitis and rupture, Acta Orthop Belg 55:457–460, 1989. 75. Hicks JH: The mechanics of the foot. II. The plantar aponeurosis and the arch, J Anat 88:25–30, 1954. 76. Hintermann B, Valderrabano V, Kundert HP: Lengthening of the lateral column and reconstruction of the medial soft tissue for treatment of acquired flatfoot deformity associated with insufficiency of the posterior tibial tendon, Foot Ankle Int 20:622–629, 1999. 77. Hirose CB, Johnson JE: Plantar flexion opening wedge medial cuneiform osteotomy for correction of fixed forefoot varus associated with flatfoot deformity, Foot Ankle Int 25:568–574, 2004. 78. Hochman M, Reed MH: Features of calcaneonavicular coalition on coronal computed tomography, Skeletal Radiol 29:409–412, 2000. 79. Hogan JF: Posterior tibial tendon dysfunction and MRI, J Foot Ankle Surg 32:467–472, 1993. 80. Holmes GB Jr, Mann RA: Possible epidemiological factors associated with rupture of the posterior tibial tendon, Foot Ankle 13:70–79, 1992.

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81. Houck JR, Nomides C, Neville CG, Samuel Flemister A: Effect of Stage II posterior tibial tendon dysfunction on deep compartment muscle strength: a new strength test, Foot Ankle Int 29:895–902, 2008. doi:10.3113/FAI.2008.0895. 82. Neville C, Flemister A, Houck JR: Effect of AirLift PTTD brace on foot kinematics with stage II posterior tibial tendon dysfunction. Orthop Sports Phys Ther 39:201–209, 2009. doi:10.2519/ jospt.2009.2908. 83. Hsu TC, Wang CL, Wang TG, et al: Ultrasonographic examination of the posterior tibial tendon, Foot Ankle Int 18:34–38, 1997. 84. Imhauser CW, Siegler S, Abidi NA, Frankel DZ: The effect of posterior tibialis tendon dysfunction on the plantar pressure characteristics and the kinematics of the arch and the hindfoot, Clin Biomech (Bristol, Avon) 19:161–169, 2004. 85. Jahss MH: Spontaneous rupture of the tibialis posterior tendon: clinical findings, tenographic studies, and a new technique of repair, Foot Ankle 3:158–166, 1982. 86. Janisse DJ, Wertsch JD, Del Toro DR: Foot orthoses and prescription shoes. In Redford JB, Basmajian JV, Trautman P, editors: Orthotics, clinical practice and rehabilitation Technology, New York, 1995, Churchill Livingstone, pp 64–65. 87. Jeng CL, Bluman EM, Myerson MS: Minimally invasive deltoid reconstruction for stage IV flatfoot, Foot Ankle Int 32:21–30, 2011. doi:10.3113/FAI.2011.0021. 88. Jeng CL, Vora AM, Myerson MS: The medial approach to triple arthrodesis. Indications and technique for management of rigid valgus deformities in high-risk patients, Foot Ankle Clin 10:515– 521, vi–vii, 2005. 89. Johnson KA, Strom DE: Tibialis posterior tendon dysfunction, Clin Orthop Relat Res 239:196–206, 1989. 90. Bridgeman JT, Zhang Y, Donahue H, et al: Estrogen receptor expression in posterior tibial dysfunction: a pilot study, Foot Ankle Int 31:1081–1084, 2010. doi:10.3113/FAI.2010.1081. 91. Kadakia AR, Haddad SL: Hindfoot arthrodesis for the adult acquired flat foot, Foot Ankle Clin 8:569–594, x, 2003. 92. Kapandji I: The physiology of the joints, New York, 1970, Churchill Livingston, pp 170–194. 93. Karasick D, Schweitzer ME: Tear of the posterior tibial tendon causing asymmetric flatfoot: radiologic findings, AJR Am J Roentgenol 161:1237–1240, 1993. 94. Kaye RA, Jahss MH: Tibialis posterior: a review of anatomy and biomechanics in relation to support of the medial longitudinal arch, Foot Ankle 11:244–247, 1991. 95. Keenan MA, Peabody TD, Gronley JK, Perry J: Valgus deformities of the feet and characteristics of gait in patients who have rheumatoid arthritis, J Bone Joint Surg Am 73:237–247, 1991. 96. Kennedy JC, Willis RB: The effects of local steroid injections on tendons: a biomechanical and microscopic correlative study, Am J Sports Med 4:11–21, 1976. 97. Kettelkamp DB, Alexander HH: Spontaneous rupture of the posterior tibial tendon, J Bone Joint Surg Am 51:759–764, 1969. 98. Key JA: Partial rupture of the tendon of the posterior tibial muscle, J Bone Joint Surg Am 35:1006–1008, 1953. 99. Khazen G, Khazen C: Tendoscopy in stage I posterior tibial tendon dysfunction, Foot Ankle Clin 17:399–406, 2012. doi:10.1016/j.fcl.2012.06.002. 100. Khoury NJ, el-Khoury GY, Saltzman CL, Brandser EA: MR imaging of posterior tibial tendon dysfunction, AJR Am J Roentgenol 167:675–682, 1996. 101. Kirkham BW, Gibson T: Comment on the article by Downey et al, Arthritis Rheum 32:359, 1989. 102. Koutsogiannis E: Treatment of mobile flat foot by displacement osteotomy of the calcaneus, J Bone Joint Surg Br 53:96–100, 1971.

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103. Kulig K, Burnfield JM, Requejo SM, et al: Selective activation of tibialis posterior: evaluation by magnetic resonance imaging, Med Sci Sports Exerc 36:862–867, 2004. 104. Kulik SA Jr, Clanton TO: Tarsal coalition, Foot Ankle Int 17:286– 296, 1996. 105. Kulowski J: Tendovaginitis (tenosynovitis), general discussion and report of one case involving the posterior tibial tendon. J Missouri State Med Assoc 33:135–137, 1936. 106. Kumar SJ, Guille JT, Lee MS, Couto JC: Osseous and nonosseous coalition of the middle facet of the talocalcaneal joint, J Bone Joint Surg Am 74:529–535, 1992. 107. Langenskiöld A: Chronic non-specific tenosynovitis of the tibialis posterior tendon, Acta Orthop Scand 38:301–305, 1967. 108. Lapidus PW: Kinesiology and mechanical anatomy of the tarsal joints, Clin Orthop Relat Res 30:20–36, 1963. 109. Lapidus PW, Seidenstein H: Chronic non-specific tenosynovitis with effusion about the ankle; report of three cases, J Bone Joint Surg Am 32:175–179, 1950. 110. Leboucq H: De la soudure congenitale de certains os du tarse, Bull Acad Royale Med Belg 4:103–112, 1890. 111. Lee MF, Chan PT, Chau LF, Yu KS: Tarsal tunnel syndrome caused by talocalcaneal coalition, Clin Imaging 26:140–143, 2002. 112. Lemley FR, Neville C: Effect of ankle foot orthotic devices on foot kinematics in Stage II posterior tibial tendon dysfunction, Foot Ankle Int 33:406–414, 2012. doi:10.3113/FAI.2012. 0406. 113. Lipscomb P: Non-suppurative tenosynovitis and paratendinitis, Instr Course Lect 7:254, 1950. 114. Malicky ES, Crary JL, Houghton MJ, et al: Talocalcaneal and subfibular impingement in symptomatic flatfoot in adults, J Bone Joint Surg Am 84:2005–2009, 2002. 115. Mann RA: Tendon transfers and electromyography, Clin Orthop Relat Res 85:64–66, 1972. 116. Mann RA: Acquired flatfoot in adults, Clin Orthop Relat Res 181:46–51, 1983. 117. Mann RA: Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon, J Bone Joint Surg Am 78:780–792, 1996. 118. Mann RA: Flatfoot in adults. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, St Louis, 1999, Mosby, pp 733–767. 119. Mann RA: Posterior tibial tendon dysfunction. Treatment by flexor digitorum longus transfer, Foot Ankle Clin 6:77–87, vi, 2001. 120. Mann RA, Beaman DN, Horton GA: Isolated subtalar arthrodesis, Foot Ankle Int 19:511–519, 1998. 121. Mann R, Inman VT: Phasic activity of intrinsic muscles of the foot, J Bone Joint Surg Am 46:469–481, 1964. 122. Mann R, Specht T: Posterior tibial tendon rupture. Presented at the Annual Winter Meeting of the American Orthopedic Foot and Ankle Society, Las Vegas, Nev, 1982. 123. Mann RA, Thompson FM: Rupture of the posterior tibial tendon causing flat foot. Surgical treatment, J Bone Joint Surg Am 67:556–561, 1985. 124. Marcus RE, Pfister ME: The enigmatic diagnosis of posterior tibialis tendon rupture, Iowa Orthop J 13:171–177, 1993. 125. McCormack AP, Varner KE, Marymont JV: Surgical treatment for posterior tibial tendonitis in young competitive athletes, Foot Ankle Int 24:535–538, 2003. 126. McMaster PE: Tendon and muscle ruptures. Clinical and experimental studies on the causes and location of subcutaneous ruptures, J Bone Joint Surg 15:705, 1933. 127. Michelson J, Conti S, Jahss MH: Survivorship analysis of tendon transfer surgery for posterior tibial tendon rupture, Orthop Trans 16:30–31, 1992.

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128. Michelson J, Easley M, Wigley FM, Hellmann D: Posterior tibial tendon dysfunction in rheumatoid arthritis, Foot Ankle Int 16:156–161, 1995. 129. Miller SD, Van Holsbeeck M, Boruta PM, et al: Ultrasound in the diagnosis of posterior tibial tendon pathology, Foot Ankle Int 17:555–558, 1996. 130. Momberger N, Morgan JM, Bachus KN, West JR: Calcaneocuboid joint pressure after lateral column lengthening in a cadaveric planovalgus deformity model, Foot Ankle Int 21:730–735, 2000. 131. Monto RR, Moorman CT 3rd, Mallon WJ, Nunley JA 3rd: Rupture of the posterior tibial tendon associated with closed ankle fracture, Foot Ankle 11:400–403, 1991. 132. Mosca VS, Bevan WP: Talocalcaneal tarsal coalitions and the calcaneal lengthening osteotomy: the role of deformity correction, J Bone Joint Surg Am 94:1584–1594, 2012. 133. Mosier SM, Lucas DR, Pomeroy G, Manoli A 2nd: Pathology of the posterior tibial tendon in posterior tibial tendon insufficiency, Foot Ankle Int 19:520–524, 1998. 134. Mosier-LaClair S, Pomeroy G, Manoli A 2nd: Operative treatment of the difficult stage 2 adult acquired flatfoot deformity, Foot Ankle Clin 6:95–119, 2001. 135. Mueller TJ: Acquired flatfoot secondary to tibialis posterior dysfunction: biomechanical aspects, J Foot Surg 30:2–11, 1991. 136. Myerson, MS: Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon, Instr Course Lect 46:393–405, 1997. 137. Myerson MS, Badekas A, Schon LC: Treatment of stage II posterior tibial tendon deficiency with flexor digitorum longus tendon transfer and calcaneal osteotomy, Foot Ankle Int 25: 445–450, 2004. 138. Myerson MS, Corrigan J: Treatment of posterior tibial tendon dysfunction with flexor digitorum longus tendon transfer and calcaneal osteotomy, Orthopedics 19:383–388, 1996. 139. Myerson M, Solomon G, Shereff M: Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease, Foot Ankle 9:219–225, 1989. 140. Ness ME, Long J, Marks R, Harris G: Foot and ankle kinematics in patients with posterior tibial tendon dysfunction, Gait Posture 27:331–339, 2008. 141. Niki H, Ching RP, Kiser P, Sangeorzan BJ: The effect of posterior tibial tendon dysfunction on hindfoot kinematics, Foot Ankle Int 22:292–300, 2001. 142. Nyska M, Parks BG, Chu IT, Myerson MS: The contribution of the medial calcaneal osteotomy to the correction of flatfoot deformities, Foot Ankle Int 22:278–282, 2001. 143. Petersen W, Hohmann G, Pufe T, et al: Structure of the human tibialis posterior tendon, Arch Orthop Trauma Surg 124:237– 242, 2004. 144. Petersen W, Hohmann G, Stein V, Tillmann B: The blood supply of the posterior tibial tendon, J Bone Joint Surg Br 84:141–144, 2002. 145. Phillips GE: A review of elongation of os calcis for flat feet, J Bone Joint Surg Br 65:15–18, 1983. 146. Pineda C, Resnick D, Greenway G: Diagnosis of tarsal coalition with computed tomography, Clin Orthop Relat Res 208:282– 288, 1986. 147. Plattner PF: Tendon problems of the foot and ankle. The spectrum from peritendinitis to rupture, Postgrad Med 86:155–162, 167–170, 1989. 148. Pomeroy GC, Pike RH, Beals TC, Manoli A 2nd: Acquired flatfoot in adults due to dysfunction of the posterior tibial tendon, J Bone Joint Surg Am 81:1173–1182, 1999. 149. Harish S, Kumbhare D, O’Neill J, Popowich T: Comparison of sonography and magnetic resonance imaging for spring ligament abnormalities: preliminary study, J Ultrasound Med 27: 1145–1152, 2008.

150. Premkumar A, Perry MB, Dwyer AJ, et al: Sonography and MR imaging of posterior tibial tendinopathy, AJR Am J Roentgenol 178:223–232, 2002. 151. Raikin SM, Winters BS, Daniel JN: The RAM classification: a novel approach to adult acquired flatfoot, Foot Ankle Int 17:169–181, 2012. doi:10.1016/j.fcl.2012.03.002. 152. Rathbun JB, Macnab I: The microvascular pattern of the rotator cuff, J Bone Joint Surg Br 52:540–553, 1970. 153. Rosenberg ZS: Chronic rupture of the posterior tibial tendon, Magn Reson Imaging Clin N Am 2:79–87, 1994. 154. Rosenberg ZS, Jahss MH, Noto AM, et al: Rupture of the posterior tibial tendon: CT and surgical findings, Radiology 167: 489–493, 1988. 155. Ross JA: Posterior tibial tendon dysfunction in the athlete, Clin Podiatr Med Surg 14:479–488, 1997. 156. Alvarez RG, Marini A, Schmitt C, Saltzman CL: Stage I and II posterior tibial tendon dysfunction treated by structured nonoperative management protocol: an orthosis and exercise program, Foot Ankle Int 27:2–8, 2006. 157. Saltzman CL, Brandser EA, Berbaum KS, et al: Reliability of standard foot radiographic measurements, Foot Ankle Int 15: 661–665, 1994. 158. Saltzman CL, el-Khoury GY: The hindfoot alignment view, Foot Ankle Int 16:572–576, 1995. 159. Sammarco VJ, Magur EG, Sammarco GJ, Bagwe MR: Arthrodesis of the subtalar and talonavicular joints for correction of symptomatic hindfoot malalignment, Foot Ankle Int 27:661– 666, 2006. 160. Sangeorzan BJ, Mosca V, Hansen ST Jr: Effect of calcaneal lengthening on relationships among the hindfoot, midfoot, and forefoot, Foot Ankle 14:136–141, 1993. 161. Sarrafian SK: Anatomy of the foot and Ankle, Philadelphia, 1983, JB Lippincott, pp 43–61, 216–219, 375–425. 162. Schaffer JJ, Lock TR, Salciccioli GG: Posterior tibial tendon rupture in pronation–external rotation ankle fractures, J Trauma 27:795–796, 1987. 163. Scranton PE Jr: Treatment of symptomatic talocalcaneal coalition, J Bone Joint Surg Am 69:533–539, 1987. 164. Sijbrandij ES, van Gils AP, de Lange EE, Sijbrandij S: Bone marrow ill-defined hyperintensities with tarsal coalition: MR imaging findings, Eur J Radiol 43:61–65, 2002. 165. Silver RL, de la Garza J, Rang M: The myth of muscle balance. A study of relative strengths and excursions of normal muscles about the foot and ankle, J Bone Joint Surg Br 67:432–437, 1985. 165a. Smith JW: Blood supply of tendons, Am J Surg 109:272–276, 1965. 166. Solomon LB, Ruhli FJ, Taylor J, et al: A dissection and computer tomograph study of tarsal coalitions in 100 cadaver feet, J Orthop Res 21:352–358, 2003. 167. Song SJ, Lee S, O’Malley MJ Deltoid ligament strain after correction of acquired flatfoot deformity by triple arthrodesis, Foot Ankle Int 21:573–577, 2000. 168. DeOrio JK, Shapiro SA, McNeil RB, Stansel J: Validity of posterior tibial edema sign in posterior tibial tendon dysfunction, Foot Ankle Int 32:189–192, 2011. doi:10.3113/FAI.2011.0189. 169. Stein RE: Rupture of the posterior tibial tendon in closed ankle fractures. Possible prognostic value of a medial bone flake: report of two cases, J Bone Joint Surg Am 67:493–494, 1985. 170. Stephien M: The sheath and arterial supply of the tendon of the posterior tibialis muscle in man, Folia Morph (Warsz) 32:51–61, 1973. 171. Stormont DM, Peterson HA: The relative incidence of tarsal coalition, Clin Orthop Relat Res 181:28–36, 1983. 172. Streb HS, Marzano R: Conservative management of posterior tibial tendon dysfunction, subtalar joint complex, and pes planus deformity, Clin Podiatr Med Surg 16:439–451, 1999.

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173. Sung IH, Lee S, Otis JC, Deland JT: Posterior tibial tendon force requirement in early heel rise after calcaneal osteotomies, Foot Ankle Int 23:842–849, 2002. 174. Supple KM, Hanft JR, Murphy BJ, et al: Posterior tibial tendon dysfunction, Semin Arthritis Rheum 22:106–113, 1992. 175. Sutherland DH: An electromyographic study of the plantar flexors of the ankle in normal walking on the level, J Bone Joint Surg Am 48:66–71, 1966. 176. Swiontkowski MF, Scranton PE, Hansen S: Tarsal coalitions: long-term results of surgical treatment, J Pediatr Orthop 3:287– 292, 1983. 177. Teasdall RD, Johnson KA: Surgical treatment of stage I posterior tibial tendon dysfunction, Foot Ankle Int 15:646–648, 1994. 178. Tellisi N, Lobo M, O’Malley M, et al: Functional outcome after surgical reconstruction of posterior tibial tendon insufficiency in patients under 50 years, Foot Ankle Int 29:1179–1183, 2008. 179. Toolan BC, Sangeorzan BJ, Hansen ST Jr: Complex reconstruction for the treatment of dorsolateral peritalar subluxation of the foot. Early results after distraction arthrodesis of the calcaneocuboid joint in conjunction with stabilization of, and transfer of the flexor digitorum longus tendon to, the midfoot to treat acquired pes planovalgus in adults, J Bone Joint Surg Am 81:1545–1560, 1999. 180. Trevino S, Gould N, Korson R: Surgical treatment of stenosing tenosynovitis at the ankle, Foot Ankle 2:37–45, 1981.

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181. Uchiyama E, Kitaoka HB, Fujii T, et al: Gliding resistance of the posterior tibial tendon: Foot Ankle Int 27:723, 2006. 182. Varner KE, Michelson JD: Tarsal coalition in adults, Foot Ankle Int 21:669–672, 2000. 183. Wacker JT, Calder JD, Engstrom CM, Saxby TS: MR morphometry of posterior tibialis muscle in adult acquired flat foot, Foot Ankle Int 24:354–357, 2003. 184. Wacker JT, Hennessy MS, Saxby TS: Calcaneal osteotomy and transfer of the tendon of flexor digitorum longus for stage-II dysfunction of tibialis posterior. Three- to five-year results, J Bone Joint Surg Br 84:54–58, 2002. 185. Wechsler RJ, Schweitzer ME, Deely DM, et al: Tarsal coalition: depiction and characterization with CT and MR imaging, Radiology 193:447–452, 1994. 186. Wertheimer SJ, Weber CA, Loder BG, et al: The role of endoscopy in treatment of stenosing posterior tibial tenosynovitis, J Foot Ankle Surg 34:15–22, 1995. 187. Wilde PH, Torode IP, Dickens DR, Cole WG: Resection for symptomatic talocalcaneal coalition, J Bone Joint Surg Br 76:797–801, 1994. 188. Williams BR, Ellis SJ, Deyer TW, et al: Reconstruction of the spring ligament using a peroneus longus autograft tendon transfer, Foot Ankle Int 31:567–577, 2010. 189. Woll TS: Posterior tibial tendon dysfunction, West J Med 159:485–486, 1993. 190. Yao L, Gentili A, Cracchiolo A: MR imaging findings in spring ligament insufficiency, Skeletal Radiol 28:245–250, 1990.

Chapter

Pes Cavus Fabian G. Krause, Gregory P. Guyton

CHAPTER CONTENTS ETIOLOGY CHARCOT-MARIE-TOOTH DISEASE POLIOMYELITIS Patterns of Foot Deformity in Polio Hindfoot Cavus Forefoot Cavus Other Deformities OTHER NEUROLOGIC LESIONS POSTTRAUMATIC CAVOVARUS FOOT DEFORMITIES CONGENITAL PES CAVUS Clubfoot Residuals The Idiopathic Cavus Foot EVOLUTION OF DEFORMITY BIOMECHANICAL CONSEQUENCES OF PES CAVUS Physical Examination INVESTIGATIONS Conservative Treatment Surgical Treatment Decision Making Soft Tissue Procedures (Video Clips 47, 49, and 51) Bony Procedures (Video Clips 48, 50, 75, and 118) Outcome

1361 1361 1363 1363 1363 1364 1364 1364 1364 1365 1365 1365 1365 1366 1368 1369 1370 1370 1370 1370 1374 1380

Pes cavus describes a foot with a high arch that maintains its shape and fails to flatten out with weight bearing. By majority, the components of pes cavus are an increased calcaneal pitch and varus of the hindfoot, plantar flexion of the medial forefoot, and adduction of the entire forefoot. The predominant deformity in pes cavus may be in the hindfoot, the forefoot, or a combination of both. A precise radiographic definition of pes cavus is difficult because the deformity is made up of various components in the forefoot and hindfoot. ETIOLOGY

Although the specific etiology of any cavus foot varies with the disease process, all forms result from muscle imbalance. Historical attempts to attribute all forms of cavus foot to a single neurologic lesion have proven

overly simplistic. Bentzon2 and Hallgrimsson16 in 1939 proposed that extrinsic muscle imbalance underlay all deformities. In 1959, duch*enne9 subsequently proposed that the deformity results from an imbalance between the extrinsics and the intrinsics. Neither approach is fully satisfactory; a cavus foot is best thought of as an end result that a variety of subtle neurologic lesions can produce. Brewerton et al5 specifically looked at the cause of pes cavus in a series of 77 patients and found subtle neurologic defects in 66% of them, leaving a large group of “idiopathic” cases. Of these, 11 of the 26 patients had a family history of pes cavus, and 7 of the 26 had nonspecific abnormalities upon electromyographic and nerve conduction velocity examination. Most cases of idiopathic pes cavus likely represent a very subtle neurologic lesion that is below clinical detection. Roughly half of the detectable lesions are variants of Charcot-Marie-Tooth disease, but a host of other less common conditions can also be discovered (Table 26-1).19 Neurologic referral is mandatory in situations that might point toward a correctable lesion of the spinal cord, such as a syrinx or spinal cord tumor. These include rapid progression, hyperreflexia, clonus, or significant asymmetry between sides in motor pattern or deformity. A new diagnosis of central neurologic disease is not uncommon in foot and ankle practice. CHARCOT-MARIE-TOOTH DISEASE

Charcot-Marie-Tooth disease (CMT) should at least be considered in every patient who presents with pes cavus. CMT is not, in fact, a single disease but rather a heterogeneous group of disorders caused by inheritable defects in any of several constituent proteins of the myelin sheath of peripheral nerve. The disorder was described in general terms by the great French neurologist Jean Martin Charcot and his pupil Marie in 1886 and independently by Tooth in England later that year.6,44 Originally, Charcot attributed the disorder to a spinal defect, and it was Tooth’s subsequent work that correctly classified it as a peripheral nerve disorder. The disease is the most common inheritable defect of peripheral nerves, but approximately half of the time it represents a new sporadic chromosomal recombination error. 1361

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Table 26-1 Etiology of Pes Cavus Classification I. Neuromuscular A. Muscle disease B. Afflictions of peripheral nerves and lumbosacral spinal nerve roots C. Anterior horn cell disease of spinal cord

D. Long-tract and central disease

II. Congenital

III. Traumatic

Specific Etiology Muscular dystrophy Charcot-Marie-Tooth disease Spinal dysraphism Polyneuritis Intraspinal tumor Poliomyelitis Spinal dysraphism Diastematomyelia Syringomyelia Spinal cord tumors Spinal musculature atrophy Friedreich ataxia Roussy–Lévy syndrome Primary cerebellar disease Cerebral palsy Idiopathic cavus foot Residual of clubfoot Arthrogryposis Residuals of compartment syndrome Crush injury to lower extremity Severe burn Malunion of fractured foot

Modified from Ibrahim K: Pes cavus. In Evarts CM, editor: Surgery of the musculoskeletal system, New York, 1990, Churchill Livingstone, pp 4015–4034.

The nomenclature associated with CMT is confusing because of the historical lack of understanding of its cause. The archaic term peroneal muscular atrophy (PMA) was supplanted by Dyck and Lambert, who developed an extensive classification of inheritable motor neuropathies based upon their electrodiagnostic patterns in the 1960s and 1970s.12 Their scheme refers to a series of seven hereditary motor sensory neuropathies (HMSN-I through HMSN-VII). Since 1990 there has been an explosion of understanding of the specific genetic defects underlying the CMT disorders,4 leading to a new and still evolving reclassification of the disease. CMT-1 is the most common form and accounts for more than 50% of all cases. It is autosomal dominant and demonstrates slow nerve conduction velocities (NCVs) in the range of 10 to 30 m/sec as a result of demyelination. CMT-1 can be further subdivided. CMT-1A accounts for 80% of CMT-1 cases and is the single most common form of the disease in general. Curiously, it is usually caused by a segmental trisomy along chromosome 17. The area contains the gene for peripheral myelin protein-22 (PMP-22), whose function remains unknown. Although some cases have been linked to alternative point mutations in PMP-22, the segmental trisomy responsible for most cases indicates CMT can be produced from a gene dosage effect. This chromosomal 1362

aberration is inheritable in an autosomal dominant fashion, but many cases seem to represent sporadic chromosomal recombination events. CMT-1B accounts for 5% to 10% of CMT-1 patients and is associated with a point mutation in the myelin P0 gene. The phenotype is associated with a particularly aggressive form of the disease. CMT-1C represents the small remainder of CMT-1 patients in whom the genetic defect is still unknown. CMT-2 is the second most common general form of the disease and represents 20% of patients. It is autosomal dominant like CMT-1 but has dramatically different electrical findings: NCVs are near normal, and there is no evidence of demyelination. Four separate chromosomal loci have been identified, but the product proteins involved remain unknown. In general, the course of CMT-2 is more indolent than that of CMT-1. CMT-X shows an X-linked inheritance pattern; male patients are affected and female patients are either unaffected or mildly affected carriers. It is found in 10% to 20% of all CMT cases and is associated with defects in yet another myelin constituent protein, connexin 32. CMT-4 is an autosomal recessive form of the disease and is quite rare. It in fact encompasses a large number of described genetic defects on different chromosomal loci; no product proteins have yet been described. The foot deformities in CMT do not result from absolute weakness of the motor units powering the foot but of their relative imbalance. Initiation of the deformity likely results from an imbalance of the failing foot intrinsics and the preserved extrinsics.3 Subsequently, a specific pattern of extrinsic motor weakness is common in CMT in which the anterior and lateral compartment musculature is selectively affected, with certain curious exceptions. The disease almost always affects the peroneus brevis but spares the peroneus longus. This was first observed clinically by Mann and Hsu33 and subsequently confirmed by Tynan et  al,45 who demonstrated that the cross-sectional area of the peroneus longus was preserved on magnetic resonance imaging (MRI) of patients with the disease. An additional oddity can be observed in the anterior compartment musculature; the extensor hallucis muscle can be spared while the anterior tibialis is affected. This occurs despite the more distal location of the extensor hallucis longus (EHL) and their shared peroneal innervation. The reasons for the unusual patterns of motor weakness in CMT remain poorly understood. The selective denervation affects certain muscles in the anterior and lateral compartments, and only very late posterior compartment involvement is seen. Denervation in CMT progresses very differently from a classic symmetric polyneuropathy, such as that encountered in diabetes. At least some speculation has been centered upon the possibility that some element of nerve compression can play a role.14 Regardless of the cause of the patterns of weakness, each of the deformities of the disease can be explained in

Pes Cavus ■ Chapter 26

Table 26-2 Foot Deformities in Charcot-Marie-Tooth Disease Deformity

Weak Agonist Muscle(s)

Intact Antagonist Muscle(s)

Action

Equinus

Tibialis anterior

Plantar flexion

Adduction and hindfoot varus Plantar flexion of the first ray Toe deformities

Peroneus brevis

Gastrocnemius–soleus complex (triceps-surae) Tibialis posterior

Tibialis anterior

Peroneus longus

Foot intrinsics

Long toe flexors

Hallux claw toe

Foot intrinsics

EHL and FHL

Plantar flexes the first ray, creates a secondary forefoot cavus Clawing occurs as the extrinsic forces are unmodified by the intrinsics; also depresses the metatarsal heads and accentuates cavus Severe hallucal clawing occurs when a spared EHL is used to assist a weak tibialis anterior dorsiflex the foot

Adducts the foot, inverts the subtalar joint

From Guyton GP, Mann RA: The pathogenesis and surgical management of foot deformity in Charcot-Marie-Tooth disease, Foot Ankle Clin 5:317–326, 2000. EHL, extensor hallucis longus; FHL, flexor hallucis longus.

the form of a weak agonist muscle and a more normally functioning antagonist (Table 26-2). There is no evidence of spasticity in the motor units that remain innervated. The functional peroneus longus serves to plantar flex the first ray while the denervated anterior tibialis fails to provide any counterbalancing dorsiflexion. The first metatarsal head is depressed and a forefoot cavus results. Next to a relative talus dorsiflexion, an equinus contracture develops as the Achilles tendon (triceps surae) is unopposed by the anterior tibialis. In addition, the toe extrinsics force the toes into a clawed position that is not counterbalanced by the denervated foot intrinsics. This also serves secondarily to depress the metatarsal heads and raise the arch. The supination and adduction of the foot is worsened because the posterior tibialis is unopposed by the weakened peroneus brevis. In cases with sparing of the EHL, the claw toe deformity of the hallux is worsened even more dramatically because the patient uses the EHL to dorsiflex the foot and compensate for the weak anterior tibialis. It is rare in clinical practice to encounter a patient at such an early stage of disease that the foot is entirely supple with no hindfoot or forefoot contractures. However, rebalancing the foot through tendon transfers can help prevent the development of further deformity if it is done early enough.38 For instance, the overpull of the peroneus longus that forces the forefoot into cavus can be eliminated by transferring the tendon to the peroneus brevis. This also serves to help oppose the tibialis posterior and prevent adduction. The emphasis in early-stage surgery on CMT should be on tendon transfers rather than lengthening motor units. Because the long-term outcome of CMT is one of progressive, inexorable weakness, strength should be preserved whenever possible. POLIOMYELITIS

The last great epidemic of polio in the United States occurred in New England in 1955. Although the residual

effects of the disease are now encountered with increasing rarity, it still serves as a useful model of a process that can produce either a forefoot cavus or a hindfoot cavus.8 Paralytic polio is the result of a ribonucleic acid (RNA) virus that primarily affects the thalamus, hypothalamus, motor centers of the brain stem and cerebellum, and the anterior tracts of the spinal cord. There is a wide variety of clinical presentations depending upon what portions of the central nervous system (CNS) are affected, but as a practical matter the lower extremity weakness patterns of polio come from a strikingly selective destruction of the anterior motor neurons in the spinal cord itself, preserving function both proximal and distal to the lesion. After an initial incubation period of 6 to 20 days, the acute phase of the disease is associated with the most dramatic paralysis and lasts approximately 7 to 10 days. Clinically detectable weakness usually occurs when more than 60% of the motor neurons to a muscle group are affected. Muscle function can recover gradually thereafter; the most substantial gains occur in the first 4 months, and some return of function is usually seen up to 2 years after the illness. Patterns of Foot Deformity in Polio Hindfoot Cavus The gastrocnemius–soleus complex is the critical variable in determining what variety of foot deformity will develop. The classic cavus foot deformity resulting from polio is that of a hindfoot cavus associated with a dramatically high calcaneal pitch angle. This is the result of the paralysis of the gastrocnemius–soleus complex with preservation of the remainder of the posterior compartment, the intrinsic foot musculature, and the anterior tibialis. When appropriate tension is missing from the Achilles tendon, the long toe flexors still function to depress the metatarsal heads, raising the arch. The intrinsics foreshorten the distance between the metatarsals and the calcaneus, functioning much like a bowstring to raise 1363

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the calcaneal pitch. The result is a vertical posture of the calcaneus. Forefoot Cavus A lesion slightly higher in the spinal cord can spare the gastrocnemius–soleus complex but affect the tibialis anterior selectively. This situation results in two particular imbalances that drive depression of the first ray and a forefoot cavus. First, just as in CMT, the peroneus longus is unopposed and directly plantar flexes the first ray. Second, the extensor hallucis longus is still functional and serves as an accessory dorsiflexor of the foot. This creates a claw toe as the foot is pulled up through the toe rather than the usual midfoot insertion of the tibialis anterior. The claw toe deformity itself also serves to depress the metatarsal head. Other Deformities Because the motor neuron destruction in poliomyelitis is often patchy and recovery is sometimes incomplete, the patterns of motor weakness cannot always be so neatly categorized. When the tibialis posterior is affected, either alone or in combination with the tibialis anterior, the result is a progressive planovalgus foot rather than a cavus foot. Rarer still is isolated involvement of the peroneals, which usually results in a very mild cavus foot dominated more by varus of the hindfoot with attendant instability of the ankle. The critical lesson is that, like all peripheral neural lesions, the motor weakness patterns in polio all must be evaluated and treated individually.

