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BAXTER’S THE FOOT AND ANKLE IN SPORT Copyright # 2008, 1995 by Mosby, Inc., an affiliate of Elsevier Inc.
ISBN: 978-0-323-02358-0
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. 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 the practitioner, relying on their own experience and knowledge of the patient, 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 assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher Library of Congress Cataloging-in-Publication Data Baxter’s the foot and ankle in sport / [edited by] David A. Porter, Lew C. Schon.—2nd ed. p. ; cm. Rev. ed. of: The foot and ankle in sport / edited by Donald E. Baxter. c1995. ISBN 978-0-323-02358-0 1. Foot—Wounds and injuries. 2. Ankle—Wounds and injuries. 3. Foot—Abnormalities. 4. Ankle—Abnormalities. 5. Sports injuries. I. Baxter, Donald E. II. Porter, David A., 1959- III. Schon, Lew. IV. Title: Foot and ankle in sport. [DNLM: 1. Ankle Injuries. 2. Foot Injuries. 3. Ankle—abnormalities. 4. Foot Deformities. 5. Sports Medicine—methods. WE 880 B355 2007] RD563.F638 2007 617.50 85044 dc22 2007022810 Acquisitions Editor: Emily Christie Editorial Assistant: Faith Brody Project Manager: David Saltzberg Design Direction: Lou Forgione
Printed in USA Last digit is the print number: 9 8 7 6 5 4 3 2 1
......................................... CONTRIBUTORS
Abrao M. Altman, MD Professor, Orthopaedics Santa Cecilia University Orthopaedic Surgeon Casa de Saude de Santos Santos, Brazil
Michael W. Bowman, MD, FACS Clinical Assistant Professor Department of Orthopaedic Surgery University of Pittsburgh Consultant, Pittsburgh Steelers Football Club Pittsburgh, Pennsylvania
Robert B. Anderson, MD Chief, Foot and Ankle Service Department of Orthopaedics Carolinas Medical Center Charlotte, North Carolina
W. Grant Braly, MD Clinical Professor, Foot and Ankle Fellowship Foundation for Orthopaedic Athletic and Reconstruction Research Department of Orthopaedic Surgery University of Texas Health Science Center at Houston Clinical Assistant Professor Department of Orthopaedic Surgery Baylor College of Medicine Active Staff, Orthopaedic Surgery Texas Orthopaedic Hospital Houston, Texas
Donald E. Baxter, MD Former Clinical Professor of Orthopaedic Surgery Head of Foot and Ankle Surgery Director of Foot and Ankle Fellowship Programs Baylor College of Medicine University of Texas Medical School Houston, Texas Christoph Becher, MD Center for Knee and Foot Surgery/Sports Trauma ATOS Clinic Center Heidelberg, Germany Kim L. Bennell, BAppSci (physio), PhD Professor Centre for Health, Exercise and Sports Medicine University of Melbourne School of Physiotherapy Melbourne, Australia Gregory C. Berlet, MD, FRCSC Chief, Section of Foot and Ankle Department of Orthopaedics The Ohio State University Fellowship Director Orthopaedic Foot and Ankle Center Columbus, Ohio
Peter Brukner, MBBS, FACSP Associate Professor in Sports Medicine Centre for Health, Exercise and Sports Medicine University of Melbourne Melbourne, Australia Thomas O. Clanton, MD Professor and Chairman Department of Orthopaedic Surgery The University of Texas Health and Science Center at Houston Team Physician, Rice University Team Orthopaedist, Houston Texans Team Physician, Houston Rockets Houston, Texas J.A. Colombier, MD Foot and Ankle Surgery Clinique de l’Union Toulouse, France
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Erin Richard Barill, PT, ATC Director of Rehabilitation Indianapolis Colts Indianapolis, Indiana
Contributors
Michael J. Coughlin, MD Director, Idaho Foot and Ankle Fellowship Boise, Idaho Clinical Professor, Department of Orthopaedic Surgery and Rehabilitation Oregon Health Science University Portland, Oregon Private Practice of Orthopaedic Surgery St. Alphonsus Regional Medical Center Boise, Idaho Past President, American Orthopaedic Foot and Ankle Society P.A.J. DeLeeuw, PhD Fellow Department of Orthopaedics Academic Medical Centre University of Amsterdam Amsterdam, The Netherlands A. Lee Dellon, MD Professor of Plastic Surgery and Neurosurgery The Johns Hopkins University Baltimore, Maryland Clinical Professor of Plastic Surgery, Neurosurgery and Anatomy University of Arizona Tucson, Arizona Director, the Dellon Institutes for Peripheral Nerve Surgery Jonathan C. Dick, MB, BCh, BAO, LRCP & SI Associate Lecturer School of Medicine University of Queensland Brisbane, Australia Peter H. Edwards, Jr., MD Senior Attending Orthopaedic Surgery Ohio Orthopedic Center of Excellence Columbus, Ohio David G. Ford, C. Ped Board Certified Pedorthist Orthopaedic Sports Medicine Birmingham, Alabama Carol Frey, MD Fellowship Co-Director Foot & Ankle West Coast Orthopedic & Sports Medicine Foundation Manhattan Beach, California
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Kevin B. Gebke, MD Assistant Professor of Clinical Family Medicine Primary Care Sports Medicine Fellowship Director IU Center for Sports Medicine Family Medicine Indiana University Indianapolis, Indiana Sandro Giannini, MD Professor Orthopaedics Bologna University Chief of VI Department Istituti Ortopedici Rizzoli Bologna, Italy John S. Gould, MD Professor of Surgery Division of Orthopaedic Surgery University of Alabama at Birmingham Chief of Medical Staff UAB Highlands Hospital Birmingham Clinical Professor Orthopaedic Surgery University of South Alabama Mobile, Alabama J. Speight Grimes, MD Assistant Professor Orthopedic Surgery Texas Tech University Health Sciences Center Lubbock, Texas Florian W. Gruber, MD Resident 1st Orthopaedic Department Orthopedic Clinic Gersthof Vienna, Austria William G. Hamilton, BSE, MD Senior Attending Orthopaedic Surgery St. Luke’s Roosevelt Hospital Assistant Attending Orthopaedic Surgeon The Hospital for Special Surgery Clinical Professor of Orthopaedic Surgery College of Physicians & Surgeons Columbia University New York, New York Travis W. Hanson, MD Foot and Ankle Surgery & General Orthopaedics KSF Orthopaedic Center Houston, Texas
Contributors
Hong-Geun Jung, MD, PhD Associate Professor Attending Staff Surgeon Department of Orthopedic Surgery, Foot and Ankle Service Konkuk University School of Medicine Seoul, South Korea Jon Karlsson, MD, PhD Professor of Orthopaedics and Sports Traumatology Department of Orthopaedics Sahlgrenska University Hospital Goeteborg, Sweden Moosa Kazim, MD, FRCS (C) Director, Department of Sports Medicine Orthosports Medical Center Dubai, United Arab Emirates John G. Kennedy, MD, FRCS (Ortho) Assistant Professor of Orthopaedic Surgery Cornell University Ithaca Attending Surgeon Foot and Ankle in Sports Hospital for Special Surgery New York, New York Cesar Khazen, MD Foot and Ankle Surgeon Department of Orthopaedic Surgery Hospital de Clinicas Caracas Caracas, Venezuela Gabriel Khazen, MD Foot and Ankle Surgeon Department of Orthopaedic Surgery Hospital de Clinicas Caracas Caracas, Venezuela Daniel E. Kraft, MD Assistant Clinical Professor Pediatrics Indiana University Methodist Sports Medicine Clinic Indianapolis, Indiana
Rover Krips, MD, PhD Department of Orthopaedic Surgery Academic Medical Center University of Amsterdam Amsterdam Afdelind Orthopaedie Diaconessenhuis Leiden Leiden, The Netherlands Kyung-Tai Lee, MD Professor, Chief Foot and Ankle Service Department of Orthopedics Eulji University Hospital Seoul, South Korea Thomas H. Lee, MD Assistant Clinical Professor Department of Orthopaedics The Ohio State University Columbus, Ohio Nicola Maffulli, MD, PhD, FRCS Sports Med, Ltd. The London Independent Hospital London Professor of Trauma and Orthopaedic Surgery University of Keele School of Medicine University Hospital of North Staffordshire Stoke-on-Trent, United Kingdom Ansar Mahmood, MB, ChB, MRCS Specialist Registrar in Trauma & Orthopaedic Surgery University of Keele School of Medicine Registrar in Trauma & Orthopaedics Queens Hospital Burton Burton-upon-Trent, United Kingdom Roger A. Mann, MD Associate Clinical Professor Orthopaedic Surgery University of California School of Medicine San Francisco Director Foot and Ankle Fellowship Oakland, California John V. Marymont, MD Associate Professor Chief, Foot & Ankle Section Baylor College of Medicine Staff Physician Methodist Hospital Houston, Texas
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Christopher W. Hodgkins, MD Orthopaedic Fellow Foot and Ankle Surgery Hospital for Special Surgery New York, New York
Contributors
Peter B. Maurus, MD Orthopaedic Surgeon, Foot and Ankle Surgery Mercy Hospital Steindler Orthopedic Clinic Iowa City, Iowa William C. McGarvey, MD Associate Professor Director of Foot and Ankle Surgery Department of Orthopaedic Surgery University of Texas-Houston Health Science Center Houston, Texas Eyal Melamed, MD Foot and Ankle Service Department of Orthopaedics B Rambam Medical Center Foot and Ankle Clinic Kelalit HMO Polyclinic Kiriat Bialik Haifa, Israel Secretary, Israeli Foot and Ankle Society Larry L. Nguyen, MD Orthopaedic Surgeon Physician OrthoArkansas, P.A. Little Rock, Arkansas James A. Nunley, MD J. Leonard Professor and Chief of the Division of Orthopaedics Department of Surgery Duke University Durham, North Carolina Padraic R. Obma, MD Resident, Orthopaedic Surgery Indiana University School of Medicine Indianapolis, Indiana Yong-Wook Park, MD, PhD Professor of Orthopaedics Hangang Sacred Heart Hospital Seoul Professor of Orthopaedics Chunchon Sacred Heart Hospital Chunchon Supervisor of Orthopaedics The Armed Forces Medical Command Yangju, South Korea Mihir M. Patel, MD Fellow, Foot and Ankle Service Department of Orthopaedic Surgery The Hospital for Special Surgery New York, New York
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Glenn B. Pfeffer, MD Director, Foot and Ankle Center Cedars-Sinai Medical Center Los Angeles, California Terrence Philbin, DO Assistant Clinical Professor Department of Orthopaedics The Ohio State University Medical Director of Foot and Ankle Orthopaedics Grant Hospital Columbus, Ohio David A. Porter, MD, PhD Voluntary Clinical Associate Faculty Orthopaedics, Indiana University Indianapolis Adjunct Clinical Associate Professor of Health, Kinesiology and Leisure Studies Foot and Ankle Consultant Purdue University West Layfayette Foot and Ankle Consultant Indianapolis Colts Indianapolis Foot and Ankle Consultant Co-Director Department of Research and Education Methodist Sports Medicine – The Orthopedic Specialists Indianapolis, Indiana Anthony S. Rhorer, MD Director, Orthopaedic Trauma Scottsdale Healthcare President Sonoran Orthopaedic Trauma Surgeons Scottsdale, Arizona Gregory A. Rowdon, MD Team Physician Purdue University West Lafayette, Indiana G. James Sammarco, MD Volunteer Professor Orthopaedic Surgery University of Cincinnati Cincinnati SportsMedicine and Orthopaedic Center Cincinnati, Ohio V.J. Sammarco, MD Co-Director Foot and Ankle Fellowship University of Cincinnati Cincinnati SportsMedicine and Orthopaedic Center Cincinnati, Ohio
Contributors
Mikael Sansone, MD Resident, Department of Orthopaedics Sahlgrens University Hospital Gothenburg, Sweden Scott T. Sauer, MD Clinical Instructor Department of Orthopaedic Surgery Georgetown University School of Medicine Washington, DC Terence S. Saxby, FRACS (Ortho) Consultant Orthopaedic Surgeon Brisbane Foot and Ankle Center Brisbane, Australia Robert C. Schenck, Jr., MD Professor and Chairman Department of Orthopaedic Surgery University of New Mexico School of Medicine Albuquerque, New Mexico Lew C. Schon, MD Assistant Professor Department of Orthopaedic Surgery The Johns Hopkins University Baltimore Clinical Associate Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Georgetown University Medical Center Washington, DC Director of Foot and Ankle Services Department of Orthopaedic Surgery The Union Memorial Hospital Baltimore Active Staff, Part Time Department of Orthopaedic Surgery The Johns Hopkins Medical Institutions Baltimore, Maryland Scott B. Shawen, MD, MAJ(P), MC Assistant Professor Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland Director, Orthopaedic Foot & Ankle Surgery Orthopaedics & Rehabilitation Walter Reed Army Medical Center Washington, DC Staff Orthopaedic Surgeon Surgery Kimbrough Ambulatory Care Center Fort Meade, Maryland
Roman A. Sibel, MD Fellow, Foot and Ankle Department of Orthopaedics The Hospital for Special Surgery New York, New York Yasuhito Tanaka, MD Assistant Professor Department of Orthopaedic Surgery Nara Medical University Kashihara, Japan David D. Taylor, MD Sports Medicine Fellow Methodist Sports Medicine Indianapolis, Indiana Hajo Thermann, MD, PhD Professor, Trauma Department Hannover Medical School Hannover Center for Knee and Foot Surgery/Sports Trauma ATOS Clinic Center Heidelberg, Germany Craig Ives Title, MD Department of Orthopaedics Lenox Hill Hospital New York, New York C. Niek van Dijk, MD, PhD Head Department of Orthopedic Surgery Academic Medical Center Amsterdam, The Netherlands Francesca Vannini, MD Department of Orthopaedic Surgery Bologna University Consultant, VI Department Istituti Ortopedici Rizzoli Bologna, Italy Sergio Vianna, MD Chief, Section of Foot and Ankle Surgery Instituto Nacional de Traumato-Ortopedia Rio de Janeiro, Brazil Veronica Vianna, MD Member, Section of Foot and Ankle Surgery Instituto Nacional de Traumato-Ortopedia Rio de Janeiro, Brazil Xu Xiangyang, MD Professor Department of Orthopaedics Shanghai Jiaotong University Medical College Ruijin Hospital Shanghai, China ix
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Melanie Sanders, MD Leesburg, Virginia
Contributors
Zhu Yuan, MM Attending Doctor Department of Orthopaedics Ruijin Hospital Shanghai Jiaotong University Shanghai Orthopaedics Institute Shanghai, China Mohammed S. Zafar, BSc, MBBS, MRCS Specialist Registrar in Trauma and Orthopaedic Surgery University of Keele School of Medicine Staffordshire University Hospitals Birmingham Selly Oak Hospital Birmingham, United Kingdom
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Chaim Zinman, MD The Bruce Rappaport Faculty of Medicine Technion-Israel, Institute of Technology Chairman, Department of Orthopaedics B Rambam Medical Center Haifa, Israel Jerett Zipin, DO Attending Sports Medicine Health Care Partners Pasadena, California
......................................... P R E F A C E
treatment. The chapter on the subtalar joint has been expanded and the ever elusive topic of subtalar instability has been addressed and hopefully clarified. We have added a chapter on new advances in the treatment of the foot and ankle. We have tried to focus more on the rehabilitation needs in the chapter on Unique Problems in Sports and Dance. We have also added a new chapter on the principles of rehabilition for the foot and ankle. The advancements in treatment for athletic injuries to the foot and ankle have continued to explode. We have therefore updated each chapter to keep the clinician at the forefront of this exciting field. We have tried to keep the length similar so as to be an easy access for all health care providers. The field of sports medicine of the foot and ankle has become global in its scope, therefore the reader will note a more international flavor to the authorship of this edition. We hope you enjoy this edition of the foot and ankle in sport. We have enjoyed working with our contributor friends and colleagues in the field of foot and ankle sports medicine. We have also enjoyed thinking of our readers and their needs and interests. We hope this edition meets all your interests, needs, and expectations.
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The original volume of The Foot and Ankle in Sport by Don Baxter has become a widespread authority on the diagnosis and treatment of athletic injuries to the foot and ankle. It is an ominous task to improve on this text. In fact, our attempt with the second edition is to update the already authoritative text and provide the same authoritative resource today. We have decided to keep the basic format with sections on Athletic Evaluation, Sports Syndromes, Anatomic Disorders, Unique Problems in Sports and Dance and a section on shoewear, orthoses, and rehabilitation. We hope you have enjoyed this approach and find it helpful to your treatment of athletes and sports enthusiasts. We have memorialized the chapter provided by the late Ken Johnson, MD, by having one of his former fellows compile this chapter. We have expanded the chapter on trauma to focus on the treatment of ankle fractures (both acute and stress), midfoot ligamentous injuries and occult fractures of the foot and ankle. We have included a chapter on the problematic stress fractures also. The section on ankle injuries has been focused more closely on ankle instability, ankle sprains, and their updated
........................................... C H A P T E R 1 Assessment and treatment of the elite athlete: helpful hints and pertinent pearls Donald Baxter and Lew Schon CHAPTER CONTENTS ...................... #1. Look at the big picture #2. ‘‘Conservative treatment was exhausted’’ may mean only that the athlete and medical team were exhausted
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#12. Plan twice, cut once
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#13. A stealthlike incursion should leave ne’er a trace
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#14. Minimize surgery and maximize recovery
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#3. Conservative care may not conserve resources
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#15. Identify injuries that are at high risk for failure
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#4. Patience and relative rest are virtues
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#16. A little instability can go a long way: keep both eyes open
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#5. Think about the nerves
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#17. When is it okay to ‘‘spare the rod and spoil the athlete’’?
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#18. Work backward in establishing a return to sport protocol
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#19. Everyone loves a winner
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#20. It is better to have no publicity than bad publicity
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Conclusion
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#6. The tarsal coalition can be the great masquerader
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#7. Timing should never be underrated
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#8. Location, location, location
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#9. Despite #8, it is better to be lucky than good
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#10. A quick fix may buy time
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#11. Sometimes it is better to go for the base hit
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Although this textbook contains sections on specific entities, there are broader themes that must be considered. The authors have compiled a list of their favorite pearls and highlighted them with case presentations. The list is by no means profound or comprehensive, but like a mantra recited during meditation, it still can be a source of inspiration or focus. These points cut across many situations and can facilitate the assessment and care of the elite athlete.
#1. LOOK AT THE BIG PICTURE The proper history and physical examination is completed by keeping the big picture in mind and obtaining contributory static and dynamic factors that affect the athlete. This approach includes appreciating the patient’s experience with the condition or injury; the character of the symptoms; the duration and onset of the problem; aggravating and ameliorating factors; and a description of the specific offending activity. In
addition, other general sports activities should be noted, such as details about the gear; the surfaces; the opponents, teammates, and partners (dance); and the sporting environment. Training factors should be documented, especially the duration, intensity, and frequency of events, as well as the warm up and cool down. Motivational drives and the way that the condition is perceived relative to future ambitions are enlightening. Nutritional issues, general health, medical history, medications, vitamins and supplements, and prior surgeries or traumas often may be revealing. The physical examination should be performed accordingly, taking both wide and focused perspectives and juxtaposing the examination with static and dynamic appraisals. The athlete should be observed during normal standing, walking, and sitting, as well as running or performing the particular maneuvers of the sport or dance. The musculoskeletal system, especially the lower extremities, warrants evaluation, because any one area can affect the foot and ankle and the clinician may find clues that are useful to determining a diagnosis and treatment. The
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Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
synthesis of these protean elements can be challenging but carries a high reward for observing the human body at its finest physical performance.
#2. ‘‘CONSERVATIVE TREATMENT WAS EXHAUSTED’’ MAY MEAN ONLY THAT THE ATHLETE AND MEDICAL TEAM WERE EXHAUSTED In treating the elite athlete, as with treating any athlete or patient, there is an evaluation process that must include conservative consideration of all options before invasive treatment may be instituted. The orthopaedic foot and ankle and or sports medicine subspecialist must know the condition, its etiology, and its natural course. Timing relative to the disease state and the activity requirements is critical and must influence the approach. Operative treatment might be considered with the elite athlete, whereas conservative treatment would be used with the high school athlete and nonathlete having the same problem. Although simple and complex nonsurgical techniques exist for every orthopaedic malady, do not assume that the solution was applied appropriately or completely for the elite athlete. Often, a thorough evaluation of the dynamic and static conditions that contribute to the problem has not been synthesized to design a customized, multitiered approach best suited to the individual. As with surgery, there are ‘‘tricks and moves’’ that can render the standard treatment into a tour de force cure. Often the effort, including reassessments and tweaking of the protocol, can be more laborious and frustrating than an operative endeavor. Finally, despite good intentions, it must be remembered that nonoperative treatment carries risks and can be considered a waste of valuable time and resources. It is the norm for multiple opinions to be offered regarding treatment of elite athletes, and it is preferable for everyone involved, including the team physician, agent, and so forth, to agree with the treatment recommended by the clinician. With that said, the following cases illustrate straightforward and unglamorous conservative interventions that carried little risk but made a major, beneficial impact. A Major League Baseball player presented with a chronic, overuse strain of his left great toe. He was a left-handed pitcher, and the left great toe was being subluxed into a lateral valgus position during push-off. The problem was diagnosed as a form of a turf-toe, more specifically a sprain of the medial sesamoidal phalangeal ligament and the medial head of the flexor hallucis brevis tendon. After talking to the trainer, agent, team doctor, and orthotist, we designed and custom made a spacer to fit between the great toe and the
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second toe. After a slow start to the season and requisite reassurance, the pitcher won 22 games using a simple device (Fig. 1-1). Another Major League Baseball player had ankle and hindfoot symptoms that were felt to limit his hitting. The ankle and hindfoot examination was unremarkable, with good stability, alignment, and strength. An examination of the whole musculoskeletal system brought to light an obvious genu varus, which resulted in varus of the ankle and the subtalar joint. When watching him simulate his swing, we noted that his ankle would subtly invert. By placing an off-the-shelf lateral wedge into the shoe, the player was able to get a better stance and more stability while batting and was able to increase his batting average significantly, winning the major league batting title (Fig. 1-2). A professional quarterback asked for the opinion of three foot and ankle subspecialists. His ruptured Achilles tendon had been repaired one season before the examination. The repair had stretched out and did not allow adequate push-off. After careful discussion by the three orthopaedists who saw the quarterback simultaneously, it was decided to treat the elongated and weak tendon conservatively with an ankle-foot orthosis (AFO). This AFO was made with a plantar assist by using an anterior tibial stop for the AFO (Fig. 1-3). The Hall of Fame quarter back played three
Figure 1-1 Hallux valgus toe spacer is a useful means of conservative treatment for a metatarsophalangeal (MTP) capsular or ligamentous injury.
#3. Conservative care may not conserve resources
#3. CONSERVATIVE CARE MAY NOT CONSERVE RESOURCES
more seasons with a similar brace and never had additional surgery to the Achilles tendon. A top-level and highly paid National Basketball Association (NBA) star sustained within 1 year three sequential injuries to his Achilles tendon that were diagnosed as partial tears. Following each injury, addressed by brief bouts of conservative treatment (physical therapy [PT], nonsteroidal anti-inflammatory drugs [NSAIDs], and rest), he was aggressively encouraged to continue to play despite persistent pain, swelling, and dysfunction. His third injury during the playoffs was the most incapacitating, both physically and emotionally. He lost faith in his doctors, whom he felt had allowed him to be reinjured by trivializing his trauma as insignificant. Much to the frustration of the team management, doctors, and fans, he decided to wait for complete resolution of the swelling, pain, and weakness before resuming play and missed numerous games. Further opinions were sought to bring the situation to resolution. The nonsurgical solution that we initiated satisfied all parties and permitted return with protection. A flexible plastic molded poster shell AFO, fabricated for each game (to avoid sudden and potentially catastrophic fatigue failure of the device), reduced the strain on the Achilles tendon while allowing somewhat restricted and controlled mobility. With the device, he returned to play after a 6-month hiatus and experienced progressive restoration of confidence while the injury continued to heal (Fig. 1-4).
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Figure 1-2 Several views of wedged heel shock absorbers, Anti-Shox by Apex (Teaneck, NJ).
Many stress fractures of the talus and other bones seen on magnetic resonance imaging (MRI) have healed after months of treatment but without surgery. Occasionally these fractures can become long, drawn-out, chronic affairs. The cost of a prolonged convalescence can be overwhelming to the athlete and the team. With this potential for a long recovery, it is typical to use a bone stimulator, despite uncertainty that one truly is needed. Thus whereas the cost may be prohibitive in the nonelite athlete population, it can be justified for the elite performer. An example of the economic impact of the conservative option is provided. A 2-mm, displaced supinationeversion II fibular fracture occurred in a top-level National Hockey League player immediately preseason (Fig. 1-5, A through C). He had no deltoid or syndesmotic tenderness. There were concerns about potential hardware prominence interfering with the skate if an open reduction internal fixation (ORIF) were performed. This would delay return to play until after the hardware was removed. Given the nature of this injury to heal quickly and uneventfully, it was decided to treat the ankle fracture without surgery. The ankle was placed in a cast and the player was kept nonweight bearing for 6 weeks, then given a removable, off-the-shelf, boot brace. He resumed conditioning and ankle strengthening progressively with low-impact activity and then subsequently began skating. At 3 months, he still had tenderness, focal edema, and warmth, and could not skate aggressively or confidently enough to perform choppy sprints or to make quick stops and precision turns. He also was concerned about getting checked and sustaining a complete fracture. The x-ray and computed tomography (CT) scan (Fig. 1-5, D) performed at 3 months showed approximately 20% healing along the proximal posterior aspect. All parties were frustrated, and the team suffered without his talent. Treatments discussed included operative and nonoperative modalities. Among all parties—trainers, manager, team doctor, and the patient—it was agreed that we perform shock wave treatment of the delayed union with the Sonocur extracorporeal machine (which requires no local or general anesthetic), begin an EBI bone stimulator (EBI, Parsippany, NJ), and fabricate a custom-molded, plastic AFO that could be worn in a sneaker. The patient continued to advance in his low-impact skating and nonskating workout, using the brace and bone stimulator when not conditioning. By two additional months, the fracture had progressed to 60% healing and the symptoms had abated to allow return to aggressive skating during the playoffs (Fig. 1-5, E and F).
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Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-3 The Toeoff splint made of carbon graphite (Camp Scandinavia, Helsingborg, Sweden). The Toeoff is an AFO with an anterior tibial shell connected to a foot plate. The brace is open posteriorly.
#4. PATIENCE AND RELATIVE REST ARE VIRTUES A world record holder in the 100 meters had plantar fasciitis and could not compete for 12 months. He cross trained with water running, biking, and lower impact activities to stay in shape. Ultimately, with the use of
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an Achilles stretching protocol, orthotic devices, and a night splint, the fascia finally healed and he recovered. It was a year filled with many office visits and requests for a quick fix. Great runners and elite athletes often find it difficult to be patient. No one knows when or if the condition will resolve. On our side is the knowledge that most cases of plantar fasciitis (more than 90%) respond to conservative modalities by 12 months.
#5. Think about the nerves
The risk of an unusual complication following plantar fascia release and the loss of spring and push-off in this sprinter were outweighed by the benefits of a potentially faster recovery, given the demands of his sport. Of course, 20/20 hindsight is everything.
#5. THINK ABOUT THE NERVES Many patients with a deep posterior compartment syndrome have pain at one specific area. This pain usually
Figure 1-4 AFO for Achilles tendinitis. (Courtesy of John Rheinstein CPO, New York, NY and Otto Bock Healthcare, Minneapolis, MN.)
Figure 1-5 (A-C) Lateral, mortise, and anteroposterior (AP) radiograph of the initial supination-eversion severity rating II fracture in this professional hockey player.
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(continued)
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Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
;
Figure 1-5 cont’d. (D) The player was still symptomatic and a sagittal computed tomography (CT) scan at 3 months shows insufficient bridging of the fracture site. (E) Lateral x-ray at 5 months.
is isolated to the lower edge of the gastrocnemius on the medial side of the leg. With a history of chronic pain in this compartment and a negative scan, exercise compartment testing to rule out exertional compartment syndrome is recommended. On occasion, despite normal pressures, a local fascial release has been performed at the lower gastrocnemius, releasing what we have considered to be an isolated high tarsal tunnel
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syndrome. Occasionally, a specific nerve conduction test and electromyogram (EMG) can pick up a delay of the tibial nerve in the leg. However, because the nerve entrapment is a functional entrapment from a hypertrophied muscle and a squeezing effect on the nerve, the nerve conduction is not always positive. The symptoms may result from a compressed tibial nerve, rather than from lack of oxygen to leg muscles.
#5. Think about the nerves
Figure 1-5 cont’d. (F) Sagittal CT scan at 5 months shows bridging of >60%.
permit the cramping to subside and the leg pain to resolve. Similarly, an athlete with what appears to be lateral exertional compartment syndrome may be suffering from superficial peroneal nerve entrapment. This may present with normal compartment pressures. One should be aware that this condition may occur because of an unstable ankle. In the latter cases, not only does 9
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We have treated several elite athletes, particularly track runners, who have presented with a cramping-type sensation in the posterior calf in the midline area. After a full evaluation of standard posterior calf pain (deep venous thrombosis [DVT], exertional compartment syndrome, muscle tear, and so forth), we have attributed the pain to a sural nerve fascial constriction. Releasing fascia around the sural nerve in this isolated area may
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Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
a superficial peroneal nerve have to be released, but the unstable ankle must be repaired as well. There are anatomic variations of this nerve, and it may lie within the lateral or anterior compartments or both. The jogger’s foot is more common than most physicians realize. The medial plantar nerve may become entrapped at an isolated area at the knot of Henry. Abnormal range of motion may lead to a squeezing effect by the hypertrophied abductor hallucis muscle. A minimal incision releases the medial plantar nerve; because it is relatively deep, care must be taken to avoid damage. The anterior tarsal tunnel syndrome also is fascinating because the deep peroneal nerve may be irritated for several reasons. It can be compressed because of a functional instability of the ankle or the talonavicular joint. The treatment includes a minimal release by cutting the inferior edge of the retinaculum and then carefully removing dorsal bone from the talus or navicular bone (Fig. 1-6). The lateral branch of the deep peroneal nerve may be compressed by the fascia of the extensor brevis muscle, causing a sinus tarsi pain. This is an often-overlooked cause of the sinus tarsi syndrome. In this situation, the nerve should be released where it is focally tender, typically dorsal and medial to the sinus tarsi itself. The fascia of the extensor brevis muscle can be the causative structure, but the physician always must evaluate for ankle instability, as well. We do not recommend transecting this nerve branch as a means of reducing the pain. Interdigital nerves are either entrapped and cut by the edge of the transverse metatarsal ligament or bulbous from chronic compression and scarring of the nerve. If the entrapment is treated before the nerve becomes ‘‘scarred and bulbous,’’ then a simple release of the intermetatarsal ligament may be considered. If the nerve is bulbous, we prefer to remove the
affected nerve, proximal to the transverse metatarsal ligament.
#6. THE TARSAL COALITION CAN BE THE GREAT MASQUERADER When treating the younger, promising, future elite athletes, remember to consider the possibility of a tarsal coalition. Unlike the descriptions in the literature that portray the peroneal spastic flat foot, the tarsal coalitions in athletic individuals present as chronic ankle sprains; chronic calcaneal, navicular or talus stress fractures; posterior tibial tendinitis; tarsal tunnel syndrome; sinus tarsi syndrome; peroneal tendinitis; ankle impingement; or even Achilles tendinitis. They rarely have peroneal spasticity and typically do not have deformities. Often, subtalar motion will be restricted but may not be eliminated. The x-rays may not show the coalition because they may be incomplete, fibrous, or cartilaginous. MRI, CT scan, and/or technetium (Tc) bone scan may be needed to identify the site and extent of the coalition (Fig. 1-7).
#7. TIMING SHOULD NEVER BE UNDERRATED Some of the hardest injuries to treat include the nondisplaced navicular stress fracture, the nondisplaced medial-malleolar stress fracture, the nondisplaced Lisfranc strain, and the high ankle sprain. With many of these injuries, bone stimulators, cast immobilization or bracing, rest, careful PT, and, occasionally, well-placed percutaneous screws are invaluable. Yet the most influential factor is time. Insufficiency in this latter element may lead to more complicated problems, such as displaced fractures or dislocations, and a need for complex surgery.
#8. LOCATION, LOCATION, LOCATION
Figure 1-6 Lateral radiograph of a dorsal osteophyte on naviculum caused a deep peroneal neuralgia.
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A stress fracture of the navicular or medial malleolus generally is more ominous than a middle-lower onethird junction fibula stress fracture. Although the former stress fractures are more likely to preclude athletics, certain stress fractures, such as the latter, can be managed less aggressively. A world record-holding, female, middle distance runner presented with a fibular stress fracture 4 cm above ankle joint. She had excellent strength; good hip, knee, leg, and ankle biomechanics; and no ankle instability
#11. Sometimes it is better to go for the base hit
Figure 1-7 Coronal magnetic resonance imaging (MRI) of a medial subtalar facet tarsal coalition in a young dancer with hindfoot pain. She was referred for evaluation of insertional Achilles tendinitis. She had tenderness medially along the posterior tibial tendon, laterally in the sinus tarsi, and posteriorly by the retrocalcaneal bursa. Following resection of the coalition, all three zones of tenderness resolved.
#9. DESPITE #8, IT IS BETTER TO BE LUCKY THAN GOOD One National Collegiate Athletic Association (NCAA) center for a Final Four basketball team sustained a nondisplaced navicular fracture. The athlete used both a high-intensity ultrasound machine and a bone stimulator for a month before gradually resuming play with an arch support. Two months after the injury, he played in the National Championship game without advancing to a complete fracture. This was a risky choice; a better option would have been to fix the fracture percutaneously without open grafting, in order to minimize the
surgical trauma while reinforcing the weakened bone. The odds were not in our favor, but luck was. After the season, two small screws and a bone graft were used in the navicular, preventing reoccurrence in a 5-year professional basketball career (Fig. 1-8).
#10. A QUICK FIX MAY BUY TIME Unlike the aforementioned case, an NCAA college basketball center presented with a nonhealing proximal second metatarsal fracture (about 1.5 cm distal to the metatarsocuneiform [MTC] joint) several weeks before the beginning of the season. The decision was made to place a screw across the fracture percutaneously and drill the nonunion site. Eight weeks later, the center was able to return to play. At the end of the season, the symptoms were escalating to the preseason level. After the season, the fracture underwent open bone grafting and insertion of a larger screw, and full recovery was permitted during the off season (Fig. 1-9).
#11. SOMETIMES IT IS BETTER TO GO FOR THE BASE HIT A middle distance runner was felt to have first tarsometatarsal (TMT) instability with hallux valgus, second 11
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medially or laterally. She had some forefoot supination that was felt to cause a valgus moment at her ankle while she was striding. After careful analysis of her condition, it was agreed that she could, with use of a semirigid orthotic, run one race that she and her trainer felt was essential for her preparation for the World Championships. The plan was that, following this event, she would then do easy training for two and a half weeks before her next big race. During the event, not only were the symptoms controlled but she had the greatest race of her career, winning the world championship as her Eastern European challenger fell, chasing her at the finish.
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-8 (A) Centrally located navicular stress fracture seen on the anteroposterior (AP) x-ray (arrow). (B) Sagittal magnetic resonance imaging (MRI) demonstrates edema in the naviculum.
metatarsophalangeal (MTP) subluxation, and lesser metatarsal overload. A Lapidus procedure with MTC fusion was recommended to correct the deformity. Because most of the symptoms were at the bunion and the runner could not take off more than 8 to 12 weeks, a chevron bunionectomy was performed, ignoring the first TMT instability. The runner did have a recurrence 10 years later, but that was after he had participated in
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two Olympics and set an American record on the roads (Fig. 1-10).
#12. PLAN TWICE, CUT ONCE Treatments should be reviewed and rereviewed and should stand up to scrutiny readily provided by the
#13. A stealthlike incursion should leave ne’er a trace
Figure 1-8 cont’d. (C and D) Two small screws were inserted from the medial pole.
it does permit concerted preoperative appraisal. Any ‘‘wasted’’ time often will be recouped intraoperatively or postoperatively.
#13. A STEALTHLIKE INCURSION SHOULD LEAVE NE’ER A TRACE Our philosophy with the elite athlete is to restore the anatomic structure with the least surgery possible and
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athlete, family, coach, trainer, and agent. Similarly, when devising a surgical plan, it always is useful to review all the other alternatives for one’s own benefit, even though one may have a preferred treatment that has worked well in the past. One should think about how the plan or the alternatives will affect any associated conditions, the rehabilitation, return to sport, and lifelong function beyond sports. Even though the exercise of mapping out the screw placement or osteotomy is tedious or may be considered remedial,
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-9 (A) An anteroposterior (AP) x-ray reveals the second metatarsal stress fracture in this basketball player that became symptomatic just before the season. (B-D) Magnetic resonance imaging (MRI) demonstrates the proximal fracture. (E) Intraoperative fluoroscan shows the insertion of the screw in a minimally traumatic fashion that permitted him to start the season. Toward the end of a relatively asymptomatic season, his symptoms increased and he underwent open bone grafting and insertion of a larger screw. Full recovery occurred in the off season.
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#15. Identify injuries that are at high risk for failure
#14. MINIMIZE SURGERY AND MAXIMIZE RECOVERY
then use a functional recovery. When surgery is performed, the tissues should be minimally disturbed. One should know where to go, not dissect widely, avoid disrupting soft tissue planes, save neurovascular structures, do the repair, and take care on the way out. Postoperative management should allow rehabilitation without compromising the integrity of the reconstruction. Initially a half-cast or U-splint and posterior splint are used, followed by removable bracing with early range of motion. This is especially important with Achilles tears. One gifted sprinter ruptured his Achilles tendon in the finals of the Olympic 100 meters. With a minimal incision and limited exposure, the Achilles was sutured. The anterior fat pad was reapposed, and the paratenon was repaired. Early plantarflexion range of motion was instituted postoperatively. The sprinter was kept in equinus for 1 month in a plantarflexed brace. Walking without the brace was permitted by 10 weeks. Progressive impact activities were permitted with careful monitoring by an excellent trainer/therapist. The sprinter was running aggressively by 9 months, and, by 1 year, full-out sprinting was comfortable. The sprinter came back in 18 months and ran the fastest 60-m indoor race of the year despite this potentially career-ending injury.