OTHER NEUROLOGIC LESIONS

Although CMT and polio represent the most historically prominent etiologies of the cavus foot, a wide variety of other lesions can lead to the deformity. Friedreich ataxia is a familial progressive ataxia in which posterior column function is steadily lost.36 It occurs in an autosomal recessive form with an earlier age of onset (11.75 years) and in a dominant form with a later age of onset (20.4 years). No cases of onset after the age of 25 have been reported. The disease is usually associated with pronounced and progressive symmetric cavus foot deformities with severe claw toe formation. In numerous instances, the foot deformities have been the presenting complaint. A heterogeneous group of hereditary cerebellar ataxias are also associated with cavus foot, but they are less easy to categorize than Friedreich ataxia, which primarily shows spinal cord involvement. Roussy-Lévy syndrome is a rare syndrome of cavus foot, sensory ataxia without obvious long-tract signs, peripheral motor atrophy, and kyphoscoliosis. Because it shares characteristics of both diseases, it was poorly differentiated from Friedreich ataxia and CMT for many years.37 The onset occurs very early in childhood and runs a relatively benign course. 1364

Spinal muscular atrophy is a heterogeneous group of disorders that are usually present from birth but have some late-onset forms.41 They are characterized by an inexorably progressive loss of anterior motor neuron cells. The disorders are characterized by hypotonia and can be associated with the cavus foot deformity, although it is rarely the presenting feature. Structural spinal cord disease often manifests with cavus foot deformity and requires a high degree of suspicion to detect. In particular, the unexplained onset of a progressive bilateral cavus deformity, or essentially any unilateral deformity, should warrant an imaging workup. Spinal cord tumors are notorious for their early absence of symptoms, and foot deformity might be the initial complaint. Syringomyelia is a cavitation in the center of the spinal cord that usually occurs in the cervical cord but can also interrupt the neural pathways to the lower extremities and result in spasticity or deformity. Diastematomyelia is a rare disorder in which a spicule of bone or fibrous band sagittally divides the spinal canal in the thoracic or high lumbar regions and separates the spinal cord into two pieces, each surrounded by dura. Because the cord and axial skeleton grow at different rates, a traction myelopathy very slowly develops as the child matures. The findings can be subtle, but making the diagnosis is critical. Spinal dysraphism in all its forms (spina bifida, myelocele, myelomeningocele) is certainly more common and can manifest with a variety of postural foot disorders depending upon the particular patterns of involvement. Fortunately, the diagnosis is almost always well established early in life. Cerebral palsy is, by definition, a static encephalopathy and can result in a variety of foot deformities, including pes cavus. Although the neurologic lesion is not progressive, the flexibility of the postural disorders deteriorates with time. POSTTRAUMATIC CAVOVARUS FOOT DEFORMITIES

Any traumatic condition that leads to an imbalance of the intrinsic and extrinsic foot musculature can lead to a cavus deformity. The deep posterior compartment of the leg is most commonly involved in traumatic compartment syndromes, and a Volkmann contracture in that location will lead to a cavus foot with a prominent claw toe component. Crush injuries of the leg and severe burns or soft tissue loss can also have the same result, both from direct injuries to the musculature and indirectly through tibial nerve injury. Compartment syndromes confined to the foot most commonly occur with calcaneus fractures or with crush injuries to the forefoot; they have been associated with the late development of claw toes but not with cavus deformity. Several forms of fracture malunion can also result in a fixed cavovarus deformity. Most commonly, a talar neck fracture with substantial medial comminution can fall

Pes Cavus ■ Chapter 26

into a varus malunion. This substantially limits subtalar joint eversion and leads secondarily to the calcaneus assuming a varus malalignment. Alternatively, a varus hindfoot can result from residual deformity from an intraarticular calcaneus fracture or even medial impaction of the tibial plafond. CONGENITAL PES CAVUS

Clubfoot Residuals The cavus foot deformity is one of four components of the congenital clubfoot, easily remembered by the mnemonic CAVE (cavus, adductus, varus, equinus). Adult clubfoot residuals encountered after childhood casting usually result from a failure of early casting to adequately elevate the first ray before abducting the foot about the fulcrum of the talar head as described by Morcuende et al.35 The most severe deformities that result from improper casting technique are usually not those of residual cavus but of a rocker-bottom foot that results when the equinus is inappropriately corrected while the calcaneus remains locked under the talus; the foot then dorsiflexes through the midfoot rather than through the ankle. A wave of enthusiasm for surgical clubfoot correction in the 1970s and 1980s is also now yielding residual effects in the adult foot and ankle population. The results of clubfoot correction surgery have proved to be substantially less reliable than once thought.30,42 A patient presenting with problems with a postsurgical clubfoot is just as likely to have overcorrection into planovalgus as residual undercorrection in cavovarus. The one constant in the surgically corrected clubfoot is a remarkable amount of stiffness in adults. In a dynamic gait analysis study, Huber and Dutoit18 specifically identified late subtalar stiffness as the primary feature associated with a poor result after childhood clubfoot surgery. It is rare that anything short of triple arthrodesis can be entertained to address the residual complaints. The Idiopathic Cavus Foot Despite the litany of potential known causes of the cavus deformity, the largest single group of cases encountered is symmetric and has no known cause. They can manifest because of stiffness in the hindfoot, stress fractures along the lateral column, recurrent ankle instability, or, commonly, for symptoms totally unrelated to the conformation of the arch. EVOLUTION OF DEFORMITY

Pes cavus must be viewed as a spectrum of deformities in which the underlying abnormality is that of an elevated longitudinal arch, but after that a variety of bony and soft tissue deformities can be present. The spectrum can range from a mild cavus foot, with flexible claw toes as the only significant clinical problem, to a severe fixed deformity,

Figure 26-1 Pes cavus with a predominant hindfoot deformity. Note the dramatically high pitch angle of the calcaneus.

with altered weight bearing, callosities, lateral ankle laxity, stress reactions, and pain. The shape of the foot varies with the cause and duration of the motor imbalance that created the deformity. When muscular imbalance in pes cavus begins before maturation of the skeleton, there can be substantial change of healthy osseous morphology. After skeletal maturity, there is usually little or no change in the morphology.1 The cavus foot is best understood by systematically analyzing the bone deformities, the soft tissue deformities, and the specific muscle functions that are imbalanced. The bony deformity may be predominantly in the hindfoot, the forefoot, or a combination of both. A hindfoot cavus describes an elevated pitch of the long axis of the calcaneus, which is usually greater than 30 degrees in a cavus foot (Fig. 26-1). Hindfoot cavus was a very common deformity in the era of widespread poliomyelitis; the focal nature of the disease in the anterior horn cells of the spinal cord often led to gastrocnemius weakness but sparing of the tibialis anterior and often the foot intrinsics. The resultant imbalance of forces then often led to dramatic calcaneal pitch angles and subsequent soft tissue contractures. Pure hindfoot cavus is now less common, while hindfoot varus is a predominant finding in pes cavus with underlying neurologic disease. Elevated calcaneal pitch is still encountered as a component of a combined deformity in the idiopathic cavus foot with no clear neurologic cause. Most neurologic cavus deformities are thought to occur from a forefoot-driven hindfoot varus resulting from a muscle imbalance as in CMT. The peroneus longus tendon is a direct antagonist to the tibialis anterior tendon. Often spared by the neuropathy, the strong peroneus longus muscle overpowers the affected tibialis anterior and initializes the deformity by plantar flexion of the medial forefoot (Fig. 26-2). The tibialis posterior muscle induces the hindfoot varus, and the Achilles tendon further enhances the varus stress secondary to the plantarflexed first ray and varus heel alignment, which alters the 1365

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Figure 26-2 Left pes cavus of Charcot-Marie-Tooth patient with a predominant forefoot deformity. A, The driving force is the plantar-flexed and adducted forefoot, clinically seen as depression of the first metatarsal head. The radiograph demonstrates plantar flexion and adduction of the first metatarsal relative to the axis of the talus (talo–first metatarsal angle). B, Bilateral plantar flexion of the first metatarsal accompanied by a varus heel deformity. C, Some cases demonstrate a more generalized forefoot deformity with generalized forefoot equinus.

transmission of axial forces through the ankle joint. With inversion of the hindfoot, the lateral foot supinates and the peroneus longus muscle further plantar flexes the first ray to restore the tripod position and a plantigrade foot.1 Soft tissue contracture converts a flexible to a fixed cavus deformity over time. Toe deformities are thought to occur from early degeneration of the intrinsic muscles of the foot. Because the lumbricals are not acting to stabilize the metatarsalphalangeal (MTP) joint (intrinsics effect: MTP flexion, proximal interphalangeal [PIP] and distal interphalangeal [DIP] extension), the unopposed extensor digitorum longus hyperextends the unstable lesser toes at the MTP level while the flexor digitorum longus and brevis flex the phalanges.1 The plantar-flexed metatarsal heads and plantar fascia shortening amplify forefoot plantar flexion. The deformities might be as mild as flexible clawing of the MTP joints in association with mild flexion of the interphalangeal joints, or they can manifest as fixed claw toe deformities. Once severe fixed claw toe deformities are present, the forces from the extrinsic toe extensors serve to hold the metatarsal heads in a plantar-flexed position (Fig. 26-3). Of importance, the plantar fat pad is displaced distally in severe cases as the toes pull up into extension. Not only are the metatarsal heads driven plantarward by the deformity, but they are also deprived of their normal cushioning layer of fat. 1366

The plantar fascia commonly develops a contracture with time in all forms of cavus foot. It is anatomically much thicker on the medial aspect of the foot, and as the contracture develops, it not only holds the longitudinal arch in an elevated position but also holds the forefoot adducted and keeps the calcaneus inverted (Fig. 26-4). Although some bony procedures can secondarily relax the plantar fascia by altering the shape of the arch, they are not always adequate by themselves. Early in the development of many cases of forefoot cavus the deformities remain relatively flexible. The arch might not flatten while standing, but muscle forces are holding it in position rather than bone and joint contractures. This is typical, for instance, of a very young patient with Charcot-Marie-Tooth disease. The subtalar joint compensates for the forefoot deformity by falling into a varus alignment (Fig. 26-5). As the disease progresses, the capsule and interosseous ligament of the subtalar joint become contracted, and the once-flexible hindfoot deformity becomes fixed. BIOMECHANICAL CONSEQUENCES OF PES CAVUS

The mechanics of all variants of the foot are similar. The axes of the talus and the calcaneus are more collinear. The talar head remains over the anterior process of the

Pes Cavus ■ Chapter 26

Figure 26-3 Metatarsophalangeal (MTP) joint deformities. A, Mild claw toes of the right foot with a near-normal left foot. B, Examples of severe clawing of the MTP joints, including clawing of the hallux from the use of the extensor hallucis longus as an accessory dorsiflexor.

Figure 26-4 Contracture of the plantar fascia contributes to and fixes the deformity. The tight medial band of the plantar fascia holds the forefoot in adduction and the hindfoot in varus. A, Cavus foot demonstrates adduction of the forefoot, an elevated longitudinal arch, and varus of the calcaneus. B, Radiograph demonstrating severe adduction of the forefoot.

calcaneus, and the navicular moves to a superior instead of a medial position to the cuboid; the subtalar joint axis is more vertical; and the Chopart joint function is impaired.1 When the hindfoot is locked in inversion, there is less subtalar and transversal tarsal motion during gait than in the normal foot. The ability of the foot to absorb the impact of walking by pronation during the

early part of stance phase is diminished, and the first metatarsal head and the lateral border of the foot are overloaded.1 A cavus foot is always stiffer than one of normal conformation. The relative dorsiflexion of the talus within the ankle mortise is caused by plantar flexion of the medial forefoot, limits ankle dorsiflexion, and is accompanied by 1367

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Figure 26-5 Varus heel deformity. A, In cases of forefoot-driven cavus, the varus heel is initially present as the natural standing posture of the heel when the first ray is plantar flexed and adducted. With time, the hindfoot deformity can become fixed. The presence of the deformity can be best assessed from behind. B, An axial view of the calcaneus demonstrates marked varus deformity. C, The Coleman block test can be used to demonstrate persistent flexibility of the hindfoot. If the heel can be forced into valgus by weight bearing on a block supporting only the lateral column of the foot, the subtalar joint remains flexible. In this case, the cavus can be corrected by addressing the forefoot deformity alone.

anterior ankle impingement. Together with the hindfoot varus position, relative talus dorsiflexion is thought to contribute to an increased anteromedial contact stress in the ankle joint. The association between lateral ankle instability, cavovarus deformity, and ankle arthritis has been discussed in the literature.13,46 A significant pressure increase and reduction of the area loaded in the ankle joint was also demonstrated in simulated pes cavus and is considered to lead to ankle arthritis in long-standing deformities with, but also without, lateral ligament instability.24 In the forefoot, the weight-bearing area beneath the metatarsal heads and heel pad is decreased, leading to substantially higher plantar pressures in both locations. In addition, because of the clawing and hyperextension of the MTP joints, the toes do not participate in weight bearing during toe-off, and power is diminished. The plantar fascia normally functions as a passive windlass mechanism to elevate the longitudinal arch, plantar flex 1368

the metatarsals, and invert the calcaneus. In the cavus foot, all three of these conditions are present permanently, and the plantar fascia becomes contracted. The muscle weakness patterns seen around the foot vary with the cause of the condition, but adduction of the forefoot is commonly seen when the posterior tibialis is active in the presence of a weak peroneus brevis. Metatarsus adductus exacerbates the already considerable tendency for excessive pressure in the lateral column of the foot, and stress reactions of the fifth metatarsal can result. Physical Examination The patient encounter begins with a careful history of the condition and a detailed family history. Generalized lateral column pain seems to be the most common presenting symptom associated with the cavus foot. Frequently, patients report ongoing lateral hindfoot instability despite one or more previous lateral hindfoot

Pes Cavus ■ Chapter 26

ligament repairs or reconstructions that failed later because the predisposing hindfoot statics were not corrected. The patient’s gait is carefully observed for the nature of ground contact, the position of the heel, and the position of the toes during stance. Any fall of the heel toward further varus as weight transfers onto the limb should be noted by observing the patient walk from behind. During swing phase, the examiner should check for the possibility of a footdrop and the use of the extensor hallucis longus as an accessory dorsiflexor, leading to a co*ck-up deformity of the first MTP joint. The heel pad could be seen easily from the front (“peek a boo”) with the patient standing and feet aligned straight ahead. In a normal foot, the heel pad is not visible on the medial side of the foot when viewed from the front because of the slight amount of valgus positioning of the average heel, which places the heel pad behind the normal hindfoot. The relative position of the hindfoot to the forefoot must be noted along with the rigidity of that relationship. The normal hindfoot will be positioned in slight valgus when standing flat and deviate into varus when rising onto the toes. The patient is asked if he or she experiences a subjective instability in the tiptoe position. The Coleman block test can be used to determine the ability of the hindfoot to fall back into an appropriate valgus posture. The heel alone or heel and lateral column of the foot are supported on a small flat wooden block while the forefoot or the medial column, respectively, remain unsupported. If the hindfoot is not fixed and the deformity is being driven by a first ray fixed in plantar flexion, the calcaneus will noticeably tilt into valgus when viewed from behind. In theory, a foot that exhibits flexibility on the Coleman block test can be corrected by working on the forefoot deformity alone. With the patient seated, the examiner observes active and passive range of motion of the ankle, subtalar, transverse tarsal, and MTP joints. The forefoot should also be examined after manual correction of the hindfoot varus deformity to assess the amount of fixed forefoot pronation and to determine the need for medial metatarsals dorsiflexion osteotomies. Limited and painful ankle dorsiflexion may demonstrate anterior or anteromedial ankle impingement because of the relative talar dorsiflexion within the ankle mortise. The hindfoot is assessed for any chronic ligamentous incompetence. Clinical signs of the lateral border overload range from calluses to proximal diaphyseal or metaphyseal fractures of the lateral metatarsals. Peroneal tendon pathology, including tears and subluxation, are commonly present, as is tightness of the gastrocnemius–soleus complex. Muscle function is very carefully assessed and documented for evaluation disease progression. Special attention should be paid to the ability of the peroneus longus to selectively plantar flex the first ray because this can point to the potential for a tendon transfer to effectively assist in treatment. A patient who does not carry a known

neurologic diagnosis should also undergo a neurologic screening, including testing for long-tract signs, reflexes, hamstring tightness, and any asymmetry. Intrinsic wasting is usually easier to pick up in the upper extremity, and in suspected cases of CMT or other systemic peripheral neuropathies, an examination of the intrinsic musculature of the hands is in order. Subtle disease can usually be discerned in the loss of muscle mass and strength of the first dorsal interosseous along the radial border of the second metacarpal. The patient exhibits weakness in abducting the index digit away from the midline with the rest of the hand held in a neutral position to isolate the intrinsics. Because of the very subtle findings associated with structural disease of the spinal cord, substantial unexplained asymmetry or rapid progression of the deformity warrants a neurologic referral and corresponding imaging. INVESTIGATIONS

Standing anteroposterior (AP) and lateral radiographs of the foot and ankle are essential. A line drawn down the axis of the talus should pass through the axis of the first metatarsal on both AP and lateral weight-bearing images of the foot in the normal situation. The axes should ordinarily be collinear, 0 degrees ± 5. The lateral talo–first metatarsal angle (the Meary angle) can be used to assess the severity of a forefoot plantar flexion, whereas, as opposed to other measured angles, the extent appears to correlate with the development of anteromedial ankle arthritis.24 The AP talo–first metatarsal angle defines the amount of forefoot adductus. The calcaneal pitch angle is elevated in cases of hindfoot cavus. Further findings on the lateral radiographs are an increased navicular height, an increased Hibbs angle (measured by a line through the axis of the calcaneus and the first metatarsal—in normal feet the angle is 45 degrees, and in cavus feet, it is near 90 degrees), and a posterior fibula with a “flat-topped” talus. The latter appearance is an artifact because in pes cavus a standard lateral view is in fact an oblique view. On the AP radiograph of the foot, the talocalcaneal angle is almost parallel in moderate and severe hindfoot varus. The presence of any associated metatarsus adductus should be noted by drawing of the AP talo–first metatarsal angle because this can require some degree of additional surgical attention or limit the degree of correction that can be achieved. The extent and progression of any ankle arthritis and talar tilt is recorded on extra AP and lateral standing ankle radiographs. The Saltzman view can be added to assess the angles of the tibiotalar and the subtalar joint. Computed tomography (CT) examination with the foot supported in the typical 90-degree position, with sagittal and coronal reformats, and three-dimensional modeling rules out occult degenerative joint disease and tarsal coalitions. MRI or ultrasound can occasionally be helpful to reveal any inflammation, splitting, or tears of the tendons. MRI can also detect early cartilage 1369

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degeneration and osteochondral lesions when arthritis is not yet visible on plain radiographs or CT. A digital dynamic pedobarography can be helpful to determine a pathologic plantar pressure distribution. Associated changes are the lateralization of the line of center of pressure and increased zone of pressure under the first metatarsophalangeal joint in case of a plantarflexed first metatarsal. Conservative Treatment Many cases of cavus deformity represent stable or slowly progressive deformities that are appropriately managed, at least initially, by nonoperative means. In the case of an adolescent with progressive deformity and a still-supple foot, however, there may be much to be lost by delay. Soft tissue surgery alone might manage the deformity early in the course of the disease, avoid ankle arthritis, and prevent the necessity of osteotomies or fusions. A stretching program to maintain motion is an important component of conservative management, particularly in cases of neurologic origin. Eversion and dorsiflexion should be emphasized. Metatarsalgia might be an early presenting complaint from uncovering of the metatarsal heads as claw toes develop. Accommodative manufactured shoes with extra-depth toe boxes can be of substantial benefit. Orthoses are a valuable adjunct to the conservative treatment of cavus feet. The reduced weight-bearing area in cavovarus feet is enlarged with orthotic devices. Typical custom foot orthotics for cavus may include an elevated heel to accommodate a tight gastrocnemius muscle and a recess under the first metatarsal head to accommodate the plantar-flexed first ray and allow some degree of hindfoot eversion.34 A forefoot wedge, beginning just lateral to the first metatarsal recess, extends to the lateral border of the device to mirror the forefoot pronation. Basically, the more fixed the cavus deformity is, the less likely is much benefit from orthoses, and discomfort and calluses may develop in supported areas. Once the deformity becomes fixed, patients tolerate corrective orthoses poorly. For lateral ankle instability, a high-top boot or an off-the-shelf ankle brace offer hindfoot stabilization. Lace-up braces are easier to fit inside a shoe or boot and stabilize the ankle comparably to plastic upright braces. Preexisting ankle instability usually worsens by higharched orthoses amplifying hindfoot varus. Severe muscle weakness is usually treated with fulllength custom ankle–foot orthoses (AFOs) to prevent foot drop. The integration of orthotic modifications into the AFO improves proprioception and ankle stability more than the brace alone. Many patients can be managed by hinged AFOs with dorsiflexion assistance to allow a much more normal gait pattern. In some cases of equinus deformity, full clamshell braces or casts are needed because the strong or unopposed plantar flexors will overcome the correction obtained with a posterior brace or anterior strap. 1370

Surgical Treatment Decision Making The goal of surgical management is to produce a plantigrade, stable foot, to alleviate discomfort, and to improve function. Surgical realignment should be recommended when signs of tendon or hindfoot joint degeneration arise, resulting from recurrent hindfoot instability or elevated hindfoot joint contact stresses by varus alignment. Earlier surgery may be appropriate due to lateral column pain or progressive deformity. Basics of dynamic and static realignment are that tendons contributing to the deformity should be transferred to a more functional location (i.e., peroneus longus to brevis), contracted structures should be released to allow restoration of normal foot shape (i.e., plantar fascia), and osteotomies are preferred over arthrodesis of nonarthritic joints to help realign the foot to a more functional position (calcaneal osteotomy instead of corrective subtalar fusion). If the deformity is fixed, however, an arthrodesis might be necessary to produce a plantigrade foot. There is no simple boilerplate approach applicable to all cavus feet. A suggested algorithm is provided in Figure 26-6. The key to surgical decision making is to adopt procedures that are necessary to match each specific deformity. It is not uncommon to have a foot with a combination of fixed and supple deformities; a particular case might require a combination of bone and soft tissue procedures. Soft Tissue Procedures PLANTAR FASCIA RELEASE (STEINDLER STRIPPING) The contracted plantar fascia plays a major role in maintaining height of the longitudinal arch and varus positioning of the calcaneus in the patient with pes cavus. Release and stripping of the plantar fascia often help to reduce the height of the longitudinal arch in patients who retain some degree of flexibility (Video Clip 47).43 At times, the procedure may be carried out in conjunction with a lateralizing calcaneal osteotomy, a triple arthrodesis, or a first metatarsal osteotomy. Surgical Technique 1. The patient is placed in a supine position. The normal external rotation of the lower extremity provides adequate visualization of the foot. A tourniquet is used around the thigh. 2. An oblique skin incision is made, starting distal to the weight-bearing area of the calcaneal fat pad and passing over the contracted plantar fascia. This incision does not put the medial calcaneal branches to the heel pad at risk of being cut. 3. The incision is deepened through the fat, exposing the plantar fascia on the plantar aspect of the foot as well as medially over the fascia of the abductor hallucis muscle.

Pes Cavus ■ Chapter 26

Pes cavovarus

Flexible?

Yes (Coleman block positive)

No (Coleman block negative)

Plantar flexed medial forefoot? => Step 1: MT I (II, III) dorsiflexion osteotomy => Step 2: PL to PB transfer => Step 3 (rarely): release of planter fascia

Standard OR-steps => Lateralizing calcanealosteotomy => PL to PB transfer => MT I (II, III) dorsiflexion osteotomy

Persistent hindfoot varus? => Lateralizing calcaneal osteotomy

Ankle arthritis? => Anterior ankle arthrotomy, cheilectomy

Equinus deformity? => Achilles-lengthening or gastrocnemius recession

Persistent plantar flexion of medial forefoot? => Plantar fascia release

Further options: => Repair/reconstruction of lateral hindfoot ligaments => PL to PB transfer, TA-lateralization or TP to PB transfer with neurologic etiology

Persistent forefoot deformity? => Forefoot reconstruction 1st toe clawing? => Jones procedure

Advanced or severe hindfoot arthritis? => Instead of or in addition to lateralizing calcanealosteotomy: realigning subtalar, double, or triple arthrodesis

Equinus deformity? => Achilles-lengthening or gastrocnemius recession

Further options: => Repair/reconstruction of lateral hindfoot ligaments => TA-lateralization or TP to PB transfer with neurologic etiology Figure 26-6 Pes cavovarus treatment algorithm. PB, Peroneus brevis tendon; PL, peroneus longus tendon; TA, tibialis anterior tendon; TP, tibialis posterior tendon.

4. The origin of the plantar fascia is transected while tension is being applied to it by dorsiflexing the MTP joints. In this way, the plantar fascia will separate as it is cut. Often, some deeper septa must be carefully transected. The lateral plantar nerve passes just distal to the cut, so the surgeon must be cautious when transecting the septa. 5. After releasing the plantar fascia, the surgeon palpates along the medial aspect of the foot, particularly in a severely deformed case, to release the superficial and deep fascia surrounding the abductor hallucis muscle. This is a very important part of the release, particularly

in cases involving significant adduction of the forefoot. 6. Once the cuts have been made by blunt dissection and stretching the fascia, the wound is carefully inspected to ensure that no tight bands of fascia remain, either on the plantar aspect of the foot or along the abductor muscle. Postoperative Care The patient is placed into a short-leg compression dressing incorporating plaster splints. The sutures are removed in 12 to 14 days, after which the patient is placed in a 1371

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Figure 26-7 co*ck-up deformity of the first metatarsophalangeal joint from the use of the extensor hallucis longus as an accessory dorsiflexor with a weak anterior tibialis. A, Resting. B, With active attempted dorsiflexion of the ankle.

short-leg cast. Weight bearing is begun as tolerated, whereas 4 weeks of immobilization is usually adequate if plantar fascia release is carried out as an isolated procedure. FIRST-TOE JONES PROCEDURE The procedure is used to correct a hyperextension deformity of the first MTP joint caused by weakness of the tibialis anterior. Although the EHL is also located in the anterior compartment and is innervated more distally than the tibialis anterior, its function can be spared in a surprising number of conditions. In modern practice, this is usually seen in CMT or variants of cerebral palsy, but it was historically common in polio.22 In these cases, the EHL is functioning as an accessory dorsiflexor of the ankle joint, which results in hyperextension of the MTP joint and secondary flexion of the interphalangeal joint (Fig. 26-7). Moving the insertion of the EHL tendon into the base of the first metatarsal facilitates dorsiflexion of the ankle and also relieves the co*ck-up deformity of the MTP. To prevent a floppy first toe, a fusion of the interphalangeal joint is usually performed. Surgical Technique 1. The procedure is carried out with the patient supine. A tourniquet is used around the thigh (Fig. 26-8 and Video Clip 51). Interphalangeal Joint Arthrodesis 2. An elliptic skin incision is centered over the dorsal aspect of the interphalangeal joint of the hallux. The collateral ligaments are cut to expose the articular surfaces. 3. The extensor hallucis longus tendon is freed from its retinacular attachments along its mediolateral aspect. 4. The surfaces of the interphalangeal joint are removed with a power saw to create two flat surfaces. The interphalangeal joint is placed in a few degrees of plantar flexion and neutral varus/valgus alignment. 5. A 2.5-mm hole is drilled in an antegrade manner from proximal to distal through the midportion of the 1372

Skin incision

Screw

Figure 26-8 The first-toe Jones procedure moves the pull of the extensor hallucis longus (EHL) tendon from the great toe to the neck of the first metatarsal. Interphalangeal joint arthrodesis of the hallux is then performed to prevent a floppy toe. The procedure aids the ability of the EHL to serve as an accessory dorsiflexor and helps eliminate depression of the first metatarsal head. (From Mann RA, Coughlin MJ: The video textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions.)

distal phalanx. Where the drill bit begins to pressure the skin on the tip of the toe, a generous transverse incision is made to prevent maceration of the tissue. 6. The drill bit is removed and brought back through the hole from distal to proximal. Holding the interphalangeal joint in a reduced position, the surgeon extends the drill hole into the proximal phalanx. 7. The hole is measured. A 4.0-mm solid-shaft cancellous lag screw or headless screw is inserted, providing compression to the arthrodesis site. 8. A Kirschner wire (K-wire) may be placed obliquely across the interphalangeal joint to control any rotational forces. This is removed after approximately 4 weeks. Extensor Hallucis Longus Tendon Transfer 9. A longitudinal incision is made over the dorsal aspect of the first metatarsal.