#15. IDENTIFY INJURIES THAT ARE AT HIGH RISK FOR FAILURE Stress fractures of the medial malleolus, especially vertical type stress fractures, need a vertical repair, not a
Figure 1-11 Spring ligament repair. The torn spring ligament is seen after the posterior tibial tendon sheath is opened. The triangular open arrow demonstrates the posterior tibial tendon, the solid arrow points to the naviculum, and the open arrow shows the talonavicular ligament and spring ligament. The inset displays the ligament being held by forceps.
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Figure 1-10 Preoperative x-ray of an elite runner with hallux valgus and second metatarsophalangeal (MTP) joint instability who ultimately had a chevron bunionectomy instead of a Lapidus and second MTP joint procedure, as recommended elsewhere.
A pole vaulter missed the pit, landing on his foot in abducted fashion. This led to the development of a spring ligament/deltoid complex detachment. Ecchymosis and tenderness were noted medially anterior to the medial malleolus. The foot assumed an abducted posture with bulging around the talonavicular joint. The posterior tibial tendon had excellent strength with full inversion power 45 degrees past the midline against resistance. An MRI showed changes in the spring ligament. Intervention with an anatomic and secure repair was critical to the pole vaulter’s future career. The reconstruction was accomplished through a 4-cm incision (Fig. 1-11). After the torn spring ligament was exposed at its navicular insertion, the edges and thinned portions were debrided. The proximal medial aspect of the pole of the navicular was roughened, establishing a cancellous bleeding surface through which an osseous suture anchor was placed, thereby avoiding inadvertent talonavicular joint penetration. A splint was applied following surgery. This was replaced by a brace that was worn for 16 weeks. A heel lift was used for 6 to 8 weeks subsequently. Rehabilitation succeeded in permitting this athlete to resume his career and to set the American pole vault record on his repaired foot.
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
horizontal repair. If a horizontal typical medial malleolar screw is used in a vertical stress fracture of the medial malleolus, the stresses are not adequately removed to allow healing, making it possible for the fracture to recur and the screw to break. For that reason, a buttress plate on the medial malleolus should be used to relieve the vertical stresses (Fig. 1-12). One sprinter with an injured ankle and a medial malleolar stress fracture was treated with nonweight-bearing activity and with conservative care for 2 months. His ankle healed, and he went on to have a 15-year career, including an Olympic appearance 12 years later, and no further stress fractures occurred (Fig. 1-13). Other athletes have had these vertical fractures, particularly those with some genu varus or heel varus. There is an inordinate amount of stress placed through the medial malleolus, and conservative care will not suffice. In these vertical fractures, extending above the articular cartilage, the stress fracture should be curetted and small local bone graft should be injected; then a medial buttress plate should be used to remove the vertical stresses.
Figure 1-12 This medial malleolar stress fracture was unrecognized and went on to complete fracture. Notice the medial talar osteophyte. The fracture was fixed with horizontally placed compression screws and an Ace Depuy (Warsaw, IN) fibular plate.
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An NBA guard had a vertical stress fracture with a medial malleolar screw and bone graft. The fracture healed; however, the following year, an additional fracture occurred in the same area and had to be fixed with a buttress plate and bone graft (Fig. 1-14). Following treatment, the NBA guard has been able to play for 3 years with no further problems, playing 30 out of 48 minutes in each game. Functional problems with biomechanical stresses need repair, eliminating those stresses that caused the injury.
#16. A LITTLE INSTABILITY CAN GO A LONG WAY: KEEP BOTH EYES OPEN Some joints are susceptible to ligamentous damage that can present with occult instability and therefore are often overlooked. Nearly all physicians can identify lateral ankle ligamentous injuries, but what about the spring ligament, the anterior deltoid, the Lisfranc ligament, or instability of the MTP joint’s plantar plate? A turf-toe injury of the great toe is a diagnosis that may represent many anatomic problems. The standard great toe strain, a first- or second-degree turf-toe, often can be treated by using rigid plate inserts in the shoe and taping the great toe. If there is a complete rupture or thirddegree turf-toe type injury, there may be complete separation of the sesamoids from the proximal phalanx with rupture of the sesamoidal phalangeal ligament(s); or there may be a complete rupture of the adductor or abductor tendon from the base of the proximal phalanx of the great toe with or without collateral ligament injury, causing marked laxity of the first metatarsal phalangeal joint. There can be diastasis of a bipartite sesamoid or disruption of the flexor hallucal brevis tendons from the sesamoids. In these cases, performing bilateral anterior draw maneuver and checking flexor hallucis longus (FHL) and flexor hallucis brevis (FHB) function may reveal the deficit. Further testing with a varus or valgus stress also is helpful, as well. X-rays and MRIs can show irregular position of the sesamoids with ligament and/or tendon rupture. These instabilities can result in problems cutting, pivoting, running, and jumping. Long term, if unaddressed, the joint subjected to nonphysiologic shear stresses will suffer degenerative changes. If recognized early, the condition can be repaired and the cycle of deterioration halted. Although the rehabilitation period is 6 to 9 months, return to top performance is possible (Fig. 1-15). The plantar plate injury in the lesser MTP joints also can be a ‘‘small’’ problem with grave consequences if the joint subluxates or, even worse, dislocates. This is particularly true when there is a long second metatarsal. Again, early recognition with the anterior draw test and varus/valgus stresses is paramount. Although further
#16. A little instability can go a long way: keep both eyes open
Figure 1-13 The magnetic resonance imaging (MRI) showed this medial malleolar stress fracture that healed following conservative treatment.
Figure 1-14 fracture.
(A) The x-ray shows a medial malleolar stress (continued)
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subluxation of the second metatarsophalangeal joint may be prevented by initially treating a plantar plate strain of the metatarsal phalangeal joint (including plantarflexion stretching of the extensor tendon by use of a metatarsal pad and toe taping), surgical repair may be warranted. Once the plantar plate stretches out significantly, either acutely or chronically, surgery must be considered (Fig. 1-16). In this case, a second MTP dislocation and hallux valgus were treated with a ChevronAkin osteotomy and open reduction of the dislocation. The second MTP joint was stabilized with a 0.62 pin, which was left in place for 3 weeks. In the patient with a long second metatarsal and unstable MTP joint, we do an oblique osteotomy to shorten the metatarsal (Fig. 1-17). Why do some fibular stress fractures and high ankle sprains lead to diastasis of the ankle joint, whereas other fractures of the fibula do not? (Fig. 1-18). At times, incompetence of the anterior deltoid ligament or spring ligament is to blame. When rotary ankle injury occurs with or without fibula fracture, one should check for tenderness in the anterior deltoid (Fig. 1-19). If there is excessive swelling and tenderness over the anterior deltoid or spring ligament, a repair should be considered in the high-performance athlete. If the anterior deltoid ligament is torn from the medial malleolus or off the
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-14 cont’d. (B) After fixation with a single screw, the fracture ultimately failed and the complete fracture was treated with bone graft and medial malleolar plating with a Synthes tibial plate.
the medial malleolus or the navicular to repair the torn anterior deltoid. If there is some question about whether the diastasis needs support, a diastasis screw should be used after the anterior deltoid has been fixed.
#17. WHEN IS IT OKAY TO ‘‘SPARE THE ROD AND SPOIL THE ATHLETE’’?
Figure 1-15 Sagittal magnetic resonance imaging (MRI) demonstrates the rupture of the plantar plate (solid arrow shows retracted sesamoid; open arrow points to intact flexor hallucis longus [FHL] tendon, which is directly plantar to the rupture of the sesamoid phalangeal ligament).
navicular attachment, the ankle is allowed to rotate out of the ankle mortise. Unfortunately, if a diastasis screw is placed across the tibiofibular joint, the talus will continue to sublux forward in the ankle mortise. In severe injuries of the ankle in which there is a lateral malleolar fracture and a diastasis, consider repairing the injury by plating the distal fibula and putting anchors in either
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Midtibial chronic stress fractures with the ‘‘dreaded black line’’ usually respond to drilling without the need for bone grafting (Fig. 1-20). We have success with ballet dancers with a minimal drilling of the isolated tibial stress fracture under x-ray control. Dancers have gone on to long careers without reoccurrence of the stress fractures once this tibial stress fracture heals from isolated drilling. It is imperative for the ballet dancer or the athlete to avoid torque for 2 to 3 months before or after the drilling process so that the stress fracture does not lead to a complete catastrophic fracture.
#18. WORK BACKWARD IN ESTABLISHING A RETURN TO SPORT PROTOCOL One should realize that designing an appropriate return to the sports program requires not only an appreciation
#18. Work backward in establishing a return to sport protocol
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Figure 1-16 In this case, a second metatarsophalangeal (MTP) dislocation and hallux valgus was treated by open reduction and pinning of the second in conjunction with a Chevron-Akin osteotomy. The joint was stabilized with a 0.62 pin across the MTP joint that was left in place for 3 weeks.
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-17 (A and B) This ultra-marathon runner had been treated conservatively for a progressively more symptomatic second hammertoe, second metatarsophalangeal (MTP) subluxation, and hallux valgus. (C) Return to running was 10 weeks with this distal chevron osteotomy coupled with a distal second metatarsal oblique osteotomy and proximal interphalangel fusion.
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#20. It is better to have no publicity than bad publicity
elliptical trainer. At 6 weeks postoperatively, an Airsport or lace-up ankle brace is applied, allowing for more mobility. Dancing at the barre is permitted but releve´ beyond the 40-degree plantarflexed position must be avoided so as not to stretch the repair. At 10 to 12 weeks, the releve´ restrictions are gradually lifted, but full pointe should not be achieved until 14 weeks. Once full range of motion permits completion of the barre exercises without pain or swelling, the dancer may begin center work. The dancer should initially avoid pirouettes, large jumps, or leaps. As soon as the dancer masters the smaller jumps and rapid weight shift from side to side, he or she can advance to performing faster movement combinations that incorporate the pirouettes and jumps, ideally by 18 weeks. To reach the target release date, the dancer should be able to handle a full class and rehearsal by 20 weeks. During rehabilitation, the trainer, teacher, and/or orthopaedist must continuously assess the dancer’s signs and symptoms to ensure that the reconstruction is not undone as these new stresses are introduced.
of the competition or performance schedule but an assessment of the timing and requirements of a reconditioning program. The clinician should learn from the athlete, trainer, and coach what milestones and competencies are achieved in the typical preseason routine and how long they take to be mastered. Next, knowing the magnitude of the injury and requisite recovery to nonathletic baseline, one should anticipate the tasks and time for reestablishing the athletic baseline. Along the way, the clinician should determine what testing or standards will be used to permit safe advancement to the next level of activity. A good example is a ballet dancer with chronic ankle instability who undergoes a lateral ligament reconstruction. To return to high-level dance, he or she must achieve not only full range of motion, strength, stability, and proprioception but also endurance. In our basic protocol, the athlete is off the foot and in a posterior splint for 10 to 14 days after surgery. Then a boot brace is applied and the athlete is allowed to be fully weight bearing. During this time, a strengthening program is initiated and the ankle can be put through a range of motion from maximum dorsiflexion to 30 to 40 degrees of plantarflexion, avoiding any inversion. Cardiovascular workout can be achieved using an exercise bike or
#19. EVERYONE LOVES A WINNER The easy cases that require little worry and intervention are a pleasure to recap and ponder. The challenge is to stay engaged with the ones that are not following the typical pathway. One should be prepared to get additional advice. At the least, the clinician should step back, clear the mind of any assumptions, and acquire new or revisit old information about the case. This process of providing oneself with a second opinion generally is productive and will allow the less successful recoveries to switch to the winning category.
#20. IT IS BETTER TO HAVE NO PUBLICITY THAN BAD PUBLICITY It is the athlete’s business to converse with the public through the media. The clinician must respect the wishes of the patient and his or her team for confidentiality. These days it is the law. The clinician’s glory will come in a quieter manner long after the fans have lost intense interest as the athlete manages to return without a relapse or reinjury through the season. One should let the agents, athletes, and team handle the press. In addition, a worse situation is the negative press associated with failure or a complication, whether or not the physician was responsible.
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Figure 1-18 Fibula stress fractures need to be evaluated for medial ankle ligamentous instability and occult syndesmotic instability. Although pain can be the best guide, stress views and a magnetic resonance imaging (MRI) may be helpful.
CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-19 (A) This is an athlete whose magnetic resonance imaging (MRI) demonstrated a fibula stress fracture (open arrow); (continued)
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#20. It is better to have no publicity than bad publicity
Figure 1-19 cont’d. (B) Regular arrow shows fracture. There also is edema of the talus dome laterally, deltoid signal abnormalities, and changes in the anterior tibial fibular ligaments (open arrow shows the syndesmotic injury). (continued)
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CHAPTER 1
Assessment and treatment of the elite athlete: helpful hints and pertinent pearls
Figure 1-19 cont’d. (C) The coronal MRI views demonstrate the syndesmotic injury (regular and open arrows).
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Conclusion
CONCLUSION The elite athlete presents a wide variety of challenges that require a keen knowledge of anatomy, biomechanics, physiology of healing, and psychology to interpret. Usually the physician and athlete are surrounded
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Figure 1-20 The white arrow delineates the ‘‘dreaded black line’’ of the established tibial stress fracture.
by issues, trainers, coaches, agents, team physicians, owners, and other consultants who influence the interaction. The big picture is visualized so that the static and dynamic factors can be assessed. Odd conditions present with uncharacteristic symptoms, and standard conditions may manifest in peculiar ways. The physician should think profoundly to determine the diagnosis and then create a customized treatment algorithm that incorporates conservative and surgical modalities. One should provide honest and evidence-based opinions. The timing obviously is important. Being cost conscious is laudable, but the cost of a conservative or surgical treatment sometimes is dwarfed by the cost of missed games and bad seasons. If an operation is warranted, it should be well conceived, striving for a biomechanically logical and anatomically sound reconstruction with limited surgical trauma. Postoperative rehabilitation and return to sport or dance should be mapped and reassessed along the way to avoid a setback. Communication should flow to the patient and his or her immediate family and should involve the trainers, therapists, coaches, and agents as permitted by Health Insurance Portability and Accountability Act (HIPAA). The media should be directed to contact the player or his or her designee. Most importantly, one should keep an open and creative mind, work hard, treat people with dignity, and enjoy the journey. Once the athlete, the trainer, and the agent see positive outcomes, other cases will follow and the physician will slowly develop a good reputation for being a doctor who treats winners.
........................................... C H A P T E R 2 Impingement syndromes of the foot and ankle William G. Hamilton, Mihir M. Patel, and Roman A. Sibel CHAPTER CONTENTS ...................... Introduction
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Specific anatomic areas
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General technique tips for osteophyte removal
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References
43
INTRODUCTION ‘‘Impingement’’ is derived from the Latin verb impingere, meaning ‘‘to force against.’’ The periosteum is composed of two layers: the superficial (fibrous layer) and the deep (cambium) layer. The cambium layer has osteogenic potential. This can be seen following conditions that strip the periosteum from the underlying bone (e.g., tumors and fractures). In impingement, one bone’s repetitively striking the other can stimulate the cambium layer to form osteophytes. Once the osteophytic prominence forms, impingement occurs more easily, so that the impingement spur, once formed, often increases in size and eventually may break off, forming a loose body. Conservative treatment should be aimed at breaking this repetitive cycle so that the impingement spurs do not enlarge and produce irritation. In ballet we tell the dancer not to ‘‘hit bottom’’ in the plie´ (knee-bend) when he or she lands from a jump and the ankle is forced into maximal dorsiflexion. These restrictions often are difficult to follow or are too restrictive. Therefore if the symptoms warrant, and conservative treatment is not working, surgery usually is indicated.
GENERAL TECHNIQUE TIPS FOR OSTEOPHYTE REMOVAL 1. Get adequate exposure and visualization. If one is using the arthroscope and struggling, one should open it up and do the job right.
2. Make the skin incisions carefully to avoid incisional neuromas. Nothing is more discouraging than a good clean-out that is spoiled by a hypersensitive scar. 3. Be sure to get all the osteophytes out; there can be hidden spurs or more than one. If there is any doubt, it is best to take an x-ray in the operating room at the end of the case to make sure nothing has been missed.
SPECIFIC ANATOMIC AREAS The interphalangeal joint of the hallux Dorsal impingement with spur formation similar to that seen in the first metatarsophalangeal (MP) joint can occur in this joint. It can be a sign of degenerative joint disease (DJD) but usually is secondary to stiffness and lack of motion in the adjacent MP joint. When hallux rigidus forms in the first MP joint, the interphalangeal (IP) joint will be forced into excessive dorsiflexion in an attempt to compensate for the lack of motion in the proximal joint. At times this can be dramatic. I once saw a female dancer who was born with congenital ankylosis of both first MP joints. They were totally rigid. She had Grecian (Morton’s) feet with short first rays and had developed 90 degrees of dorsiflexion in her IP joints so that she had a full demipointe releve´. Rigidity in this joint can be treated similarly to the condition found in the first MP joint. One should remember, however, that this joint is forgiving, and surgery is rarely necessary.
CHAPTER 2
Impingement syndromes of the foot and ankle
The lesser metatarsophalangeal joints Dorsal impingement in these joints usually is associated with Freiberg’s disease.1 This condition is no more common in athletes and dancers than it is in the general population. One should remember, however, that it can be symptomatic for as long as 6 months before it appears on x-ray and should be considered in unexplained metatarsalgia in young patients. A bone scan or magnetic resonance imaging (MRI) usually will confirm the diagnosis before plain radiographic changes are evident. Freiberg’s infarction comes in the following four variations.1 Type I The head of the metatarsal (MT) dies and then heals by ‘‘creeping substitution’’ (Phemister2). In this form it may heal completely, with little or no collapse, leaving the articular surface intact and almost as good as it was before the event occurred. Surgery often is not necessary.
Figure 2-1 A rare case of multiple Freiberg’s disease.
Type II The head collapses during revascularization and the articular surface settles and remains intact, but peripheral osteophytes form along the dorsal margin of the joint, limiting dorsiflexion. This type is amenable to a dorsal clean-out (cheilectomy), which should leave the joint intact and restore dorsiflexion. (The surgeon should remember to remove more bone than he or she thinks is necessary when performing this operation.) Type III The head collapses and the articular surface loosens and falls into the joint, leaving the joint totally destroyed. Obviously simply removing the osteophytes will not suffice in this case—an arthroplasty is required. All the necrotic bone must be excised from the MT head and all the dorsal osteophytes must be removed. Usually the plantar portion of the head is left when this has been done. The surgeon should be generous in the excision to permit full dorsiflexion later, but the entire MT head should not be removed. Either a dorsiflexion osteotomy of the MT head or a capsular arthroplasty, similar to the one described for use in the first MP joint, can be useful in this situation. Type IV Multiple heads are involved in the process (Fig. 2-1). This type is rare and actually may be a form of epiphyseal dysplasia. Each MT head must be evaluated and treated individually. A Freiberg-like syndrome can occur in the fifth MT head following a nondisplaced or minimally displaced fracture of the distal MT shaft, similar to the ‘‘boxer’s fracture’’ of the fifth metacarpal (Fig. 2-2).
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Figure 2-2 ‘‘Boxer’s fracture’’ of the distal fifth metatarsal (arrow).