Pes Cavus ■ Chapter 26

10. The extensor tendon, which was previously freed distally, is now freed proximally and delivered into the wound. 11. A transverse drill hole is made and cleaned in the distal portion of the first metatarsal. The size is selected to snugly fit the tendon. 12. The extensor hallucis longus tendon is passed through the drill hole and sutured onto itself, holding the ankle in 10 degrees of dorsiflexion and placing a moderate amount of tension on the tendon transfer. Postoperative Care The patient is placed into a short-leg compression dressing incorporating plaster splints. A popliteal block can be useful to control postoperative pain. The sutures are removed at 10 to 12 days, and the patient is placed in a short-leg walking cast for 4 weeks. At 6 weeks postoperatively, ambulation as tolerated is allowed. If the interphalangeal joint fusion is not complete at that time, an additional period of ambulation in a postoperative shoe may be necessary.

brevis. A 2-0 coated polyester suture (Ethibond; Ethicon360, Menlo Park, Calif.) is used to join the tendons. If other procedures are to be carried out on the foot, the final tensioning and suture of the tendon is saved until the end of the case. Postoperative Care The foot is placed in a short-leg compression dressing reinforced with plaster splints. After 10 to 12 days, the sutures are removed and a short-leg weight-bearing cast is applied. If no other procedures are being performed, a transition to regular footwear is usually made after a total of 4 to 6 weeks of immobilization.

PERONEUS LONGUS TO BREVIS TRANSFER Many cases of cavus foot, particularly in CMT, are associated with preserved function of the peroneus longus muscle in the presence of a failing tibialis anterior.15 This pulls the first ray plantarward and leads to a forefoot cavus deformity as well as a secondary hindfoot varus. A transfer of the peroneus longus to the peroneus brevis can dramatically improve the situation by both weakening the plantar pull on the first metatarsal and augmenting the function of the usually failing peroneus brevis.

TIBIALIS ANTERIOR LATERALIZATION The transfer of the insertion of the anterior tibial tendon to the lateral cuneiform is a very powerful step of the dynamic realignment when sufficient strength remains in the tendon. It provides both hindfoot stability and lateral shift of the ankle center of force by changing the strong inversion moment into a light eversion moment while still maintaining dorsiflexion power. Minimal risk of overcorrection is present with transfer of the tendon to the lateral cuneiform, and the procedure is technically simpler than the split anterior tibialis transfer previously advocated.17 A long history of the procedure exists in the treatment of mild clubfoot residuals after cast correction by the Ponseti method.35 However, because transferred muscles generally lose one fifth of their strength, tibialis anterior muscle strength of at least 4 of 5 preoperatively is required for a reasonable effect, and the procedure may not be appropriate in cases of CMT.47

Surgical Technique 1. The surgery is carried out with the patient supine. A small bump under the ipsilateral hip can facilitate access to the lateral aspect of the foot. A thigh tourniquet is used (Video Clip 49). 2. A 4-cm incision is made over the anterior margin of the peroneus longus on the lateral aspect of the foot as it courses toward the cuboid to turn underneath the foot. This incision is then deepened through the subcutaneous fat to access the peroneus brevis. Care should be taken to avoid injury to the sural nerve, which usually passes through the proximal aspect of the incision. 3. The peroneus longus and peroneus brevis each lie in separate sheaths in this area, and they must be released to access the tendons. The peroneus longus crosses underneath the brevis and is not always easy to find. 4. The peroneus longus is then cut as far distally as possible as it makes the turn around the cuboid to pass underneath the midfoot. If an os peroneum is present in the tendon, it is excised and the cut is made through this area. 5. The foot is held in maximum eversion, and the peroneus longus is woven two or three times in Pulvertaft fashion through the distal aspect of the peroneus

Surgical Technique 1. The procedure is carried out with the patient supine. A tourniquet is used around the thigh. 2. A medial longitudinal 3- to 4-cm incision is made from the tuberosity of the navicular to the base of the first metatarsal, and the tendon is released at its insertion to bone. 3. A second 3- to 4-cm longitudinal anterior incision is made slightly above the superior extensor retinaculum. The retinaculum is incised as needed to pull out the tendon. 4. The tendon end is grasped with a thick nonabsorbable suture. It is then rerouted subcutaneously to the level of the lateral cuneiform and pulled out through a third 3-cm longitudinal incision centered over the lateral cuneiform. 5. There the fibers of the extensor digitorum brevis muscle are bluntly separated, and the correct entry point of the bone tunnel (dorsolateral edge of the center of the lateral cuneiform) is verified fluoroscopically. 6. A 6-mm hole is drilled from there through all the cuneiforms to the medial cuneiform, and the tendon is drawn into this tunnel until appropriate tension is obtained. It is fixed by transosseous suture at the 1373

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medial cuneiform and into the surrounding soft tissues at the lateral entry. Alternatively, a dorsal to plantar tunnel can be created through the lateral cuneiform and fixation achieved with an interference screw. Postoperative Care A short-leg compression dressing reinforced with plaster splints is applied. The sutures are removed after 12 to 14 days, and a short-leg weight-bearing cast is applied. If this is the only procedure, a transition to regular footwear is usually made after a total of 4 to 6 weeks of immobilization. Results and Complications Patients who undergo tibialis anterior transfer were seen to have a lower mean talo–first metatarsal angle than those who had not, suggesting that, in its native position, the tibialis anterior may contribute to cavus.47 In general, tendon tranfers result in a decrease in their overall strength. The tibialis anterior also typically loses strength with progression of the Charcot-Marie-Tooth disease, and over time, the transfer may become less effective. CLAW TOE CORRECTIONS Associated claw toe deformities are common in pes cavus. Often, dynamic claw toes resolve with realignment of the hindfoot and midfoot deformity. Treatment of the claw toe deformity depends upon whether a fixed or flexible deformity is present. With fixed deformity at the MTP joints, release of the extensor tendons and joint capsules is required. To hold the toes in the neutral position, usually a flexor tendon transfer needs to be done. With fixed deformity of the proximal interphalangeal joint (hammer toe), a proximal interphalangeal joint arthrodesis or a DuVries phalangeal arthroplasty with removal of the distal portion of the proximal phalanx is indicated. Some authors prefer one of the latter two procedures as the standard procedure because they have a similar effect on the long flexor tendons, require less dissection, and are more reliable, particularly in neurologic diseases.29 However, if the claw toe deformity is passively correctible, a flexor tendon transfer alone usually suffices. The surgical techniques for flexor tendon transfer (Girdlestone procedure), DuVries phalangeal arthroplasty to correct a hammer toe, and release of the MTP joints in a fixed contracture are described in Chapter 7 (Video Clip 75). LATERAL LIGAMENT REPAIR/RECONSTRUCTION Regardless of the repair or reconstruction technique to restore lateral hindfoot stability, the operation will likely fail when hindfoot varus static is not realigned at the same time. The association of lateral ligamentous hindfoot instability, cavus deformity and ankle arthritis has been made by various authors who all advise not only correction of the deformity with osteotomies and tendon transfers but also lateral hindfoot ligament reconstruction to prevent recurrence.13,40,46 1374

The surgical techniques for lateral hindfoot ligament repair and reconstruction are described in Chapter 30. Bony Procedures OSTEOTOMIES At times, a specific bony deformity is present in pes cavus that significantly impairs the patient’s ability to maintain a plantigrade foot, but the remainder of the foot remains relatively supple. This usually takes the form of a fixed varus deformity of the hindfoot or a fixed plantar flexion of the first ray. If the fixed deformity can be corrected, a plantigrade foot can be achieved without an arthrodesis. In general, an osteotomy that includes the first metatarsal or calcaneus or both is carried out in conjunction with a plantar fascia release and peroneus longus to brevis tendon transfer. DORSIFLEXION OSTEOTOMY OF THE FIRST RAY Particularly in cases of CMT, plantar flexion of the first metatarsal can become fixed, with a resultant fixed forefoot valgus deformity. This forefoot equinus deformity can also involve the second and, rarely, the third metatarsal. As a result of this deformity, as the head of the first metatarsal contacts the ground, the forefoot is twisted into an inverted position. If this is associated with a varus deformity of the calcaneus, a weak peroneus brevis muscle, or a contracted plantar fascia, dramatic increases in stress on the lateral ankle ligaments can result. This stress can lead to chronic lateral ankle ligament instability over time. Dorsiflexion of the first ray is achieved either by a dorsally closing osteotomy of the medial cuneiform (reversed Cotton osteotomy), by a corrective first metatarsocuneiform arthrodesis when the joint is arthritic, or by a dorsally closing osteotomy of the first metatarsal. DORSIFLEXION OSTEOTOMY OF THE FIRST METATARSAL In general, a first metatarsal osteotomy is carried out not as an isolated procedure but as part of a more comprehensive cavus foot correction. In the patient with mild and flexible deformity, sometimes only a plantar fascia release and a dorsiflexion osteotomy of the first metatarsal are required. More often, however, a calcaneal osteotomy, plantar fascia release, and first metatarsal osteotomy are done together. The first-toe Jones procedure can also be added without complication. In a similar but more powerful technique, a dorsiflexion of the first ray can also be achieved by removal of a dorsally based wedge of the medial cuneiform (reversed Cotton osteotomy), whereas the osteotomy is sometimes difficult to close because of the Lisfranc ligament. Surgical Technique 1. The patient is placed in a supine position. If this is an isolated procedure, the first metatarsal osteotomy can be carried out under an ankle block only. If it is part

Pes Cavus ■ Chapter 26

of a more comprehensive cavus foot correction, general anesthesia is used (Video Clip 50). 2. An incision is made over the dorsal aspect of the first metatarsal, starting over the medial cuneiform and ending over the distal third of the metatarsal. 3. The incision is deepened to the extensor tendon, which is immobilized and retracted medially or laterally. 4. The metatarsocuneiform (MTC) joint is identified, and the proposed osteotomy site is marked on the bone starting about 1.5 cm distal to the joint (Fig. 26-9A and B). 5. A 2.7-mm or 3.5-mm screw is centered in the proximal portion of the metatarsal above the proposed osteotomy.

6. A 0.062-inch K-wire is used to make a transverse drill hole in the dorsal part of the metatarsal 1 cm distal to the osteotomy. 7. The osteotomy is a dorsal closing wedge that usually removes 4 to 6 mm of bone, depending upon the degree of plantar flexion of the first metatarsal that must be corrected. 8. The first cut is made parallel to the MTC joint. A convergent cut is then made distally, aiming for the plantar cortex. Care is taken to leave the plantar cortex intact. A greenstick fracture is made as the osteotomy is closed, resulting in a more stable construct than if the cuts were fully completed. It is better to undercut the osteotomy than to remove too large a segment.

Following osteotomy

Axis of first metatarsal

Figure 26-9 Technique of the dorsiflexion osteotomy of the first metatarsal. A, A dorsally based wedge of bone is removed approximately 1 cm distal to the first metatarsocuneiform joint. The plantar fascia is often released when carrying out this procedure for a cavus foot. B, A 3.5-mm screw is placed in the proximal fragment to serve as a post. C, The osteotomy site is closed down, and the plantar aspect of the foot carefully palpated. If the first metatarsal is still too plantar flexed, a larger wedge is removed. D, The osteotomy site is fixed by placing a length of 22-gauge wire through a transverse drill hole in the distal fragment and then fixing it to the screw. E and F, Preoperative and postoperative radiographs demonstrate dorsiflexion of the first metatarsal after proximal osteotomy. (From Mann RA, Coughlin MJ: The video textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions.)

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9. After the osteotomy has been created, the plantar cortex is loosened by rocking the bone back and forth until the dorsal gap can be closed (Fig. 26-9C). 10. To determine whether enough bone has been removed, the ankle is brought up into dorsiflexion and the forefoot is carefully evaluated, comparing the level of the first and fifth metatarsals in relation to the long axis of the leg. The surgeon must imagine that the foot is in a plantigrade position and that the first and fifth metatarsals are on the same plane. 11. If the size of the osteotomy cut is correct, internal fixation is inserted. 12. A piece of 22-gauge wire is passed through the transverse drill hole that was made distal to the osteotomy site in step 6. The wire is then brought up around the screw head in the proximal portion of the metatarsal and tightened with a wire twister while the osteotomy is held closed (Fig. 26-9D). 13. Once the osteotomy site has been completely closed, the bottom of the forefoot is again carefully examined. If the degree of dorsiflexion is adequate, the surgeon may proceed with closure of the wound. If it is not adequate, the wire is removed and more bone is removed from the osteotomy site (Fig. 26-9E). Alternatively, a 3-hole 2.0 DCP is used to compress the osteotomy site by eccentric drilling. 14. Occasionally, the second metatarsal needs to be dorsiflexed, which is done using the same procedure. 15. The foot is placed in a compression dressing. If this is the only procedure being carried out, splints are not required.

In the presence of a horizontal ankle joint line and a cavus foot, it appears more reasonable to redistribute the ankle joint contact forces by realigning the foot deformity rather than by creating a new deformity, that is, with a supramalleolar osteotomy. Furthermore, this would create additional problems in the forefoot by accentuating the plantar flexion of the first ray. Calcaneal osteotomies act by shifting the ground contact point and, consequently, the weight-bearing axis through the ankle joint. They are particularly useful in patients with recurrent hindfoot sprains as a result of heel varus and can be used with either a supple or a stiff subtalar joint.34 The lateralizing calcaneal osteotomies also lateralize the lever arm of the Achilles tendon during toeoff. The contribution of the Achilles tendon toward the tibialis posterior is thus reduced in favor of the peroneus brevis. From recent static biomechanical studies, there is evidence that in simulated pes cavus common lateralizing calcaneal osteotomies substantially contribute to normalize the elevated contact stress in the anteromedial ankle joint, which is thought to cause ankle arthritis in longstanding pes cavus.24 Osteotomies that include lateralization of the tuberosity, including a simple slide and the Z-osteotomy with additional lateralization of the tuberosity,23 reduced contact stresses more effectively than, for instance, the Z-osteotomy without additional lateralization of the tuberosity32 and are therefore recommended for moderate-to-severe hindfoot varus realignment. Both the Dwyer osteotomy and its modifications with translation, as well as the Z-osteotomy, can accomplish correction of hindfoot varus and are described below.

Postoperative Care A popliteal block can be useful to control postoperative pain. If this is the only procedure being carried out, the patient is permitted to ambulate as tolerated in a postoperative shoe. If it is done in conjunction with other procedures, the patient is placed in a short-leg non– weight-bearing cast. In general, the osteotomy heals in approximately 6 weeks, after which ambulation is permitted as tolerated.

DWYER CALCANEAL OSTEOTOMY WITH OPTIONAL LATERAL AND/OR DORSAL TRANSLATION Surgical Technique 1. The patient is placed in a lateral or in a supine position with a bolster beneath the ipsilateral hip for adequate exposure of the lateral aspect of the calcaneus. A tourniquet is used on the thigh. 2. The skin incision is perpendicular to the axis of the calcaneus, begins about 2 cm posterior to the tip of the fibula, and is carried obliquely past the tip of the fibula toward the plantar aspect of the calcaneocuboid joint (Fig. 26-10A and Video Clip 48). 3. The deep incision is carried just below the peroneal tendon sheath, and the calcaneus is exposed as required. Care is taken not to injure the sural nerve. Dorsally and plantarly, the soft tissues are stripped off to place Hohman retractors. 4. A transverse osteotomy is made in the calcaneus that starts about 2 cm posterior to the posterior facet of the subtalar joint and runs in line with the skin incision, perpendicular to the calcaneus axis. If possible, the medial cortex of the calcaneus is left intact. 5. A second cut is now created, removing a pie-shaped wedge of bone from the lateral aspect of the calcaneus. The size of the wedge depends upon the severity of the

CALCANEAL OSTEOTOMIES Patients with a moderate-to-severe cavus deformity usually have a varus deformity of the hindfoot. A fixed varus deformity is treated with the lateralizing calcaneal osteotomy, that is, as described by Dwyer,10,11 Malerba and De Marchi,32 or Knupp.10,11,23,32 Whenever possible, realigning osteotomies are preferred over arthrodesis. If the patient lacks adequate dorsiflexion and has a high calcaneal pitch angle (a hindfoot cavus), a Samilson39 osteotomy is carried out to allow the calcaneal tuberosity and the attached Achilles tendon to slide vertically, thereby effectively lengthening the gastrocnemius–soleus complex and correcting the effective pitch angle of the calcaneus. These procedures are usually carried out with a plantar fascia release and a first metatarsal osteotomy. 1376

Pes Cavus ■ Chapter 26

varus deformity. Usually, 5 to 7 mm of calcaneus is removed with the second cut (Fig. 26-10B). 6. Once the second cut is completed, a greenstick fracture is made on the medial side of the calcaneus by manipulating the fragments back and forth. The osteotomy is then closed. Sometimes, temporary insertion of a stout pin into the posterior tuberosity can serve as a joystick to facilitate closing the osteotomy. The

Line of osteotomy

Postoperative Care The patient is placed into a short-leg compression dressing incorporating plaster splints. A popliteal block can be useful in controlling postoperative pain. The sutures are removed 10 to 12 days after the procedure, and a short-leg non–weight-bearing cast is applied. Ambulation is permitted in the cast 4 weeks after the procedure, and casting is discontinued 8 weeks postoperatively if radiographs demonstrate union.

Skin incision

Pin fixation

Figure 26-10 The Dwyer calcaneal osteotomy. A, Skin incision is made along the inferior margin of the peroneal tendons, with caution taken to avoid injury to the sural nerve. B, A lateral closing wedge of bone is taken of sufficient size to correct the deformity. C, Fixation is achieved with a longitudinal pin, a longitudinal screw, or a lateral staple. (From Mann RA, Coughlin MJ: The video textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions.)

position of the bone is carefully evaluated. If an inadequate degree of correction has been obtained, more bone needs to be removed. This may result in substantial hindfoot shortening. Alternatively, the tuberosity is fully osteotomized. This allows further correction in two planes, including further lateralization of up to 7 mm for more severe deformities and vertical translation to reduce the calcaneal pitch. Vertical translation accomplishes the goals of the “Samilson” osteotomy, an operation designed purely to address the excessive calcaneal pitch in poliomyelitis.22 7. The osteotomy site is fixed with single or multiple 5.0- to 7.3-mm screws placed down the long axis of the calcaneus through a separate stab incision (Fig. 26-10C). If a screw is used, it should be placed lateral to the midline, and the patient should be warned that it may require later removal if it irritates the back of the foot against the heel counter of a shoe.

Results and Complications The postoperative results after a Dwyer calcaneal osteotomy are usually most satisfactory in mild-to-moderate hindfoot varus (Fig. 26-11). Occasionally, the sural nerve becomes entrapped in scar tissue or disrupted, which can create a problem for the patient. Sometimes it is difficult to judge whether adequate bone has been removed. The surgeon must attempt to line up the calcaneus with the long axis of the leg when trying to decide if a sufficient degree of correction has been achieved. The only significant error that can be made when performing this procedure is to fail to remove sufficient

Figure 26-11 Preoperative (A) and postoperative (B) radiographs demonstrate the results of the Dwyer calcaneal osteotomy. The tarsal canal is visible on end preoperatively, indicating a varus deformity of the heel, whereas the position of the subtalar joint changes once the heel is brought into valgus.

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bone, leaving the hindfoot in varus. In cases that require much correction, removal of large wedges may result in substantial hindfoot shortening, whereas the moment arm of the Achilles tendon is decreased, weakening toeoff. Alternatively, the tuberosity may be fully osteotomized and lateralized 6 to 8 mm. Because translation of the calcaneal ground contact point by lateral sliding is more effective than rotation by lateral closing wedges, translating or combined translatingrotating osteotomies are usually preferable for the realignment of more severe hindfoot varus.28 Z-OSTEOTOMY23,32 Surgical Technique 1. The patient is placed in a supine position with a bolster beneath the ipsilateral hip or in the lateral position for adequate exposure of the lateral aspect of the calcaneus. A tourniquet is used on the thigh. 2. The skin incision is perpendicular to the axis of the calcaneus, begins about 3 cm posterior to the tip of the fibula, and is carried obliquely past the tip of the fibula toward the plantar aspect of the calcaneocuboid joint (Figs. 26-12 to 26-14 and Video Clip 118). 3. The deep incision is carried just below the peroneal tendon sheath, and the calcaneus is exposed as required. Care is taken not to injure the sural nerve.

Dorsally and plantarly, the soft tissues are stripped off to place Hohman retractors. The exposure of the calcaneus should extend from its dorsal aspect behind the fibula to just proximal to the calcaneocuboid joint. 4. Hohman retractors are used to protect the soft tissues. K-wires should be inserted and checked under fluoroscopy to ensure that the osteotomy is appropriately positioned and perpendicular to the calcaneal axis. The horizontal part of the osteotomy is about 2 cm long and parallel to the plantar fascia. The anterior vertical cut is made 1 to 2 cm posterior and parallel to the calcaneocuboid joint, and the posterior vertical cut is placed in the posterior half of the cavity of the tuberosity. Sparing the Achilles insertion is important. 5. Four K-wires are then used to define the corners of the wedge to be removed. The base of the wedge is 8 to 10 mm in width, depending on the desired amount of correction. The wedge is mobilized with the oscillating saw and osteotomes without harming the soft tissues. A laminar spreader is used to mobilize the osteotomy. The lateral gap is then carefully closed as described by Malerba and De Marchi.32 An additional lateral displacement of the tuberosity fragment (6-10 mm) is done as described by Knupp et al.23 An option is that the calcaneus can also be lengthened by displacing the tuberosity posteriorly.

Translation

Rotation

Figure 26-12 The Z-osteotomy with removal of a laterally based wedge of 8 to 10 mm (A), according to Malerba (rotation of the ground point). A more powerful correction is achieved with additional lateralization of the tuberosity (B) according to Knupp and Hintermann (rotation and translation of the ground point). (Modified from Krause FG, Sutter D, Waehnert D, et al: Ankle joint pressure changes in a pes cavovarus model after lateralizing calcaneal osteotomies. Foot Ankle Int 31:741-746, 2010. Used with permission.)

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Pes Cavus ■ Chapter 26

nerves themselves do not appear noticeably enlarged by the eye, CMT nerves may be slightly thicker and more sensitive to compression compared with normal nerves.14 A routine release of the nerve’s compartment (inferior flexor retinaculum) when performing a lateralizing calcaneal osteotomy for hindfoot varus in patients with CharcotMarie-Tooth disease is therefore recommended.27 Consolidation of the osteotomy is reported to be fast and reliable, and most patients show consolidation on the radiographs 6 weeks postoperatively.

Figure 26-13 Preoperative Saltzman hindfoot view of a hindfoot varus. Intraoperative lateral and axial fluoroscopy, and postoperative Saltzman hindfoot view after a Z-osteotomy of the calcaneus with lateralization of the tuberosity, according to Knupp and Hintermann. A peroneus longus to brevis tendon transfer and a dorsiflexion osteotomy of the first metatarsal were added. (Courtesy M. Knupp, MD, Department of Orthopaedic Surgery, Kantosspital Liesthal, Switzerland. Used with permission.)

6. The osteotomy is secured with one or two K-wires. The desired correction is carefully evaluated clinically and under fluoroscopy. The osteotomy site is fixed by one or two 3.5-mm or larger screws placed down the long axis of the calcaneus through a separate stab incision. Postoperative Care The patient is placed into a short-leg compression dressing incorporating plaster splints. A popliteal block can be useful in controlling postoperative pain. The sutures are removed 10 to 12 days after the procedure, and a short-leg non–weight-bearing cast is applied. Partial weight bearing is permitted in the cast 3 to 4 weeks after the procedure, and casting is discontinued 6 to 8 weeks postoperatively if radiographs demonstrate union. Results and Complications Transient and irreversible tibial nerve palsy after lateralizing calcaneal osteotomies has been described.27 Particularly after large corrections in CMT cases and posttraumatic cases, the rate is substantial. Although the

MIDTARSAL OSTEOTOMIES Various types of midfoot osteotomies have been proposed for the patient with a forefoot equinus or anterior cavus deformity with the apex located at the Chopart and midtarsal joints. These include the Cole osteotomy, which consists of removing a dorsal wedge of bone from the navicular, cuneiforms, and cuboid.7 A similar, more distal osteotomy has been proposed by Japas, in which a V-shaped osteotomy is made within the tarsal bones.21 The distal portion is then depressed to allow the forefoot to be brought out of its equinus position. Although, in theory, midfoot osteotomies are preferred because they correct a typical deformity closer to its apex than a basilar osteotomy of the first metatarsal, in practice, this is not the case. Inevitably, all variations of the midfoot osteotomies result in multiple intraarticular cuts that can lead to early arthritis. The residual deformity from the much safer extraarticular osteotomy through the first metatarsal is well tolerated, and this approach should be universally preferred. Midfoot procedures should be reserved for patients who already have arthritis, and the joints should then be arthrodesed in conjunction with the cavus correction. ARTHRODESIS PROCEDURES The triple arthrodesis is the requisite operation for more severe, fixed postural deformities of the hindfoot of any kind. In the cavus foot, it is important to remember that other procedures, such as a first metatarsal osteotomy or Jones procedure, can be carried out in addition to a triple arthrodesis if the conditions warrant. Routine joint preparation and cartilage removal often prove adequate for milder degrees of deformity. Because the posterior facet of the subtalar joint is approached from the lateral side, there is a natural tendency to remove more bone laterally and position the calcaneus toward valgus using standard techniques, just as one would perform a triple arthrodesis for hindfoot arthritis. Long-term follow-up studies of standard triple arthrodesis for patients with Charcot-Marie-Tooth disease and cavus deformity have shown a high incidence of osteoarthritis of the remaining foot joints after this procedure. One study reported degenerative changes of the ankle and midfoot in 77% and the need for subsequent ankle arthrodesis for the treatment of degenerative joint disease in 20% after an average follow-up of 20 years.48 Also, a literature review reveals poor results in as many as 47% 1379

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

157.9° (22.1°) 75.0° (105.0°)

82.6° (97.4°)

171.9° (8.1°)

25.0° (155.0°)

24.1° (155.9°)

Figure 26-14 Preoperative anterior (A), oblique (B), and posterior (C) photographs and postoperative anteroposterior (D) and lateral (E) weight-bearing radiographs of a 56-year-old male patient with idiopathic pes cavus and grade III anteromedial ankle arthritis. Operative deformity correction included a lateralizing sliding osteotomy of the calcaneal tuberosity, dorsiflexion osteotomy of the first metatarsal, peroneus longus to brevis transfer, and lateral malleolus shortening osteotomy to reduce the varus tilt of the talus. No progression of the ankle arthritis was seen at latest follow-up 4 years postoperatively.

of patients, recurrence rates of 9% to 20%, nonunion in 6% to 33% of patients, and incomplete correction of the deformity in as many as 70% of patients. Because hindfoot joints usually are already stiff in severe cavus deformities, there is little, if any, motion loss after a triple arthrodesis.34 Therefore reducing the foot into normal heel valgus with a triple arthrodesis may result in further plantar flexing an already plantar-flexed first ray in long-standing deformities. The ankle will tip into varus postoperatively if this is not corrected with a dorsiflexion osteotomy. A satisfactory plantigrade position is essential for good results.34 Outcome Few level III and IV studies have been published that assess the outcome of operative treatment of mainly fixed neurologic and idiopathic cavus deformities. Because of various etiologies and the limited number of patients treated, the reader is unable to draw definite conclusions. Nevertheless, each study offers some information about successful operative treatment and the pitfalls of certain treatment choices. The natural course of the disease without operative treatment has not yet been described. The surgeon must therefore thoughtfully apply the lessons learned from the available literature. An overview is given in Table 26-3. The outcome of various procedures reveals significant improvements of function and relief of pain and about two thirds good and excellent results, even in the long term. Worse outcome 1380

after cavus realignment is reported when advanced ankle arthritis stage II and above is present preoperatively, indicating the importance of detecting ankle arthritis early and preventing its progression.20,26 Another study revealed an association of radiographic evidence of ankle arthritis with a higher Foot Function Index (FFI) pain subscore, which suggests that arthritis prevention may have a greater impact on patient outcome than achievement of radiographic alignment.47 The unfavorable combination of recurrent lateral ankle sprains or chronic instability and hindfoot varus as commonly seen in pes cavus likely increases the risk for accelerated ankle arthritis, but it is also common in patients without instability because of elevated anteromedial ankle contact stresses in pes cavus.24,46 To prevent arthritis progression, a more aggressive dynamic and static realignment with slight overcorrection is recommended. Worse outcomes after surgery have also been reported for patients with neurologic as opposed to idiopathic pes cavus. Despite appropriate pes cavus realignment, neurologic patients appear to suffer more from pain and activity impairments.31 After joint-preserving realignment surgery, cavus patients were seen to have a slower gait velocity and lower cadence, but the proportion of time spent in stance and swing phase was near that of normal individuals.47 Although patients may have some deformity recurrence postoperatively, most are able to wear normal shoes and do not need orthoses.47

21 ft 15 pts

13 ft 10 pts 9 ft 8 pts

41 ft 25 pts

19 ft 15 pts

22 ft 22 pts

29 ft 23 pts

13 ft 13 pts

Sammarco et al, 2001

Fortin et al, 2002 Vienne et al, 2007

Ward et al, 2008

Kroon et al, 2009

Irwin et al, 2010

Maskell et al, 2010

Krause et al, 2013

Idiopathic 7 Neuropathic 6

All idiopathic

Idiopathic 11 Neurologic 4

Idiopathic and residual clubfoot All neurologic

All idiopathic

All neurologic

Etiology

Rigid

Flexible and rigid

Flexible

Flexible and rigid Flexible

Flexible

Flexibility

Stage 1-3

Group 1 stage 0-1 Group 2 stage 2-3 None

None

Stage 0-2

Stage 1-3

None

Ankle Arthritis at Surgery

A, B, C, D, E, J

A, B, C, D, G, H

2xA, B, C, E, F, G, I

B, C, G, H, K

A, C, D

A, B, D, F

A, B, H

Procedure

312 (26 years)

Mean Follow-up (months)

AOFAS: from 45 to 71

AOFAS: from 45 to 90

SF36 mental: 50 SF36 physical: 38 FFI pain: 35 FFI disability: 41 FFI activity limit: 22 AOFAS: 83 FFI pain: 13 FFI activity limit: 13 AOFAS group 1: 86, group 2: 59 VAS: 21 and 40 resp.

Karlsson score: from 33 to 82 AOFAS: from 57 to 87

AOFAS: from 46 to 89 Maryland Foot Score: from 72 to 90

Outcome (Mean)

Talo–first metatarsal angle from 9.9 to 2.4 degrees

Talo–first metatarsal angle from 22 to 17 degrees Arthritis progression mainly in group 2

OA most often in TMT 1 joints

Not reported

Lateral talo–MT I angle decreased 6.5 degrees Arch height decreased 6.8 mm Not reported

Radiographic Findings at Follow-up

III

Evidence

AOFAS, American Orthopaedic Foot and Ankle Society; EHL, extensor hallucis longus; FFI, Foot Function Index; IP, interphalangeal; OA, osteoarthritis; pts, patients; SF36, 36-item short Form Health Survey; TMT, tarsometatarsal; VAS, visual analog scale. Operative procedures: A, lateralizing calcaneal osteotomy, B, first metatarsal dorsiflexion osteotomy; C, peroneus longus to brevis transfer; D, lateral ligament reconstruction; E, Achilles lengthening tenotomy; F, anterior ankle debridement (cheilectomy) for osteotphytes; G, EHL transfer (Jones procedure) and IP fusion; H, plantar fascia release; I, tibialis posterior transfer to lateral cuneiform; J, gastrocnemius recession; K, tibialis anterior transfer to lateral cuneiform; L, deltoid ligament release; M, fibula osteotomy.

Number

Author

Mean Age at Surgery

Table 26-3 Pes Cavus Outcome Studies of the Last Decade

Pes Cavus ■ Chapter 26

1381

Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

REFERENCES 1. Aminian A, Sangeorzan BJ: The anatomy of cavus foot deformity, Foot Ankle Clin 13:191–198, v, 2008. 2. Bentzon PGK: Pes cavus and the m. peroneus longus, Acta Orthop Scand 4:50, 1933. 3. Berciano J, Gallardo E, Garcia A, et al: New insights into the pathophysiology of pes cavus in Charcot-Marie-Tooth disease type 1A duplication, J Neurol 258:1594–1602, 2011. 4. Bertorini T, Narayanaswami P, Rashed H: Charcot-Marie-Tooth disease (hereditary motor sensory neuropathies) and hereditary sensory and autonomic neuropathies, Neurologist 10:327–337, 2004. 5. Brewerton DA, Sandifer PH, Sweetnam DR: “Idiopathic” pes cavus: an investigation into its aetiology, Br Med J 2:659–661, 1963. 6. Charcot JM, Marie P: Sur une forme particulaire d’atrophy musculaire progressive souvent familiale débutant par les pieds et les jambes et atteignmant plus tard les mains, Rev Med 6:97–138, 1886. 7. Cole WH: The treatment of claw foot, J Bone Joint Surg Am 22:895–908, 1940. 8. Dhillon MS, Sandhu HS: Surgical options in the management of residual foot problems in poliomyelitis, Foot Ankle Clin 5:327–347, 2000. 9. duch*enne GB: The physiology of motion (trans EB Kaplan), Philadelphia, 1959, WB Saunders. 10. Dwyer FC: Osteotomy of the calcaneum for pes cavus, J Bone Joint Surg Br 41:80–86, 1959. 11. Dwyer FC: The present status of the problem of pes cavus, Clin Orthop 106:254–275, 1975. 12. Dyck PJ, Lambert EH: Lower motor and primary sensory neuron diseases with peroneal muscular atrophy. I. Neurologic, genetic, and electrophysiologic findings in hereditary polyneuropathies, Arch Neurol 18:603–618, 1968. 13. Fortin PT, Guettler J, Manoli A: Idiopathic cavovarus and lateral ankle instability: recognition and treatment implications relating to ankle arthritis, Foot Ankle Int 23:1031–1037, 2002. 14. Guyton GP: Peroneal nerve branching suggests compression palsy in the deformities of Charcot-Marie Tooth disease, Clin Orthop Relat Res 451:167–170, 2006. 15. Guyton GP, Mann RA: The pathogenesis and surgical management of foot deformity in Charcot-Marie-Tooth disease, Foot Ankle Clin 5:317–326, 2000. 16. Halgrimsson S: Pes cavus, seine Behandlung und einige Bemerkungen uber seing Aetiologie, Acta Orthop Scand 10:73, 1939. 17. Henderson CP, Parks BG, Guyton GP: Lateral and medial plantar pressures after split versus whole anterior tibialis tendon transfer, Foot Ankle Int 29:1038–1041, 2008. 18. Huber H, Dutoit M: Dynamic foot-pressure measurement in the assessment of operatively treated clubfeet, J Bone Joint Surg Am 86-A:1203–1210, 2004. 19. Ibrahim K: Pes cavus. In Evarts CM, editor: Surgery of the musculoskeletal system, New York, 1990, Churchill Livingstone, pp 4015–4034. 20. Irwin TA, Anderson RB, Davis WH, Cohen BE: Effect of ankle arthritis on clinical outcome of lateral ankle ligament reconstruction in cavovarus feet, Foot Ankle Int 31:941–948, 2010. 21. Japas LM: Surgical treatment of pes cavus by tarsal V-osteotomy. Preliminary report, J Bone Joint Surg Am 50:927–944, 1968. 22. Jones R: An operation for paralytic calcaneocavus, Am J Orthop Surg 5:371, 1908. 23. Knupp M, Horisberger M, Hintermann B: A new Z-shaped calcaneal osteotomy for 3-plane correction of severe deformity of the hindfoot, Tech Foot Ankle Surg 7:90–95, 2008.

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24. Krause F, Windolf M, Schwieger K, Weber M: Ankle joint pressure in pes cavovarus, J Bone Joint Surg Br 89:1660–1665, 2007. 25. Krause FG, Henning J, Pfander G, et al: Cavovarus foot realignment to treat anteromedial ankle arthrosis, Foot Ankle Int 34:54– 64, 2013. 26. Krause FG, Klammer G, Benneker LM, et al: Biochemical T2* MR quantification of ankle arthrosis in pes cavovarus, J Orthop Res 28:1562–1568, 2010. 27. Krause FG, Pohl MJ, Penner MJ, Younger AS: Tibial nerve palsy associated with lateralizing calcaneal osteotomy: case reviews and technical tip, Foot Ankle Int 30:258–261, 2009. 28. Krause FG, Sutter D, Waehnert D, et al: Ankle joint pressure changes in a pes cavovarus model after lateralizing calcaneal osteotomies, Foot Ankle Int 31:741–746, 2010. 29. Krause FG, Wing KJ, Younger AS: Neuromuscular issues in cavovarus foot, Foot Ankle Clin 13:243–258, vi, 2008. 30. Kremli MK: Fixed forefoot adduction after clubfoot surgery, Saudi Med J 24:742–744, 2003. 31. Kroon M, Faber FW, van der Linden M: Joint preservation surgery for correction of flexible pes cavovarus in adults, Foot Ankle Int 31:24–29, 2010. 32. Malerba F, De Marchi F: Calcaneal osteotomies, Foot Ankle Clin 10:523–540, vii, 2005. 33. Mann DC, Hsu JD: Triple arthrodesis in the treatment of fixed cavovarus deformity in adolescent patients with Charcot-MarieTooth disease, Foot Ankle 13:1–6, 1992. 34. Manoli A, Graham B: The subtle cavus foot, “the underpronator,” Foot Ankle Int 26:256–263, 2005. 35. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV: Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method, Pediatrics 113:376–380, 2004. 36. Pandolfo M: Friedreich ataxia, Semin Pediatr Neurol 10:163–172, 2003. 37. Pareyson D: Differential diagnosis of Charcot-Marie-Tooth disease and related neuropathies, Neurol Sci 25:72–82, 2004. 38. Roper BA, Tibrewal SB: Soft tissue surgery in Charcot-MarieTooth disease, J Bone Joint Surg Br 71:17–20, 1989. 39. Samilson RL: Crescentic osteotomy os calcis for calcaneovarus feet. In Bateman JE, editor: Foot science, Philadelphia, 1976, WB Saunders, p 18. 40. Sammarco GJ, Taylor R: Combined calcaneal and metatarsal osteotomies for the treatment of cavus foot, Foot Ankle Clin 6:533–543, vii, 2001. 41. Schmalbruch H, Haase G: Spinal muscular atrophy: present state, Brain Pathol 11:231–247, 2001. 42. Simbak N, Razak M: Residual deformity following surgical treatment of congenital talipes equinovarus, Med J Malaysia 53(Suppl A):115–120, 1998. 43. Steindler A: Operative treatment of pes cavus: stripping of the os calcis, Surg Gynecol Obstet 24:612–615, 1917. 44. Tooth HH: The peroneal type of progressive muscular atrophy, London, 1886, HK Lewis. 45. Tynan MC, Klenerman L, Helliwell TR, et al: Investigation of muscle imbalance in the leg in symptomatic forefoot pes cavus: a multidisciplinary study, Foot Ankle 13:489–501, 1992. 46. Valderrabano V, Hintermann B, Horisberger M, Fung TS: Ligamentous posttraumatic ankle osteoarthritis, Am J Sports Med 34:612–620, 2006. 47. Ward CM, Dolan LA, Bennett DL, et al: Long-term results of reconstruction for treatment of a flexible cavovarus foot in Charcot-Marie-Tooth disease, J Bone Joint Surg Am 90:2631– 2642, 2008. 48. Wetmore RS, Drennan JC: Long-term results of triple arthrodesis in Charcot-Marie-Tooth disease, J Bone Joint Surg Am 71:417– 422, 1989.

Chapter

Diabetes Jeffrey E. Johnson, Sandra E. Klein, James W. Brodsky CHAPTER CONTENTS BACKGROUND AND HISTORY PATHOPHYSIOLOGY Metabolic Control Neuropathy Angiopathy Structural Changes COMMON CLINICAL PROBLEMS ASSOCIATED WITH DIABETES Ulceration Classification of Diabetic Foot Ulcerations Charcot Neuropathic Arthropathy Temporal Staging of Charcot Neuropathic Arthropathy Anatomic Classification of Charcot Arthropathy Skin and Nail Disorders Infection DIAGNOSIS Physical Examination Neurologic Evaluation Vascular Evaluation Radiographic Examination Plain Radiographs Magnetic Resonance Imaging Computed Tomography Bone Scans and Labeled White Blood Cell Scans [18F]-2-Fluoro-2-Deoxy-D-Glucose–Positron Emission Tomography TREATMENT APPROACHES Patient Education Team Approach Neuropathy Topical Therapies Treatment of Motor Neuropathy Nerve Release for Treatment of Sensory Polyneuropathy Total-Contact Casting Footwear and Shoe Insoles Wound/Ulcer Management Activity Modification Local Wound Care Surgical Treatment Specific Ulcerations and Treatment Wound Closure and Soft Tissue Reconstruction

1385 1386 1386 1386 1387 1388 1388 1388 1390 1393 1396 1396 1399 1400 1405 1405 1406 1407 1409 1409 1410 1410 1411 1412 1412 1412 1412 1413 1413 1415 1415 1417 1425 1431 1432 1433 1433 1434 1441

Infection Cellulitis Abscess Osteomyelitis Hyperbaric Oxygen Treatment of Charcot Arthropathy Pharmacologic Therapy Surgical Treatment Timing of Operative Treatment Surgical Techniques Unique Considerations in the Treatment of Ankle Neuropathic Arthropathy Surgical Decision Making for Charcot Ankle Charcot Ankle Arthropathy Associated with an Open Wound Unstable Ankle Deformity Patterns Multijoint Arthropathy Ankle Fractures in the Diabetic Patient Ankle Fracture Treatment Options and Rationale Postoperative Management: Prolong Length of Immobilization Amputation

1443 1444 1444 1444 1450 1450 1455 1455 1455 1455 1459 1460 1460 1461 1462 1467 1468 1469 1471

BACKGROUND AND HISTORY

Diabetes mellitus was described in the medical writings of fifth century BC Greece, and the name itself is from the Greek (dia, through; bainein, to go; melitos, honey). It was diagnosed by the sweet taste of patients’ urine, their excessive thirst, and the agony of their inevitable death.273 Although the method of diagnosis was slightly less crude by the beginning of the 20th century, little else changed in the natural history or course of this disease for 2500 years. Only with the discovery of insulin by Banting and Best in 1922 did the modern era of diabetes as a nonfatal chronic disease begin. Since that landmark discovery, medicine has unfolded the myriad multisystem complications by which this disease is now well known. The American Diabetes Association currently estimates the population of diabetic patients in the United States is more than 25 million and rising as the average age in the United States increases, because the incidence of diabetes increases with age.96 The Centers for Disease Control and Prevention estimates that over a quarter of these are 1385

Part VII ■ Diabetes

undiagnosed cases.96 Foot problems, especially infections, are the most common disorder, necessitating hospital admission. More than 60% of nontraumatic lower limb amputations occur in patients with diabetes.96 The diabetic foot and its complications are encountered by practitioners in many different specialties, as well as by the orthopaedic surgeon, because of its prevalence in the same patient population who, for example, require total joint replacement. The complications of diabetes also affect such ordinary orthopaedic problems as fractures of the foot and ankle. The incidence of diabetes has increased dramatically in people older than 40 years, and an estimated 26% of the population older than age 65 is affected. The cost in morbidity, mortality, and time lost from work and family is enormous. The economic impact of diabetic foot problems and their sequelae on the health care system is mammoth.15,139,298 A review of diabetic patients in a medical clinic showed a 68% incidence of some form of foot disease. Most problems were mild, with very early changes, such as callus formation (51%) and hammer toes (32%); some were more apparent as sources of eventual injury and disease, such as sensory (34%) and autonomic (25%) neuropathy; however, all represented the early requisites that can lead to later problems of ulceration and infection.190 The severity of the complications of diabetes in the foot is not necessarily related to the severity of the disease itself. The majority of complications occur in patients with type 2 diabetes mellitus (T2DM), who account for the large majority of the diabetic population. Despite the advances in the field of diabetic foot care, including better control of hyperglycemia, the discovery of a multitude of new antibiotics, advanced surgical and nonsurgical techniques for vascular reconstruction, dissemination of knowledge on the relief of pressure to treat ulcerations, and new diagnostic modalities for evaluating tissue oxygenation in the extremities, the treatment of problems of the diabetic foot remains obscure, if not puzzling, to many physicians and surgeons. PATHOPHYSIOLOGY

Metabolic Control Diabetes is a metabolic disease resulting from inadequate insulin secretion, decreased responsiveness to insulin, or both. The hyperglycemic state experienced in diabetes is considered multifactorial, but most specialists agree that the long-term control of blood glucose levels reduces a patient’s risk for the known long-term complications of diabetes, such as vascular disease, nephropathy, retinopathy, and neuropathy.198 Careful control of blood glucose levels is critical for prevention as well as treatment of diabetic foot pathology. All diabetic patients should be followed closely by a primary care physician or endocrinologist experienced in the treatment of diabetes. 1386

Figure 27-1 Insensitivity resulting from neuropathy allowed this patient to step on a broken nail. The patient did not recognize the injury until a severe infection occurred.

Neuropathy Neuropathy, especially sensory neuropathy, is the preeminent source or initiating event of almost all ulcerations and most infections (Fig. 27-1). Peripheral vascular disease often coexists with neuropathy and contributes to poor or delayed healing, but it is seldom the initiating event. Vascular insufficiency causes tissue ischemia and can produce gangrene, prevent healing because of marginal nutrition of tissue, or even cause ischemic pain. However, the loss of protective sensation combined with acute trauma, recurrent trauma, repetitive trauma, or even microtrauma leads to most instances of soft tissue breakdown in the diabetic foot.35,61,125,238 The exact cause of diabetic neuropathy remains to be fully elucidated; however, autopsy studies have indicated that changes in the vasa nervorum, with resulting ischemia to the nerves, are the major pathway. The two theories regarding these microvascular changes in the nerves postulate the accumulation of sorbitol and intraneural accretion of advanced products of glycosylation. The only current possible treatment involves enzymatic blocking of the biochemical path toward sorbitol, but the efficacy of this treatment remains unproved.29 For all practical purposes at this time, neuropathy remains an irreversible condition that tends to progress gradually, and it lies at the heart of most foot disease in the diabetic patient.379 Risk of developing neuropathy is associated with poorer glucose control, age, and height.6,298 Brand and Ebner wrote a pioneering paper in 1969 describing the importance of pressure in the development of insensitive hands and feet. This study called for objective methodology to quantify pressure and heralded the development of this area of investigation.64 Research using optically based52,53,57,135,149 and electronically based92,155 pressure measurement systems have

Diabetes ■ Chapter 27

demonstrated abnormal, increased pressures under the diabetic foot that have been postulated for so long but could not be measured or quantified before these developments.18 One early study57 used the optical pedobarograph to examine patients with neuropathy for abnormal plantar pressures, defined as pressures greater than 10 kg/cm2. The same patients, when examined 3 years later, showed that some of these pressure areas resolved, whereas new ones appeared in others; 5 of 6 patients in the group of 39 who developed ulcers developed them in the areas identified previously as locations for abnormal pressure. In a study by the same group,83 14 of 44 patients thought clinically not to have neuropathy were discovered to have abnormal plantar pressures.57 When tested for vibratory sensation and sensory nerve conduction, these patients showed significantly decreased function, which suggests that the pathologic pressures that lead to ulceration can occur in conjunction with neuropathy but at a point before the neuropathy itself is apparent. A study comparing diabetic patients who have a history of ulcerations with diabetic controls without such a history revealed that both the severity of neuropathy and the peak pressures under the foot were greater in the group who had ulcerations.360 A number of studies have examined the effect of peripheral neuropathy on postural stability and gait. Studies examined both a subjective history of falling as well as biomechanical function in standing and in walking.89 Peripheral neuropathy, regardless of the cause, was demonstrated to be associated with an increased risk of falling.323 The abnormalities appear greater in standing and balance than in gait.91,351 Clinically, it is important to keep in mind that balance is a function of three factors: proprioception, which is affected by peripheral neuropathy in the lower extremities; vision; and the vestibular system. The first two factors can be damaged by complications of diabetes, namely, peripheral neuropathy and retinopathy. Therefore the physician should be aware of the risk of balance issues when both of these complications are present. Autonomic neuropathy produces a loss of normal sweating in the skin of the foot. This leads to stiff, dry, scaly skin that cracks easily because of its inflexible quality. Cracks in thickened skin, and especially in the stiff calluses on the sole, propagate into and through the dermis to open pathways for infection (Fig. 27-2). Loss of normal skin temperature regulation is also a result of autonomic neuropathy. A blunted response in diabetic extremities to increased temperature demonstrates this autosympathectomy effect and is thought to contribute to infection and injury.158 Autonomic neuropathy, as measured by blood flow variability and vasoconstrictor response, was demonstrated to be associated with foot ulceration in diabetic patients with neuropathy.162 Motor neuropathy is expressed as a loss of function and contracture of the intrinsic muscles of the foot that leads to the classic claw toe deformities (Fig. 27-3). These

Figure 27-2 Dry, scaly skin associated with autonomic component of diabetic peripheral neuropathy.

Figure 27-3 Clawing of toes associated with motor component of diabetic peripheral neuropathy. Hyperextended metatarsophalangeal joint increases pressure under metatarsal heads, and flexed proximal interphalangeal joint increases risk of ulceration on dorsum of toes.

changes predispose to ulcerations on the dorsum of the digits. The claw toe deformity contributes to a second area of ulceration as well because it increases pressure beneath the metatarsal head as the pressure of the base of the hyperextended proximal phalanx pushes down on the metatarsal head through its intact but contracted tendons.150 Magnetic resonance imaging (MRI) in neuropathic patients has demonstrated extensive atrophy of the intrinsic foot muscles, which precedes clinical hammer toe deformity.80 Mononeuropathy, most often affecting the peroneal nerve, can produce unilateral or bilateral footdrop, which is often unrecognized until the patient has developed a fixed equinus deformity. The equinus position increases pressure on the forefoot and thus contributes to ulceration of the forefoot or the distal end of a partial foot amputation. Angiopathy Arteriosclerotic disease is more common and more severe in diabetic than in nondiabetic patients.275 The calcification of atherosclerotic plaques in nondiabetic patients is patchy and occurs within the intimal layer of the vessel. In contrast, the characteristic calcification in diabetic arteries is circumferential and diffusely distributed along the vessel length and occurs within the tunica media of the 1387

Part VII ■ Diabetes

arteries. This produces the typical lead pipe appearance of calcified arteries on radiographs and can be seen in large and small vessels alike. It is often visible out to the vessels of the midfoot or even the toes. These calcified vessels are noncompliant and brittle. They produce artifactual elevation of Doppler pressure measurements in the lower extremities and make vascular reconstruction problematic at the time of anastomosis of a saphenous vein bypass graft into this stiff tissue. No evidence, however, indicates that calcification per se, rather than occlusion, is directly responsible for decreased perfusion in the foot.101 Proximal occlusive vascular disease does occur in diabetic patients in the aortic, iliac, and femoral vessels, and vascular reconstruction of these proximal lesions is often required to salvage foot lesions. It is critical to remember that the diabetic patient with a dysvascular lower limb may have arterial disease in the proximal and distal parts of the arterial tree. However, the vascular involvement in the distal part of the lower extremity of the diabetic patient is unusual and different from the nondiabetic patient’s because of the diffuse pattern of involvement that occurs below the popliteal artery trifurcation. The widespread, multisegmental occlusion of these small arteries usually requires dilation or bypass procedures down to the level of the ankle. The procedures are done to whichever, if any, of the anterior tibial, posterior tibial, or peroneal arteries is patent and has adequate runoff at the ankle level. Furthermore, the diabetic limb is unusual because of the common involvement of the major arteries of the foot by the atherosclerotic process, unlike in the nondiabetic extremity. Occlusive changes may be variable at different levels of the limb, with diminished toe pressures in a foot that has a reasonable dorsalis pedis or posterior tibial pulse. Much has been made of so-called small-vessel disease or microvascular changes of the diabetic foot. However, recent studies question the reality of small-vessel disease at the subarteriolar level. The occlusive nature of this supposed entity in the absence of large-vessel occlusion remains undocumented and unproved. In addition, adequate correlation has not been proved between the known changes in capillary permeability and basem*nt membrane thickening in the diabetic foot and the physiologic events of gangrene and infection.262 Actual measurement of blood flow in diabetic patients with supposed smallvessel disease failed to show a difference when compared with control subjects with and without peripheral neuropathy from other causes; this led the investigators to conclude that toe lesions were caused by changes of neuropathy and that the lesion of “microvascular disease” remains unproved.196 Structural Changes Stiffness and callous formation within the skin have also been found to be factors associated with ulceration. Whether the callous formation represents a true independent variable or is another expression of pressure is not proved. Measures of plantar tissue stiffness or plantar skin 1388

hardness remain to be defined with regard to their clinical relevance.121,229,286 The thickness of plantar tissue has been suggested to be related to the magnitude of peak plantar pressures in diabetic patients,4,166 although in one study, the soft tissue thickness was not greater in control subjects than in diabetic subjects.324 Recent studies by Abboud et al3 on muscle dysfunction provide fascinating new information with regard to a dynamic component of increased foot pressure leading to ulceration. Diabetic patients were shown to have a greater period of contact pressure and a measurable delay in initiation of contraction of the tibialis anterior. The authors postulated that late firing of the ankle dorsiflexors resulted in reduced control of foot contact after heel strike.3 New study methodology continues to be consistent with the basic clinical principle that ulceration requires both pressure and neuropathy. Foot pressures alone do not predict foot ulcerations.119,243 Another mechanical factor that has been investigated concerns structural changes within the foot itself. Authors have shown a decreased plantar muscle thickness consistent with motor neuropathy, as well as changes in metatarsophalangeal (MTP) joint extension and increased MTP joint arthropathy that may be contributing to the development of ulcerations. These measurements appear to represent a structural measurement for the effects of autonomic and motor neuropathy described earlier.324 However, the relationship of static foot structure to plantar pressure and ulceration formation is yet to be fully defined.90 Biochemical changes in the periarticular tissues, especially of the small joints (e.g., in the hand and foot), have been noted to produce thickened skin, diminished range of motion, and joint contractures in diabetic patients (Fig 27-4).231 Recent studies have demonstrated similar changes producing abnormal joint mechanics in the feet and ankle.136,319 Subtalar motion is decreased in diabetic patients and, to a greater degree, in those with a previous history of ulceration than in those who have not had foot ulcers.126 It is not possible to state that this represents a causeand-effect relationship between joint stiffness and the ulcerations. Some suggest that the limited joint mobility syndrome itself leads to increased plantar pressures.150,282,326 One study found an association with Charcot arthropathy, although it was unclear whether the limited joint mobility syndrome was an effect rather than a cause.104 COMMON CLINICAL PROBLEMS ASSOCIATED WITH DIABETES

Ulceration Ulcerations of the diabetic foot are the single most common problem for which medical assistance is sought. The economic burden of diabetic ulcers is significant even in a multidisciplinary clinic specifically designed for efficient care of diabetic patients.15,328 The lifetime risk of developing a diabetic foot ulcer has been reported at 15%, with an annual incidence of 2%.59,355

Diabetes ■ Chapter 27

Figure 27-4 Limited joint mobility syndrome in diabetes, causing permanent contractures of fingers.

The natural history of these lesions varies by location, size, and depth. Plantar ulcers are caused by weightbearing pressure, whereas dorsal and side ulcers are usually caused by shoe pressure. Ulcers of greater size and especially of greater depth are more difficult to treat. However, the outcome of ulcerations and their treatment is often unpredictable. A number of epidemiologic studies have examined risk factors for the development of diabetic ulceration. Abbott et al1 showed that a number of factors were independently related to the risk of developing a new foot ulcer: prior ulceration of the foot, abnormal neuropathy disability score, previous foot treatment, inability to feel the 10-g monofilament, reduced pulses, foot deformities, abnormal reflexes, and age. These authors concluded that the neuropathy disability score, pulse palpation, and monofilament testing were the three most important tests in routine screening, although an accurate history of prior ulceration was even more highly associated.1,2 More recent investigation by Lavery et al245 identified seven common pathways to ulceration. Factors most significantly associated with ulceration included neuropathy, deformity, callus, elevated peak pressure, peripheral vascular disease, penetrating trauma, and footwear-related issues. Several authors have shown the importance of psychosocial problems, such as alcohol addiction and divorce, as well as the duration of diabetes and poor metabolic control.65 Boyko et al60 showed that foot deformities, reduced foot perfusion, poor vision, and sensory and autonomic neuropathy were independently related to the development of foot ulcers. A second study by Reiber et al60 showed that trauma, neuropathy, and deformity were important causes of ulceration.321 These authors also found increased risk with greater body mass. However, other authors found that body mass was unrelated or a

poor predictor of risk.65,92 Apelqvist et al11,14 showed that peripheral vascular disease is a high-risk factor for amputation. This is compounded by other medical problems such as nephropathy, which was measured in terms of proteinuria. The development of ulcerations was associated in these studies with age and other diabetic complications, including retinopathy. The International Working Group on the Diabetic Foot developed a system of risk classification that predicts clinical outcomes of foot lesions in diabetic patients.301 In this classification, group 0 were patients without neuropathy, group 1 were patients with neuropathy but without foot deformity or peripheral vascular disease, group 2 were patients with neuropathy and either deformity or peripheral vascular disease, and group 3 were patients with a history of foot ulceration or lower extremity amputation. A prospective case-control study showed that the classification was associated with ulceration and amputation rates.301 A principle to remember is that once an ulcer occurs in the diabetic patient, it signifies that the patient has now reached a level of peripheral neuropathy at which the feet will always be at equal or greater risk in the future. Several epidemiologic studies have documented that the presence or prior occurrence of an ulcer is one of the major risk factors for new ulceration and for amputation in the diabetic patient.1,11,14,60 Sensory neuropathy alone does not cause breakdown but acts in combination with pressure. All neurotrophic ulceration is caused by these two factors combined. Brand62 elegantly demonstrated with animal models that repetitive trauma produces tissue inflammation that then progresses to tissue necrosis, even in the absence of ischemia. Both the inflammation and necrosis was confirmed histologically. This is mechanical breakdown of the tissue. Repetitive low-level trauma, which is not excessive for a given repetition but is abnormal in the number of repetitions permitted (as a result of the lack of sensation) causes tissue breakdown by eventually exceeding the threshold of soft tissue tolerance. Brand summarized the concepts in a review that emphasized the importance of patient awareness and understanding of the “tenderized foot.” His three principles were the severity and localization of sensory loss on the foot, the magnitude of forces on the foot, and the quantity of repetition (walking distance) of the forces necessary to lead to tissue inflammation and breakdown.63 Objective scientific methods have now corroborated the assertions that ulcerations are the result of a combination of pressure and neuropathy, such as the study comparing plantar pressures in a group of diabetic patients and a group of patients with rheumatoid arthritis. Each had abnormal pressures under the foot in about the same degree and incidence, but only the diabetic patients had plantar ulceration corresponding to the presence of neuropathy, and ulceration did not occur in the patients with arthritis.268 Plantar ulcerations almost always correspond to areas of underlying bony prominence in the foot, which 1389

Part VII ■ Diabetes

Figure 27-5 Examples of pressure ulceration at various locations on bony prominences. A, Fifth metatarsal head. B, Dorsum of proximal interphalangeal joint of hammer toe. C, Medial sesamoid and first metatarsal head. D, Exostosis of midfoot (type 1) Charcot joint, as well as intermediate metatarsal heads.

Figure 27-6 Ulceration over dorsolateral aspect of fifth toe caused by pressure from shoe.

explains why most ulcers occur under the metatarsal heads, the medial sesamoid, and the base of the fifth metatarsal; over the proximal interphalangeal joint of claw toes; and so on (Fig. 27-5A-D). Although ulcerations can occur under calluses, which are themselves the result of pressure, the underlying pressure rather than the calluses themselves is the risk factor.110 In contrast to plantar ulcerations, which are caused by intermittent pressure, the ulcerations on the dorsum and medial and lateral sides of the foot are usually caused by constant pressure exerted by a shoe. This can produce an ulcer even more quickly, even within 1 hour of wearing a poorly fitting shoe. The surgeon must correctly recognize this as the cause of ulcers to address the issue of footwear (Fig. 27-6). Classification of Diabetic Foot Ulcerations Several wound classifications systems have been proposed for the diabetic foot.20,212,241,361 The classification system developed in the 1970s at Rancho Los Amigos Hospital in California by Wagner and Meggitt, otherwise known as the Wagner classification, has been the most widely used and accepted grading system for lesions of the diabetic foot (Table 27-1).82,384 Numerous authors have since worked to improve the 1390

Figure 27-7 Grade 1 ulcer under midfoot Charcot prominence. The ulcer is superficial and filled with granulation tissue.

Table 27-1 Wagner Classification for Diabetic Foot Ulcerations Wagner Grade 0 1 2 3 4 5

Clinical Characteristics Preulcerative or postulcerative lesion Partial or full-thickness superficial ulceration (Fig. 27-7) Ulceration that probes to tendon or capsule (Fig. 27-8) Deep ulceration to bone Partial foot gangrene Whole foot gangrene

Diabetes ■ Chapter 27

understanding of wounds, particularly diabetic foot wounds, and much progress has been made. The Wagner classification, however, through its history and its simplicity, has provided a basis for communication and comparison among physicians and investigators in this area. The original Rancho Los Amigos classification presented the first widely referenced classification of diabetic foot

Figure 27-8 Grade 2 ulcer. Note the deep exposed tissue of the tendon and joint capsule.

lesions. However, limitations of this system exist in light of further experience. Specifically, all lesions of the diabetic foot from grade 1 ulcers to grade 5 gangrene do not occur along a natural continuum. Although this may often be true for the grade 1 ulcer, which progresses to the grade 3 lesion of osteomyelitis, this is not the case with grades 4 and 5. Grades 4 and 5 are vascular lesions or descriptions of the vascular status of the foot and are not necessarily related to the nature or progression of the wounds described by the lesser grades. Vascular disease can and should be graded as well, but a relationship does not necessarily exist between the depth of ulcerative lesions (grades 0, 1, 2, and 3) and the dysvascularity of the foot (grades 4 and 5). Moreover, the grade 5 foot is no longer a foot problem but belongs in the domain of salvage of the proximal portion of the leg. The ischemic lesions of grades 4 and 5 can exist separately from the lesser grades or coincide with any of them. For example, a grade 4 foot (partial gangrene) could include a forefoot that is otherwise grade 0 (no break in the skin and soft tissue) or grade 1 (superficial lesion). In addition, there are not necessarily pathways backward and forward from each grade of lesion. For example, grade 4 feet (partial gangrene) cannot be reversed to grade 3. The depth-ischemia classification68 is a modification of the Wagner-Meggitt classification (Fig. 27-9). The purpose of this modified classification is to make the classification easier to use by separating the evaluation of the wound from the evaluation of the perfusion of the foot; to clarify the distinctions among the grades, especially between grades 2 and 3; and to simplify the task of correlating

DEPTH

Grade 0 No break in skin

Grade 1 Superficial ulcer

Grade 2 Exposed tendons, joints

Grade 3 Exposed bone and/or abscess/ osteomyelitis

ISCHEMIA

Grade A No ischemia

Grade B Ischemia not gangrenous

Grade C Partial foot gangrene

Grade D Complete gangrene

c JW BRODSKY, MD, 1998 Figure 27-9 Classification of depth and ischemia in diabetic foot lesions.