Lesser MP joint instability Metatarsalgia is not common in the young, healthy athletic population. When it is encountered, one should suspect either early Freiberg’s disease or MP instability.1 This subtle problem often goes unrecognized because the x-rays are normal. The patient presents with isolated metatarsalgia. There is plantar tenderness under the MT head and dorsal tenderness where the phalanx subluxes on top of the head when the patient releve´s or goes up on the ball of the foot. The subluxated phalanx pushes the head of the metatarsal downward, producing the metatarsalgia, the so-called dropped metatarsal. It is recognized easily on physical examination if one remembers to observe for it. The Lachman test of the MP joint will be positive.1 The base of the proximal phalanx is grasped in the fingers, and a dorsal-plantar force is applied. The instability is recognized easily
Specific anatomic areas
inflammatory medication; and, if necessary, giving the patient one or two (at most) intra-articular injections of steroids. If this fails, exploration and appropriate surgery are indicated. Surgical options include (1) extensor tendon lengthening with resection of the plantar condyles of the MT head, (2) Girdlestone-Taylor3 procedure, (3) DuVries-type arthroplasty,3 and (4) resection arthroplasty with partial syndactyly to the adjacent digit.
Lachman test of the metatarsophalangeal (MP)
when the phalanx subluxes on the top of the MT head (Fig. 2-3). Conservative treatment consists of padding to unload the painful MT head and taping or wearing a toe retainer to try to control the instability (Fig. 2-4). It often is a frustrating situation for the dancer or athlete because he or she does not want to undergo surgery, but once the ligaments and plantar plate are stretched, they can be tightened again only by surgery. The surgical options for this problem in a dancer are tricky. The usual operations for this condition (stabilizing procedures such as the Girdlestone-Taylor operation3) are inappropriate for athletes because they stabilize the joint but also limit dorsiflexion—an unacceptable solution for dancers, gymnasts, and so forth. We have had success in a limited number of dancers and athletes with a resection arthroplasty and partial syndactyly, especially in the fourth MP joint, which seems especially prone to this problem. As previously noted, one should not remove too much of the proximal phalanx (one-fourth to one-third at most), and one should remove the plantar condyles of the MT head, use a toe wire, and remove it early (2 weeks).
Idiopathic synovitis Idiopathic synovitis4 is characterized by MP swelling, the so-called sausage toe. Its cause is controversial. (It usually is not caused by systemic inflammatory diseases, but of course these must be ruled out.) It usually is associated with laxity of the joint and MP instability. Whether the looseness irritates the joint and leads to chronic synovitis or the synovitis loosens the joint is not known. Conservative therapy involves stabilizing the joint by using tape or toe retainers (see Fig. 2-4); having the patient reduce activities and take anti-
Figure 2-4 instability.
Taping to control metatarsophalangeal (MP)
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Figure 2-3 joint.
Medial midfoot impingements True impingements in the midfoot are rare. Occasionally, accessory ossicles can be seen between the bases of the metatarsals or the cuneiforms; symptoms may warrant their removal. These bones, more often than not, will be asymptomatic. An isolated osteophyte on the dorsum of the midfoot occasionally can cause entrapment of the deep peroneal nerve or irritation of the extensor hallucis longus (EHL) tendon as they pass over it. Initially, extra padding on the undersurface of the tongue of the shoe may resolve pain. If this fails, removal of the osteophyte may be necessary. The painful accessory navicular is not due to an impingement and is discussed in Chapters 8, 14, and 27.
CHAPTER 2
Impingement syndromes of the foot and ankle
Lateral midfoot impingements In the lateral midfoot, three related conditions are a combination of impingement and subluxation: (1) derangement of the cuboid—base of the fourth and fifth metatarsal joints, (2) cuboid subluxation, and (3) sinus tarsi syndrome. Subluxation of the cuboid5 and derangement of the cuboid—base of the fourth and fifth metatarsal joints— often are seen together. The subluxing cuboid is a common but poorly recognized condition. It presents as lateral midfoot pain and an inability to ‘‘work through’’ the foot. Pressing on the plantar surface of the cuboid in a dorsal direction is painful. The normal dorsal-plantar joint play is reduced or absent when compared with the uninjured side. (Because of this immobility, the condition sometimes has been referred to as a ‘‘locked cuboid.’’) Often there is a shallow depression on the dorsal surface, a palpable fullness on the plantar aspect of the cuboid, and subtle forefoot valgus. Documentation by x-ray, computed tomography (CT) scan or MRI is difficult because of the normal variations found in the relationship between the cuboid and its surrounding structures. The diagnosis must be made on the basis of the history and physical findings. Treatment involves recognition of the pathology and manual reduction by a therapist or physician familiar with the condition and follow-up to be certain that it remains in place. Therapists and orthopaedists involved in the care of athletes and dancers should be aware of the subluxed cuboid and be able to recognize it when it occurs. When the cuboid subluxes plantarward, the bases of the fourth and/or fifth metatarsals often are elevated, causing the head of the fourth metatarsal to be depressed (Fig. 2-5, Table 2-1). There usually are two types of cuboid subluxations: acute and chronic/recurrent. Treatment consists of recognition and manual reduction by a therapist familiar with the condition. The cuboid then must be held in place by taping and padding for several weeks to prevent recurrence. If the subluxation has gone unrecognized and the joint has been subluxed for any length of time, reduction can be difficult. The forefoot valgus must be corrected and the lateral column lengthened manually before the reduction can be performed. In the chronic condition, it may not be possible to keep the cuboid reduced if it goes in and out at random. In these cases, athletes often can be taught to reduce the subluxation themselves (Fig. 2-6). Sinus tarsi syndrome4 is a controversial condition that produces pain deep in the sinus tarsi that increases with activity and is exacerbated by impact (jumping and running) and pronation. It is often, but not always, a sequel to a sprained ankle. On physical examination, there is discrete tenderness, or a ‘‘trigger point’’ deep in the
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Figure 2-5 A ‘‘dropped’’ fourth metatarsal head resulting from elevation of its base. (From Marshall PM, Hamilton WG: Am J Sports Med 20:170, 1992.)
sinus tarsi, and forceful abduction-pronation of the heel and midfoot may be painful. The condition usually can be confirmed with an injection of 0.5 ml of lidocaine into the trigger point. If the pain is relieved by the local anesthetic, a second injection of 0.15 ml of corticosteroids often can be highly effective. The condition is thought to have several etiologies: (1) soft tissue entrapment or partial tear of the interosseous talocalcaneal ligament, (2) osteophyte impingement (Fig. 2-7), (3) neural entrapment (motor nerve to the extensor digitorum brevis [EDB]), (4) degenerative arthrosis,
Table 2-1 Cuboid subluxation
Symptoms
Signs
Lateral midfoot pain
Tender plantar mass
Weakness in push-off
Decreased joint play
Inability to ‘‘work through’’ the foot
Shallow depression over the cuboid
Function limited by pain
Subtle forefoot abduction
Specific anatomic areas
from bleeding into the joint in conjunction with an ankle sprain, can cause residual symptoms after the sprain has healed. Conservative treatment consists of anti-inflammatory medication, physical therapy, a medial heel wedge or arch support to open up the sinus tarsi, and, if necessary, the previously mentioned cortisone injection. If symptoms persist and the diagnosis has been confirmed with lidocaine injection, surgical exploration and clean-out is indicated. This is one area in which an injection— if placed in the right spot—often is dramatically effective and will avoid surgery. Finally, the sinus tarsi syndrome often is found in conjunction with lateral ankle ligament laxity, and, in these cases, sinus tarsi exploration and debridement should be considered if ankle ligament reconstruction is planned. More about the subtalar joint can be found in Chapter 15.
Figure 2-7
Reduction of a subluxed cuboid by the patient.
Sinus tarsi syndrome; note osteophytes (arrow).
and (5) arthrofibrosis. It can be difficult to differentiate this syndrome from subtalar dysfunction, and osteophytes can be found in the sinus tarsi that are not causing symptoms. The two areas are anatomically close together. One of the best ways to differentiate one from the other is to pay close attention to subtalar motion. Mann and Coughlin3 have shown how important subtalar motion is to normal foot mechanics. Subtle loss of this motion, such as arthrofibrosis of the subtalar joint
Anterior (medial, central, lateral) Anteromedial ankle pain often comes from impingement of the anterior portion of the medial malleolus against an impingement spur on the medial shoulder of the talus. This spur is hard to see on x-ray because it cannot be visualized on standard lateral radiographs. However, nonweight-bearing, oblique x-rays of the foot may detect these spurs. The spur often can be palpated on physical examination and should be looked for in any anterior ankle clean-out. It is easy to miss, the ‘‘hidden spur.’’ To visualize and resect this spur arthroscopically, the surgeon must hold the ankle in dorsiflexion. Anterocentral is the location of the classic anterior ankle impingement. It comes in the following four types: 1. Spurs are primarily on the lip of the tibia. This type is ideal for arthroscopic debridement. Under direct vision, the lip of the tibia can be removed 33
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Figure 2-6
The ankle When considering ankle impingement, one should remember the basic anatomy of the ankle. The talus sits sidesaddle on the os calcis so that the axis of the talus is roughly in line with the first web space of the foot and the axis of the os calcis is in line with the fourth web space (Fig. 2-8). In dorsiflexion, bony impingement occurs anteromedially between the neck of the talus and the anterior lip of the tibia. In plantarflexion, bony impingement occurs posterolaterally between the os calcis and the posterior lip of the tibia. Therefore anteromedial and posterolateral problems usually are associated with bony impingement, whereas anterolateral and posteromedial problems usually are soft tissue in origin (there is no bony impingement in these areas). The anterior ankle is an extremely common location for impingement, but impingements can be found in all quadrants around the ankle: anterior, lateral, posterior, and medial.
CHAPTER 2
Figure 2-8
Impingement syndromes of the foot and ankle
Axis of talus versus axis of os calcis.
fairly easily with a thin osteotome or burr. Care should be taken not to damage the dome of the talus, either by holding the ankle in maximal dorsiflexion or by using an osteotome with blunt edges, as described by Scranton and McDermott.6 2. Spurs are primarily on the neck of the talus. This type is more difficult to treat with the arthroscope, because the osteophytes often are within the capsular insertion on the neck of the talus, and it is necessary to strip off the capsule distally to visualize the pathology. It is easy to miss some of the osteophytes; therefore intraoperative imaging may be needed to ensure adequate removal. 3. Spurs are present on both the lip of the tibia and the neck of the talus, sometimes with loose bodies that have broken off the osteophytes. This type is common and is the most difficult to deal with. In the early 1980s, I thought professional dancers would return to dancing sooner if their anterior debridement could be done with the arthroscope. I found that, in all but the most uncomplicated cases, it took 3 months for them to return whether the operation was performed with the arthroscope or with a small anterior arthrotomy. Use of the arthroscope often was taking more than an hour and required an x-ray to be certain that I had not missed anything, whereas the arthrotomy took 30 to 40 minutes and rarely required intraoperative imaging. I thought that I was doing a better job, with less surgical time, with the open technique. I have therefore gone
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34
back to a small anterior arthrotomy on these complex cases, with the use of a headlamp and ArmyNavy retractors to allow adequate visualization. 4. Multiple anterior osteophytes can be present secondary to frank osteoarthritis of the ankle. Anterior clean-out in these cases is of questionable effectiveness and probably should not be performed for this condition. Anterolateral ankle pain usually is not due to bony impingement because the tibia and talus do not come together in this location. Difficulties in this area usually are due to one of two conditions: Basset’s ligament and Ferkel’s phenomenon. Basset’s ligament7 is an abnormal distal slip of the anterior tibiofibular ligament extending so far distally on the lateral malleolus that the lateral shoulder of the talus impinges against it when the ankle is plantarflexed (Fig. 2-9). It is difficult to diagnose but, when present, can be resected with the arthroscope. Ferkel’s phenomenon8 is an accumulation of scar tissue and synovitis in the anterolateral gutter of the ankle, usually following trauma. It causes symptoms similar to Basset’s ligament and also is amenable to arthroscopic debridement. Anterior syndesmosis pathology usually is not the result of impingement but can cause anterolateral ankle pain that is exacerbated by dorsiflexion of the ankle because the wide portion of the talus spreads the malleoli and places tension on the anterior tibiofibular ligament. There are three types of pathology: 1. A sprain of the syndesmosis, the ‘‘high ankle sprain’’ sometimes can take an extraordinarily long time to heal.
Figure 2-9 Basset’s ligament. (Arthroscopic view seen from the medial portal.)
Specific anatomic areas
Figure 2-10 Fracture of the anterior process of the os calcis.
misdiagnosed as an ankle sprain, because routine plain radiographs often are read as normal. CT is the study of choice for diagnosis. Surgical treatment options range from excision to open reduction internal fixation (ORIF), depending on the size of the fragment.14 Talus pathology is covered in more detail in Chapter 14. 4. An accessory ossicle, the os subfibulare, which had been asymptomatic, can be loosened by injury and become symptomatic. 5. Avulsion fractures of the tip of the fibula can become trapped in or under the lateral ankle joint and become symptomatic. The bony fragment often is in the insertion of the calcaneofibular ligament. If it is small, it should be excised and the stump of the ligament sutured into the tip of the lateral malleolus. If it is large, it often can be reattached with a screw or K-wire. Infrequently the same situation can be found at the anterior edge of the lateral malleolus at the insertion of the anterior talofibular ligament (ATFL) (Fig. 2-11).
Figure 2-11 Fracture of the tip of the fibula trapped under the lateral malleolus.
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2. The Tillaux fracture is an avulsion fracture of the insertion of the distal tibiofibular ligament into the tibia. On rare occasions, the avulsion can occur on the fibular side. 3. Synovial hernias into rents in the tibiofibular ligament have been described.9 The lateral ankle can be a complex site of pain and discomfort, and an accurate diagnosis in this area can be difficult. Symptoms in this area often have their onset following ankle sprains. The original trauma often can be mild—for example, a first-degree sprain with no resultant lateral instability. Cuboid subluxation and the sinus tarsi syndrome were discussed earlier. Other conditions to consider are as follows: 1. The ‘‘meniscoid’’ of the ankle10 is thought to be soft tissue trapped between the lateral shoulder of the talus and the lateral malleolus. McCarroll et al.11 described this lesion in four soccer players who had a history of frequent ankle sprains and, after failing conservative treatment, underwent arthroscopic debridement of the lesion. After appropriate rehabilitation, all four returned to competition with cessation of symptoms, with one player having only rare pain. 2. An avulsion fracture of the anterior process of the os calcis12 is not an impingement. It is an avulsion fracture of the origin of the EDB and EHB. It usually can be seen on an x-ray (Fig. 2-10) and diagnosed on physical examination by the specific tenderness at the anatomic site or pain with pronation-supination of the forefoot. Persistent symptoms may warrant excision of the fragment (see Fig. 2-10). 3. Fracture of the lateral process of the talus13 also can cause impingement beneath the lateral malleolus. This fracture has been labeled the ‘‘snowboarder’s fracture’’ for its increased incidence in this patient population. A high index of suspicion is required to identify this injury, often
CHAPTER 2
Impingement syndromes of the foot and ankle
Impingement under the tip of the fibula following os calcis fractures is a common complication of this injury. Often it is difficult to differentiate the impingement pain from subtalar joint pain. A small injection of a local anesthetic beneath the tip of the lateral malleolus, but not into the subtalar joint, can indicate how much of the pain is coming from the impingement, versus an arthritic subtalar joint. If the pain relief with the local anesthetic is dramatic, it might be worthwhile to excise this portion of the os calcis before recommending subtalar arthrodesis (Fig. 2-12). For a more detailed discussion of calcaneal fractures, refer to Chapter 5. Peroneal dysfunction, although not an impingement, also can produce pain in this area and should be considered in the differential diagnosis. This includes peroneal subluxation, longitudinal splits in the tendons,15 and even fracture of the os perineum with retraction of the peroneus longus16 (Fig. 2-13). Posterior ankle pain is common in athletes such as dancers, gymnasts, soccer players, and skaters who must work or kick in the equines position. A review of posterior ankle anatomy will help to explain the two common pain syndromes found in this area (Tables 2-2 and 2-3).
Figure 2-12 Impingement under the tip of the fibula, following a fracture of the os calcis and lateral malleolus.
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The posterior aspect of the talus has two tubercles: the medial and the lateral (Fig. 2-14). The lateral tubercle is the origin of the posterior talofibular ligament. The tubercle can be small or large. When it is large it is referred to as the posterior process of the talus or Stieda’s process. In 7% to 11% of people, this posterior process is separate from the talus and connected by a fibrous synostosis; then it is called the os trigonum (OT).17 The OT is the second most common accessory bone in the foot, the accessory navicular being the most common.18 Bony impingement can occur posterolaterally when the trigonal process or OT is compressed between the posterior lip of the tibia and superior portion of the os calcis in extreme plantarflexion (Fig. 2-15). The flexor hallucis longus (FHL) tendon passes through the fibro-osseous tunnel between the two posterior tubercles as it runs from its origin on the fibula (laterally) to its insertion in the distal phalanx of the hallux (medially) (Fig. 2-16). Chronic tendinitis and dysfunction within this tunnel can produce posterior medial pain, ‘‘dancer’s tendinitis.’’19-22 Thus there usually are two sources of posterior ankle pain: lateral (trigonal impingement) and medial (FHL tendinitis), or a combination of the two.
Posterolateral ankle pain The posterior impingement syndrome of the ankle, or talar compression syndrome,21,23,24 is the natural consequence of full weight bearing in maximal plantarflexion of the ankle in the demi-pointe or full pointe position, especially if an OT is present. It presents as posterolateral pain in the back of the ankle when the posterior lip of the tibia closes against the superior border of the os calcis. It can be confirmed on physical examination by tenderness behind the peroneal tendons in the back of the lateral malleolus (it often is mistaken for peroneal tendinitis) and pain with forced passive plantarflexion of the ankle, the ‘‘plantarflexion sign.’’ This syndrome is often, but not always, associated with an OT or trigonal process in the back of the ankle. As previously noted, the posterior aspect of the talus normally has two tubercles: the medial and the lateral. Between the two lie the fibro-osseous tunnel and the FHL tendon (Fig. 2-17). Most people who have an OT are not aware of its presence, and the posterior impingement syndrome is rare in most athletes. In dancers it may or may not be symptomatic, and the degree of symptoms is not always related to its size. Large OTs can be minimally symptomatic and small ones sometimes can be disabling. Usually the symptoms are mild and, on the whole, the OT often is more asymptomatic than symptomatic. Many world-famous ballerinas have asymptomatic OTs, and they work with them without any trouble. It is important to stress this fact to the dancer when discussing the problem, because
Specific anatomic areas
Retraction of the os peroneum (arrow), following rupture of the peroneus longus tendon.
Table 2-2 FHL tendonitis versus posterior impingement of the ankle
FHL tendonitis
Posterior impingement
Posteromedial
Posterolateral
Tenderness over FHL tendon
Table 2-3 Medial versus lateral posterior ankle pain in athletes and dancers
Posteromedial
Posterolateral
FHL tendinitis
Tenderness behind fibula
Posterior impingement (OT syndrome)
Soleus syndrome
Pain or triggering with motion of the hallux
Pain with plantar flexion of the ankle
Fx. trigonal process (Shepherd’s fracture)
PT tendonitis
Peroneal tendonitis
Thomasen’s sign14
Plantar flexion sign
Pseudomeniscus syndrome
Mistaken for PT tendonitis
Mistaken for peroneal tendonitis
Posteromedial fibrous tarsal coalition
FHL, flexor hallucis longus; PT, posterior tibial.
FHL, flexor hallucis longus; Fx., fracture; OT, os trigonum; PT, posterior tibial.
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Figure 2-13
CHAPTER 2
Impingement syndromes of the foot and ankle
Figure 2-16 Medial anatomy of the flexor hallucis longus. Figure 2-14
Figure 2-15
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38
Anatomy of the posterior talus.
Posterior impingement on the os trigonum.
the condition often is overdiagnosed by paramedical practitioners, who may recommend surgery unnecessarily, perhaps because of the dramatic appearance of the bone on x-ray. It is seen best on a lateral view of the ankle en pointe or in full planter flexion (Fig. 2-15). The diagnosis can be confirmed, if necessary, by injecting 0.5 ml of a local anesthetic into the posterior soft tissues behind the peroneal tendons. If the pain that was present is relieved by this small injection, the diagnosis is almost certain. Treatment of the posterior impingement syndrome should be graded. The first step, similar to the treatment for tendinitis, is modification of activities (‘‘Don’t do what hurts!’’), nonsteroidal anti-inflammatory drugs (NSAIDs—if the dancer is older than age 16), and physical therapy. In cases in which this approach has failed, or the symptoms recur, an injection of 0.25 to 0.5 ml of a mixture of a long-acting and a short-acting corticosteroid often can give dramatic and permanent relief of symptoms. This can be done accurately with the use of sonography. Before injecting the steroid preparation, the clinician should confirm the diagnosis with a local anesthetic. If the local anesthetic does not relieve the symptoms, there is no point in injecting the steroids. It should be stressed that the OT usually is not a surgical problem; most dancers with an OT do not need to have it removed surgically. Occasionally, the OT does cause enough disability to warrant surgical excision, but, as with most elective surgery, it is indicated only after the failure of conservative treatment in a serious dancer at least 16 years of age or older. If the problem is an isolated OT with no medial symptoms, it can be approached posterolaterally between the FHL and the peroneal tendons (with the
Specific anatomic areas
Tibialis anterior Extensor hallucis longus Extensor digitorum longus
Talus
Tibia Fibula Tibialis posterior Flexor retinaculum
Superior peroneal retinaculum
Flexor digitorum longus
Os trigonum
Flexor hallucis longus Achilles tendon
Figure 2-17 Superior view of relationship of flexor hallucis longus to os trigonum.
Excision of the OT using the lateral approach Under anesthesia, the patient is placed in the lateral decubitus or prone position with a pneumatic tourniquet on the leg or thigh over cast padding. Because dancers have increased external rotation of the hip, it is extremely difficult to perform this operation with the patient supine. A curvilinear incision is made at the level of the posterior ankle mortise in line with the posterior border of the peroneal tendon sheath. The sural nerve is identified or carefully avoided in the subcutaneous tissues. The dissection is carried down to the interval between the peroneal tendons laterally and the muscle belly of the FHL medially. A posterior capsular incision then is made with the ankle in neutral or slight dorsiflexion. The OT or trigonal process (a Stieda process) can be found on the superior surface of the posterior talus, just on the lateral side of the FHL tendon, between the ankle and subtalar joints. It has attachments on all its sides: (1) superior—the posterior capsule of the talocrural joint; (2) inferior—the posterior talocalcaneal ligament, at times thick and fibrous; (3) medial—the FHL tunnel with its sheath; and (4) lateral—the origin of the posterior talofibular ligament. The bone can be removed by circumferential dissection. One should be careful not to stray too far medially—the posterior tibial nerve rests on the FHL tunnel. The proximal entrance of the FHL tunnel can be opened if there are muscle fibers attaching distally on the FHL tendon that crowd into the tunnel when the hallux is brought into dorsiflexion (see Tomasen’s 39
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sural nerve protected). Not infrequently, there is a combined problem of FHL tendinitis and posterior impingement. The posteromedial approach is used in these patients so that the neurovascular bundle can be isolated and protected. A tenolysis of the FHL and removal of the adjacent OT then can be performed safely. Other causes of posterolateral ankle pain include the following: 1. A previously asymptomatic OT may become persistently symptomatic following an ankle sprain, resulting from disruption of its ligamentous connections and a subtle shift in position. 2. Posterior impingement can follow an ankle sprain that stretches out the lateral ligaments that hold the talus under the tibia in the releve´.22 As the talus slips forward, the posterior lip of the tibia comes to rest on the os calcis. The treatment for this type of posterior impingement is to tighten the lateral ankle ligaments (preferably by the Brostro¨m-Gould procedure).25 If the drawer sign can be corrected, the posterior impingement usually disappears. 3. A posterior pseudomeniscus or plica in posterior ankle,22 with or without an OT, can cause the posterior impingement syndrome in the absence of an OT or ligament laxity. We have seen buckethandle tears in this structure causing locking and other mechanical symptoms that are seen more often in the knee than the ankle.
CHAPTER 2
Impingement syndromes of the foot and ankle
sign10). One should not dissect medial to the FHL tendon without adequate visualization; the posterior tibial nerve lies directly medial to the FHL tendon. The surgeon should check thoroughly for loose bodies; I have found them even in the FHL tunnel. The foot should be brought into maximal plantarflexion to look for any residual impingement. At times it is necessary to remove more of the posterior lateral tubercle. Often there is a facet on the cephalad portion of the os calcis that articulated with the OT, and this can be large enough to impinge against the posterior lip of the tibia after the OT has been removed. Careful hemostasis will prevent a postoperative hematoma, which can delay recovery and make early motion difficult for the patient. A layered closure then is performed with plain catgut suture with the ankle in neutral dorsiflexion. We usually close the wound with a running absorbable suture and SteriStrips. The patient is placed in a bulky dressing, and weight bearing with crutches is begun as tolerated. Early motion is essential to prevent fibrosis and resultant limited range of motion. The dancer is encouraged to swim and progress to barre exercises as discomfort subsides. Average return to full dancing is 2 to 3 months.
Posteromedial ankle pain Tendinitis of the FHL tendon behind the medial malleolus of the ankle is so common in dancers that it is known as dancer’s tendinitis.19-22,26 The FHL is the ‘‘Achilles tendon of the foot’’ for the dancer. It passes through a fibro-osseous tunnel behind the talus like a rope through a pulley. As it passes through this pulley, it is easily strained. When this occurs, rather than moving smoothly in the pulley, it begins to bind. This binding causes irritation and swelling, which, in turn, causes further binding, irritation and swelling—setting up the familiar cycle: because it is swollen and irritated, it binds; and because it binds, it is swollen and irritated. If a nodule or partial tear is present, triggering of the big toe may occur. This is known as hallux saltans (Fig. 2-18). At the extreme, the tendon may become completely frozen in the sheath, causing pseudo hallux rigidus. This tendinitis typically responds to the usual conservative measures. Rest is an important component of the therapy so that the chronic cycle previously described can be broken. NSAIDs can help, but they should be used only as part of an overall treatment program and not as medicine to kill the pain so that the patient can continue dancing and ignore the symptoms. As with other tendon problems, steroid injections should be avoided in the office setting because of the danger of injecting the steroid into the tendon. However, diagnostic and therapeutic injections can be performed into the FHL tendon sheath more accurately and safely under sonographic control. On some occasions, in professional or high-level amateur dancers and
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Figure 2-18 A nodule in the flexor hallucis longus (FHL) tendon causing triggering of the great toe; ‘‘hallux saltans.’’
athletes, FHL tendinitis may be recurrent and disabling. In refractory cases, operative tenolysis may be indicated, but only after failure of conservative therapy. The situation is similar to de Quervain’s stenosing tenosynovitis in the wrist. FHL tendinitis usually occurs behind the medial malleolus, but occasionally it can be found at the knot of Henry under the base of the first metatarsal where the flexor digitorum longus (FDL) crosses over the FHL, and under the head of the first metatarsal where it passes between the sesamoids. A fibrous subtalar coalition may be present in the posteromedial ankle, mimicking FHL tendinitis or tarsal tunnel syndrome. This condition should be suspected when there is less than normal subtalar motion on physical examination. The differential diagnosis of posterior ankle pain includes the following: 1. Posterior process (Shepherd’s)27 fracture; nondisplaced or stress. 2. FHL tendinitis (dancer’s tendinitis). 3. Peroneal tendinitis. 4. Posteromedial localized talocalcaneal coalition. 5. Osteoid osteoma. Operative treatment is indicated when conservative therapy has failed. The posterior clean-out can be performed from either the medial or lateral side of the
Specific anatomic areas
Tenolysis of the FHL and excision of the OT from the medial approach This procedure can be performed with the patient supine because dancers usually have increased external rotation of the hip and knee that allows easy visualization of the posterior ankle from the medial side. A bloodless field is desirable, so we use a tourniquet on the thigh over cast padding. For this reason, the procedure cannot be performed with the patient under local anesthesia or ankle block. A curvilinear incision is made over the neurovascular bundle behind the medial malleolus beginning just above the superior border of the os calcis and continuing to a line just posterior to the tip of the medial malleolus (Fig. 2-19, A). This incision should be made carefully. The deep fascia and lacinate ligament in this area often are thin. If the incision is made too enthusiastically, the surgeon may find himself or herself in the midst of the neurovascular bundle before he or she had planned to be there. The deep fascia then is divided carefully to avoid damage to the artery and nerve beneath it. At this point one must decide whether to go in front of the bundle or behind it. The posterior approach can take the surgeon into the variable neural branches to the os calcis. It is safer to go anteriorly to the bundle. All branches of the tibial nerve at this level go posteriorly, thus the safe plane is between the posterior aspect of the medial malleolus and the neurovascular bundle. The bundle can be taken down off the malleolus by blunt dissection (Fig. 2-19, B). Often there are several small vessels here that need to be ligated, but once the bundle is mobilized it can be held with a blunt retractor such as a loop or Army-Navy retractor (never with a rake) (Fig. 2-19, C). The posterior tibial nerve is much larger than one expects; it usually is about the size of a pencil (Fig. 2-19, D). The surgeon should examine the nerve and the artery and note where they each divide into medial and lateral plantar branches as they leave the tarsal canal. It is not unusual for either the artery or the nerve, or both, to divide above this area, leading to reduplication within the tunnel.
There also may be reduplication of the tendons—the flexor hallucis accessorius. With the neurovascular bundle retracted posteriorly, the FHL is identified easily by moving the hallux (Fig. 2-19, E). The thin fascia overlying the muscle fibers of the FHL is opened proximally, and a tenolysis is performed by opening the sheath from proximal to distal. Usually it is stenotic and tough, and the FHL often can be seen entering it at an acute angle. Care should be taken distally because the FHL tunnel and the nerve are close together here. As the tenolysis approaches the area of the sustentaculum tali, the sheath thins so that there no longer seems to be anything to divide. The tendon should be retracted with a blunt retractor and inspected for nodules or longitudinal tears. If present, these should be carefully debrided or repaired. At this point the FHL can be retracted posteriorly with the neurovascular bundle. The OT or trigonal process will be found just on the lateral side of the FHL tunnel. If the posterior aspect of the talus cannot be visualized, a capsulotomy should be performed. If there is difficulty in visualizing the OT, it helps to identify the superior border of the os calcis and the subtalar joint (by moving the os calcis into adduction and abduction). The subtalar joint then is dissected from medial to lateral, and this will take the surgeon underneath the OT. Once identified, it can be removed by circumferential dissection. Care should be taken to stay on the bone when performing this part of the procedure. This can be somewhat difficult, especially if the OT is large. Once it is removed, the posterior ankle joint should be inspected for remnants, bone fragments or loose bodies, soft tissue entrapment, or a large articular facet on the upper surface of the os calcis that articulated with the OT. If this articulation is large, it may need to be removed with a thin osteotome. The FHL sheath is not closed. The wound then is irrigated, checked for any residual impingement by putting the foot in maximal plantarflexion, and closed in layers with plain catgut and with the ankle in neutral flexion. We begin weight bearing as tolerated with crutches as soon as possible and proceed with swimming and physical therapy when the wound is healed. If the tenolysis is performed without excision of the OT, the recovery period is about 6 weeks. If the OT is removed along with the tenolysis, the recovery time is 8 to 12 weeks. It is important to get patients moving early to prevent stiffness. In dancers with a rather large OT, it is necessary to warn them that, once it is removed, the ankle does not just drop down into maximal plantarflexion. They must realize that the bone has been there since they were born, and removing it does not lead to immediate motion. The increased plantarflexion is obtained slowly and can be accompanied by many strange symptoms, both anteriorly and posteriorly, as the soft tissues adjust to the new range of motion. 41
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Achilles tendon. The lateral approach should be used if the patient has an isolated posterior impingement without a history of FHL tendinitis or medial difficulties. A medial incision in indicated if the patient has a combined problem of FHL tendinitis and posterior impingement, or if he or she primarily has FHL tendinitis with an incidental OT that the surgeon wishes to remove along with an FHL tenolysis. The medial incision is safer and more utilitarian because one can work safely on the lateral side from the medial approach, but it is dangerous to work medially from the lateral approach because the neurovascular bundle cannot be isolated and protected from the lateral side.
CHAPTER 2
Impingement syndromes of the foot and ankle
Figure 2-19 (A) Posteromedial incision. (B) Neurovascular bundle beneath a thin layer of fascia. (C) Neurovascular bundle taken down from the posterior medial malleolus. (D) Posterior tibial nerve protected with a blunt retractor. Underneath lies the flexor hallucis longus (FHL) sheath. (E) FHL sheath opened.
The medial ankle Posterior tibial tendinitis, so common in athletes, is rare in dancers—an example of altered kinesiology producing altered patterns of injury. Working primarily in the equinus position produces less stress on the posterior tibial tendon but more on the FHL tendon as it passes
...........
42
through its pulley behind the medial malleolus. In addition, dancers are selected for, and usually have, cavus feet, which are less prone to posterior tibial (PT) tendinitis. Indeed, more often than not, a dancer diagnosed with PT tendinitis, on careful examination, will be found to have FHL tendinitis instead (dancer’s tendinitis).
References
Table 2-4 Differential diagnosis of medial ankle pain in athletes and dancers Most common
PT tendonitis (athletes) FHL tendonitis (dancers)
Common
Deltoid ligament strain
Rare
FDL tendonitis Soleus syndrome
FDL, flexor digitorum longus; FHL, flexor hallucis longus; PT, posterior tibial.
treatment. On rare occasions, a fracture of the medial tubercle or disruption of an accessory navicular can occur. In this setting, the injury should be treated in a short-leg walking cast or cam walker boot for 4 to 6 weeks to prevent the injury from becoming chronic. Strains of the spring ligament and plantar fascia can be mistaken for medial ankle pain, but a careful physical examination should make the diagnosis apparent. A rare cause of medial ankle pain is an unrecognized fracture of the colliculus located on the medial portion of the posterior tibia. This occult injury can be difficult to diagnose. It usually can be documented by a bone scan and CT scan. Another cause of medial pain just above the medial malleolus is the soleus syndrome.28 This presents as chronic pain resembling a shin splint but is too far distal on the posteromedial tibial metaphysis to be a true shin splint. It is caused by an abnormal slip in the origin of the soleus muscle. The condition, similar to the exertional compartment syndrome, is much more common in athletes than dancers. It usually responds to conservative therapy, but, on rare occasions, release of the tight band may be necessary. In summary, treatment of dancers can be as challenging as it is rewarding. Dancers often have unusual difficulties related to the altered kinesiology required by their individual dance form—ballet, modern dance, jazz, tap, ethnic, Broadway, and so forth. A thorough understanding of these movements will help guide the physician to the cause of the disability, particularly in the setting of overuse injuries. This knowledge, coupled with a careful physical examination, is essential for the accurate diagnosis and treatment of the dancer, who is both athlete and artist.
REFERENCES 1. Thompson FM, Hamilton WG: Problems of the second metatarso-phalangeal joint, Orthopedics 10:83, 1987. 2. Phemister DB: Necrotic bone and the subsequent changes which it undergoes, JAMA 64:211, 1915. 3. Mann RA, Coughlin MJ: Surgery of the foot and ankle, ed 6, St Louis, 1993, Mosby Year Book. 4. Taillard W, et al: The sinus tarsi syndrome, Int Orthop 5:117, 1981. 5. Marshall PM, Hamilton WG: Cuboid subluxation in ballet dancers, Am J Sports Med 20:169, 1992. 6. Scranton PE, McDermott JE: Anterior tibiotalar spurs: a comparison of open versus closed debridement, Foot Ankle 13:125, 1992. 7. Bassett FH, et al: Talar impingement by the anteriorinferior tibiofibular ligament, J Bone Joint Surg 72-A:55, 1990. 8. Ferkel RD, et al: Arthroscopic treatment of anteriorlateral impingement of the ankle, Am J Sports Med 19:440, 1991. 9. McLaughlin HL: Trauma, Philadelphia, 1960, WB Saunders. 10. Tomasen E: Diseases and injuries of ballet dancers, Denmark, 1982, Universitetsforlaget I.Arhus.
43
...........
Medial sprains of the ankle are rare because the medial structures are strong and rigid in comparison with the lateral ones. Persistent symptoms on the medial side may be due to an unrecognized fracture of the sustentaculum tali, which can be picked up on a bone scan, or to a localized fibrous tarsal coalition. Sprains of the medial ankle do occur, usually from landing off balance with sudden pronation, but again, this is more likely to produce a sprain of a portion of the deltoid ligament than a strain of the PT tendon, although this can occur. The sprain usually affects the portion of the ligament under tension when the force was applied: the anterior deltoid if the foot was in equinus, the middle deltoid if the foot was plantigrade, and the posterior portion if the foot was in dorsiflexion (rare). An accessory bone, the os subtibiale, may be present in the deep layer of the deltoid; this bone can be involved in the sprain, becoming symptomatic when it had not been before. The treatment of these medial sprains and strains in the acute phase consists of the usual RICE regimen (i.e., rest, ice, compression, and elevation), an aircast stirrup brace, crutches if necessary, and physical therapy. An x-ray should be taken to rule out bone or physeal injury. Recovery usually is uneventful. Occasionally a trigger point can form in the deltoid, usually around a chip fracture or accessory ossicle. These may require a corticosteroid injection if they do not respond to conservative therapy. Only rarely will surgical excision be necessary. Nodules may form on the EDL or PT tendons following medial strains, but these usually are asymptomatic. In dancers, the most common cause of pain around the medial malleolus comes from ‘‘rolling in’’ (pronating) to obtain proper turnout (Table 2-4). This produces a chronic strain on the deltoid ligament, particularly the deep portion, and is one of many overuse syndromes seen in dancers. Contusion of the medial prominence of the tarsal navicular can occur. This usually happens when one foot is brought forward past the other and, as it passes the navicular, strikes the medial malleolus of the other ankle. These contusions usually heal with symptomatic
CHAPTER 2
Impingement syndromes of the foot and ankle
11. McCarroll JR, et al: Meniscoid lesions of the ankle in soccer players, Am J Sports Med 15:255, 1987. 12. Harburn T, Ross H: Avulsion fracture of the anterior calcaneal process, Phys Sports Med 15, 1987. 13. Hawkins LG: Fractures of the lateral process of the talus, J Bone Joint Surg 52A:991, 1970. 14. Valderrabano V, et al: Snowboarder’s talus fracture: treatment outcome of 20 cases after 3.5 years, Am J Sports Med 33:871, 2005. 15. Sammarco JG, DiRaimondo CV: Chronic peroneus brevis tendon lesions, Foot Ankle 9:163, 1989. 16. Thompson FM, Patterson AH: Rupture of the peroneus longus tendon, report of three cases, J Bone Joint Surg 71-A:293, 1989. 17. Grant JCB: A method of anatomy, Baltimore, 1985, Williams & Wilkins. 18. Sarrafian SK: Anatomy of the foot and ankle, Philadelphia, 1983, JB Lippincott. 19. Hamilton WG: ‘‘Dancer’s tendonitis’’ of the FHL tendon, Durango, CO, 1976, American Orthopedic Society for Sports Medicine. 20. Hamilton WG: Tendonitis about the ankle joint in classical ballet dancers; ‘‘Dancer’s tendonitis’’, J Sports Med 5:84, 1977.