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Infected?

Dysvascular? Doppler screening

Figure 27-10 Principles of care for the diabetic foot. Note two columns representing the two major issues of infection and vascularity. Once the dysvascular limb has been revascularized, the level of infection is determined and treated. CT, computed tomography, MRI, magnetic resonance imaging; TM, transmetatarsal.

Infected and not dysvascular

Dysvascular with or without infection

MRI, CT, roentgenogram (bone scan may or may not be helpful)

Vascular consultation

Vascular

Osteomyelitis

Abscess

Cellulitis

Reconstructable

Excision or ablation of infected bone

Drain and debride

Intravenous antibiotics

Balloon angioplasty, distal arterial bypass, or proximal large vessel reconstruction

Toe, ray, or TM amputation or partial-foot amputation (often delayed primary closure)

Partial amputation sometimes necessary for exposed bone, tendon

appropriate treatments with the proper grade of lesion. This revision of the classification of the lesions of the diabetic foot, combined with the treatment flowchart (Fig. 27-10), makes the decision-making path clearer and this information more accessible than with the Wagner algorithms.382 With the depth-ischemia classification, the soft tissue first is inspected and graded with a number grade, and then the limb and foot are evaluated for perfusion. The first step is based primarily on inspection of the foot and its wound or ulcer. Grade 1 lesions are superficial without exposure to sight or to the air of any deep structure. Grade 2 lesions are deeper by virtue of exposure of tendon or joint capsule, with or without infection. Grade 3 lesions are the deepest, composed of exposed bone, deep infection, abscess, or osteomyelitis (Fig. 27-11A and B). Determination of these three basic wound grades is based on the simple physical examination consisting of visualization and gentle probing of the wound with a sterile blunt instrument. The other numeric grade, grade 0, identifies a foot that has no open wound but is considered at risk for future or recurrent ulceration. These feet are defined as being at risk because the patient has a history of previous ulceration, 1392

Infected

Not reconstructable

Not infected

Debridement

Appropriate amputation level

now healed, or has the components for future ulceration, that is, neuropathic insensitivity with or without foot deformity. Once the examiner has assigned a numeric grade to the foot, the second step is to assign the letter grade by evaluating the limb perfusion (see Fig. 27-9). Grade A identifies the foot without clinically significant ischemia and does not require vascular evaluation or intervention. Grade B is the widest category in the ischemia portion of the classification. This foot has diminished perfusion but is not gangrenous. Grade B feet require a screening test, such as arterial Doppler studies or transcutaneous oxygen measurements. Depending on the outcome of these screening tests, vascular reconstruction might be indicated. Grade C feet have partial gangrene, and grade D feet have complete gangrene. Grades C and D require vascular evaluation to determine the appropriate level of healing and the possible need for vascular bypass to achieve healing of that amputation. A great advance has been the University of Texas classification.241 It is the same as the depth–ischemia classification in its definitions of wound depth and separation of that from evaluation of ischemia (Table 27-2). The advantage of this classification is that it includes

Diabetes ■ Chapter 27

grading systems, relatively little has been investigated regarding the important issue of the anatomic location of the lesion.253 Ulcer characteristics (classification) are still more important than ulcer site as a determinant of healing.13 In general, lesions of the forefoot, especially distal to the distal third of the metatarsal, have a much lower associated mortality and much higher limb salvage than more proximal lesions of the foot, even though the actual healing time of the proximal and distal lesions may be similar.225 In general, hindfoot lesions are associated with a higher incidence of serious problems and a greater risk of amputation. This type of prognostic generalization puts into perspective the increased seriousness of lesions of the midfoot and hindfoot and should aid the orthopaedic surgeon in patient counseling. In addition, transtibial amputation, which is a more common consideration for many severe hindfoot lesions, has been associated with a higher morbidity and mortality rate than more distal amputations.79

Charcot Neuropathic Arthropathy

B Figure 27-11 Grade 3 ulceration (A) with underlying osteomyelitis (B). Table 27-2 University of Texas Ulcer Classification Grade

Clinical Characteristics

0 1 2 3

Preulcerative or postulcerative lesion Partial or full-thickness superficial ulceration Deep wound that involves tendon or capsule Wound penetrating bone or joint

Stage A B C D

Clean wound Nonischemic infected wound Ischemic noninfected wound Ischemic infected wound

consideration of infection. The authors have called the presence of infection or ischemia “stages” of each grade (or depth). The stage A is neither infected nor ischemic. Stage B is infected but not ischemic. Stage C is ischemic but not infected. Stage D is both ischemic and infected. A study comparing original Wagner classification and the University of Texas classification system showed that the latter is superior.295 Other studies have attempted to validate the relevance of the classification system to the severity and outcomes of wounds and have found the classification to be predictive.21 Authors other than the originators have found that stage rather than grade corresponds best with outcome; the presence of infection and ischemia are more strongly predictive of outcome than the depth of the wound.295 Although much attention has been given to the depth of the diabetic foot lesion, as expressed in past and new

Charcot neuroarthropathy (CN), also known as a Charcot joint, is a noninfective bone and joint destructive process that occurs in association with a peripheral neuropathy. Diabetes mellitus (type 1 and 2) is the leading cause of CN in the developed world, having surpassed syphilis, which was the original cause of neuroarthropathy at the time that these joints were first described by Jean Martin Charcot in 1868 when he reported on tabes dorsalis (neuropathic arthropathy of the knee). Worldwide, especially in underdeveloped countries, leprosy, or Hansen disease, is also a major cause of CN. Although diabetes mellitus is the most common cause, other causes of peripheral neuropathy, including alcoholic peripheral neuropathy, Charcot-Marie-Tooth disease, and idiopathic peripheral neuropathy, are also associated with CN. The major problem with CN is the development of deformities of the foot and ankle that cause difficulty with shoe fitting and marked alteration in the load applied to the plantar foot or medial or lateral ankle during weight bearing. These changes lead to an increased propensity for ulceration in the high-pressure areas. Once established, these ulcers may become a portal of entry for bacteria and thus may result in superficial or deep infection, which may further lead to a need for amputation. Neuropathic arthropathy may create joint instability, especially at the ankle and hindfoot, which may result in loss of the plantigrade position of the foot and the development of progressive varus, valgus, equinus, or calcaneus deformity. Jordan was the first to recognize the association of the peripheral neuropathy of diabetes with a Charcot joint with his case report in 1936.220 Experimental documentation of the relationship of neuropathic joint destruction and loss of normal sensation was first elucidated in 1917 in a study by Eloesser,144 in which he selectively denervated single limbs of cats with otherwise normal sensation to produce Charcot joints in only those limbs. Other 1393

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studies have focused on the cellular and biochemical role of bone destruction and bone formation.169,291,344 Epidemiologic data for Charcot neuropathic arthropathy (CNA) is limited; however, several studies have indicated that the annual incidence of CNA is less than 1% (0.1-0.85%).147,244,356 However, given the 25.8 million people in the United States with a diagnosis of diabetes (8.5% of the population),96 the upward trend of this incidence and the increasing longevity of patients with the disease, the number of patients with Charcot arthropathy will continue to increase. Patients with CN experience increased morbidity and decreased quality of life. Dhawan et al130 reported that diabetic patients with CN had lower physical component scores than patients with end-stage renal disease on hemodialysis, cardiovascular disease, Parkinson’s disease, and these scores were one standard deviation lower than patients with diabetes in general. Patients with CN are at a high risk for amputation (7%) even if no ulceration is present initially; however, this risk for amputation increases to 28% if an ulceration is present at the time of first evaluation. Because this condition is still often overlooked and many cases are misdiagnosed, it is likely that the incidence is higher than previously reported. The percentages of men and women with Charcot arthropathy are about equal, and the average duration of diabetes before the occurrence of the Charcot arthropathy is more than 10 years; however, the range of duration of diabetes is 0 to 45 years. Charcot joints of the feet occur bilaterally in approximately 30% of patients. No preponderance of type 1 diabetes (T1DM) patients are affected, but the percentage of T1DM patients (16%)71 might reflect a somewhat higher fraction of T1DM patients than in the diabetic population as a whole, which is 5% to 10%.9 The pathophysiology of Charcot neuroarthropathy is poorly understood. Charcot’s idea of a “trophic” effect on the joints was replaced in the 20th century with two basic theories of the cause of neuroarthropathy. The first theory is neurotraumatic destruction and hypothesizes that the joint destruction, fractures, and collapse of the foot occur as the result of cumulative mechanical trauma, which could be minor trauma, major trauma, or unrecognized microtrauma in a joint that has been rendered insensitive to proprioception and pain. This initial traumatic event activates a process that is exacerbated by continued weight-bearing activity because the patient lacks the guarding, off-loading, and activity modification that individuals with normal sensation exhibit. Eventually, the mechanical breakdown of the bone or joint occurs, resulting in a repair process that is hampered by continued weight-bearing activity, which produces a clinical picture similar to a hypertrophic nonunion.218 The second theory is neurovascular destruction and postulates that secondary to trauma or some other trigger, a state of regional hyperemia is generated by an overactive vasomotor autonomic neuropathy. Dysregulation of regional blood flood as a result of this autosympathectomy results in bone 1394

resorption and ligamentous weakening that promotes a mechanical breakdown of the bone or joint dislocation.28,78 Recent studies suggest that the bone resorption observed during the Charcot process may be mediated by cytokine stimulation of osteoclasts and progenitor cells.37,159,314,404 Release of these proinflammatory cytokines (tumor necrosis factor-α [TNF-α] and interleukin1β) leads to increased expression of the polypeptide receptor activator of nuclear factor–κβ ligand (RANKL) from various local cell types. RANKL stimulates maturation of osteoclasts from osteoclast precursor cells via a nuclear transcription factor (NF-κβ). In a typical fracture, this rise in proinflammatory cytokines is relatively short lived because of the pain and subsequent splinting of the bone. However, in the person who develops a neuropathic fracture, the loss of pain sensation does not limit the activity of the individual, and continued ambulation causes ongoing repetitive trauma to the limb. It has been suggested that this results in continual production of proinflammatory cytokines, RANKL, NF-κβ, and osteoclasts, which in turn leads to continuing osteolysis.210,325 Despite these advances, neither theory has been shown to completely explain this complex phenomenon, and our understanding of the exact mechanisms that results in CN remains poorly understood. One unifying theory is yet to be elucidated, although it likely includes elements of both neurotraumatic and neurovascular theories. Risk factors associated with the development of Charcot neuroarthropathy include somatic and autonomic neuropathy, osteopenia, renal impairment,218 and other factors, such as obesity, ankle equinus contracture, muscle imbalances resulting from denervation of extrinsic, and intrinsic musculature and increased activity level have been proposed.305 Reduced peripheral but not axial bone mineral density (BMD) has previously been demonstrated in patients with Charcot neuroarthropathy213,404 However, BMD measures were correlated with type of neuropathic pattern and found that a fracture-type pattern was associated with BMD deficiency and a dislocation-type pattern was associated with a normal BMD.189 In this study, the data did not appear to change whether or not measures of systemic or regional BMD were used. Also noted was that the fracture patterns predominated at the ankle and forefoot, whereas dislocations predominated at the midfoot.189 However, many fundamental questions remain, such as why do some diabetic patients with neuropathy develop ulceration, and others develop Charcot neuroarthropathy? Why do some Charcot feet ulcerate, and others with apparently greater deformity and greater plantar pressure never develop ulcerations (Figs. 27-12 and 27-13)? In one study, Stevens et al368 found that the neuropathy in patients with diabetic CN had different characteristics than ulcer patients. Charcot patients had impaired cold perception but relatively preserved warm perception, compared with loss of both in ulcer patients. Light-touch perception (as tested with monofilaments) was preserved in the Charcot patients but not in the ulcer patients. Vascular response of the hallux skin to heating was also

Diabetes ■ Chapter 27

Figure 27-12 A 57-year-old man with an 8-year history of type 2 hindfoot Charcot that never ulcerated and was treated with custom-molded cushioning insoles. The patient fell while working in his barn, sustaining fracture of talar body. This healed uneventfully after open reduction and internal fixation, and he resumed his outdoor work.

greater in Charcot patients. Of note, Charcot neuroarthropathy is not typically seen in a dysvascular patient, further implicating the role of vascular mechanisms in the etiology of this disorder. In summary, the neural and vascular characteristics of the foot are complex, and how they interact to produce the clinical disorders that are exhibited by the patient with diabetes is yet to be described. Despite the ever-increasing numbers of Charcot joints, this problem is still often overlooked, underdiagnosed, and often poorly managed. In the scenario of cellulitis and foot ulceration, CN is often confused with infection, further delaying the diagnosis and appropriate treatment. Clinically, most Charcot neuropathic joints/fractures manifest with a history that includes trauma and impaired sensation caused by the neuropathy. The density of the sensory neuropathy is not necessarily related to the severity of the diabetes, its duration, or whether it is type 1 or type 2. Some of the worst cases of a Charcot joint may occur in patients with mild type 2 diabetes treated with oral hypoglycemic agents or diet modification alone. In occasional patients, the Charcot joint might even be the first manifestation of previously undiagnosed diabetes. The trauma may be microtrauma (e.g., abnormal gait causing increased pressure with each footstep as a result of poor sensory feedback from the limb), minor trauma (e.g., bumping the foot),358 or major traumatic event (e.g., a fall or a twisting injury to ankle).107 The trauma may be recognized or unrecognized; it may be subacute or chronic. The Charcot joint can manifest as a fracture,111,191,234 dislocation,186,250,290 fracture-dislocation, or subluxation. In the earliest stages, it can simply manifest as a hot, red, swollen foot. Infection (commonly osteomyelitis) in the Charcot foot or ankle occurs as the result of extension from a soft tissue focus, usually an ulcer as a result of

C Figure 27-13 A, Plantar view of healed midfoot ulceration resulting from Charcot arthropathy. B, Lateral radiograph. C, Ulcer was managed with custom insoles and off-the-shelf walking shoes.

pressure at a bony prominence. One diabetic center reported a 17% annual incidence of ulceration among 115 diabetic patients with Charcot arthropathy.73,240 The physician who first sees a patient in the early stages of the development of the Charcot process may be tempted to diagnose the changes in the bone as osteomyelitis; indeed, the distinction may be difficult given the erosive changes diffusely through the bone, sometimes accompanied by new bone formation. One subtle but valuable hallmark of a neuropathic fracture is that it lacks 1395

Part VII ■ Diabetes

Figure 27-14 Histologic section from a Charcot joint demonstrates bony detritus within the synovial tissue.

the surrounding osteopenia that typically occurs in osteomyelitis.322 When the distinction between osteomyelitis and Charcot bone changes cannot easily be made, the definitive study in the past has been biopsy of the bone through an incision away from any associated ulcer or skin breakdown. The specimen should be submitted to the laboratory for aerobic and anaerobic cultures; part of the bone specimen should be submitted to the pathologist for examination of histologic evidence of osteomyelitis or Charcot changes. Provided that the specimen was sampled from near or at a joint, the histology can reveal the pathognomonic changes of Charcot joint destruction, that is, bone particles embedded within the synovium (Fig. 27-14). Osteomyelitis can be distinguished by the acute and chronic inflammatory cells within the marrow spaces, with or without associated osteonecrosis and fibrosis in the marrow. An excellent example of the complexity of treating Charcot arthropathy is in a patient with a neuropathic ankle fracture that has undergone progressive bone destruction with the development of deformity and a nonplantigrade foot. The deformity can become so great that treatment in a total-contact cast (TCC) or ankle–foot orthosis (AFO) is impossible. The foot is skewed off the end of the leg, and massive soft tissue breakdown, infection, and amputation are imminent. Cases of severe varus or valgus deformity at the ankle or combined deformity at the ankle and the hindfoot are more common. Reconstruction is indicated to realign the foot to make it plantigrade and to control the pressure on the soft tissue that causes breakdown. Temporal Staging of Charcot Neuropathic Arthropathy Eichenholtz143 described three stages of development of the Charcot joint that represent its temporal course from the initial events to eventual healing. Stage I is characterized by an acute inflammatory process in which the primary radiographic finding is fragmentation, the synonym for stage I.214,215 It is associated with hyperemia, 1396

Figure 27-15 Placing the hands of the examiner on each foot will detect even small differences in skin temperature, which may indicate inflammation over a Charcot joint. This is a helpful clinical method for monitoring the response to cast treatment of acute Charcot neuroarthropathy. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

and the joint typically is swollen, hot, and erythematous. The difference in limb temperature can easily be detected by placing one hand of the examiner on each foot, and even small differences in temperature can be detected indicating inflammation over a Charcot joint (Fig. 27-15). On radiographs, the bone shows dissolution, fragmentation, and dislocation. Stage II, known as coalescence, is typified by the beginning of the reparative process, as signified by a diminution of the edema, warmth, and redness and the radiologic finding of new bone formation. This coalescing new bone forms at the site of the initiating fracture and bone destruction or even at the site of dislocation in the absence of a major fracture. Stage III is characterized by bony consolidation and healing, usually with residual deformity. This is sometimes a confusing picture because the joint may be enlarged despite the resolution of edema in this last stage. Although the acute Charcot process may be reactivated in the same limb, this is the exception rather than the rule; this usually occurs in stage II rather than in stage III, when solid bony healing has occurred. However, there is evidence that once the patient enters stage III, there is a continued slow “creep” of deformity over time. In a group of 15 Charcot patients monitored for 2 years and compared with matched diabetic patients without Charcot and normal subjects, the medial column deformity worsened during the first 6 months, and the lateral column deformity continued to collapse over the 2 years of the study.183 Anatomic Classification of Charcot Arthropathy The classification of Charcot joints of the foot and ankle into anatomic categories has been described by multiple authors (Harris and Brand, 1966; Cofield, 1983; Brodsky, 1993; Sammarco and Conti, 1998; Schon et al, 1998).42,69,178,334,342 These classifications are clinically

Diabetes ■ Chapter 27

useful for defining the broad categories and patterns of destruction as well as a method for studying progression and natural history of this often devastating disorder. The Brodsky classification is based on which of the four anatomic areas is predominantly affected by the Charcot process, as judged by the findings on plain radiographs; therefore it requires some judgment by the clinician about which area of the foot has the greatest involvement, especially when multiple areas of the foot are involved.69,75 Type 1 involves all or portions of the midfoot, including the metatarsocuneiform and naviculocuneiform joints. Type 1 joints are the most common and represent about 60% of Charcot feet. Type 2 Charcot joints represent those in which the main changes are within the hindfoot, that is, any or all of the triple joints of the subtalar complex: the subtalar, calcaneocuboid, and talonavicular joints. Type 2 accounts for 30% to 35% of the Charcot joints. Types 3A and 3B are relatively minor groups numerically, although they behave quite differently. Type 3A joints represent those in which the predominant changes are within the ankle joint, and often lead to significant deformity, disability, and complications and frequently require surgical treatment or significant bracing. Type 3B Charcot feet are those that develop a pathologic fracture of the tubercle of the calcaneus with secondary deformity and collapse of the distal portions of the foot. Figure 27-16 illustrates the types of Charcot joints. The vast majority of Charcot joints of the foot and ankle (90%-95%) are represented by type 1 (midfoot group) and type 2 (hindfoot group). The remaining two types are less common and more often associated with discrete

traumatic incidents, such as a major ankle fracture in the case of type 3A Charcot joints. Schon et al342 developed a classification specifically for midtarsus deformities based on 109 patients with acquired midtarsus deformities (from both neuropathic and nonneuropathic etiologies) combining anatomic location and severity of collapse. Anatomic locations were determined by radiography and divided into types I to IV: I, tarsometatarsal; II, naviculocuneiform; III, perinavicular; and IV, transverse tarsal (calcaneocuboid and talonavicular) (Fig. 27-17).342 The severity (or stage) of collapse was judged clinically by observing the foot. Stage A was a minimal deformity with loss of arch height but no “rocker” or negative arch; stage B has greater deformity than A—with an obvious plantar prominence; stage C (Fig. 27-18)342 was severe destruction of both medial and lateral columns, with a midfoot prominence more plantar than a line extrapolated from the heel to the ball of the foot beneath the metatarsal heads.342 Although considerable overlap clearly occurs in the natural history of the different types of Charcot joints and between different classification systems, there are clear patterns of behavior and progression for the different types.75 The Brodsky type 1, or midfoot, Charcot group is typified by the development of symptomatic plantar midfoot bony prominences, a shorter average period of immobilization required for bony healing, and lower likelihood of requiring long-term immobilization (of a year or more) in a cast or brace (Fig. 27-19). These patients have rocker-bottom feet and severe midfoot valgus deformity and bony protuberances that produce increased pressure, leading to serious and persistent ulcerations on

Type 3

Type 2

Type 3

Type 2 Type 1

Type 1

Figure 27-16 Dorsal (A) and lateral (B) views showing anatomic classification of Charcot’s joints of the tarsus. Type 1 (midfoot) involves the tarsometatarsal and naviculocuneiform joints. Type 2 (hindfoot) involves the subtalar, talonavicular, or calcaneocuboid joints. Type 3A (ankle) involves the tibiotalar joint.

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Type I Type IV

Type II Type III

Type II Type I

Type IV

Type III

Figure 27-17 Graphic illustration of the types of deformities (I-IV). A, Anteroposterior view. B, Lateral view. (Modified from Schon LC, Weinfeld SB, Horton GB, Resch S: Radiographic and clinical classification of acquired midtarsus deformities. Foot Ankle Int 19:394-404, 1998.)

the medial and lateral borders and especially on the plantar surface of the foot. Using the Schon classification, Bevan and Tomlinson,42 in a review of 19 patients (24 feet), found that only patients with a lateral talar-first metatarsal angle of greater than 27 degrees had an ulcer. Other characteristics of midfoot Charcot include a higher proportion of hypertrophic bony changes and a lower incidence of erosive bony changes than found in Brodsky type 2 feet. Type 1 feet tend to settle into a stable but deformed shape, and thus patients are most likely to present late when they have already reached Eichenholtz stage II of osseous coalescence or even stage III of bony healing, even without having been treated. These Charcot feet are most likely to require treatment of ulcerations, either with TCCs and AFO braces or by surgical resection of the underlying bony prominences causing the ulcers (Fig. 27-20). By contrast, the type 2, or hindfoot, group is typified by the development of chronic, persistent skeletal instability, often associated with the anecdotal phrase “bag of bones.” These patients are less likely to develop ulcerations from symptomatic bony prominences, but bony prominences do occur in about a third; they are more likely to require long periods of immobilization until Eichenholtz stages II and III of bony consolidation are finally reached. The average period of immobilization, almost 2 years, is also longer in type 2 feet than in type 1 feet. The association of type 2 Charcot joints 1398

with long-term immobilization of 1 year or longer is also statistically significant. These patients are more likely to have persistent enlargement that cannot be easily contained in normal footwear and that produces a shift of the entire foot off of the weight-bearing axis of the leg. Type 3A joints, in which the changes are in the ankle itself, are similar to the hindfoot (type 2) group, with the formation of chronic swelling and instability, requiring immobilization for an average of more than a year to achieve bony healing. Type 3 joints develop chronic enlargement and shortening and can then drift into varus or valgus deformities and lead to pressure over the malleoli with subsequent ulcerations, infection, and osteomyelitis. Thus type 3A, or ankle, Charcot joints experience a combination of both the major problems—bony prominences and instability (Fig. 27-21A and B). The principle is that the closer the area of neuropathic joint destruction is to the axis of weight bearing in the limb (i.e., the more proximal the area of the Charcot change), the longer the immobilization and the greater the propensity for producing long-term instability.71 Type 3B, or os calcis, Charcot joints occur in patients who develop a pathologic fracture in the tubercle of the calcaneus that later leads to secondary collapse of the foot. In contrast to the three other types of Charcot joints, in which the primary process is articular, in type 3B feet, the changes occur primarily with a fracture whose mechanical effect results in secondary, more distal joint

Diabetes ■ Chapter 27

Skin and Nail Disorders Stage A

Stage B

Stage C

Figure 27-18 Clinical staging of degree and deformity. (Modified from Schon LC, Weinfeld SB, Horton GB, Resch S: Radiographic and clinical classification of acquired midtarsus deformities. Foot Ankle Int 19:394-404, 1998.)

Figure 27-19 Lateral radiograph of a type 1, or midfoot, Charcot joint.

changes. These patients are treated with shoe modifications after relatively short periods of immobilization. Similar cases have been reported sporadically.114 The association of symptomatic bony prominences with type 1 Charcot joints and the association of long-term instability (greater than 1 year) with type 2 Charcot joints are statistically significant.71

Care of the skin and nails is an essential part of the routine care of the diabetic foot.68,202 The reduction in eccrine sweat gland function and loss of skin thermoregulation that occurs as a result of autonomic neuropathy can cause the skin of the foot to become excessively dry and thus more susceptible to cracks and splits. These fissures in calluses propagate down into the dermis and may lead to infection. The patient should be instructed, as a part of the daily or twice-daily routine inspections, to apply moisture-restoring skin lotion to dry areas of the skin. Care should be taken to avoid moistening between the toes, where the skin is least likely to become scaly and where excessive moisture leads to maceration. Special lotions for diabetic feet are available in drug stores, although inexpensive products such as petroleum jelly, vegetable shortening and “udder balm” (containing lanolin) are also effective. Products containing alcohols should be avoided because they can cause further drying of the skin. Application of a very thin layer of a moisturizer immediately after bathing can seal in the hydration absorbed by the skin during the bath or shower. For excessively scaly skin and thick areas of callosity, products containing 10% to 20% urea may be used to help breakdown thickened areas. Care of the nails requires a few special instruments to be kept in the clinic (Fig. 27-22A-E). It is usually most convenient to keep the instruments together in a sterile tray; extras of the most frequently used instruments can be wrapped separately, especially peel-packed single-use scalpel blades. The double-action bone rongeur, although a surgical instrument, has many advantages for trimming the nails in diabetic patients, for whom nail disease can be the initiating event of more serious foot problems. The rongeur is sharp enough and can generate enough force to clip thickened nails without twisting or cracking the nail or its attachments. The rounded beaks can be used to protect and push the soft tissue away from the cutting edges. Extremely hard nails should be nibbled away a bit at a time. The anvil-type nail splitter has a flat lower jaw that is pushed under the nail to separate it from the nail bed and is most useful for removing the medial or lateral edge of a nail that is incurvated or ingrown. The sharp, triangular upper jaw splits the nail by coming together with the flat anvil portion. This is the safest way to remove a nail margin for an acutely infected and ingrown toenail while avoiding cutting the nail bed below, which could lead to infection or inflammation of the underlying bone of the distal phalanx. The Freer elevator is useful for lifting up the split portion of the nail and for separating the nail from the overlying eponychial fold. A straight hemostat is also useful for clamping the edge of the nail after it has been cut longitudinally and rotating it out of the nail fold rather than pulling on the nail, which is more traumatic to the nail fold. The nail curet is used for gently debriding a corner of the nail, where it is compressing the adjacent soft tissue. A motorized hobby drill, fitted with 1399

Part VII ■ Diabetes

a sandpaper disc or drum, can be used in the clinic to debride onychomycotic nails and to smooth plantar calluses. Special care must be taken to avoid injury to the skin, but when properly used, this technique can be easier and safer than trimming and paring with cutting tools. The diabetic patient can be instructed in how to perform some of the nail debriding techniques at home with the use of an emery board but should not use power equipment on their feet. Care of the skin and nails can be practiced in the clinic and taught to the patient and family. Although the surgeon should examine the diabetic patient for nail problems and be skilled in performing the various procedures needed to manage nail complications, different members of the diabetic foot care team can teach and perform these routine nail care tasks that are critical to

minimizing complications. Designation of a nurse, physician’s assistant, medical assistant, or technician is important in planning for complete care of the feet of diabetic patients (Box 27-1). Infection Unlike many other orthopaedic infections, most diabetic foot infections are polymicrobial.105,264,336,378,392 Impairment of leukocyte function has been documented in diabetic patients.31,278 This represents a defect in handling infection once it is established, but not necessarily a greater susceptibility to infection. In major infections of the diabetic foot, proper culture technique, including culture for anaerobic organisms is critical to successful treatment. The ideal selection of an antibiotic regimen is based on

Left Right

Peak plantar pressure off-loading by 71%

Figure 27-20 A, This patient has a Brodsky type 3 Charcot neuroarthropathy of the ankle and hindfoot. Shown are the plantar pressure measurements with and without the Gillette calf lacer ankle–foot orthosis (AFO) fitted with a custom accommodative total-contact insole as shown in the top right panel. In the left panel, note the high peak pressures while walking barefoot and the significant (71%) reduction of peak pressures measured in the shoe with the Gillette brace attached. A graphic representation of the peak pressures without the brace is illustrated in the middle panels, and the step-by-step measurements of peak pressure in the shoe with walking are illustrated in the bottom horizontal panel.