...........
44
21. Hamilton WG: Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the os trigonum in ballet dancers, Foot Ankle 3:74, 1982. 22. Hamilton WG: Foot and ankle injuries in dancers. In Yokum L, editor: Sports clinics of North America, Philadelphia, 1988, Williams & Wilkins. 23. Howse AJG: Posterior block of the ankle joint in dancers, Foot Ankle 3:81, 1982. 24. Quirk R: The talar compression syndrome in dancers, Foot Ankle 3:65, 1982. 25. Hamilton WG, Thompson FM, Snow SW: The modified Brostro¨m procedure for lateral ankle instability, Foot Ankle 14:1, 1993. 26. Hamilton WG: Ballet, In Reider B, editor: The school-age athlete, Philadelphia, 1991, WB Saunders. 27. Shepherd FJ: A hitherto undescribed fracture of the astragalus, J Anat Physiol 17:79, 1882. 28. Michael RH, Holder LE: The soleus syndrome, Am J Sports Med 13:87, 1985.
........................................... C H A P T E R 3 Stress fractures: their causes and principles of treatment Peter D. Brukner and Kim L. Bennell CHAPTER CONTENTS ...................... Introduction
45
Differential diagnosis
68
Epidemiology
46
Treatment
68
Risk factors for stress fractures
52
Conclusion
70
Diagnosis
63
References
70
INTRODUCTION Physical exercise has beneficial effects on a number of physiologic systems, including the skeleton. However, unwise training practices, combined with potential risk factors, may harm these systems. A stress fracture represents one form of breakdown in the skeletal system.1 It can be defined as a partial or complete fracture of bone that results from the repeated application of a stress lower than that required to fracture the bone in a single loading situation.2
Historical perspective Stress fractures were first described in 1855 by Briethaupt, a Prussian military physician who observed foot pain and swelling in young military recruits unaccustomed to the rigors of training. He considered it to be an inflammatory reaction in the tendon sheaths resulting from trauma and called the condition Fussgeschwulst. It was not until the advent of radiographs that the signs and symptoms were attributed to fractures in the metatarsals.3 The condition then became known as a ‘‘march’’ fracture because of the close association between marching and the onset of symptoms. Stress fractures were first noticed in civilians in 1921 by Deutschlander,4 who reported six cases in women. However, it was not until 1956, more than a century following their identification in military recruits, that they were recognized in athletes.5 A variety of terms have been used over time to describe stress fractures. These include march fractures, Deutschlander’s fractures. pied force´, fatigue fractures, or
crack fractures.4,6-10 Virtually all of these terms have been intended to describe some etiologic attribute of the stress injuries of bone. In recent years the most commonly used term has been stress fracture. Following the radiographic description of metatarsal stress fractures, many theories were set forth to explain the etiology of this injury. Most of the reports were based on series that were small, and the theories proposed were concerned with either mechanical factors, such as spasm of the interossei, or flat feet,4,11,12 or with inflammatory reactions, such as nonsuppurative osteomyelitis.7,8
Etiology of stress fractures It is now recognized that the development of a stress fracture represents the end product of the failure of bone to adapt adequately to the mechanical loads experienced during physical activity. Ground reaction forces and muscular contraction result in bone strain. It is these repetitive strains that are thought to cause a stress fracture. Bone normally responds to strain by increasing the rate of remodeling. In this process, lamellar bone is resorbed by osteoclasts, thereby creating resorption cavities that subsequently are replaced with more dense bone by osteoblasts. Because there is a lag between increased activity of the osteoclasts and osteoblasts, bone is weakened during this time.13,14 If sufficient recovery time is allowed, bone mass eventually increases. However, if loading continues, microdamage may accumulate at the weakened region.14,15 Remodeling is thought to repair normally occurring microdamage.16,17 The processes of microdamage accumulation and bone remodeling, both resulting from bone
CHAPTER 3
Stress fractures: their causes and principles of treatment
strain, play an important part in the development of a stress fracture. If microdamage accumulates, repetitive loading continues, and remodeling cannot maintain the integrity of the bone; a stress fracture may result.15,18,19 This may occur because the microdamage is too extensive to be repaired by normal remodeling, because depressed remodeling processes cannot adequately repair normally occurring microdamage, or because of some combination of these factors.18
EPIDEMIOLOGY Stress fractures have been reported to occur in association with a variety of sports and physical activities. Clinical impression suggests that stress fractures are more common in weight-bearing activities, particularly those with a running or jumping component. However, it is difficult to compare the incidence of stress fractures in different sports or to identify the sport or activity with the greatest risk because of a lack of sound epidemiologic data. This section reviews the descriptive epidemiology of stress fractures. Most of the literature in this area pertains to female runners and to male military populations. There is no information about stress fracture rates in the general community.
Stress fracture injury rate ............................................................. Stress fracture rates in athletes Studies investigating stress fracture rates in athletes are shown in Table 3-1.20-31 Of these, only two allow a direct comparison of annual stress fracture rates in different sporting populations.28,29 Johnson et al.28 conducted a 2-year prospective study to investigate sports-related injuries in collegiate male and female athletes. In total, 34 stress fractures were diagnosed during the study period. Track accounted for 64% of stress fractures in women and 50% of stress fractures in men. The stress fracture incidence rate (expressed as a case rate) in males was highest for track (9.7%), followed by lacrosse (4.3%), crew (2.4%), and American football (1.1%). The stress fracture incidence rate in women was highest for track athletes (31.1%), followed by crew (8.2%), basketball (3.6%), lacrosse (3.1%), and soccer (2.6%). No athlete sustained a stress fracture in fencing, hockey, golf, softball, swimming, or tennis. Goldberg and Pecora29 reviewed medical records of stress fractures occurring in collegiate athletes during a 3-year period. Approximate participant numbers were available to allow calculation of estimated incidence case rates in each sport. The greatest incidence occurred in softball (19%), followed by track (11%), basketball (9%), lacrosse (8%), baseball (8%), tennis (8%), and gymnastics (8%). However, participant numbers were small in some of these sports, possibly leading to a bias in incidence rates.
...........
46
Both studies suggest that track athletes are at one of the highest risks for stress fracture. However, because neither expressed incidence in terms of exposure, it may not be strictly valid to compare the risk of stress fracture in such diverse sports. To our knowledge, there is only one athlete study that has expressed stress fracture incidence rates in terms of exposure.24 This 12-month prospective study followed a cohort of 95 track and field athletes. Results showed an overall rate of 0.70 stress fractures per 1000 training hours. Further research is needed to quantify incidence rates in this manner to allow more valid comparison between studies. Retrospective studies have measured stress fracture rates in specific sporting populations, mostly runners and ballet dancers.20-23,25-27,29-31 Variation in reported rates reflects differences in methodology, particularly cohort demographics and method of data collection. A history of stress fracture has been reported by 13% to 52% of female runners. The lowest rate was found in one study that included recreational, as well as competitive, runners. Ballet dancers are another population in which stress fracture rates appear high, with 22% to 45% of dancers reporting a history of stress fracture. However, most studies failed to confirm the accuracy of subject recall, a failure that may introduce bias into the figures reported. Nevertheless, it is clear that stress fracture is a relatively common athletic injury.
Stress fracture rates in the military Reports of the incidence of stress fractures in male recruits undergoing basic training for periods of 8 to 14 weeks are remarkably similar and generally range from 0.9% to 4.7%.32-40 However, in two particular studies involving the Israeli army, the reported incidence was 31%41 and 24%.42 The authors attributed this much higher incidence to several factors, including meticulous follow-up, a high index of suspicion, and the use of the radioisotope bone scan for diagnosis. In addition, asymptomatic areas of uptake on bone scan also were classified as lesions, and this would inflate the reported figures. Stress fracture rates in female military recruits during basic training generally are higher than those in males, ranging from 1.1% to 13.9%.32,33,35,37,39,43 Stress fracture recurrence rates Clinically it seems that recurrence of stress fractures at new sites is common. In female track and field athletes, half of those who reported a history of stress fracture had experienced a stress fracture on more than one occasion.23 However, few studies have reported recurrence rates in either athletes or the military. When male and female track and field athletes were followed prospectively for 1 year, 60% of those who sustained a stress fracture had a previous stress fracture history.24 The athlete recurrence rate in this study was particularly high at 12.6%. A large number of male
Stress fracture (SF) rates in athletes expressed as participant rates unless otherwise stated
Reference
Study design
Population
Subject sex & number
Method of data collection
Resp rate of quest (%)
Observation period
Diagnosis of SF
SF rate (%)
R
Collegiate distance runners
240-F
Self-admin. question
24
Hx
x-ray or BS
37.0
Brunet et al., 199021
R
Recreational/ competitive runners
375-F 1130-M
Self-admin. question
NS
Hx
NS
13.2-F 8.3-M
Cameron et al., 199222
R
State/ national level runners
263-F 287-M
Self-admin. question
67
Hx
NS
26.6-F 28.0-M
Bennell et al., 199523
R
Track & field athletes
53-F
Self-admin. question
100
Hx
x-ray, BS, or CT
51.5 84.9*
Bennell et al., 199624
P
Track & field athletes
46-F 49-M
Monitoring
NA
1 yr
BS þ CT
21.7-F 20.4-M 30.4-F* 24.5-M*
Warren et al., 198625
R
Professional ballet dancers
40-F
Self-admin. question
100
Hx
x-ray or BS
45.0 67.5*
Frusztajer et al., 199026
R
Ballet dancers
45-F
Interview þ question
100
1 yr
NS
22.0
Kadel et al., 199227
R
Professional ballet dancers
54-F
Self-admin. question
100
Hx
x-ray or BS
31.5 50.0*
Johnson et al., 199428
P
Collegiate athletes
321-F 593-M
Monitoring
NA
2 yr
x-ray or BS
6.9-F*{ 2.0-M*{
Epidemiology
Barrow & Saha, 198820
(Continued)
47
............
Table 3-1
48
............
CHAPTER 3
Stress fracture (SF) rates in athletes expressed as participant rates unless otherwise stated (cont’d)
Reference
Study design
Population
Subject sex & number
Method of data collection
Resp rate of quest (%)
Observation period
Diagnosis of SF
SF rate (%)
Goldberg & Pecora, 199429
R
Collegiate athletes
1200-F 1800-M
Review of medical records
NA
3 yr
x-ray or BS
2.7-F*{ 1.4-M*{
Pecina et al., 199030
R
Elite ice skaters
42 M/F
Self-admin. question
100
Hx
NS
21.0
Dixon & Fricker, 199331
R
Elite gymnasts
74-F 42-M
Review of medical records
NA
10 yr
x-ray or BS
27.0-F* 14.3-M*
From Bennell KL, Brukner PD: Epidemiology and site specificity of stress fractures, Clin Sports Med 16:183, 1997. BS, Bone scan; CT, computed tomography; F, females; Hx, history; M, males; NA, not applicable; NS, not stated; P, prospective cohort; quest, questionnaire; R, retrospective cohort; resp, response. *Stress fracture rates expressed as case rates: number of stress fractures per 100 athletes. {Annual incidence.
Stress fractures: their causes and principles of treatment
Table 3-1
Epidemiology
Comparison of stress fracture rates in different age groups It is unclear whether age, as an independent factor, influences the risk of stress fracture because results in the military are conflicting and there are no studies in athletes investigating the incidence of stress fractures in different-aged individuals engaged in identical training. In a retrospective cohort study of 20,422 military recruits, review of clinical records found a positive association between increasing age in the range 17 to 34 years and the incidence of stress fractures in both men and women.35 Similar results, even after adjusting for pretraining physical activity, were reported by Gardner et al.36 in a large prospective study. These suggest that increasing age, within the range studied, may be associated with a higher incidence of stress fractures. It is surmised that this may be because bone of older individuals is less resistant to fatigue failure.45,46 However, a prospective study by Milgrom et al.42 in the Israeli army contradicts the hypothesis that stress fracture incidence increases with age in military recruits. For each year of increase in age from 17 to 26 years, the risk for stress fracture at all sites decreased by 28%. The authors suggested that the decreasing risk with age may be related to increased structural maturity, increased bone density, larger cross-sectional moment of inertia, or changes in bone quality in the older recruits. It also is possible that injury-prone older individuals may be less likely to apply for military training. However, it should be noted that the number of recruits older than the age of 19 was very small in this study. A case series of 1407 patients presenting to a sports medicine center found that stress fractures or periostitis comprised a greater percentage of injuries in the ‘‘younger’’ group (mean age of 30 years), compared with that in the ‘‘older’’ group (mean age of 57 years).47 However, because of the study design, it is not known whether this reflects selection of stress fracture-resistant individuals in the older group, modification of training regimens to lower musculoskeletal stress, or an independent age effect on stress fracture development. Comparison of stress fracture rates in men and women It often is suggested that women sustain a disproportionately higher number of stress fractures than men. The
relative risk of stress fracture for women compared with men from studies in which stress fracture rates can be directly compared is shown in Table 3-2. In the military, reported incidence rates during an 8-week training period vary from 1.1% to 13.9% in women and from 0.9% to 3.2% in men. These studies consistently show that female recruits have a greater risk of stress fracture than male recruits, with relative risks ranging from 1.2 to 10.32,33,35,37,39,43 This increased risk persists even when training loads gradually are increased to moderate levels and when incidence rates are separated by age and race. The most likely explanation for these findings in the military is lower initial physical fitness in the female recruits. Other possible reasons include differences in bone density and geometry, gait, biomechanical features, body composition, and endocrine factors, particularly estrogen status. In contrast, a gender difference in stress fracture rates is not as evident in athletic populations.21,22,24,28,29,31 Studies either show no difference between male and female athletes or a slightly increased risk for women, up to 3.5 times that of men (see Table 3-2). A possible confounding variable is that, unlike the military, in which the amount and intensity of basic training is rigidly controlled, it is difficult to assume equivalence of training between men and women in most of these studies. However, Bennell et al.24 found no significant difference between gender incidence rates even when expressed in terms of exposure. Women sustained 0.86 stress fractures per 1000 training hours, compared with 0.54 in men. It is feasible that a gender difference in stress fracture risk is reduced in athletes because female athletes may be more conditioned to exercise than female recruits; hence the fitness levels of male and female athletes may be closer.
Comparison of stress fracture rates in different races Both male and female Caucasians appear to be at greater risk for stress fractures than blacks, with relative risks ranging from 2.3 to 24 (Table 3-3). This may be related to higher bone density in blacks48 or to different biomechanical features that may be protective against stress fractures.49 Relative frequency of stress fractures as a proportion of total injuries Numerous case series have reported that stress fractures comprise between 0.7% and 15.6% of all injuries sustained by athletic populations.31,50-54 In those investigating runners only, the relative frequency is much higher, ranging from 6.0% to 15.6%. In track and field athletes, stress fractures appear to comprise a large proportion of overuse injuries: 34.2% in women and 24.4% in men reported by one study,24 and 42.0% by men and women combined in another.50 In elite gymnasts, stress fractures comprised 18.3% of overuse injuries 49
...........
military recruits were followed for a minimum of 1 year after basic training.44 The recurrence rate of stress fractures at a different site in those who had sustained a stress fracture during basic training was 10.6%. In the control group of 60 recruits who did not develop a stress fracture during basic training, the incidence of stress fracture after basic training was only 1.7%. This finding could indicate the persistence of risk factors in susceptible individuals.
50
............
CHAPTER 3
Relative risk of stress fracture for women compared with men from studies in which stress fracture rates can be directly compared
Variable
Brunet et al., 199021
Cameron et al., 199222
Johnson et al., 199428
Goldberg & Pecora, 199429
Zernicke et al., 199393
Type of study
R
R
P
R
NS
Sport population
Runners*
Runners
Variety{
Variety{
Runners
Age, females
33
NS
18–22
18-22
18-22
Age, males
39
NS
8-22
18-22
18-22
Female number
375
263
321
1200
NS
Male number
1130
287
593
1800
NS
Observation
History
History
2 yr
3 yr
12 months
Data collection
Q
Q
Clinic
Records
NS
Response rate
NS
67%
NA
NA
NS
% of SF, females
13.2
26.6
6.9
2.7
20-25
% of SF, males
8.3
28.0
2.0
1.4
10.0
Relative risk F:M
1.6
0.95
3.5
1.9{
2.2
From Bennell KL, Brukner PD: Epidemiology and site specificity of stress fractures, Clin Sports Med 16:179, 1997. NA, Not applicable; NS, not stated; P, prospective; Q, questionnaire; R, retrospective. *Mainly novice runners. { Collegiate athletes. { Population at risk was estimated, therefore providing an approximate incidence rate.
Stress fractures: their causes and principles of treatment
Table 3-2
Population
Study design
Number C
Number B
SF rates C (%)
SF Rates B (%)
Relative risk C vs. B
Brudvig et al., 198335
Military
R
NS
NS
1.1
0.2
4.7*
Gardner et al., 198836{
Military
P
2050
975
1.6{
0.7{
2.3*
Milgrom et al., 199442
Military
P
765
18
24.8
0.0
24.8*
Brudvig et al., 198335
Military
R
NS
NS
11.8
1.4
8.5*
Barrow & Saha, 198820
Athletes
R
220
12
39.0
17.0
2.3
Reference Men
Women
From Bennell KL, Brukner PD: Epidemiology and site specificity of stress fractures. Clin Sports Med 16:187, 1997. NS, Not stated; P, prospective cohort; R, retrospective cohort. *Statistically significant difference between races. { Blacks include all racial and ethnic groups apart from whites. { Stress fracture rates expressed as case rates: number of stress fractures per 100 recruits.
Epidemiology
51
............
Table 3-3 Studies investigating the rates and relative risk of stress fractures (SFs) comparing caucasians (C) and blacks (B). All rates are expressed as participant rates unless stated
CHAPTER 3
Stress fractures: their causes and principles of treatment
in women and 9.2% in men.31 It seems that the relative frequency of stress fractures is greater in female than in male athletes. The variation in results probably reflects differences in the composition of each case series.