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Left Right

Peak plantar pressure off-loading by 81%

Figure 27-20, cont’d B, This patient has a Brodsky type 1, Schon type IV, midfoot Charcot neuroarthropathy with similar plantar pressure measurements, with and without the Gillette calf lacer AFO with custom insole, as shown in the top right panel. In the left panel, note the high peak pressures while walking barefoot and the significant (81%) reduction of peak pressures measured in the shoe with the Gillette brace attached. (A and B, Courtesy David Sinacore, PhD, Washington University Program in Physical Therapy, unpublished data.)

culture results whenever possible. With the ever-increasing problems of drug resistance, drug-sensitivity testing is a crucial part of the culture process. The most typical combination of organisms includes the triad of gram-positive cocci (e.g., staphylococci, group B streptococci, and enterococci), gram-negative aerobic rods (e.g., Escherichia coli, Enterobacter, Proteus, and Pseudomonas spp.), and anaerobes (e.g., Bacteroides fragilis and other Bacteroides spp., Clostridium spp., and peptostreptococci). Various and differing combinations of organisms are common. An infection can be caused by a single organism. When this occurs, it is usually a gram-positive bacterium or sometimes a gram-negative bacterium, but it is almost never an anaerobe alone.105,270 Antibiotic resistance is a major concern in diabetic foot infections.123 Now the population faces the ominous

problems of emergent strains of vancomycin-resistant enterococci and staphylococci (VRSA), a problem that threatens to be as serious as, or more serious than, methicillin-resistant Staphylococcus aureus (MRSA). Close attention to the pattern of antibiotic sensitivity of infecting organisms is recommended. Consultation with an infectious diseases specialist should be sought in these cases. In general, these infections require the early involvement of a multidisciplinary team of care providers.235 Gas may be present in the soft tissue with diabetic foot infections. However, it is very seldom caused by the Clostridium perfringens of classic gas gangrene. Most gas in the soft tissue is caused by aerobic organisms, including gram-positive cocci, such as group B streptococci or enterococci, or by mixed gram-negative rods.41 When gas is demonstrated in the soft tissue either clinically or on 1401

Part VII ■ Diabetes

Figure 27-21 Type 3 Charcot joint with tibiotalar involvement, bony enlargement, and varus. This patient is 7 years from onset and wears a posterior shell ankle–foot orthosis lined with Plastizote. A, Anterior clinical view. B, Posterior clinical view. C, Anteroposterior radiograph. D, Lateral radiograph.

radiographs, an immediate Gram stain of the exudate is the most expeditious way to determine whether this is true gas gangrene. True gas gangrene demonstrates grampositive rods on the Gram stain. Gas in the soft tissue also occurs in necrotizing fasciitis, an extremely serious and often fatal disorder that produces rapidly progressive tissue necrosis that can extend proximally at an alarming rate. Fortunately, the latter is uncommon, and most gas in the soft tissue of diabetic foot infections is caused by the more ordinary pathogens. Not only is the proper culture technique important, but the quality of material from which the culture is obtained is crucial as well. Organisms obtained by taking superficial swabs from the surface of ulcers, sinus tracts, and the outside layer of a deep wound have been proved to correlate poorly with the microbiology of the deep tissues of the wounds.336,337,347 Although some correlation often occurs, there is often a superficial colonization of organisms other than those responsible for the deep disease below. For major wounds, especially those that require surgical debridement, cultures must be obtained by techniques other than simple swabbing of the wound. The most reliable technique is to biopsy the tissue intraoperatively from deep in the wound. In the outpatient setting of the clinic or office, curettage and culture of the 1402

base of the ulcer have been shown to yield greater concordance with deep cultures compared with simply swabbing the surface. Deep or even curetted cultures are not always possible or practical to obtain, but they should be especially considered in deep or difficult wounds. The purpose of emphasizing the types of cultures and techniques for gathering cultures is that the choice of antibiotic and the duration of therapy often depend on this information. Antibiotic selection is sometimes unavoidably empiric, and usually it is initially empiric and based on the most likely combination of organisms. Once culture reports have been obtained, the antibiotic regimen can usually be modified to the specific sensitivity patterns of adequately obtained specimens. Patients who are admitted to the hospital for treatment of severe diabetic foot infections have usually already been treated as outpatients with oral antibiotics. This is often tantamount to partial antibiotic treatment in that the patient often has received enough antibiotic to suppress the new cultures but not sufficient antibiotic to cure the infection. This can lead to considerable confusion when the culture report returns as “negative,” suggesting that no active infection exists at all, or the culture report reflects a superficial colonization unrepresentative of the smoldering infection below. Often, it is also necessary to

Diabetes ■ Chapter 27

Figure 27-22 Instruments for diabetic foot care in the outpatient clinic. Basic instrument set. A, Left column: two small curved hemostats, Freer elevator, and larger clamp; right column: anvil-type nail splitter, small curette, forceps, and iris scissors. B, Nail splitter, curette, and Freer elevator enlarged. C, No. 17 scalpel for trimming keratotic lesions. D, A motorized drill for sanding calluses and nails. E, Handheld Doppler for arterial examination.

stop all oral antibiotics for 1 to several days preoperatively to enhance the surgical cultures. Even with this measure, some of the cultures will be negative. With suspected or known osteomyelitis, it is desirable to submit a bone specimen for histologic examination as well as a specimen and cultures for aerobic and anaerobic cultures. These should be in addition to aerobic and anaerobic cultures of the soft tissue. When bone is resected in the diabetic foot, it can undergo pathologic examination for microscopic evidence of infection within the bone. The surgeon should specifically request that the pathologist “examine the bone for histologic evidence of osteomyelitis.” This is usually illustrated by the presence of inflammatory cells acutely or chronically within the marrow space. The histologic substantiation of the presence or absence of osteomyelitis may be basis for determining the length of treatment with intravenous (IV) antibiotics, as well as the choice of antibiotic regimens. On the other hand, the classic regimen that mandates 6 full weeks of IV antibiotic therapy for all cases of bone

infection does not apply uniformly to all cases. Those guidelines are most appropriate and are most applicable to cases in which the infected bone cannot be resected or clean margins cannot be obtained. In many cases of diabetic foot infection, the entire bone, or region of the bone, and the surrounding soft tissue can be removed. When this is the case, an early transition to oral antibiotics can often be made. Surgical site infections represent another area of concern in diabetic patients. Higher rates of surgical site infection have been reported in patients with diabetes undergoing foot and ankle surgery when compared with patients without diabetes.400 Peripheral neuropathy, Charcot arthropathy, smoking, and length of surgery were all found to be risk factors for surgical-site infection. Wukich et al399 identified a 10-fold increase in risk of postoperative infection in patients with complicated diabetes (neuropathy, peripheral vascular disease, previous foot ulcer, or Charcot neuropathy) compared with patients without diabetes. Patients with uncomplicated 1403

Part VII ■ Diabetes

Box 27-1 Patient Instructions for Diabetic Foot Care Understand the Problem ■ Understand that the loss or absence of normal, protective sensation is the cause of most diabetic foot problems. What you cannot feel may hurt you. ■ Remember that vigilance is the best way to prevent foot problems. Inspecting Your Feet ■ Inspect your feet daily. ■ Use a mirror or have a companion inspect your feel for you if you are unable to see each part of your foot because of poor vision or poor flexibility. ■ Look carefully all over each foot for cracks, blisters, bruises, reddened spots, cuts, and ulcers. Make sure the skin between your toes is not excessively moist. Washing Your Feet ■ Bathe your feet daily with warm water and mild soap. ■ Always test the temperature of the water with either your arm or your hand, as long as it is not also affected by neuropathy, or have someone else test the water. Remember that you may burn your foot and not even feel it. ■ Dry gently and carefully between the toes. Blot, do not rub. ■ Do not soak your feet unless you have been specifically instructed to do so by your physician. Beware of Burns ■ If your feet are cold at night, wear socks to bed. ■ Never use heating pads, hot water bottles, or any other heat sources to warm your feet. Irreparable damage can be done in a minute. ■ Never walk on hot surfaces, such as sandy beaches or on the cement around swimming pools without shoes because this can also cause damage to your skin. Skin Care ■ Apply a very thin coat of lubricating oil or cream, such as petroleum jelly or specialty diabetic moisturizers, after bathing in order to keep your skin moist. Consult your physician for the type of lubricant you should use. ■ Do not apply creams, lotions, or ointments between the toes. ■ Do not use adhesive tape directly on the feet, as this can cause tears to your skin, which can lead to infection. ■ Avoid lotions or creams that list alcohol as one of the first three ingredients. Nail Care ■ Trim nails straight across. Do not attempt to dig out the corners of the nails. ■ Filing the nails daily reduces the frequency of clipping, but avoid rubbing dry skin. ■ Have a family member help with nail care if you have poor eyesight. ■ Consult your physician if the nails are too thickened or are hard to trim. Calluses and Corns ■ Use a pumice stone or foot file to reduce calluses gently at bath time, while your foot is damp. Have a family member assist you if you are vision impaired. ■ Do not use chemical agents or strong antiseptic solutions to remove corns or calluses because these can cause burns. Do not cut corns.

1404

■

Some corns and calluses can only be removed professionally, especially if you have severely impaired circulation.

Stockings and Socks ■ It is important that you always wear properly fitting stockings or socks. ■ Padded socks help to reduce pressure on the foot. ■ Look for socks that are made of an acrylic/cotton blend. This material will reduce friction on the skin. ■ Do not wear mended stockings. ■ Avoid stockings and socks with elastic tops or garters and avoid those with seams. ■ Wash and change your socks or stockings daily. Wearing Shoes ■ Never walk barefoot, even around the house. ■ Do not wear shoes without socks. ■ Inspect the inside of your shoes daily for foreign objects, nail points, torn lining and rough areas. ■ Changing shoes during the day can reduce the risk of pressure problems. ■ Do not use hard devices or rigid orthotics in your shoes because these can produce excessive pressures on the foot. ■ Take special precautions during the winter time. Wear wool socks and protective foot gear, such as fleecelined boots. Choosing Shoes ■ Remember that fashion is an enemy of the diabetic person with neuropathy. Many serious foot problems results from shoe pressure. ■ Do not wear sandals with thongs between the toes. ■ Inform your shoe salesman that you are diabetic. ■ Shoes sizes vary by brand and style, and feet change in width and shape with age. Shop for shoes that are properly fitted; keep in mind that they may not be the same size every time. ■ Make sure shoes are long enough and wide enough and have enough room for the toes, especially if the toes are clawed. ■ Purchase shoes in the afternoon when feet tend to be the largest. Shoes should be comfortable at the time of purchase. Do not depend on the shoe to stretch. ■ Shoes should be made of leather or fabric. Avoid hard or synthetic materials that do not stretch or breathe, such as plastic or patent leather. ■ Inspect the feet frequently when wearing new shoes. Wear new shoes no more than 1 hour the first day. ■ Consult a pedorthist or other professional to have your shoes properly fitted if you have neuropathy, significant foot deformity, or if you have had serious foot problems in the past. Your Responsibility ■ Do not smoke. Smoking will decrease the amount of blood that gets to your feet. ■ It is important that you see your physician regularly, and be sure that your feet and the areas between the toes are examined at each visit. ■ Inform your foot and ankle specialist that you are diabetic. ■ Notify your foot and ankle specialist at once should you develop a blister or sore on your foot.

Diabetes ■ Chapter 27

diabetes were not found to have a significant increase in their risk. DIAGNOSIS

Physical Examination Orthopaedic physical examination of the diabetic patient should include an evaluation at least up to the level of the knee. Both lower extremities should always be examined together. Disease on the less severely affected limb is often overlooked simply from a failure to check both. The examiner initially observes the patient’s gait and notes any abnormalities at the proximal limb and pelvic levels. The shoes should be inspected to observe patterns of wear and to look and feel for foreign objects such as protruding staples or nails. The examiner should record the palpable examination of the pulses and the warmth and hair growth of the skin and should examine between the toes. Clinically significant skin and nail abnormalities should be noted, including erythema, edema, breaks in the skin, and nail deformities. Ulcerations should be measured accurately for size and depth. Tracing the margins of the ulcer on a clear piece of acetate and copied onto the chart is a technique that allows easy comparison of ulcer size from one clinic visit to the next (Fig. 27-23A and B). Digital

B Figure 27-23 A, Clear (unexposed and developed) x-ray film and indelible felt marker used to trace patient’s ulcer for recording on chart. B, Example of visual record created on chart to document progressive shrinking (healing) of ulcer.

photography is now frequently used to document ulcer size and progression of healing in electronic medical records. The process begins with visual inspection of the wound, particularly looking for exposed deep structures (e.g., tendon, joint) that would signify a grade 2 lesion. Next, gently probing the wound with a blunt, sterile instrument reveals whether the wound communicates to the deeper structures, especially to the underlying bone. If bone can be probed through the ulcer, there is a high probability of osteomyelitis, making it a grade 3 lesion.170,242 Bony prominences and structural deformities, such as claw toes, bunions, hindfoot varus, collapse of the longitudinal arch, and gross changes in the foot’s shape, such as occurs with neuropathic arthropathy, are important to note. Restriction of range of motion may be important information relative to present or future ulceration. A patient with a hot, red, swollen foot may be difficult to diagnose clinically; this may represent cellulitis, an abscess, or an acute and acutely inflamed neuropathic arthropathy. The swelling will not quickly recede, but a simple test can help to distinguish clinically between the erythema of cellulitis and the dependent rubor of a Charcot joint before resorting to a battery of tests. The dependent rubor of an inflamed Charcot joint recedes after a few minutes of elevation of the foot higher than the level of the heart, with the patient in the supine position, whereas the erythema of cellulitis does not. This is particularly helpful with an early neuropathic arthropathy that has produced minimal or no discernible changes on plain radiographs. The clinical signs of Charcot or neuropathic arthropathy depend on whether it is acute or subacute. The acute Charcot joint can mimic other causes of acute inflammation. The foot or ankle (or both) is always swollen, with varying degrees of increased warmth and erythema. The differential diagnosis for the acutely swollen, hot, red foot in a diabetic patient includes cellulitis, abscess formation, or an early Charcot joint before the appearance of radiographic changes. The signs of a subacute or chronic Charcot joint are proportionately less than those of acute inflammation and proportionately more than those of deformity, with varying severity of radiographic changes. The definitive sign of the Charcot joint is architectural disruption of the structure of the foot, whether in a single joint surface or across half the foot. When the midfoot is involved, the foot is usually widened, with bony prominences on the plantar surface or medial and lateral borders of the foot. In some cases, the longitudinal arch collapses or even reverses to produce the classic rocker-bottom foot (Fig. 27-24A and B). As the longitudinal arch collapses, the dynamic effect of the Achilles tendon is altered by loss of the normal calcaneal pitch, that is, its relative plantar flexion compared with normal (Fig. 27-25). The bony protuberances are clinically important because they can cause neuropathic ulceration, either on the plantar surface 1405

Part VII ■ Diabetes

B Figure 27-24 Rocker-bottom foot. A, Clinical appearance. B, Lateral radiograph.

Achilles

Normal

Calcaneal pitch

Achilles

Loss of calcaneal pitch Figure 27-25 Normal calcaneal pitch (angle relative to the floor) (top) is lost in patients with a Charcot collapse of the arch (bottom). This leads to a mechanical disadvantage for the Achilles tendon.

from the pressure of walking and standing or on the medial or lateral border of the foot from the pressure of footwear. The change in the shape of the foot makes shoe fitting difficult. Severe proximal deformities can result, such as deviation of the foot on the leg into severe, 1406

uncorrectable varus or valgus. The extreme pressure on the malleoli, heel, or hindfoot can lead to ulceration, infection, osteomyelitis, and eventual amputation. The symptoms of the Charcot joint are also affected by its acute or chronic nature. The classic Charcot joint, resulting from tabes dorsalis, was well known by the epithet of “painless swelling.” However, about half the patients present with a chief complaint of pain,71 although the pain is not commensurate with the severe destruction seen in the limb. Most patients with Charcot arthropathy are ambulatory when they first present; they often exhibit a severity of bone and joint destruction that would render a person with a sensate limb incapacitated and immobile. The symptoms may be related to the patient’s suddenly or gradually noticing a change in the shape of a foot or a difficulty with shoes no longer fitting. Most often and more than any other symptom, patients note tenacious swelling made worse by weight bearing but usually never resolving entirely. Patients with severe bone destruction and instability seldom complain of “giving way” or other symptoms that relate to the loss of structural integrity of the ankle or hindfoot, the areas where this is most likely to occur (see the section on classification). The reason for this presumably is the loss of a normal proprioceptive sense. Neurologic Evaluation The effects of sensory, motor, and autonomic neuropathy, including toe deformities and dry, flaking, cracked skin, should be investigated. It is reasonable to begin testing with pinprick, light touch, and position sense examinations. However, more reproducible methods are the objective threshold tests of neurologic function that can be done with a range of techniques that continue to be developed. These include Semmes-Weinstein and other types of monofilaments (Fig. 27-26A and B), temperature testing, or vibratory methods, electric stimulators, and motor nerve conduction velocity studies.54,86,159,296,309 Vibratory perception thresholds using electrical devices have been shown to be characteristic of diabetic neuropathy and associated with diabetic foot ulceration.54 The biothesiometer and the modification called the neuro thesiometer are the devices used for measuring vibration perception threshold (VPT).403 Vibratory testing has been incorporated into the development of neuropathy scores used to assess patients clinically. The Michigan Diabetic Peripheral Neuropathy Score (DPNS) has three components: sensory, motor, and reflexes. The sensory impairment is assessed by using vibration perception with a tuning fork, together with pressure testing using a 10-g Semmes-Weinstein monofilament. Motor testing includes finger-spread extension of the great toe and ankle dorsiflexion. Reflex testing includes the biceps, triceps, quadriceps, and Achilles reflexes. These tests of VPT and the Michigan DPN scores have been shown to be clinical predictors for foot ulceration.2,402

Diabetes ■ Chapter 27

Figure 27-27 Semmes-Weinstein 5.07 monofilament testing.

B Figure 27-26 A, Set of graduated filaments is seen from the side. B, Semmes-Weinstein monofilaments for sensory threshold testing.

A comparison of these different threshold methods has demonstrated approximately comparable sensitivity in identifying patients with advanced peripheral neuropathy that might lead to ulceration. However, the use of Semmes-Weinstein monofilaments is most commonly used is and shown to be reasonably specific.365 Currently, the monofilaments are the least expensive and most widely used method in an everyday clinic situation.44 They are placed on the skin as perpendicular as possible to the surface, and pressure is applied until the filament begins to buckle slightly (Fig. 27-27). With eyes closed, the patient is asked to signal when she or he feels the stimulus. There are limitations to the use of monofilaments. They can be affected by temperature, the amount of pressure applied can vary by large factors if the filament is applied obliquely to the skin, and the application of the filament to a callus or thickened rind around an ulcer can interfere with perception. One study detailed the characteristics of the monofilaments, showing differences depending upon manufacturer and number of cycles of repetitive use.51 At this time, however, they are the most economical, most easily used, most widely accepted, and generally most reproducible method for threshold neurologic testing of the insensitive foot. Research on use of the monofilaments continues, but investigators have attempted to determine an absolute value of sensibility that represents the presence or absence of protective sensation in the neuropathic foot. A number of sources have suggested that this is equivalent to the

ability to feel the 5.07 monofilament, which is equivalent to application of a 10-g force. This threshold is most commonly referred to as a 10-g threshold. Although the 5.07 Semmes-Weinstein monofilament is widely held as the standard for adequate sensation to prevent ulceration, some of this is based on extrapolated data.46 One study showed that a simplified monofilament test using a 4.5-g monofilament indicates protective sensation in diabetic patients.333 Moreover, the monofilaments are still only an approximation, and some researchers note that about 10% of patients who have sensation at the 5.07 level still develop neuropathic changes, such as ulceration or a Charcot joint. Vascular Evaluation The purpose of vascular evaluation is to determine whether adequate local circulation is present to support primary healing either with or without surgical intervention.346 Patients without palpable pulses and with nonhealing wounds or ulcers, or preoperative patients with diminished pulses, usually require vascular screening. A number of available techniques have demonstrated effectiveness, including venous and arterial Doppler studies and transcutaneous oxygen measurement.30,314 Cutaneous warming, which is used often in obtaining the measurements of transcutaneous oxygen, has been reported to produce a paradoxic fall in transcutaneous partial pressure of oxygen (PO2).359 The most commonly used method is arterial Doppler ultrasound pressure measurements, despite limitations of this study to detect peripheral arterial disease. The technique is simple, reproducible, and not highly operator dependent. Although previously published guidelines by Wagner384,385 and others200,279,385 have used the Doppler pressures as criteria for wound and amputation healing, Doppler measurements are best considered as estimations and screening tests rather than absolute criteria for 1407

Part VII ■ Diabetes

Segmental pressure and Doppler study Right

Brachial

Left

180

183

Dop 8 MHz Right common femoral Gain: 96 Hz/mm Speed: 25

Dop 8 MHz Left common femoral Gain: 96 Hz/mm Speed: 25

Dop 8 MHz Right popliteal Gain: 48 Hz/mm Speed: 25

Dop 8 MHz Left popliteal Gain: 48 Hz/mm Speed: 25 1.20 220

202 1.10

1.14 209

158 0.86

Dop 8 MHz Right posterior tibial Gain: 24 Hz/mm Speed: 25

Dop 8 MHz Left posterior tibial Gain: 24 Hz/mm Speed: 25 0.49 90 1.20 0.49

63 ABI TBI

Dop 8 MHz Right dorsalis pedis Gain: 64 Hz/mm Speed: 25

0.34 1.10 0.34

Dop 8 MHz Left dorsalis pedis Gain: 48 Hz/mm Speed: 25

Figure 27-28 Doppler arterial study: pulse-volume tracings. These demonstrate pulsatile flow and the triphasic flow pattern in the femoral arteries and the right dorsalis pedis in addition to the numeric values. ABI, ankle-brachial index; DP, dorsalis pedis; PT, posterior tibial; TBI, toe brachial index.

healing. The Doppler data are expressed as the absolute pressures (in millimeters of mercury) as detected by an ultrasonic probe rather than aurally with a stethoscope. Many publications have advocated the use of the ratio of ankle or foot pressure to arm Doppler arterial pressure, where both are measured by using a pneumatic blood pressure cuff of appropriate size and readings are taken with the Doppler probe. Wagner’s original work cited a ratio of 0.45 or greater as necessary to heal diabetic foot lesions and a ratio of 0.35 to heal lesions in the nondiabetic patient with peripheral vascular disease. However, these are only rough guidelines to relative perfusion of the foot and are not absolute measures of healing potential, especially because healing is a multifactorial phenomenon. When ordering an arterial Doppler study, the physician should specify bilateral studies that include measurement of toe pressures. Copies of the waveforms or pulse-volume 1408

tracings provided in the report, together with the numeric pressure values (Fig. 27-28), are a useful adjunct. Doppler arterial readings are subject to a number of potential distortions, most commonly underestimation of the extent of vascular disease resulting from calcification of vessels.7 This calcification, produces stiffening and loss of compliance of the arterial wall. Falsely elevated pressures are observed because of the increased cuff pressure required to produce vessel occlusion in the process of taking the measurement. The Doppler pressures are intended to assess blood flow but do so indirectly by the assumption that greater pressure must be exerted to compress a vessel with greater flow. This assumption becomes inaccurate as the artery becomes more and more calcified. Pressures are often obtained in the foot and ankle that are paradoxically greater than brachial artery pressures, thus producing a ratio greater than 1.0. Ratios greater than 1.0 are an indication of vessel calcification and

Diabetes ■ Chapter 27

should serve as a warning to the surgeon that the pressures obtained are falsely elevated. It is equally important to realize that even pressures less than the arm pressure can still represent falsely elevated values because of calcification. In this situation, it is valuable to refer to the pulsevolume tracings to assess whether or not pulsatile flow exists in the foot and its quality. When the ratios and pressures are distorted by calcified vessels, at the very least, the tracings reveal the presence or absence of pulsatile flow, without which healing is unlikely to occur. Absolute toe pressures have recently been shown to be a more reliable predictor of healing than the more familiar ankle-to-arm ratios. Using ulcer healing rather than amputation healing as the criterion, Apelqvist et al12 found that 85% of patients with toe pressures greater than 45 mm Hg achieved healing, whereas none healed with an ankle pressure less than 40 mm Hg. Lower healing rates were seen in patients with incompressible arteries. Patients who complain of painful ulcers could have severe distal ischemia. The pain of neuropathy should be excluded, but it is vital to remember that neurotrophic ulcers occur as a result of a lack of sensation; they are not painful. Another source of the pain must be identified, and most often it is peripheral vascular insufficiency. Similar admonitions should be made regarding the clinical situation of the diabetic patient with neuropathy who complains of an excruciatingly painful ingrown great toenail. Most often the patient is experiencing rest ischemia, felt most severely at the most distal point in the extremity. The unsuspecting practitioner who trims the nail without first considering vascular evaluation may find that a below-knee amputation is required to complete the job. Vascular evaluation and when necessary, revascularization, should be considered before any procedure, even a “minor” one, to prevent a calamitous outcome. Once it is determined that the patient has significant vascular impairment of the limb, consultation with a vascular surgeon is appropriate. Every diabetic foot with serious ischemia needs a vascular evaluation.97 The consultant usually proceeds with an arteriogram to determine the full extent of vascular occlusion, its levels, and the possible remedies. At some centers, the invasive radiologist or vascular surgeon can perform percutaneous procedures to improve flow, such as percutaneous transluminal (balloon) angioplasty (PTA) of selected discrete lesions if there is adequate runoff distally. The key to the use of PTA is that is best for short and isolated stenotic arterial lesions. It has been more successful in aortoiliac lesion than in infrainguinal lesions.137,161 Radiographic Examination Plain Radiographs Although radiographs are the mainstay of diagnosis of osseous disorders of the diabetic foot, they are limited in sensitivity, accuracy, and the range of disorders that they

can detect. The radiograph is the first diagnostic test that is done, and the characteristic findings on plain films are worth summarizing and knowing.95 When patients present with foot or ankle pain or complaints of deformity without a concern for infection or Charcot arthropathy, radiographs frequently provide adequate information when combined with clinical examination to diagnose and treat foot or ankle pathology. When evaluating infection in the diabetic foot, plain radiographs are useful when evaluating bone directly adjacent to a known ulcer. On occasion, a foreign body in the foot will be identified on radiographs as a cause of severe infection in the foot. However, radiographs have limited sensitivity and specificity when compared with other forms of imaging when evaluating for osteomyelitis and other deep infections.335 When clinical examination combined with radiographic findings raises a concern for osteomyelitis or abscess, further imaging studies are considered. Osteolysis in the bones of a diabetic patient, especially in the distal segments, such as the phalanges, can be mistaken for osteomyelitis, even in the absence of clinical signs and symptoms of infection. The problem is further complicated by the observation that diabetic patients often fail to mount a systemic response, such as fever or elevated white blood count, to isolate infection in the distal foot. The characteristic penciling of a distal metatarsal or a vanishing phalanx is usually not associated with infection, although it is sometimes necessary to evaluate for associated infection, especially if there is an underlying ulcer. When osteolysis is neuropathic in origin in the absence of infection,408 it occurs most often in the distal part of the forefoot, usually distal to the midmetatarsal level and involving the distal metatarsals and the phalanges. The mechanism is not clearly understood but is probably related to a neurally mediated hyperemia that resorbs the bone and is caused by a loss of sympathetic nervous functional control over vasoconstriction.77 Swelling on clinical examination without skin breakdown or ulceration can lead to a diagnostic dilemma. In this case, the differentiation of infection and Charcot arthropathy is the primary goal of radiographic studies. The cardinal features of Charcot arthropathy are fractures, dislocations, bone destruction, multiple fragmentation, and an architectural disruption of one or multiple joints of the foot. The affected joint(s) may be partially or completely destroyed, not only through a loss of the articular surface and configuration, but also because of a shift of the whole relationship of the bone to other surrounding bone structures. However, one of the cardinal features of neuropathic fractures and dislocations (Charcot or neuropathic arthropathy) is the relative absence of surrounding and adjacent osteopenia when compared with an infectious process producing the same amount of bone destruction.322 Subsequent healing is demonstrated by new bone formation, both periosteal and enchondral, and often extensive bony consolidation across several tarsal or metatarsal bones. This usually produces a stable 1409

Part VII ■ Diabetes

Figure 27-29 Type 1 midfoot Charcot foot. A, Lateral radiograph. B, Anteroposterior radiograph.

foot of different shape and wider proportions than before the neuroarthropathic process began. The radiographic appearance of the Charcot joint is usually distinct and easy to recognize once it has progressed to the point of significant architectural disruption of the foot. There are combinations of fractures and dislocations; separations of the bones; new bony projections on the plantar, medial, or lateral aspects of the foot; bone compressions or disintegrations; fluffy new bone formation; and gross alterations in the skeletal anatomy. In the early stages of the Charcot joint, however, the changes may be difficult to find or are at least subtle. Some Charcot joints exhibit negative radiographic findings initially, even though clinically the process of inflammation and swelling has begun. Changes may be subtle, such as a diastasis between the bases of the metatarsals that subsequently progresses to further collapse (Fig. 27-29A and B). Magnetic Resonance Imaging MRI has been a major advance in the treatment of the diabetic foot. MRI reveals abnormalities of bone and soft tissue equally well. However, the differentiation of osteomyelitis from the marrow changes of Charcot joints is difficult.115 MRI changes are based on changes in proton activity, that is, the presence or absence of water in the tissues. Most changes in the bone on MRI are based on changes in the character of the marrow from a fat-type signal to a water-type signal because of the increased edema within the marrow. This edema is not specific and can occur from injury, infection, or neuroarthropathy alike. Although found to be highly sensitive and specific in the detection of these changes, the differentiation on MRI of osteomyelitis and neuroarthropathy in the early stages remains a challenge.222 1410

Several authors have described a distinction between neuropathic arthropathy and osteomyelitis on MRI,39,255,375 These claims must be examined carefully because there are major differences between acute and chronic Charcot changes and their appearance on MRI and radiographs. Most chronic changes can be diagnosed by simple radiographs, whereas the acute marrow changes of a Charcot joint are not pathognomonic on MRI and are easily confused with those of acute infection. In general, the diagnosis of osteomyelitis on MRI is most effective when bone marrow changes are seen in conjunction with soft tissue findings such as ulcer, abscess or a sinus tract.258,375 Preoperative imaging is especially relevant to the diagnosis of a suspected abscess. Although MRI is certainly not required for every abscess or every infected diabetic foot, its sensitivity in visualizing an abscess and changes of deep infection among the soft tissues is often valuable. Early imaging in the hospitalized patient is cost-effective by leading more quickly to the proper diagnosis.281 These images should assist the surgeon in planning drainage, including the closest location to the surface and the orientation and extent of the surgical exposure. Computed Tomography Computed tomography (CT) has been a valuable test for anatomic localization of infection and disease, such as an abscess in the deep structures of the foot. Before the advent of MRI, CT was the best technique for obtaining information on the nonosseous disease of the foot and especially of the deep structures. CT is superior to MRI in definition of details of bone anatomy, especially imaging of cortical bone. The weakness of the CT scan is the poor differentiation or wide transition zone between normal and infected tissues.339 It has since been surpassed by MRI, which is superior in its ability to differentiate a

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Figure 27-30 Infected Charcot foot: ulceration and abscess. A, Plantar view. B, Medial view. C, Dorsal view. D, Lateral radiograph. Amputation was elected for rapid healing and rehabilitation.

wider range of different tissues in their normal and abnormal states. However, CT remains a valuable test in the evaluation of bone or structural changes occurring in the setting of neuropathy arthropathy. Bone Scans and Labeled White Blood Cell Scans Technetium-99m (99mTc) bone scans and MRI are much more sensitive than plain radiographs in detecting early bone changes of osteomyelitis and Charcot neuroarthropathy.141 However, MRI is significantly more sensitive and detects osteomyelitis earlier than the bone scan. The bone scan is still considerably less costly than an MRI study in most institutions and thus still may have a place in early detection. Bone scan activity can persist for a year or longer after a fracture or other osseous change, and the pattern of positive uptake is entirely nonspecific. Negative bone scan results strongly exclude bone disease such as osteomyelitis, but a positive study is highly nonspecific.405 The clinical effectiveness of the three-phase bone scan has been shown to be low and therefore unlikely to influence decision making about treatment of the diabetic foot.209 The bone scan, the plain radiograph, or any other single study, does not represent the sine qua non in diagnosing infection or arthropathy in the diabetic foot and must be combined with clinical examination, history, and other diagnostic modalities. Surgical follow-up studies have demonstrated the inaccuracy (both poor specificity and poor sensitivity) of single studies in making the diagnosis of osteomyelitis.349 Gallium scans are too nonspecific to be helpful in making the distinction between a Charcot joint and osteomyelitis and are usually not helpful in the diagnosis of a diabetic foot. By contrast, indium-labeled white blood cells (WBCs) may be quite useful based on the greater specificity of this study for infection. A direct comparison of combined and simultaneous indium-111 (104In) and 99mTc imaging can aid in detecting the rare but

troublesome clinical problem of diagnosing a Charcot joint that might also have osteomyelitis (Fig. 27-30A to D).118,217,227,270,366 This is particularly problematic because a labeled WBC scan is the only imaging technique in which the characteristic changes of the two conditions do not almost entirely overlap. The distinction of osteomyelitis is particularly difficult to make when an ulcer, and especially an infected ulcer, overlies a Charcot deformity. The radiographic changes may be indistinguishable. In this specific but uncommon situation, some authors have advocated the use of simultaneous scanning with 99mTc and 104In. The key to this technique, according to the authors who report it, is to do both images at the same time and compare the spatial presentation of the positive areas on the two studies. If the location and size of the positive area on both scans are the same, the infection resides in the bone. If one presumes that the Charcot process is active, the positive area on the scans represents infection in the Charcot joint. If the area of uptake in the 104In scan is in the soft tissue or superficial to the area of uptake on the 99mTc bone scan, osteomyelitis is most likely not present. In theory, this technique offers the answer for detecting osteomyelitis in the patient with an ulcer overlying a Charcot joint. However, many centers have noted the difficulty in using this method successfully. Several problems exist. The most formidable is that 104In scans produce much lower radiation counts than 99mTc scans. This results in images with poor spatial resolution that are therefore difficult to interpret, especially with the combined technique just noted. Another problem is that the positive uptake on indium-labeled WBCs may be falsely positive. This can occur when the normally fatty bone marrow is activated to a hemopoietic state, and thus the presence of WBCs does not indicate the presence of infection. Simultaneous scanning with sulfur colloid can determine the 1411

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presence of activated marrow, but this then is a third agent that must be coordinated with the 99mTc and the 104 In, and cost and logistics make this largely unfeasible. Some studies have shown that nuclear scintigraphy with 104In-labeled leukocytes may be used to determine the presence of osteomyelitis in all lesions of the diabetic foot, including ulcers and Charcot joints.227,239,341,343,366 Some authors have suggested that 104In oxyquinoline scanning might even be accurate enough to be a substitute for bone biopsy.292 Previous studies have shown high sensitivity and specificity of the 104In scan.179 However, a more recent metaanalysis suggests that MRI provides nearly comparable specificity with a high level of sensitivity.133 Perhaps the greatest limitation of the 104In scan is the time and cost associated with the test. Given the relative ease of obtaining an MRI in most medical centers, the 104In scan is most useful when a true diagnostic dilemma exists. [18F]-2-Fluoro-2-Deoxy-D-Glucose–Positron Emission Tomography More recent attention has been given to FDG ([18F]-2-fluoro-2-deoxy-D-glucose)-PET (positron emission tomography) to detect osteomyelitis in the diabetic foot.289 FDG is an indicator of increased intracellular glucose metabolism. This study is associated with high sensitivity and specificity in the detection of osteomyelitis in the diabetic foot.289,335 Currently, FDG-PET studies are considered useful when MRI is contraindicated. TREATMENT APPROACHES

Patient Education It is common wisdom that education of the diabetic patient is essential. As discussed in the section on pathophysiology, neuropathy deprives the patient of the sensory input to connect them intellectually and emotionally to many of the lesions, even limb-threatening ones, of the diabetic foot. Teaching the patients and making the family aware as well of prophylactic measures seems to be indispensable in reducing the risks associated with poor outcomes. Interestingly enough, and perhaps not a surprise, studies have shown a variance in the compliance rate of patients with prescribed therapeutic shoes and other care regimens. There is certainly speculation and much suspicion that many neuropathic patients are indeed noncompliant with treatment regimens. One study in the United Kingdom showed that the patients did not wear therapeutic footwear as prescribed.230 Similar observations of noncompliance were reported in an American study.257 Studies of the use of therapeutic boots and activity have shown that patients failed to wear therapeutic boots in the home.23 Unfortunately, at least one study showed that increased knowledge did not necessarily translate into better metabolic control in the diabetic population.47 It is a 1412

legitimate question whether this applies to extremity care as well. Clearly, patient education is not just about intellectual knowledge but also about understanding the psychosocial characteristics of behavior and belief to fully influence optimal care in this and other disease states. Currently, education has been shown to decrease the incidence of foot ulceration in the short term but has not affected the overall rate of ulceration and amputation.134 Team Approach Diabetes is a multisystem disease crossing the boundaries of orthopaedic surgery, vascular surgery, endocrinology, neurology, infectious diseases, physical medicine and rehabilitation, orthotics and prosthetics, and other fields. It is difficult for any single practitioner in any one field to feel capable of managing the problem alone. Diabetes is aptly likened to the proverbial blind man feeling the different parts of the elephant. Because no cure yet exists for diabetic neuropathy or for the disease itself, treatment efforts must be directed to managing, retarding, and, it is hoped, preventing the complications of diabetes. It is an often-repeated but incontrovertible principle that the care of the diabetic foot is like no other area of orthopaedic care of the foot and ankle. The diabetic patient has many needs because the effects of the diabetes are multisystemic and thus require the expertise of many different medical specialists and subspecialists as well as those of many allied health professionals.84 The basic pathophysiologic problems of the disease often occur at the same time; to list the various members of the team of health care professionals who provide some aspect of the care of diabetic foot problems is risky because the number and range are so great. At the risk of an inadvertent omission, the team includes, at various times and according to need, orthopaedic surgeons, vascular surgeons, primary care physicians, endocrinologists, podiatrists, physical medicine and rehabilitation specialists, radiologists, neurologists, nephrologists, infectious disease specialists, nurses, physical and occupational therapists, orthotists, prosthetists, certified pedorthists, and professional shoe fitters. In the complex and sometimes frustrating task of caring for the problems of the diabetic foot, the talents and knowledge of multiple disciplines are required. Studies have documented the effectiveness of multispecialty clinics for the care of the diabetic foot.16,140 However, similar effectiveness can be achieved by use of the multiple disciplines, even when not all are physically housed in the same clinic location. The key is to consider the coordination of a team effort. Great strides will be made in the next few years in advancing the goals of improved treatment and prevention of problems of the diabetic foot. Few efforts in the field of surgery of the foot and ankle have a more tangible, beneficial effect on the life and quality of life of patients with serious systemic disease.

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Neuropathy It seems paradoxic, but the diabetic patient with diminished sensibility in the lower extremities can still experience severe pain, and both are manifestations of peripheral neuropathy. The painful neuropathy of diabetes is described variably as a burning, searing, tingling, or lancinating dysesthesia, often unrelenting or excruciating. It is often worse at night and is usually bilateral and symmetric. The treatment of this disorder most commonly falls to the neurologist, primary care physician or pain management specialist, but the orthopaedic surgeon needs to be aware of its etiology and its characteristic symptoms. The symptoms of peripheral neuropathy may be the first signs of diabetes mellitus in some patients and also are important to diagnose in patients with idiopathic peripheral neuropathy because once these diagnoses are made, treatment for their musculoskeletal problem is often altered. Treatment of painful peripheral neuropathy is usually with oral medications using classes of drugs with varying mechanisms of action. These include drugs that enhance dorsal horn inhibition such as the tricyclic antidepressants [imipramine (Tofranil), amitriptyline (Elavil), nortriptyline (Aventyl)], GABA-B agonists (Baclofen) and the anticonvulsants [gabapentin (Neurontin), pregabalin (Lyrica), phenytoin (Dilantin), carbamazepine (Tegretol),]. Other drugs work via serotonin-norepinephrine reuptake inhibition [duloxetine (Cymbalta) or by membrane stabilization such as with the local anesthetic antiarrythmic agents, [mexiletine (Mexitil)], anticonvulsants and corticosteroids,108,236,291,312 NCR#.7,53,68 All have been reported to have variable rates of success. The drugs usually must be monitored for side effects, especially drowsiness and loss of balance which could lead to increased falls in the elderly patient. The pain is often severe enough to prompt the use of opioid narcotic analgesics, which should be avoided if at all possible. However, tramadol, which is an opioid-like, centrally acting synthetic narcotic analgesic, has been confirmed to be efficacious in a randomized, controlled trial, and a follow-up study suggests that it can be used safely for up to 6 months of sustained pain relief.55,175,176 α-Lipoic acid, a free-radical scavenger antioxidant, has been shown to be efficacious in the management of painful neuropathies when administered parenterally. The results of a meta-analysis provide evidence that treatment with α-lipoic acid (600 mg/day IV) over 3 weeks is safe and significantly improves both positive neuropathic symptoms and neuropathic deficits to a clinically meaningful degree in diabetic patients with symptomatic polyneuropathy.407 A new area of research on diabetic neuropathy is examining the role of p38 mitogen-activated protein (MAP) kinase in transducing high glucose into deficits in nerve conduction velocity, which are characteristic of diabetic neuropathy. These studies suggest that increased polyol

pathway flux in diabetic animals leads to the activation of p38. This activation can mediate changes in gene transcription and cellular phenotype that are likely to underlie the observed nerve conduction velocity deficits. Agents such as insulin and aldose reductase inhibitors can prevent excess polyol pathway flux and could become helpful therapeutic agents to prevent peripheral neuropathy in patients with diabetes by preventing p38 MAP kinase activation (Figs. 27-31 and 27-32).313,371 In neuropathic pain, the empiric approach to treatment and the common use of off-label treatments attest to the clinical need for a wide range of drug choices. In general, the tricyclics and anticonvulsants are first-line drugs, and depending on side effects and efficacy, the other second-line drugs are added or substituted. The primary care physician or endocrinologist is often the most practical medical care provider to prescribe these drugs because of the potential for interactions with other drugs, side effects, and for overall coordination of care issues. In recalcitrant cases, referral to a neurologist or pain management specialist maybe indicated. Coping with painful peripheral neuropathy and compliance with treatment regimens may be enhanced with patient education about neuropathy. There are several books written by physicians or from the perspective of the neuropathy sufferer to help the peripheral neuropathy patient navigate the myriad of treatments available and to cope with the lifestyle changes associated with chronic pain.40,120,345 Topical Therapies Adjunctive topical treatments for painful diabetic peripheral neuropathy are helpful, especially in patients who have significant side effects from the systemic treatments. Delivering pain relief by this route often reduces treatment complexity and pill burden and may improve compliance with treatment.221 Atopical cream containing capsaicin, a nonprescription, naturally occurring alkaloid substance found in red peppers, depletes tissue of substance P and reduces chemically induced pain. Although several controlled studies combined in meta-analyses seem to provide some evidence of efficacy in diabetic neuropathic pain, it may be best reserved for those with localized discomfort rather than those with widespread generalized neuropathic pain.406 The lowest concentration should be used initially because the cream can cause a transient burning sensation and must be continued for at least several days to a week to judge effectiveness. Compounded drug delivery creams may also provide relief of neuropathic pain and are typically compounded with small concentrations (0.2%-6%) of various drugs, such as clonidine, gabapentin, imipramine, mefenamic acid, lidocaine, baclofen, and nifedipine. Antiinflammatory drugs can also be added. These creams can be compounded with multiple variations of these drugs and in different concentrations, but there is little data to guide the physician on which agents to use, and therefore a standard “co*cktail” of many of the drugs is the most common 1413

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Figure 27-31 A and B, 64-year-old female with diabetes mellitus and a Charcot midfoot with rocker-bottom left foot deformity with significant dorsal translation and apex plantar angulation at the naviculocuneiform joints (Brodsky type 1, Schon type II). C, Note the extent of the cuboid that protrudes below a line beneath the heel and fifth metatarsal head. D-F, Medial and lateral extensile incisions centered over the deformity. A gastrocnemius–soleus lengthening is performed at the beginning of the case to address the hindfoot equinus. G, An osteotomy is made across the malunion under fluoroscopic guidance, to resect a plantar-based wedge of bone to allow reduction of the deformity. H, Provisional fixation with pins is achieved. Note the large (temporary) pin placed transversely across the metatarsal bases to aid in the reduction maneuver. I and J, A plantarmedial plate has been applied. A dorsally placed allograft bone-block wedge has been inserted to realign the medial column of the foot. Note the anterior tendon insertion was removed to allow exposure and is “parked” along the superior aspect of the wound for later reattachment. K, A longitudinal 5.5-mm cannulated screw is placed up the metatarsal shaft to augment the fixation. L and M, Immediate postoperative radiographs with a combination of plantar-medial plating, intramedullary screws, and interfragmentary screw fixation.

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Figure 27-31, cont’d Radiographs (N and O) and clinical photograph (P), 5 years postoperatively, with a well-aligned, stable midfoot, which allowed ambulation in athletic shoes with an extended steel shank, rocker sole, and a custom total-contact insole. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

way they are prescribed, and the treatment remains quite empiric. Although the role of topical medications remains unclear, there is increasing evidence that supports the efficacy of these preparations in blocking nociceptive and neuropathic pain.221 Acupuncture5 and topical nitrates320 have also been shown to have clinical effectiveness. Some patients obtain an improvement in their symptoms during the daytime by modifying their footwear or changing shoes frequently. The use of cushioning and molded insoles in sufficiently deep shoes ameliorates, but does not eliminate, painful plantar sensations. Treatment of Motor Neuropathy Motor neuropathy exhibited by footdrop or peroneal weakness with lateral ankle instability may lead to frequent trips and falls or lateral ankle sprains. Footdrop must be investigated to determine its origin, which could include peripheral nerve injury to the peroneal nerve, motor mononeuropathy, a spinal lesion, or other central nervous system (CNS) abnormality. Treatment of a motor mononeuropathy that causes footdrop usually requires a polypropylene AFO to hold the foot in neutral dorsiflexion. Isolated lateral ankle instability from peroneal weakness may be treated with a shorter hinged or fixed ankle AFO to control coronal alignment. Usually, the patient will also exhibit sensory neuropathy; therefore the AFO should be custom-made to prevent ulcerations, with additional depth in the foot plate to accommodate a cushioning, molded foot orthosis. Surgical treatment of motor neuropathy is occasionally needed and possible only if adequate strength (minimum 4/5 power) remains in the muscle available for transfer. Tendon transfers are most commonly performed concomitantly with deformity correction procedures and may consist of a peroneus longus or posterior tibialis tendon transfer to the dorsum of the foot for loss of ankle dorsiflexion or anterior tibial tendon transfer to the dorsal-lateral midfoot for loss of peroneal strength. Achilles tendon lengthening is often needed to balance the muscle forces across the ankle and relieve an equinus

contracture. In many cases, the motor neuropathy is diffuse and no effective transfer is possible. In addition, because of the progressive nature of peripheral neuropathy, a tendon transfer may have limited long-term effectiveness and eventually require the use of an AFO. Nerve Release for Treatment of Sensory Polyneuropathy Surgical treatment of diabetic peripheral neuropathy has been advocated for relief of pain and return of sensibility in the distal extremities.127 The procedure is most commonly recommended for the lower extremity and involves neurolysis of three nerves at common sites of entrapment; the peroneal nerve at the fibular head, the superficial peroneal nerve in the distal lateral leg or dorsum of the foot, and the tibial nerve at the ankle. The rationale for the surgery is based on the increased susceptibility of the peripheral nerves to external compression because of the increased water content of the nerve as a result of glucose being metabolized into sorbitol and also the slowing of the axoplasmic flow within the nerve.127 These factors lead to external compression of the nerve which is exhibited by pain and paresthesias. Indications for this surgery include paresthesias in a dermatome (not diffuse) in a euglycemic patient, a positive Tinel sign over the nerve at the site of entrapment and failure of more traditional nonoperative treatment as outlined above.127 It has been suggested that earlier treatment, before severe axonal loss, yields better results, and several studies have reported good results with restoration of sensation in 80% of patients.127 However, despite these reports, the surgical treatment of peripheral neuropathy has not been adopted into the mainstream management for patients with diabetes mellitus. It is still unclear how many patients with diabetes require nerve release. Based on the literature on risk factors for nerve entrapment in the upper extremity, diabetes has a weak but significant (odds ratio 1.4) association with carpal tunnel release (Fig. 27-33).363 However, other factors, such as inflammatory arthritis, corticosteroid use, estrogen replacement, and 1415

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J Figure 27-32 Anteroposterior (AP) (A) and lateral (B) radiographs of a 54-year-old female with diabetes mellitus type 2, 2 weeks after sustaining a twisting injury to right foot with divergent type tarsometatarsal acute (stage 1) neuropathic arthropathy (Brodsky type 1, Schon type I). C, Intraoperative percutaneous/minimally invasive reduction technique. AP (A) and lateral (B) radiographs at 5 months postoperatively when Steinman pins are removed. Oblique (F), AP (G), and lateral (H) radiographs at years’ follow-up. I-J, Clinical photographs at 2 years’ follow-up. Patient is ambulating in in-depth shoes with a custom total-contact insole and is brace-free. (From Johnson JE, Thomson AB: Charcot neuropathy of the foot: surgical aspects. In Bowker JH, Pfeifer MA, editors. The diabetic foot, Philadelphia, 2007, Mosby, pp 473-475.)

hypothyroidism, all had risk factors higher than diabetes, further underscoring the question of how many individuals with diabetes have a clinically significant nerve entrapment of the lower extremity that would benefit from surgical release. Most of the pioneering work in this area 1416

has been by a single individual,127 and to fully adopt this surgical approach would lead to a large number of surgical procedures in a group of patients with often multiple medical comorbidities and a high risk of perioperative complications. A 2008 Cochrane review analyzed the role

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of decompressive surgery of lower extremity nerves for symmetric diabetic neuropathy. Although lack of randomization, blinding, and adequate baseline information on neuropathy or compression made the study suboptimal, the evidence reviewed suggests that the role of decompressive surgery for diabetic symmetric distal neuropathy is unproven (Figs. 27-34 and 27-35).103 In opinion of the chapter authors, there is currently insufficient data to advocate the universal screening of diabetic patients for neuropathy for purposes of multiple nerve release surgical treatment. However, this concept bears further study and is an important consideration for the neuropathic patient with pain and paresthesias who fails nonoperative treatment and has a positive Tinel sign.

Total-Contact Casting The total-contact cast is still the best and most widely used method for healing the most common type of plantar ulcerations (grade 1 ulcers). The method has proved to be efficacious and cost-effective in healing plantar ulcers caused by insensitivity. Many excellent studies have documented the efficacy of TCCs in the treatment of plantar diabetic ulcers.* Studies have demonstrated that even regular belowknee casts are effective in reducing plantar pressure, both *References 45, 46, 131, 187, 237, 279, 283, 288, 297, 310, 348, 353, 354, 385-387.

Figure 27-33 A, A 39-year-old male, 6 feet 7 inches, 370 pounds, body mass index 41.7 with type 1 diabetes mellitus and an 18-month history of a Charcot midfoot rocker-bottom foot deformity (Brodsky Type 1, Schon Type II) and plantar ulceration that has failed treatment in a Charcot restraint orthotic walker (CROW) boot with off-loading. In this case, there was no evidence of osteomyelitis, and operative treatment for correction of deformity was necessary to allow ulcer healing. Anteroposterior (B) and lateral (C) radiographs of the right foot demonstrating dorsal angulation and 100% dorsal translation of the first metatarsal relative to the first cuneiform. D, Medial midfoot exposure with a pin marking the line of the proposed osteotomy, beginning at the first cuneiform. A malleable retractor protects the dorsal neurovascular structures. Note the anterior tibial tendon insertion has been removed and “parked” at the superior end of the incision for later reattachment. E, A drill chuck is attached to a transverse pin across the metatarsal bases and is being used as a handle to aid in the reduction of the midfoot. F, Note how the forefoot was rotated out of varus, plantar flexed, and plantar translated through the osteotomy and provisionally pinned. Continued

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Figure 27-33, cont’d Lateral (G) and anteroposterior (H) intraoperative radiographs demonstrating reduction of deformity and provisional pin fixation. I and J, Intraoperative photographs after wound closure but before external fixator application. K-M, Intraoperative photographs after application of a fine-wire external fixator to augment the provisional pin fixation. The use of rigid internal fixation such as plates and screws in the setting of an open ulceration increases the risk of a deep postoperative infection.

in patients with normal feet and in those with a Charcot rocker-bottom deformity.267 Numerous studies have also investigated the mechanism by which TCCs effect pressure relief.195 Armstrong et al19 showed that areas of higher pressure required more time to heal, correlating with the role of internal bone pressure in the origin of diabetic ulcers. Two studies reported that forefoot ulcers healed faster than ulcers located more proximally on the foot, and ulcers under areas of fixed deformity took longer to heal.352,388 Higher peak plantar pressures and larger ulcers have also been associated with longer healing times.19 Pressures on the contralateral foot have been proved not to increase as a result of application of the TCC.181,247 A study by Shaw et al348 concluded that the mechanisms by which the TCC reduces forefoot pressure include transfer of approximately 30% of the weight-bearing load from the leg directly to the cast wall, increasing the load borne by the heel, and removing weight-bearing surface from the metatarsal heads by making a space with soft foam around the forefoot, inside the cast. In their model, heel pressure increased, which is consistent with clinical experience that has shown less reliable resolution of heel ulcers than forefoot ulcers in casts. Hartsell et al182 showed 1418

that a pneumatic walking brace and the TCC increased pressure under the heel while decreasing pressure under the forefoot. Other authors,388,391 however, have demonstrated the effectiveness of TCCs, even in reducing pressure in the heel region. Leibner et al249 used a different, direct measurement technique to study the mechanism of plantar unloading of the TCC. They found further evidence that the primary mechanism was not molding of the plantar surface but rather the transfer of forces to the leg, or shank, portion of the cast. Furthermore, this study revealed the unloading effect to be much greater during walking than during standing. The shape of the calf did not influence the proximal load transfer function of the calf. One plantar pressure study showed the changes in plantar pressure with changes in dorsiflexion angle of a prefabricated walking boot. Contrary to intuitive presumption, dorsiflexion at the ankle increased forefoot pressure and decreased heel pressure; conversely, plantar flexion at the ankle decreased forefoot pressure and increase heel pressure. Crenshaw et al117 speculated that the rocker sole of a walking brace functions differently than a TCC with a cast heel or cast shoe. Two studies have

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Figure 27-33, cont’d N, O: Anteroposterior (N) and lateral (O) radiographs demonstrate placement of the external fixation frame on the corrected foot deformity. P, Clinical photograph demonstrating significant reduction in plantar ulcer diameter, depth, and undermining at only 3 weeks postoperatively from correction of the midfoot deformity. Q, Five months postoperatively from midfoot osteotomy with stable midfoot. Note persistence of plantar midfoot periosteal bone formation that required later plantar exostectomy. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

revealed that the weight-bearing attachment on the plantar surface of the cast changes the pressure distribution within the cast.129,247,283 One of the confusing aspects about the TCC is that great variation exists in exact materials and technique, but all of the devices are called “TCCs.” A few studies have investigated the effects, or lack thereof, of variations in technique. Casts made with modern synthetic (fiberglass) materials have been shown to be as effective as casts made of plaster or a combination of plaster and synthetic materials.158,180 There are many published demonstrations and techniques of different methods for applying casts for neuropathic problems of the foot61,66,383 It appears that no one specific technique is more important than careful, consistent application. As with surgical procedures, familiarity and practice with a given technique seem to yield the best results. The mystique that has developed around the TCC is undeserved. The method is not unreasonably difficult, but it is necessary to have the proper material(s) (Fig.

27-36), and it is essential to pay proper attention to the details and principles of application (Fig. 27-37). The first important principle is that the cast must not be overpadded; this leads to shifting of the limb within the cast as the padding compresses in the course of use and can lead to new pressure lesions (see Fig. 27-37A-D). Second, the cast must limit toe motion. It can do this with a closed toe (see Fig. 27-37E-I) or, with the open-toe variety (Fig. 27-38), by careful molding in the dorsoplantar direction to inhibit hyperextension of the MTP joints. This helps to diminish the accentuated pressure of the metatarsal heads that occurs from the clawed (or hyperextended MTP joint) position and contributes to the persistence of the ulcer in that typical location. Third, the bony prominences and anticipated areas of high pressure should be padded with felt or foam to diminish the concentration of pressure. This includes the anterior subcutaneous crest of the tibia, the malleoli, the dorsum of the toes, the protuberance of a Charcot joint, 1419

Figure 27-34 A-C, A 70-year-old female with diabetes mellitus and a nonbraceable Charcot neuroarthropathy of ankle and hindfoot. Clinical photograph (A) and anteroposterior (B) and lateral (C) ankle radiographs demonstrate 100% lateral dislocation and 90 degrees of valgus angulation of the calcaneus in relationship to the tibia. The patient initially presented with a medial hindfoot ulcer that was healed by off-loading in a Charcot restraint orthotic walker (CROW) boot. D, Lateral non– weight-bearing radiograph of the ankle demonstrating destruction of the talar body with adequate calcaneal bone stock to consider a tibiocalcaneal (TC) fusion with a retrograde intramedullary nail. E, Anteroposterior ankle fluoroscopic image showing guidewire placement for location of flat saw cut to create stable arthrodesis surface to match against calcaneus. F, Lateral ankle fluoroscopic image showing provisional reduction of TC fusion. A flat contour is created with a microsagittal saw in the middle and posterior facet area to create a stable, flat surface for fusion with the distal tibia. Note how the anterior and posterior metaphyseal flares have also been trimmed to fit into the new “mortise” created in the calcaneus. G, Clinical photograph of completed TC fusion with closure of medial and lateral incisions. Note the medial translation of the foot relative to the tibia that is apparent because of the lack of a talar body and the need to place the calcaneus directly against the distal tibia. H, Final intraoperative lateral radiograph of the TC fusion construct. Note the plantigrade foot and the additional interfragmentary screw fixation from the talar head and neck into the anterior tibia and the calcaneal tuberosity into the posterior tibia. Lateral (I) and anteroposterior (J) ankle radiographs of the ankle at 18 months postoperatively from TC fusion. Note the healed spiral distal tibial shaft fracture that occurred around the intramedullary rod from a fall during a transfer from bed at 1 month postoperative while in a short-leg total-contact cast. K, Clinical photograph at 18 months postoperatively from TC fusion. The patient has weaned from the Gillette ankle–foot orthosis attached into an in-depth relasted shoe and is now a community ambulator. Note the sole extension and rocker sole added to the left shoe to compensate for the 3-cm leg-length discrepancy resulting from the loss of the height of the talar body. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

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and so on (see Fig. 27-37B, C, and F). Felt “donuts” or cutouts are helpful to additionally off-load high-pressure areas caused by a bony prominence or angular deformity (see Fig. 27-38B). Fourth, the foot and ankle should be positioned in a neutral plantigrade position (see Fig. 27-38) in the cast, if possible. The most common error of positioning is to allow the ankle to be casted in plantar flexion, which causes difficulty with gait, excessive recurvatum forces on the knee, increased tibial crest pressures leading to pretibial ulcers, and increased problems with toe ulcers. When the cast is completed, the patient should be able to stand in an upright position with the bottom of the cast flat against the floor and not feel the tendency to “back-knee” (see Fig. 27-38). If this occurs and is mild,

an additional amount of cast material can be placed under the heel to create a plantigrade cast. If the plantarflexion angle is greater than 5 degrees, the cast should be reapplied. Fifth, the first cast generally should be changed within 5 to 10 days because the cast functions to reduce edema, often dramatically. The first cast often becomes loose and allows the limb to shift and slide within the cast, potentially causing new abrasions, blisters, or ulcers. Subsequent casts can be at intervals of 2 to 4 weeks, or more often if treatment is for an associated ulcer that has significant drainage. If the cast is not promoting ulcer healing adequately, after checking the other principles, one can consider stiffening the plantar walking surface of the cast by incorporating a wooden platform into the outer layers

Figure 27-35 Anteroposterior (A) and lateral (B) radiographs and clinical photographs (C and D) of a 63-year-old female with nonbraceable Charcot neuropathic arthropathy of the ankle and hindfoot and a chronic medial ankle ulcer. This is the contralateral foot of the same patient illustrated in Figure 27-31. Note the severe valgus and lateral translation of the foot with dissolution of the entire talus, navicular and anterior calcaneus which precluded rigid internal fixation with an intramedullary nail. E and F, Postoperative clinical photographs after open reduction, preparation of bone surfaces of the tibia, calcaneus and remaining midfoot and pantalar fusion fixation with a hybrid external fixation frame with a combination of fine wires and half-pins. The foot plate allowed touch weight bearing for transfers and walker use during the 3 months the frame was applied. Continued

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Figure 27-35, cont’d Anteroposterior (G) and lateral (H) radiographs of pantalar fusion (minus the talus) in hybrid external fixation frame. Lateral (I) and anteroposterior (J) radiographs of pantalar fusion 6 years postoperatively. A stiff fibrous union has occurred at all the fusion surfaces, and the foot has remained well aligned beneath the tibia. K and L, Clinical photographs of both feet 2 years after pantalar fusion on the right and 5 months after midfoot arthrodesis on the left. There is no appreciable motion of the hindfoot joints. The patient has remained ulcer free without tibial stress fracture or additional Charcot neuroarthropathy over the past 6 years. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

Figure 27-36 Supplies for total-contact cast, including felt strips and pads, 14 -inch plywood shape, cast padding, self-adhesive foam, and synthetic casting tape.