Stress fracture sites ............................................................. Athletes Stress fractures are most common in bones of the lower extremity but also occur in nonweight-bearing bones, including the ribs, upper limb, and pelvis. Numerous studies have reported the anatomic distribution of series of stress fractures20,22,24,27-29,50,52,53,55-63 (Table 3-4). Although there is great variation in the percentage of stress fractures reported at each bony site, the most common sites appear to be the tibia, metatarsals, and fibula. A number of factors may influence the reported distributions of stress fractures. These include type and level of activity, gender, age, and, in particular, method of diagnosis. For example, tarsal navicular stress fractures rarely are evident on radiographs. If diagnosis is confined to radiographs, these therefore will be underreported in comparison with stress fractures at other sites. Stress fractures develop at skeletal sites that are subjected to repetitive mechanical loading during a particular activity. The site specificity of stress fractures was illustrated in a prospective study in 95 track and field athletes.24 Although stress fracture incidence rates were similar in power and endurance athletes, the site distribution differed. Power athletes (sprinters, hurdlers, and jumpers) sustained significantly more foot fractures, whereas endurance athletes (middle-distance and distance runners) sustained more long bone and pelvic fractures. In a series of 180 stress fractures, the percentage distribution of sports among the five most common sites is shown in Table 3-5.63 Dancers were the most common group sustaining metatarsal stress fractures, and track and distance runners sustained the most tibial stress fractures, whereas distance runners and dancers were prominent among fibula stress fractures. Track athletes were by far the most common among the navicular stress fractures. Pars fractures were seen in athletes in field events, racquet sports, cricket, dancing, and basketball. It therefore is apparent that different sports show typical patterns of stress fractures; these are summarized in Table 3-6.64 Other sports associated with certain stress fractures are rowing or golf (rib stress fractures), pitching (humeral fractures), and gymnastics (pars fractures). Conditioned athletes may sustain stress fractures different from those in persons unaccustomed to activity. In a series of 368 fractures, competitive athletes had stress fractures in the tibia significantly more often, whereas recreational athletes had significantly more metatarsal and pelvic bone fractures.52,58 It also has
...........
52
been reported that females sustain more metatarsal,52,58 pelvic,52,58 and navicular stress fractures28 than males. Age differences also may play a part; Matheson et al.59 found significantly more femoral and tarsal stress fractures in older athletes and more tibial and fibular stress fractures in younger athletes. However, an interaction between age and site of stress fracture was not confirmed in another large series.58
Military recruits The location of stress fractures in military personnel has appeared to change over the years, probably as a result of changes in training, with a greater emphasis on running instead of marching; changes in footwear, with athletic shoes often replacing combat boots; and changes in initial fitness levels with fitter recruits. Original reports described primarily injuries of the foot, with most diagnosed stress fractures occurring in the metatarsals.10,65 However, in the last 2 decades, a greater number of stress fractures have been found in the leg, particularly the tibia, thus more closely approximating that observed in athletic populations. In a recent prospective study in 626 male U.S. Marine Corps recruits, 27 stress fractures were sustained.40 The most common site was the tibia (41%), followed by the metatarsals (26%), the femur (19%), and the tarsals (15%). The site distribution of stress fractures in military populations has been well reviewed by Jones et al.43
RISK FACTORS FOR STRESS FRACTURES Risk factors are markers that can be used to identify athletes who are more likely to sustain a stress fracture. Preventative strategies then can be directed toward these individuals. Although the risk factors themselves may not be involved in stress fracture pathogenesis, they directly or indirectly increase the chance of a stress fracture’s developing. This occurs by their influence on either the mechanical environment of bone or the remodeling process. Although numerous risk factors for stress fractures have been proposed, research is needed to confirm anecdotal observations. Presently most studies in athletes are case series, confined to injured groups only, or are cross-sectional designs that do not allow the temporal relationship between risk factor and injury to be assessed. Methodologic issues, such as small subject numbers, different definitions of stress fractures, and failure to assess the independent contributions of risk factors also limit their usefulness. There also are few data about risk factors in male athletes. Results from large military epidemiologic studies cannot be readily generalized to athletes because of important differences in training, fitness levels, footwear, and surfaces. However, these may provide additional insights, especially given the deficiencies in the athletic literature.
Sport
No. of SF in series
Diagnosis of SF
Tibia (%)
Fibula (%)
Metatarsal (%)
Navicular (%)
Femur (%)
Pelvis (%)
Brubaker & James, 197450
Runners
17
NS
41.2
17.6
29.4
5.9
0
0
Orava, 198052
Variety
200
x-rays þ/ BS
53.5
12.5
18.0
2.0
6.0
1.5
Pagliano & Jackson, 198053
Runners
99
self-report
20.2
15.2
37.4
NS
NS
NS
Taunton et al., 198155
Runners
62
x-rays or BS
55.0
11.3
16.1
3.2
6.5
0
Clement et al., 198156
Runners
87
NS
57.5
9.2
20.7
3.4
4.6
0
Sullivan et al., 198457
Runners
57
x-ray or BS
43.9
21.0
14.0
0
3.5
10.5
Barrow & Saha, 198820
Runners
140
self-report
63.0
9.0
21.0
0.7
4.0
1.4
Hulkko & Orava, 198758
Variety
368
x-ray þ/ BS
49.5
12.0
19.8
2.5
6.3
1.9
Matheson et al., 198759
Variety
320
bone scan
49.1
6.6
8.8
NS
7.2
1.6
Courtenay & Bowers, 199060
Variety
108
x-ray or BS
38.0
29.6
18.5
4.6
2.8
0.9
Ha et al., 199161
Variety
169
x-ray or BS
31.5
10.7
7.1
4.7
12.5
4.1
Cameron et al., 199222
Runners
253
self-report
37.5
12.0
22.5
10.0
NS
NS
Risk factors for stress fractures
Reference
(Continued)
53
............
Table 3-4 Anatomic distribution of stress fractures (SFs) in athletes expressed as a percentage of the total number of stress fractures in each series
54
............
CHAPTER 3
Anatomic distribution of stress fractures (SFs) in athletes expressed as a percentage of the total number of stress fractures in each series (cont’d)
No. of SF in series
Diagnosis of SF
Tibia (%)
Fibula (%)
Metatarsal (%)
Navicular (%)
Femur (%)
Pelvis (%)
Track & field
49
x-ray, CT or BS
26.5
12.2
14.3
28.6
0
0
Kadel et al., 199227
Ballet
27
self-report
22.0
0
63.0
NS
4.0
0
Goldberg & Pecora, 199429
Variety
58
x-ray or BS
18.9
12.1
25.9
NS
10.0
3.4
Johnson et al., 199428
Variety
34
x-ray þ/ BS
38.2
0
20.6
11.8
23.5
0
Bennell et al., 199624
Track & field
26
BS & CT
45.0
12.0
8.0
15.0
8.0
4.0
Brukner et al., 199663
Variety
180
x-ray, CT or BS
20.0
16.7
23.3
20.0
3.3
1.1
Reference
Sport
Benazzo et al., 199262
From Bennell KL, Brukner PD: Clin Sports Med 16:190, 1997. BS, Bone scan; CT, computed tomography; NS, not stated.
Stress fractures: their causes and principles of treatment
Table 3-4
Risk factors for stress fractures
Table 3-5
Percentage distribution of sports among the most common stress fracture sites
Sport
Metatarsal (n ¼ 42)
Tibia (n ¼ 36)
Fibula (n ¼ 30)
Tarsal navicular (n ¼ 26)
Pars interarticularis (n ¼ 17)
Track
21.4
38.9
16.7
73.1
5.8
Jog/distance running
11.9
41.7
26.7
3.8
0
Dance
42.9
2.8
23.3
0
17.6
Australian football
4.8
8.3
10
7.7
0
Racquet sports
2.4
2.8
6.7
3.8
17.6
Field events
0
0
6.7
0
23.5
Rowing/canoeing
2.4
0
3.3
3.8
0
Triathlon
2.4
0
3.3
3.8
0
Basketball
2.4
0
0
3.8
11.8
Cricket
0
0
0
0
17.6
Aerobics
7.2
0
3.3
0
0
Field hockey
0
0
0
0
5.9
Rugby
0
2.8
0
0
0
Martial arts
2.4
0
0
0
0
Work-related
0
0
0
0
5.9
From Brukner P, et al: Clin J Sport Med 6:85, 1996.
Although Myburgh et al.71 failed to find a difference in the incidence of a family history of osteoporosis in a group of 25 athletes with stress fractures and a group without stress fractures, this may reflect the small sample. At present, there is little evidence to show that genetic factors predispose an athlete to this injury.
Menstrual disturbances Because hypoestrogenic postmenopausal women are at an increased risk of developing osteoporotic fractures, it has been suggested that stress fractures may be more prevalent in female athletes with menstrual disturbances. It is feasible that estrogen deficiency could promote stress fracture development by the following: Accelerating the process of bone remodeling, leading to weakened areas of bone because of the lag period between resorption and formation 55
...........
Genetic predisposition A large component of the variation in bone mass can be attributed to genetic factors.66 Not surprisingly, then, a family history of osteoporosis is considered to be a risk factor for low bone density and osteoporosis in both men and women.67,68 Similarly, a significant relationship between a family history of osteoporosis and yearly change in bone density has been demonstrated in studies of runners and nonrunners.69 It therefore is feasible that some individuals may be genetically predisposed to stress fractures when exposed to suitable environmental conditions, such as vigorous exercise. This was implied in a case report in which a pair of 18-year-old monozygotic twins undergoing basic military training sustained identical multiple stress fractures in the femoral and tarsal bones.70 The authors proposed that identical environmental conditions served to unmask a genetically determined deficiency in the affected bones.
CHAPTER 3
Stress fractures: their causes and principles of treatment
Table 3-6 Sports and activities commonly associated with different stress fracture sites
From Brukner PD, Khan KM: Clinical sports medicine, rev ed 2, Sydney, 2002, McGraw-Hill Book Company.
Increasing calcium excretion, resulting in greater calcium requirements that may not be adequately met by dietary intake Causing premature bone loss and hence lower bone density
...........
56
Although progesterone may be a promoter of bone formation, particularly in cortical bone,72 and luteal phase deficiency in athletes is associated with lowered progesterone levels, a possible link between luteal phase deficiency and stress fracture risk has not been sought.
Risk factors for stress fractures
*
100 Regular menses Menstrual disturbance *p <0.05
% of athletes with SF
80 *
*
60 * * 40
20
*
0 1
2
3
4
5
6
7
8
9
10 11
Figure 3-1 Studies in which the percentage of athletes with stress fractures could be compared in groups with and without menstrual disturbances. 1, Lindberg et al., 198473; 2, Marcus et al., 198574; 3, Lloyd et al., 198675; 4, Warren et al., 198625; 5, Nelson et al., 198776; 6, Barrow and Saha, 198820; 7, Myburgh et al., 199071; 8, Frusztajer et al., 199026; 9, Grimston et al., 199177; 10, Cameron et al., 199222; 11, Kadel et al., 1992.27
index and the incidence of stress fractures in 16 female runners. Conversely, Barrow and Saha20 found that lifetime menstrual history did affect the risk of stress fracture. They showed the incidence of stress fracture to be 29% in the regular group and 49% in the very irregular group. The results of a prospective study also demonstrated that those with a lower menstrual index were at greater risk of stress fracture. Myburgh et al.71 found that, although athletes with stress fractures had a higher frequency of current menstrual dysfunction than athletes without stress fractures, there was no difference in past menstrual status. This suggests that changes associated with menstrual dysfunction are reversible and do not affect future stress fracture risk if regular menses return. In summary, it would appear that there is a higher incidence of menstrual disturbances in female athletes with stress fracture than in those without. These findings have led some authors to assume that this is a direct result of decreased bone mineral density (BMD) in athletes with menstrual disturbances. However, athletes with menstrual disturbances also exhibit other risk factors, such as lower calcium intake,81 greater training load,82 and differences in soft tissue composition.83 Because these were not always controlled for in the studies discussed, it is difficult to ascertain which are the contributory factors. The relationship between age of menarche and risk of stress fracture is uncertain. Some authors have found that athletes with stress fractures have a later age of menarche,25,84,85 whereas others have found no difference.26,27,71 In a prospective study, age of menarche was an independent risk factor for stress fracture, with the risk increasing by a factor of 4.1 for every additional year of age at menarche.78 However, the mechanism for this relationship is unclear, because a later age of menarche also is associated with an increased likelihood of menstrual disturbance,86 a lower energy intake,87 decreased body fat or weight,87 and excessive premenarcheal training,86 all of which could influence stress fracture risk. Some authors have claimed that the OCP may protect against stress fracture development. Barrow and Saha20 found that runners using the OCP for at least 1 year had significantly fewer stress fractures (12%) than nonusers (29%). This was supported by the findings of Myburgh et al.71 Although no difference in OCP use was reported in ballet dancers with and without stress fractures,27 few dancers were taking the OCP. Because these studies are cross-sectional or retrospective in nature, it is not known whether the athletes were taking the OCP before or following the stress fracture episode. In addition, athletes may or may not take the OCP for reasons that in themselves could influence stress fracture risk. A prospective study did not support a protective effect of OCP use on stress fracture development.78 Nevertheless, it is not known whether the risk of stress fracture is decreased in athletes with menstrual 57
...........
Research to date has focused on the relationship between stress fracture incidence and menstrual irregularity (amenorrhea and oligomenorrhea), age of menarche, and use of the oral contraceptive pill (OCP). The findings of numerous studies suggest that stress fractures are more common in athletes exhibiting menstrual disturbances20,25-27,71,73-78 (Fig. 3-1). Although not all results were statistically significant, power may have been limited by relatively small samples in some studies. In general, athletes with menstrual disturbances had a relative risk for stress fracture that was between two and four times greater than that of their eumenorrheic counterparts. However, in ballet dancers, logistic regression analysis showed that amenorrhea for longer than 6 months’ duration was an independent contributor to the risk of stress fracture, with the estimated risk being 93 times that of a dancer with regular menses.27 The risk of multiple stress fractures also seems to be increased in those with menstrual disturbances.20,79 Clark et al.79 found that, although amenorrheic and eumenorrheic groups reported a similar prevalence of single stress fractures, 50% of the amenorrheic runners reported multiple stress fractures, compared with only 9% of those regularly menstruating. Grimston et al.80 developed a menstrual index that summarized previous and present menstrual status. They found no relationship between this menstrual
CHAPTER 3
Stress fractures: their causes and principles of treatment
disturbances who subsequently take the OCP. This is an important area for future research.
Low bone density Theoretically, low BMD could contribute to the development of a stress fracture by decreasing the fatigue resistance of bone to loading and by increasing the accumulation of microdamage.45,88 Results from a limited number of studies comparing regional bone density in military or athletic groups with and without stress fracture have been inconclusive26,40,71,77,78,84,85,89,90 (Table 3-7). The discrepancy may reflect differences in populations, type of physical activity, measurement techniques, and bone regions. However, the findings of a 12-month prospective study using dual energy x-ray absorptiometry (DEXA) to measure bone mass indicate that low bone density is a risk factor for stress fractures in women and possibly in men.78 Female athletes who sustained tibial stress fractures had 8.1% lower tibia/fibula BMD than athletes without stress fractures (p < .01). In the men, the tibial stress fracture group had 4.0% less tibia/fibula BMD than the nonstress fracture group, although this was not significant (p ¼ .17). However, it is important to note that in this study the athletes with stress fractures still had bone density levels that were similar to or greater than less-active control subjects. This implies that the level of bone density required by athletes for short-term bone health is greater than that required by the general population. Bone geometry Bone geometry influences the ability of the bone to resist mechanical loads. A prospective study of 295 male Israeli military recruits assessed the influence of bone geometry on stress fracture risk.91,92 Significantly fewer stress fractures were sustained by those with a greater mediolateral tibial width, measured using standard radiographs, than by those with a narrower tibia. This may be due to a greater area moment of inertia and hence increased ability of the bone to resist bending forces in the anteroposterior direction. However, the incidence of stress fractures did not correlate with cortical thickness. These findings were confirmed by a recent prospective study of 626 U.S. male recruits.40 Using DEXA to derive structural geometry, the authors found significantly smaller tibial cross-sectional area, smaller tibial section modulus, and smaller tibial width in the stress fracture cases. These remained after adjusting for body weight differences between groups. There are no data that investigate whether bone geometry predisposes to stress fractures in athletes. Endocrine factors Alterations in calcium metabolism could affect bone remodeling and bone density, and theoretically predispose
...........
58
to stress fracture. However, single measurements of serum calcium, parathyroid hormone, 25 OH-vitamin D and 1,25-dihydroxyvitamin D have not been found to differ between stress fracture and nonstress fracture groups in military recruits.25,71,85 This may reflect sampling procedures or the fact that many of these biochemical parameters are tightly regulated.
Nutritional status Low calcium intake may contribute to stress fracture development by directly influencing the processes of bone remodeling and bone mineralization or by indirectly affecting soft tissue composition and ovarian function. Other dietary factors, such as fiber, protein, and caffeine intake, may play a role but have not been well studied. There is limited evidence to suggest that low calcium intake may be associated with an increased risk for stress fracture.71,93 Myburgh et al.94 found a significantly lower intake of calcium in athletes with shin soreness in comparison with a matched control group. However, because exact diagnoses were not made, stress fracture may not have been the only pathology included in this group. A follow-up study in athletes with scintigraphically diagnosed stress fractures confirmed the original results.71 Current calcium intake was significantly lower in the stress fracture group, being 87% of the recommended daily intake (RDI). This is consistent with their reduced consumption of dairy products. The authors claimed that a calcium intake of greater than 800 mg/day protects against stress fracture development. Conversely, other investigators have failed to confirm the relationship between stress fractures and dietary calcium.26,27,78,84,85,95 Many ballet dancers were found to consume less than the RDI for calcium regardless of their stress fracture status,26,27 implying that other factors may be more important as risk factors in dancers. A calcium index based on the variability in calcium intake during the ages of 12 to 23 years did not differ in runners with and without stress fractures.77 In a prospective study of track and field athletes, risk of stress fracture was not associated with current calcium intake, current intake of nutrients known to influence calcium bioavailability and bone mass, or calcium supplementation use. Because the majority of athletes in this study were consuming more than the RDI for calcium, the results suggest that the relative risk of stress fracture is not influenced by daily intakes above this level. This is consistent with the concept of calcium as a threshold nutrient whereby effects on the skeleton are apparent only up to a certain level.96 However, it does not rule out an association between calcium deficiency and a higher incidence of stress fracture. There are no intervention studies assessing the effect of calcium supplementation on stress fracture incidence in
Summary of studies directly investigating the relationship between bone density and stress fractures
Reference
Study design
Subjects
Sex
Pouilles et al., 198989
CS
Military
M
Carbon et al., 199085
CS
Various athletes
Frusztajer et al., 199026
CS
Myburgh et al., 199071
Sample size
Sites
Results % diff{
41-SF 48-NSF
DPA
Femoral neck Ward’s triangle Trochanter
5.7* 7.1* 7.4*
F
9-SF 9-NSF
DPA SPA
LSp Femoral neck Distal radius Ultradistal radius
4.0* 7.0 7.7 0.0
Ballet dancers
F
10-SF 10-NSF
DPA SPA
LSp First metatarsal Radial shaft
4.1 0.0 0.0
CS
Various athletes
M/F
25-SF 25-NSF (19 F, 6 M)
DXA
LSp Femoral neck Ward’s triangle Trochanter Intertrochanter Proximal femur
8.5* 6.7* 9.0* 8.6* 5.5 6.5*
Giladi et al., 198792
P
Military
M
91-SF 198-NSF
SPA
Tibial shaft
–6.0
Grimston et al., 199177
CS
Runners
F
6-SF 8-NSF
DPA
LSp Femoral neck Tibial shaft
8.2* 7.6* 9.7
Warren et al., 199184
CS
Ballet dancers
F
14-SF 34-NSF
DPA
LSp First metatarsal Distal radius
NS NS NS
Bennell et al., 199678
P
Track & field athletes
F
10-SF 36-NSF
DXA
Upper limb Thor sp LSp Femur Tibia/fibula Foot
3.3 6.7 11.9* 2.2 4.2 6.6*
Risk factors for stress fractures
Techn
(Continued)
59
............