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(see Fig. 27-37I). The space between the cast and the board is filled in with casting material. Healing time for diabetic foot lesions, including those treated within the TCC, varies and probably depends on many factors, including the severity and depth of the ulcer, its location, the systemic variables discussed earlier, patient compliance with the treatment regimen, and most likely other, unidentified factors. Some studies have measured the healing in absolute number of days and found wide variation among patients but not between different etiologies of peripheral neuropathy.45 As always, the overriding consideration is the relief of pressure. Despite the increasing number of studies searching for more convenient and less labor-intensive methods than the TCC, it still remains the gold standard. Studies have investigated the properties and the effectiveness of prefabricated walking boots for treating plantar neuropathic ulcers, and most have shown effectiveness of the

Diabetes ■ Chapter 27

Figure 27-37 Making the total-contact cast. A, Stockinette is applied and then cut to eliminate wrinkles. B and C, Vertical felt strips are placed down the medial and lateral sides of leg and malleoli, and cast padding is applied over them. D, Felt pad for plantar surface. Note radial cuts to aid contour around the heel. E and F, Self-adhesive foam is placed over the toes and then trimmed. G and H, Casting tape is applied over all layers: stockinette, felt, cast padding, and foam. I, Plantar plywood platform is incorporated into the cast. J, Cast shoe is applied. K, Side view of closed-toe total-contact cast. L, Method of prone application to reduce equinus and varus.

boots.38,152,246,311 Some studies show equivalency in effectiveness to heal ulcers or diminish plantar pressures, some show that the boot is superior, and some that the TCC is superior.25,311 These studies are all based on the concept of off-loading as the central tenet of healing plantar ulcerations in diabetic patients and have generally been performed using subjects without deformity. These studies have revealed that devices that simulate the function of the TCC provide additional treatment alternatives; however, the treating physician must take into account many other factors, including presence of significant

deformity or ulcer, compliance, and the availability of the patient to return for repeated castings. Researchers have speculated about and investigated which are the properties that best account for the success of the TCC. The most important mechanical property is the proximal transfer of a large portion of plantar weightbearing forces to the calf and leg. Another, less recognized, property is that the cast cannot be removed, thus ensuring full-time use. Conversion of a removable walker to a nonremovable device has been shown to be an effective method of healing plantar ulcers.26 The converted 1423

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Figure 27-38 A, During application of a total-contact cast (TCC), the ankle and foot are maintained in neutral throughout the application process to avoid and equinus position. B, Felt cutouts are applied before the cast padding, to help protect bony prominences on the sides of the foot or ankle or to off-load a plantar prominence. C, As the cast is drying, a flat surface is molded to the bottom of the cast, and the ankle is maintained in neutral. D and E, If the open toe box–style TCC is applied, care is taken to ensure the cast extends beyond the tips of all the toes and that the sides of the toe box do not encroach on the toes. F, When a TCC is applied properly, with the ankle and foot in a plantigrade position, the patient should be able to stand upright comfortably with their feet together without needing to bend the knee backward. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

walking boot has potential advantages in ease of application and cost.224 The psychosocial issues that affect treatment outcomes are not easy to assess, but they clearly play a role in treatment success and failure. Some authors have addressed this issue in evaluating compliance with use of special footwear.58 Recognition of this issue has been accounted for in design of at least two studies evaluating removable walking boots.23,224 Total-contact casts do have complications,131,188 and up to 30% of patients in one study developed an ulcer during their course of treatment.173 The most common complication was a superficial abrasion, blister, or new dorsal ulcerations from pressure of the cast or movement within the cast. The two most commonly affected areas were the dorsum of the toes and the anterior border of the tibia (shin). The patient needs to be warned at the time of application that this can occur. It is usually mild and only a temporary setback, if that. Sometimes casting can continue, with modifications, to achieve additional pressure relief over the area. Often, the patient must be advised to reduce the amount of walking, especially if it has been excessive. Anterior tibial lesions can be the result of an inadequate dorsiflexion position of the ankle in the cast. 1424

As the patient progresses from the foot flat to the toe-off stage of gait, the tibia is thrust against the cast. If the cast is applied with the patient supine, the patient is required to actively hold the ankle at neutral for the application. This is tiring, and the lack of proprioception or the weakness because of the motor component of the peripheral neuropathy can make this very difficult. One solution is to apply the cast with the patient in the prone position or with the patient in a seated position with the leg hanging over the edge of the examination table and the foot supported on a foot stand with the ankle in neutral. This reduces the work for the patient and converts gravity to a force working with rather than against ankle dorsiflexion. Despite the possibility of a complication, the majority of problems created by total-contact casting are minor, and the benefits of these methods of treatment far outweigh the disadvantages. With some cast-induced ulcerations or abrasions, the patient may be left out of the cast or placed in a removable walking brace (prefabricated type) that is open or adjustable over the lesion for a week or two until the new lesions heal, and then cast treatment can usually resume. The prefabricated walking braces, most of which are outfitted with hook-and-loop (Velcro) straps and a rocker

Diabetes ■ Chapter 27

sole, are not always equivalent to a TCC, despite the studies noted earlier, for several reasons. For example, if a foot is misshapen by a Charcot joint or previous surgery, excess pressure can be applied by the rigid portion of the structure. The ability of the device to accommodate the area of excessive pressure that causes the ulcer must be assessed because casts are always custom fitted by definition. Prefabricated braces do not exert the circumferential distribution of pressure as a cast does, and thus the prefabricated brace cannot control swelling as a cast can.348 These devices play an increasing and beneficial role in the treatment of diabetic foot problems. The nuances of the use of casts and braces must be understood. A significant recurrence rate for ulcerations after totalcontact casting is well documented and probably reflects the difficulty in resolving the underlying mechanical source of the ulcer rather than a problem directly related to the casts.188,269,284 Ulcerations that occur on the plantar surface of the midfoot in the longitudinal arch in the absence of trauma are almost invariably the result of a Charcot joint, because a normal bony prominence usually is not present in the arch region, and weight-bearing ulcers usually do not develop where no bone pressure exists. Footwear and Shoe Insoles The use of proper shoes and shoe insoles constitutes a crucial part of the care of the diabetic patient with foot problems. Even the patient with a “grade 0” foot, that is, one without actual breakdown or infection but with the risk of same, needs correct and professional advice. Poorly fitting shoes and areas of concentrated plantar pressure within shoes are the most common problems that initiate the sequence of events leading to ulceration, infection, and amputation of the diabetic patient’s lower extremity, and educating the patient about this risk is paramount to ulcer prevention.259 Much scientific advancement has occurred in recent years in the study of the biomechanical function and therapeutic effects of shoes and shoe insoles. Much work remains to elucidate a truly scientific basis for treatment, but some of the principles as understood from the clinical perspective are elucidated here. Numerous studies have shown the effectiveness of therapeutic footwear in reducing the plantar pressures and in reducing the occurrence or recurrence of plantar ulceration.* The literature demonstrating the benefits of therapeutic footwear is extensive, but one paper by Reiber et al321 disputed this concept in a study that evaluated a large number of patients. The flaws of this study are numerous and substantive. First, almost half of the patients in the study had intact protective sensation and therefore were not at risk for foot injury according to currently accepted criteria. Second, the foot lesions in some of the patients were actually not neuropathic plantar ulcers. Third, the *References 81, 100, 122, 163, 192, 261, 263, 285, 338, and 381.

definition in the study of an ulcer that developed from the footwear was overly conservative. Researchers did not count 482 foot lesions. No data in the study showed that the therapeutic footwear and insoles prescribed were actually biomechanically effective in reducing plantar pressure. Next, and perhaps most important, the authors pointed out that the efficacy of the footwear and insoles actually tested in this study is questionable. A cork insole with a thin cover is an outdated treatment and below the current standard for therapeutic off-loading of the foot. Last, the authors pointed out that when reviewing only the patients who had loss of protective sensation and who were randomized to the control footwear or the therapeutic shoes with the prefabricated insoles, there was still a clear benefit of the therapeutic shoes despite the conservative definition of an ulcer. Two of the 119 patients in the therapeutic shoe group experienced shoe-related ulcer episodes, compared with 19 out of 160 patients in the control group.321 Only 58% of patients were neuropathic at entry. The principle of off-loading is that it can reduce the incidence of plantar neuropathic lesions in patients who are at risk, namely, those with neuropathy.88,98 Other researches have shown, in well-designed studies, the effectiveness of custom therapeutic insoles in off-loading areas of high pressure under the forefoot.294a Proper diabetic insoles and shoe wear remain critical tools in the prevention of foot complications in diabetic patients. The goal of footwear for the diabetic or other patient with diminished sensitivity of the feet is to help protect the foot by relieving or diminishing areas of potential pressure concentration that can lead to blistering or ulceration. A diabetic patient with dense neuropathy can develop severe ulceration in only an hour or two of wearing a poorly fitting shoe. Shoes for diabetic patients should not have to be broken in. They should be fit to the proper size when they are dispensed and not depend on stretching to achieve that fit; otherwise, soft tissues usually break down before the shoe does. Once a new pair of correctly fitted shoes has been dispensed, however, during the first few days, the shoes should be removed at intervals of gradually increasing length to inspect the skin of the feet for areas of abrasion, redness, or pressure. The shoe and insole can then be modified or replaced by the pedorthist before major skin breakdown occurs. The prescribing physician and the dispensing orthotist/pedorthist should emphasize the importance of these periodic follow-up visits to ensure that goals of the prescribed footwear are being met. The attributes of a good shoe for a diabetic patient include several characteristics. The toe box should be wide and deep enough to prevent pressure, especially against the dorsum of the proximal interphalangeal joint of hammer toes. The leather should be fairly soft and pliable so that it conforms to the foot. Inelastic materials, such as plastic, canvas, or patent leather, should be shunned because they will not conform and can cause 1425

Part VII ■ Diabetes

Figure 27-39 Broad-toed, deep commercial walking shoe with room for custom cushioning insole.

high-pressure areas. The shoe should usually have some form of adjustable closure, such as a lace-up or hook-andloop closure, because it allows more adjustment of the shoe fit. Slip-on shoes depend upon a narrow band of pressure to keep the shoe on the foot. A padded heel counter or heel backstay, especially of the pillow type, helps diminish pressure on the area of the Achilles tendon (Fig. 27-39). Techniques for shoe fitting and insole manufacture have been published, and new techniques are constantly evolving.204,357 One of the most important features of a shoe for the diabetic patient is that it should have additional depth in the dorsal-to-plantar direction. This is important to allow room for toe deformity or for placement of a custommolded protective shoe insole. This is particularly critical in patients with prior plantar ulcerations, MTP joint extension deformities, and hammer toes. The physician and surgeon should insist on immediately fitting the patient with a newly healed ulcer in some type of special footwear to protect the area of the healing. There are many options, including an extra-depth shoe with a molded insole, a polyethylene foam (Plastizote)– lined shoe, or a Carville sandal, as well as other commercially available products. Both the Plastizote shoe and the Carville sandal are lined with a forgiving, molded, or moldable surface of a cushioning polyethylene foam. Cosmetic acceptance of these two devices can be rather limited, and neither represents the final shoe to be dispensed for most patients. For a few patients with severe deformity, these are the best definitive footwear because of the cushioning nature of the entire shoe. The Carville sandal is the shoe most able to accommodate severe plantar deformity of either the forefoot or the hindfoot. It is usually manufactured by an orthotist or a certified pedorthist (Fig. 27-40A to C). The technique was developed at the Gillis W. Long National Hansen’s Disease Center in Carville, La., where a sizable population of patients with leprosy and the resulting insensitive limbs 1426

C Figure 27-40 A, Manufacture of custom-molded accommodative insoles from foamed polyethylenes (e.g., Plastizote, Aliplast, Pelite). B, Molding of heated material with weight bearing. C, Grinding edges of molded insole to shape and fit it in a shoe.

have been cared for over many years. The technique for manufacturing the sandal has been published.62 Plastizote shoes are commercially available, although durability is often limited because of the soft materials. Definitive footwear for the diabetic patient is usually an off-the-shelf extra-depth shoe, a deep walking shoe, or a wide athletic shoe (see Fig. 27-39). The liner in appropriate commercial shoes can be removed and replaced with a custom-molded insole. For patients with plantar prominences that are at risk for ulceration, additional off-loading incorporated into the foot orthosis is sig nificantly better than a soft foam insole without this added modification (Fig. 27-41). A very small minority of patients require a custom-made shoe. Custom-made shoes are sometimes required, but most patients can be

Diabetes ■ Chapter 27

Figure 27-41 A plaster mold and the resulting custom total-contact multidensity foot orthosis. Note the area of off-loading that has been created in the high-pressure area under the medial midfoot prominence. This patient will also require a wider shoe or possibly a relasted shoe to accommodate the width of the midfoot. (Courtesy Erick J. Janisse, CO, C.Ped, National Pedorthic Services, Creve Coeur, Mo., [emailprotected].)

fitted in stock shoes by a professional shoe fitter. Custommade shoes must also be made with additional depth so that the liner of the shoe can be changed periodically as it fatigues. This should be the same type of custommolded insole that lines the stock shoe so that only the liner and not the whole shoe can be replaced to accommodate minor changes in the foot. Custom shoes are occasionally needed for patients who have Charcot joints with gross disruption of foot structure. Although fully custom shoes are available for the patient who requires a shoe that is significantly wider than commercially available or requires a customized shape, they are expensive, often require weeks to fabricate, and lack the styling of a traditional shoe which limits their acceptance by many patients. However, many indepth shoes or athletic shoes can be “relasted” by removing the sole, splitting it down the middle and spreading the sole to accommodate a given foot deformity (Figs. 27-42 and 27-43).205-207 A new wider outsole is then reapplied and a custom insole to fit the shape of the foot is fabricated. This process can be done quickly by a skilled pedorthist or orthotist, avoids the expensive of a custom shoe, requires only the affected shoe to be altered and allows a wider array of shoe selections for the patient (see section on Footwear and Shoe Insoles). A custom brace can also be attached to the shoe or used to accommodate an insole molded into an AFO. The sequence of fabrication of a relasted shoe is illustrated in Figure 27-42.

Patients are generally advised to have at least two pairs of properly fitted shoes and insoles so that they can be changed in the course of heavy wear, even in the middle of a day’s activity. Although in theory this is an excellent idea, the cost of the shoes and insoles can be prohibitive for many patients, especially because many health plans do not cover the costs of therapeutic footwear, unless it is attached to a brace. The partial financial reimbursem*nt of therapeutic shoes and insoles by Medicare395,396 has been a boon to treatment and especially to prevention of diabetic foot disease. In response to the issues of cost and cosmesis, athletic or walking shoes are used in place of the more traditional orthopedic shoe. These have a more cosmetic acceptance, especially with popular styles of casual dress, and many come with a premade liner that can be removed and substituted with the custom-molded insole to afford extra space within the shoe.223,299 The role for, characteristics of, and function of the rocker-bottom sole on a shoe is less clear and is more complex than it once appeared. Benefits are reported, but there are many unanswered questions regarding size, material, height, slope, and angle of orientation of the axis of the rocker.312,340,377 Cavanagh has pointed out that the one most successful modification of shoes is to add a rigid sole with a curved (rollered) or angled (rockered) surface.94 Shoes with standard laces provide the most secure closure system for therapeutic in-depth footwear. Slip on shoes or sandals may be appropriate for short distances of walking in the home or at a pool, but for optimal offloading and to obtain the mechanical benefits of external shoe modifications such as a rocker sole, a tie shoe is recommended. Often patients have weak or insensate fingers and hands, and alternate closure devices are required on shoes and braces to allow patients to be independent with shoe or brace use (Fig. 27-44). Even though these athletic shoes are widely available, patients can greatly benefit by being fitted by a professional shoe fitter, orthotist, or certified pedorthist who is trained not only in proper shoe fitting but also in manufacturing the protective insoles. The foot must be fitted not just to the shoe but also to the combination of the shoe and the insole. The insole cannot be made as an afterthought because the shoe will have insufficient room to accommodate it, and the foot will be crowded, pressure will be created, and the problems will be exacerbated. The Pedorthic Footwear Association (PFA) offers education, training, and preparation for certification of pedorthists; the PFA provides lists of certified pedorthists in local areas. To communicate effectively with professional shoe fitters and pedorthists, physicians should be familiar with the basic glossary of shoe terms for the purposes of writing prescriptions (Fig. 27-45). The use of half-shoes, where the heel and midfoot are supported and the forefoot hangs out over the front of the shoe, is controversial. Some authors have shown that forefoot pressures are decreased in half-shoes, but others 1427

Part VII ■ Diabetes

G Figure 27-42 Steps in the fabrication process of a relasted indepth shoe. A and B, A tracing of the foot or plaster model of the patient’s foot is made to create a pattern for the “relasted” shoe. C, The original outsole of the shoe is removed, and a longitudinal cut is made through the midsole of shoe in the area corresponding to the deformity to be accommodated. The tracing pattern is then placed into the shoe, and the sole is spread until it matches the shape of the pattern. D-F, The expanded sole is wedged open, and then the gap is filled in with a high-density viscoelastic polymer or rigid expanding urethane foam to maintain the new shape. Once set, the sole is sanded flat and resoled. Often a steel shank is not needed because of the increased rigidity of the sole from the relasting process. G, Completed “relasted” shoe. Note the similarity in shape from right to left of the plaster foot mold, the tracing for the new last, and the completed resoled shoe. (Courtesy Erick J. Janisse, CO, C.Ped, National Pedorthic Services, Creve Coeur, Mo., [emailprotected].)

have pointed out the increase in pressure under the heel.87,99 In addition, many half-shoes have a negative heel built into the sole that requires the patient to have adequate ankle joint dorsiflexion, and it may also create imbalance for elderly patients. Moreover, if the patient has a plantar forefoot ulcer, TCCs and walking boots have been proved superior to the half shoe.25 The use of insoles in the shoes of patients with insensitive feet is a mainstay of conservative management, and a primary preventive measure in patients with deformity and neuropathy, especially those with a history of previous ulceration. Many types of materials, combinations of 1428

materials, and different devices have been used in the shoes of diabetic and nondiabetic patients. Most of our current prescribing regimens are based upon clinical experience. Excellent work continues in research settings on the mechanics of gait and the quantification of plantar pressures. These studies have documented the effectiveness of insoles in reducing plantar pressures under the feet of insensitive patients.70,83,154,248 Much remains to be learned about the effect of insoles and the materials of which they are composed. Current practice for diabetic patients is to use a custommolded insole made of at least two different densities of

Diabetes ■ Chapter 27

materials, at least one of which is a closed-cell polyethylene foam that has been heated and molded to the patient’s foot. Examples of the most common combinations include soft or medium Plastizote on top of a firmer Pelite, Aliplast, or Plastizote; or the Plastizote on top of a

nonmoldable material such as Poron; or viscoelastic materials such as Sorbothane, PQ, or Silipos. One direct molding method of insole fabrication consists of using two layers of heat-moldable material that are first glued together and then heated in a convection oven at about Top Line Heel counter

Tongue

Eyelet facing

Vamp

Toe cap Throat line

Insole Welt

Shank

B Figure 27-43 A and B, This patient has bilateral pes planovalgus with associated Charcot neuroarthropathy of the left midfoot, with collapse and marked forefoot abduction precluding the use of commercially available footwear. Notice the distinct difference in shape between feet and the relasted left shoe and custom insole to accommodate this deformity.

Figure 27-45 Basic anatomy of the shoe. This vocabulary is necessary for communicating shoe prescriptions.

Figure 27-44 A and B, 55-year-old male with diabetes mellitus and motor and sensory polyneuropathy, a quiescent Charcot ankle and significant hand and lower leg, ankle, and foot weakness. Note the severe hand intrinsic muscle wasting that necessitated Velcro as an alternate closure device for the Gillette calf lacer ankle–foot orthosis. (Image copyrighted by Jeffrey E. Johnson, MD, Washington University Orthopedics.)

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1430

periodic insole replacement is critical to prevention of ulcerations. Off-loading of the metatarsal heads or a plantar boney prominence is accomplished with “posting” or elevating an area of the foot that is not high pressure, to reduce the pressure in another area. A recent study indicated that a metatarsal pad needs to be placed within 6 to 11 mm proximal to the metatarsal heads to provide consistent peak pressure reduction, and improper placement will actually increase plantar pressures.184 Off-loading modifications are best performed by certified orthotists and pedorthists who will follow the patient closely to monitor the high-pressure area and make adjustments as necessary. There are significant differences in the material properties of the various insole materials and the choice of these is dependent upon multiple factors, including the weight and activity level of the patient, the presence of deformity, the hardiness of the skin of the foot, and the need for moldability. Studies on these materials have shown that the polyethylene foams were found to be the most compressive, followed by neoprene rubber (Spenco) and viscoelastic polymer (Sorbothane), with virtually no compression of the closed-cell urethane foam (PTT, Poron) (Fig. 27-46).61 In addition, merely heating the materials for purposes of creating a molded insole alters the mechanical structure of the orthotic material, which decreases its ability to disperse peak plantar loads.72 Therefore, from a clinical perspective, the attribute of compressible foams has both desirable and undesirable aspects. Greater compression means fatigue of the materials with “bottoming out” and is undesirable because of the need to replace the insole. However, it is desirable because the plantar skin is better protected than by a rigid

8 7 Thickness in millimeters

270° F for 60 to 90 seconds. The material is allowed to cool and then is molded by the weight-bearing pressure as the patient stands on the materials, which rest on top of a foam pillow (see Fig. 27-40A-C). The block is then cut, shaped, and ground on a lathe to adjust its shape and thickness to fit it into the designated shoe. Additional modifications can be made on the undersurface, such as adding a metatarsal pad or excavating the insole to provide relief for an area of high pressure. A second molding technique is to make a foam box, wax, or fiberglass impression of the foot and create a plaster mold. The mold is then used as a model over which heated layers of different density insert materials can be formed. The insert is then posted in the same manner to off-load specific areas of high pressure. The direct molding method by definition uses softer heat moldable materials, which may bottom out more quickly than the more firm materials that can be used with the plaster impression molding technique. In a multilayer insole, the softer material is placed on the upper layer close to the foot so that it will compress and fatigue more easily than the skin of the foot. This is backed with a firmer material that maintains the shape and structural integrity of the device within the shoe. Additional pressure relief can be obtained in areas of the metatarsal heads by excavating a well in the shoe under the insole and filling it with a cushioning material. Presumably, the most important function of the insole materials is the attenuation of force in the areas of local pressure concentration that threaten to lead to soft tissue breakdown. The diminution of pressure occurs as a result of the dissipation of the force of weight bearing over a wider area, the same concept that explains the function of the TCC. The insole cannot reduce the absolute amount of force distributed through the patient’s foot because this is a function of muscle action, the patient’s mass, and the gravitational field of Earth. The insole materials and shoe can slow the rate of the impact and spread those forces over a wider area, thus attenuating the hot spot of extremely high pressure. The insoles can be moved from shoe to shoe, depending on the number of appropriately fitted shoes available. Studies of numerous insole materials have documented the general effectiveness of the materials in relieving pressures.70,248 Repetitive loading, as would occur in the course of walking, results in compression and loss of thickness of the heat-molded materials made of polyethylene foam.83 This compression results in fatigue of the devices with loss of both the cushioning function and the custommolded shape that distributes force over the plantar surface. For this reason, insoles need to be replaced periodically. Longer insole life can be attained by having two pairs and alternating their use. The exact interval for replacement of diabetic insoles is highly variable, depending on the number of pairs of insoles used and the activity of the patient, but it ranges from 6 to 12 months on average. Educating the patient about the need for close monitoring of their insert wear and the need for

6 5 Plastizote (soft) Pelite (medium) PPT Spenco Sorbothane

4 3 2 0

Log number of cycles Figure 27-46 Force attenuation properties of different insole materials. (From Brodsky J, Kourosh S, Stills M: Objective evaluation of insert material for diabetic and athletic footwear. Foot Ankle 9:111-116, 1988.)

Diabetes ■ Chapter 27

material because the compressible insole gives way and spares the skin of the sole. Other qualities of the materials must be considered as well, such as the material’s ability to be molded to the foot. Viscoelastic materials, such as silicone and Sorbothane, have excellent shock attenuation, but lack moldability. For diabetic insoles, it is currently considered essential that at least the upper or closer layer be moldable. Therefore combining moldable layers of softer closed cell polyethylene foam on the top surface of the insole with less moldable materials such as polyurethane foam (PPT, Poron) or ethylvinyl acetate (EVA) in the lower layers has the advantage of providing a foot orthosis with a longer functional life that is better at resisting the compressive stress of weightbearing. The current concept is that a combination of materials probably affords the best compromise between a cushioning, molded insole and one that has durability and structural strength. Working closely with a certified pedorthist or orthotist to properly evaluate and help choose the appropriate combination of materials and who will help follow the progress of the patient is critical to the long-term success of preventative treatment. One caveat about the selection of insole materials is that the use of rigid orthoses, especially those made of hard plastics. These hard materials, commonly seen in some popular sport orthotics (Fig. 27-47A to C), are strictly contraindicated in the diabetic patient with neuropathy or a history of ulcerations. The use of rigid orthoses in the shoe of a patient with insensitivity is an invitation to disaster as a result of ulceration. The shoe insoles of the diabetic patient are meant to prevent or reduce the incidence of pressure-related problems and should be made of accommodative materials. It is important to make a specific point to the patient who is prescribed a shoe insole for the first time that he or she will most likely need to be fitted for a different shoe that is a larger size, has the appropriate last (shape), and has room for the insole. Patients might resist this because the larger appropriate-fitting shoe is perceived as too large, lacking the proper styling, or too heavy rather than as a therapeutic device. Therefore it must be explained that the use of the insole in a shoe that is too small will exacerbate the pressure problems it is meant to deter by creating increased pressure in the shoe, especially in the toe box area (see Box 27-1). Wound/Ulcer Management The first step in treating a diabetic ulcer is to classify the wound. The physician or surgeon must assess the extent of the lesion and the perfusion of the foot (see Tables 27-1 and 27-2). Most ulcers treated in an outpatient setting are grade 1. Lesions that are deeper than grade 1 usually require inpatient or surgical care, with a few exceptions. Next, it is necessary to assess whether adequate vascularity exists to promote healing. If the patient has excellent pulses, the foot is grade A (not ischemic).

C Figure 27-47 A to C, Rigid shoe inserts such as these should not be used by diabetic patients with peripheral neuropathy because of risk of injury to an insensitive foot.

If the pulses cannot be palpated or appear to be significantly diminished, vascular studies should be ordered. Based on the result of this investigation, the physician can determine if the foot is still grade A or rather is grade B (ischemic without gangrene). This can be essential data for clinical decision making because a major cause of a nonhealing, persistent chronic wound, especially an ulcer, is peripheral vascular insufficiency. Determination of grades C (partial gangrene) and D (complete foot gangrene) can be made on the basis of examination, but testing is still required to determine the severity of the ischemia and anatomic level of the occlusion. The third question that must be answered in treating an ulcer in a diabetic foot is whether it is infected. All ulcers are colonized, at least superficially, and a culture taken from a swab of the ulcer surface will reveal bacterial growth. However, an infected ulcer usually appears different: it is draining and deep (greater than grade 1), often has surrounding erythema and cellulitis, and might have associated edema and possibly lymphangitis as well. If the ulcer is significantly infected, the patient usually needs to be admitted to the hospital and started on IV 1431

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antibiotics. An internal medicine or endocrinology consultation for metabolic management and an infectious diseases consultation is usually necessary, followed by surgical debridement of the wound.256 Wound care follows general principles until such time as the wound is converted to grade 1. Several methods and systems for wound care have been studied and are practiced. The desired outcome is the same for all, namely, to achieve a clean, granulating, or primarily healing wound that has no undermining, no infection, no nonviable tissue, and no exposed tendon, joint, or bone and that is preferably shallower than it is wide. Once such a wound is achieved, clinical pressure-altering strategies are the key to healing, provided that adequate vascularity of the limb is present or has been achieved. At that time, it can be treated with the array of outpatient pressure-relieving methods (Fig. 27-48A to D). Once the questions of ulcer depth, vascularity, and infection have been satisfactorily addressed, the surgeon can focus on the key to healing ulcer lesions, namely, relief of pressure. Options for modification of weightbearing pressure include activity modifications, specialized footwear, TCCs, a prefabricated walking brace, or a custom AFO that extends to the proximal leg. The choice depends on the lesion, the clinical specifics of each patient and the prior treatment, and the anatomic location of the ulcer.

Activity Modification Studies have examined the relationship between activity level and wound healing.17,22,23,179 Scientific data are now beginning to bolster clinical intuition regarding this important aspect of healing neuropathic pressure lesions of the foot. Once again, the multifactorial nature of neuropathic ulceration is revealed as it pertains both to etiology and treatment. Unloading the foot with a crutch or a walker may be a helpful adjunct to the other mechanical methods and devices applied to the extremity. Non– weight bearing alone is not recommended. It is tiring and difficult, and it is difficult to monitor for compliance. Even the simplest tasks of daily living become perilous balancing acts for the patient attempting to function without weight bearing. Patients with neuropathy cannot perceive whether the foot is down on the floor or how hard it is pressing on the floor—yet another reason complying with instructions to modify weight bearing can be so difficult. If it is our goal to decrease weight bearing on the plantar neuropathic lesion, it is not unreasonable to use as many methods as possible at the disposal of the patient. Diabetic patients with neuropathy may have poor balance, possibly as a result of multiple factors, including diminished proprioception of the lower limbs, impaired vision, and even vestibular dysfunction.91 Creative combinations of pressure-modifying devices on the foot and leg can be

D C Figure 27-48 Different types of weight-relieving devices for diabetic foot. A, Wooden-soled postoperative shoe. B, Plastizote “healing” shoe. C, Carville sandal. D, Short-leg walking brace.

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combined with use of a wheelchair, walkers, or in selected patients, rolling walker devices (provided balance is sufficient). All of this underscores the paramount contribution of social factors in this disease. People who live alone, have an inadequate support system, or have limited resources for their activities of daily living, as well as their special medical care, have greater obstacles to overcome to achieve healing. Local Wound Care A few well-controlled prospective studies have been reported to demonstrate statistically significant differences in wound healing with certain topical treatments to diabetic ulcers.10,365,380,394 Unfortunately, these studies signify our introduction to rather than our comprehension of this field, and more questions are raised than resolved. First, statistical significance does not equate to clinical significance. In other words, even if the clinician is able to show faster wound healing, is the difference meaningful and cost-effective? Moreover, these studies do not compare the use of topical preparations with proven methods of ulcer healing, namely, pressurerelief measures such as TCCs. Clinicians know that it is impossible to ignore the role of pressure in the occurrence and recurrence of diabetic ulcerations, and this issue has yet to be adequately addressed by the wound care studies. In summary, what is removed from diabetic wounds, namely, pressure, continues to be far more important than what is put on the wounds.56 Aggressive debridement of infected and necrotic wounds is essential to achieving the quickest and most dependable healing, and no topical dressing system can substitute for this principle.302,367 Although the indications for and limitation of topical preparations remain to be clearly defined, it is still reasonable, if not prudent, to relieve pressure first and to apply a conventional dressing regimen in most cases. Surgical Treatment When ulcers fail to heal or if they recur after healing has been achieved, excessive internal bone pressure is perpetuating the ulcer. If pressure cannot be relieved externally with modified footwear, molded accommodative insoles, or TCC or walking boot treatments, then pressure must be relieved by surgical methods of modifying the bony prominences. Most surgical procedures for chronic ulceration and for infection of the diabetic foot involve relieving areas of internal bone pressure in addition to debridement of infected or nonviable tissue. There are three surgical techniques to reduce the pressure of the underlying bony prominence in neuropathic ulcers. These include resection of the prominent bone, realignment of the bone segments causing the deformity, and reconstruction to realign the deformity in a proximal segment that will result in decreased pressure distally on the midfoot or forefoot. Bone resection is the most commonly used because it is the most direct, most effective, and generally the least risky.

Surgery for the diabetic patient should never be performed cavalierly, and the patient should be shown to have adequate vascularity to support healing; otherwise, the surgery can produce further tissue necrosis. However, the presumed prohibition against any surgical procedure in the diabetic foot is unwarranted and incorrect. Failure to remove the source of the lesion is more dangerous than the judicious use of surgery to correct a deformity and relieve pressure. Surgical procedures for the relief of pressure are considered here by the anatomic region of the foot involved and by the type of lesions that occurs. Certain technical principles apply to surgical procedures for chronic and recurrent ulcerations. A separate incision is usually made away from the area of the ulcer, if possible, along the medial or lateral border of the foot or dorsally. In most cases, excision of bone through the ulcer itself should be avoided because the ulcer does not afford sufficient exposure to perform adequate debridement. Dorsal incisions are preferable to plantar incisions for bone resection, especially for treating the pressure associated with a plantar ulcer. The ulcer is debrided through a plantar approach, separate from the incision for resection of the bony prominence. The incision may be loosely closed, depending on the condition of the surrounding soft tissue and the ability to excise the infected tissue. In many instances, and especially in the presence of infection, it is best to leave the plantar ulcer open to heal secondarily after it has been debrided. If the surgeon is uncertain whether to close the incision, it may be left open; when returning the patient to the operating room for redebridement and wound irrigation in several days, the incision may be closed then. Once the surgical wounds have healed, and the deep structures of bone, joint, or tendon are no longer exposed (the wound has converted to grade 1), the ulcer should be treated with the same regimen of external pressure relief noted earlier, such as a cast. Removal of the internal source of pressure should allow healing of the ulcer thereafter. Failure of the ulcer to heal signifies that an insufficient amount of bone was resected (inadequate relief of pressure) or that another factor is responsible (e.g., residual infection, ischemia, poor nutrition).132 ACHILLES LENGTHENING There has been clinical recognition since the 1990s that there may be a role for Achilles tendon lengthening coupled with TCC treatment, in apparent recognition of the role of equinus deformity in increasing forefoot pressure.193,254 Achilles lengthening has been studied in prospective randomized trials that evaluated the role and benefit of this procedure in the treatment of recurrent plantar forefoot ulcers in the presence of diabetic neuropathy. Mueller et al284 found that there was a higher rate of healing in the group undergoing Achilles lengthening plus total-contact casting than in the group treated with total-contact casting and no Achilles lengthening. More important, these authors found that the risk for recurrence was greatly diminished (75% less at 7 months, and 1433

Part VII ■ Diabetes

52% less at 2 years) in the Achilles lengthening group. They concluded that Achilles lengthening was an effective adjunct to total-contact casting in patients with limited ankle dorsiflexion (

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