Table 3-7
60
............
CHAPTER 3
Summary of studies directly investigating the relationship between bone density and stress fractures (cont’d)
Reference
Beck et al., 199640
Study design
P
Subjects
Military
Sex
Sample size
Techn
Sites
Results % diff{
M
10-SF 39-NSF
DXA
Upper limb Thor sp LSp Femur Tibia/fibula Foot
4.9 4.1 0.8 2.9 4.0 0.3
M
23-SF 587-NSF
DXA
Femur Tibia Fibula
3.9* 5.6* 5.2
CS, Cross-sectional; DPA, dual photon absorptiometry; DXA, dual energy x-ray absorptiometry; F, females; LSp, lumbar spine; M, males; NS, not stated but not significantly different; P, prospective; SPA, single photon absorptiometry; Techn, technique; Thor sp, thoracic spine. *Statistically significant. { Results are given as the percent difference comparing stress fracture subjects (SF) with nonstress–fracture subjects (NSF).
Stress fractures: their causes and principles of treatment
Table 3-7
Risk factors for stress fractures
1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0 10
11
12
13
14
15
16
17
18
19
20
Age of menarche (years) Corrected calf girth Small
Average
Large
Figure 3-2 Plot of the probability of stress fracture at different ages of menarche for different corrected calf girths in female athletes. The plot for small corrected calf girth was calculated using the minimal value measured in the cohort; the average girth was calculated using the mean value; and the large girth was calculated using the maximal value. (From Bennell KL, et al: Am J Sports Med 24:814, 1996.)
61
...........
Anthropometry and soft tissue composition Anthropometric characteristics, such as height and weight, and soft tissue composition, such as lean mass and fat mass, theoretically could affect stress fracture risk directly by influencing the forces applied to bones98 or indirectly via effects on bone density99,100 and menstrual function.83 Unlike the military, in which anthropometric characteristics appear to be related to stress fractures incidence,40 no study in athletes has reported a difference in height, weight, body mass index, or fat mass between those with and without stress fractures.20,21,25,27,75,77,78,85 Failure to find a relationship in athletes may be due to the relative homogeneity in these characteristics, unlike the military, in which a range of somatotypes would be expected. Another explanation is that the relationship may be nonlinear. Muscles could play a dual role in stress fracture development. Some investigators consider that muscles act dynamically to cause stress fractures by increasing bone strain at sites of muscle attachment.101,102 Greater muscle mass with greater ability to generate force would be associated with an increased risk for stress fracture. Others feel that, because muscles act to attenuate and dissipate forces applied to bone,103 muscle fatigue or muscle weakness would predispose to stress fracture by causing an increase and redistribution of stress to bone.62,104 In the military, leg power was not associated with stress fracture occurrence, although the testing method was relatively crude and nonspecific.90
However, recruits with a larger calf muscle circumference developed significantly fewer stress fractures.91 This finding also was evident in female athletes, in whom every 1 cm decrease in calf girth was associated with a fourfold greater risk of stress fracture78 (Fig. 3-2). Using a biomechanical model, Scott and Winter105 calculated that, during running, the tibia is subjected to a large forward bending moment as a result of ground reaction force. The calf muscles oppose this large bending moment by applying a backward moment as they contract to control the rotation of the tibia and the lowering of the foot to the ground. The total effect is a smaller bending moment. Extrapolating from this, a stress fracture could result if the calf muscles are unable to produce adequate force to counteract the loading at ground contact and decrease excessive bone strain. The findings of a smaller calf girth in those with stress fractures tend to support the hypothesis that muscles act to protect against rather than cause stress fractures. However, there have been no studies comparing muscle mass or muscle strength, particularly peak force
Probability of SF
athletes. A randomized controlled study in male military recruits showed a similar incidence of stress fractures during a 9-week training program in 247 recruits taking 500 mg of calcium daily and in 1151 controls.97 However, because both groups had a baseline dietary calcium intake greater than 800 mg/day, this may have been sufficient to provide protection against stress fracture. Alternatively, a longer duration of calcium intervention may be necessary for effects to become apparent, particularly at cortical bone sites. Other nutrients, such as protein, total energy, phosphorus, fiber, sodium, alcohol, and caffeine could potentially affect bone health and therefore stress fracture risk. At present, no associations have been found between these and the incidence of stress fractures in athletes.26,78,84,85 Dietary behaviors and eating patterns may differ in those with stress fractures. Ballet dancers with stress fractures were more likely to diet and restrict food intake, avoid high-fat dairy foods, consume low-calorie products, have a self-reported history of an eating disorder, and have weight fluctuations down to a lower percentage of ideal body weight than those without stress fractures.26 However, scores on a validated test relating to dieting, bulimia and food preoccupation, and oral control (EAT-26) did not differ between ballet dancers or track and field athletes with and without stress fracture.25,26,78
CHAPTER 3
Stress fractures: their causes and principles of treatment
production and tendency to fatigue, in athletes with and without stress fractures. Grimston et al.106 found that, during the latter stages of a 45-minute run, females with a past history of stress fracture recorded increased ground reaction forces, whereas ground reaction forces did not vary during the run in the control group. The authors surmised that this may indicate differences in fatigue adaptation and muscle activity.
Training Repetitive mechanical loading arising from athletic training contributes to stress fracture development. However, the contribution of each training component (volume, intensity, frequency, surface, and footwear) to the risk of stress fracture has not been elucidated. Training also may influence bone indirectly through changes in levels of circulating hormones, through effects on soft tissue composition, and through associations with menstrual disturbances. Large military studies have shown that various training modifications, such as inclusion of rest periods,34,107 elimination of running and marching on concrete,33,108 use of running shoes rather than combat boots,32,108 and reduction of high-impact activity32,34,37,38,108 can decrease the incidence of stress fractures in recruits. In contrast, there is little controlled research in athletes. Most research consists of anecdotal observations or case series in which training parameters are examined only in those athletes with stress fractures. Surveys have reported that up to 86% of athletes can identify some change in their training before the onset of the stress fracture.22,29,57 Other researchers have blamed training ‘‘errors’’ in a varying proportion of cases but do not adequately define these errors.30,55,60,109 Brunet et al.21 surveyed 1505 runners and found that increasing mileage correlated with an increase in stress fractures in women but not in men. An explanation for the apparent gender difference is unclear. Australian track athletes with a past history of stress fracture tended to report more weekly hours of training and running and greater weekly distances in the 5 years preceding the study, compared with those who had never sustained a stress fracture.22 In a study of ballet dancers, a dancer who trained for more than 5 hours per day had an estimated risk for stress fracture that was 16 times greater than a dancer who trained for fewer than 5 hours per day.27 This study supports a role for training volume as a risk factor for stress fracture, but that factor may be related to increased exposure to injury. Training surface has long been considered to contribute to stress fracture development.5 Anatomic and biomechanical problems can be accentuated by cambered or uneven surfaces, whereas ground reaction forces are increased by less compliant surfaces.110,111 In a study of female runners, Zernicke et al.93 claimed that those who sustained stress fractures tended to train on harder
...........
62
surfaces but provided no further details. Other researchers also have implicated training surface or change in surface as a risk factor but do not provide substantial evidence in support.29,57 Older or worn running shoes have been related to an increase in stress fractures,36 possibly as a result of decreased shock absorption.112 However, the use of a shock-absorbing viscoelastic insole made no difference to the incidence of tibial stress fractures in rabbits113 or to the overall incidence of stress fractures in military recruits.36,44,114 It is not clear why Milgrom et al.41 found a significant insole effect limited to femoral stress fractures only. Another prospective study showed that a semirigid orthotic device significantly reduced the incidence of femoral stress fractures in recruits with high-arched feet and the incidence of metatarsal fractures in recruits with low-arched feet.115 The incidence of tibial stress fractures was not affected by the use of this orthotic device. Because the device had a hindfoot post at 3 degrees varus, altering the biomechanics of the foot, it is difficult to know whether the results of the study can be attributed to this feature or to the shock-absorption capability. In track and field, clinical observation suggests that the use of running spikes may influence the likelihood of stress fracture. However, little research has focused on the kinetic and kinematic effects of this form of footwear or on the relationship of spikes to stress fracture.
Biomechanics Biomechanical features may predispose to stress fractures by creating areas of stress concentration in bone or by promoting muscle fatigue. Although various biomechanical features have been examined in military recruits, there are few data pertaining to athletes. Failure to report measurement reliability or to analyze data appropriately makes results difficult to interpret. High arches (pes cavus) may be associated with an increased risk for stress fracture, particularly at femoral and tibial sites in male military recruits.115-117 In a prospective study, the overall incidence of stress fracture in the low-arched group was 10%, as opposed to 40% in the high-arched group.116 A similar trend was noted for tibial and femoral stress fractures. However, assessment of foot type was based on observation in a nonfunctional position, and recruits with extreme pes planus were excluded. Nevertheless, these findings were supported by a study using a contact pressure display method to provide foot-ground pressure patterns and derived stress intensity parameters.117 Although there may be a relationship between foot type and stress fracture, this may vary depending on the site of stress fracture. Using radiographs to assess foot type, femoral and tibial stress fractures were more prevalent in the presence of higher arches, whereas the incidence of metatarsal fractures was higher with lower arches.115 The authors proposed that,
Diagnosis
and using a force platform suggest a possible role for external loading kinetics and load magnitude in the development of a stress fracture.77,106 This is an important area for future research.
DIAGNOSIS In the assessment of a patient presenting with a possible diagnosis of stress fracture, there are three questions that need to be answered: 1. Is the pain bony in origin? 2. If so, which bone is involved? 3. At what stage in the continuum of bone stress is this injury? To obtain an answer to these three questions, a thorough history, precise examination, and appropriate use of imaging techniques are used. In many cases, the diagnosis of stress fracture will be relatively simple. In others, especially when the affected bone may lie deeply (e.g., femur) or the pattern of pain may be nonspecific (e.g., navicular), the diagnosis can present a challenge for the clinician.
History ............................................................. The history of the patient with a stress fracture typically is one of insidious onset of activity-related pain. Usually the pain will be described initially as a mild ache occurring after a specific amount of exercise. If the patient continues to exercise, the pain may well become more severe or occur at an earlier stage of exercise. The pain eventually may increase to the point that it limits the quality or quantity of the exercise performed or, occasionally, forces cessation of all activity. In the early stages, pain usually will cease soon after exercise is terminated. However, with continued exercise and increased severity of symptoms, the pain may persist after exercise cessation. Night pain occasionally may occur. In addition to obtaining a history of the patient’s pain and its relation to exercise, it is important to determine the presence of predisposing factors. Therefore a training or activity history is essential. In particular, note should be taken of recent changes in activity level, such as increased quantity of training, increased intensity of training, and changes in surface, equipment (especially shoes), and technique. It may be necessary to obtain information from the patient’s coach or trainer. A full dietary history should be taken; particular attention should be paid to the possible presence of eating disorders. In females a menstrual history should be taken, including age of menarche and subsequent menstrual status. A history of previous similar injury or any other musculoskeletal injury should be obtained. It is essential to 63
...........
because a low-arched foot is more flexible, it reduces the forces transmitted proximally to the tibia and femur but concentrates the forces in the foot. Limited observations in athletes tend to differ from military findings. Pes planus (pronated) was the most common foot type in athletes who presented to sports clinics with stress fractures.55,57 However, the incidence of pes planus in noninjured athletes was not assessed. In another series of stress fractures, pes planus was more common in tibial and tarsal bone stress fractures and least common in metatarsal stress fractures.59 This implies a possible heterogenous effect of biomechanical features on stress fracture risk, depending on the anatomic location of the injured region. A leg-length discrepancy is another feature that has been postulated as a potential risk factor because of resulting skeletal realignment and asymmetries in loading, bone torsion, and muscle contraction.118 Using a radiologic method to assess leg length, Friberg119 found that, in 130 cases of stress fracture in military recruits, the longer leg was associated with 73% of tibial, metatarsal, and femoral fractures, whereas 60% of fibular fractures were found in the shorter leg. In a prospective analysis, he observed a positive correlation between the degree of leg-length inequality and the incidence of stress fractures. However, no statistical analyses were performed to assess the significance of these results. A leg-length discrepancy also has been found to be associated with a significant increase in the incidence of stress fractures in athletes.21,78 Seventy percent of women who developed stress fractures displayed a leg-length difference of more than 0.5 cm, compared with 36% of women without stress fractures.78 Large prospective studies in the Israeli military have included an orthopaedic examination in addition to assessment of other risk factors for stress fractures.42,90,120 Of the biomechanical variables, only range of hip external rotation was found to correlate with the incidence of stress fracture. Soldiers in whom hip external rotation was greater than 65 degrees were at a higher risk for tibial and total stress fractures than those with a range less than 65 degrees. The risk for tibial stress fracture increased 2% for every 1 degree increase in hip external rotation range.42 However, a large prospective study in American recruits failed to confirm these findings.121 Greater forefoot varus and restricted ankle joint dorsiflexion also have been associated with an increased risk of stress fracture in military recruits.122 The only prospective study to examine a number of clinical biomechanical measurements in athletes, including range of hip rotation and ankle dorsiflexion, calf and hamstring flexibility, lower limb alignment, and static foot posture, did not find any to be useful predictors of stress fracture occurrence.78 Most studies have included static biomechanical measures, which may not adequately reflect the dynamic situation.123 Preliminary studies analyzing running gait
CHAPTER 3
Stress fractures: their causes and principles of treatment
obtain a brief history of the patient’s general health, medications, and personal habits to ensure that there are no factors that may influence bone health. It also is important to obtain from the history an understanding of the patient’s work and sporting commitments. In particular, it is important to know at what level of sport and how serious the patient is about his or her sport, as well what significant sporting commitments are ahead in the short term and medium term.
Physical examination ............................................................. On physical examination the most obvious feature is localized bony tenderness. Obviously this is easier to determine in bones that are relatively superficial and may be absent in stress fractures of the shaft or neck of femur. It is important to be precise in the palpation of the affected areas, particularly in regions such as the foot, in which there are a number of bones and joints in a relatively small area that may be affected. Occasionally redness and swelling may be present at the site of the stress fracture. There also may be palpable periosteal thickening, especially in a long-standing fracture. Percussion of long bones may result in the production of pain at a point distant from the percussion. Joint range of motion usually is unaffected except in situations in which the stress fracture is close to the joint surface, such as a stress fracture of the neck of femur. Some authors have suggested that the presence of pain when therapeutic ultrasound is applied over the area of the stress fracture is of potential use in the detection of stress fractures.124-126 Similarly it is reported that application of a vibrating tuning fork to the affected bone and subsequent increase in pain is indicative of a stress fracture. Our own experience suggests that these methods are not particularly helpful. The physical examination also must take into account the potential predisposing factors; and, in all stress fractures involving the lower limb, a full biomechanical examination must be performed. Any evidence of leglength discrepancy, malalignment (especially excessive subtalar pronation), muscle imbalance, weakness, or lack of flexibility should be noted.
Imaging ............................................................. Imaging plays an important role in supplementing clinical examination to determine the answers to the three questions mentioned at the start of this section on diagnosis. In many cases a clinical diagnosis of stress fracture is sufficient. The classic history of exercise-associated bone pain and typical examination findings of localized bony tenderness have a high correlation with the diagnosis of stress fracture. However, if the diagnosis is uncertain, or in the case of the serious or elite athlete who wishes to continue
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64
training if at all possible and requires more specific knowledge of his or her condition, there are various imaging techniques available to the clinician.
Radiography Radiography has poor sensitivity but high specificity in the diagnosis of stress fractures. The classic radiographic abnormalities seen in a stress fracture are new periosteal bone formation, a visible area of sclerosis, the presence of callus, or a visible fracture line. The diagnosis of stress fracture can be confirmed if any of these radiographic signs are present. Unfortunately, in the majority of stress fractures there is no obvious radiographic abnormality. The abnormalities on radiography are unlikely to be seen unless symptoms have been present for at least 2 to 3 weeks. In certain cases they may not become evident for up to 3 months, and in a percentage of cases never become abnormal. Isotopic bone scan (scintigraphy) If plain radiography demonstrates the presence of a stress fracture, then there seldom is any need to perform further investigations. However, in cases in which there is a high index of suspicion of stress fracture and a negative bone radiograph, the triple-phase bone scan is the next line of investigation. The bone scan is highly sensitive but has low specificity. Prather et al.127 stated that the bone scan had a true-positive rate of 100%, and false-negative scans are relatively rare.128,129 Technetium-99 methylene diphosphonate usually is used as the radionuclide substance. Other possibilities include gallium citrate (Ga 67) and indium 111-labeled leukocytes.130 The advantage of technetium-99 methylene diphosphonate (MDP) is its short half-life (6 hours), allowing a higher dose to be administered with improved resolution.131 In the first phase of the bone scan, flow images are obtained immediately after the intravenous injection of the tracer. These initial images usually are taken every 2 seconds and correspond roughly to contrast angiography, albeit with much lower spatial and temporal resolution. This first phase of the bone scan evaluates perfusion to bone and soft tissues from the arterial to the venous circulation. The second phase of the bone scan consists of a static ‘‘blood pool’’ image taken 1 minute after the injection and reflects the degree of hyperemia and capillary permeability of bone and soft tissue. Generally speaking, the more acute and severe the injury, the greater the degree of increased perfusion and blood pool activity. The third phase of the bone scan is the delayed image taken 3 to 4 hours after injection, when approximately 50% of the tracer has concentrated in the bone matrix through the mechanism of chemisorption to the hydroxyapatite crystals. On the 3-hour delayed image, the uptake of the tracer is proportional to the rate of
Diagnosis
authors postulated that this may be nonspecific stress changes related to bone remodeling,133 a false-positive finding,150 and an uncertain finding.151 Rosen et al.148 found asymptomatic uptake in 46% of cases, with focal uptake more common than diffuse uptake. Matheson et al. in Vancouver, BC,152 proposed the concept of bone strain. They noted that the radionuclide bone scan, because of its sensitivity, was able to demonstrate the adaptive changes in bone at any point in the continuum from early remodeling to stress fracture. The term ‘‘bone strain’’ was coined to reflect the true dynamic response of bone to stress and to allow the interpretation of bone changes along the continuum to be correlated with the wide range of presentations seen in clinical practice. They stated that excessive loading from overuse, abnormal biomechanics, reduced shock absorption, or altered gait produced a mechanical stress that is translated into bone remodeling via piezoelectric stimuli. The relative contribution of these factors, as well as the athlete’s activity pattern after the onset of remodeling, determines the extent of bone strain seen clinically. Pain during activity may indicate small areas of remodeling, which have low-intensity uptake on bone scan and negative x-rays. On the other hand, pain that persists after exercise and during rest may indicate more extensive remodeling, with intense uptake on scan and possibly abnormal radiographs. This concept of a continuum of bone strain’s existing both clinically and scintigraphically is now widely accepted. It is clear now that bone stress can appear as an area of increased uptake on isotope bone scan before any symptoms
Figure 3-3 Typical bone scan appearance of stress fracture of tibia.
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osteoblastic activity, extraction, and efficiency, as well as to the amount of tracer delivered per unit time or blood flow.132 The inclusion of the first and second phases of the bone scan permits the estimation of the age of stress-induced focal bony lesions and the severity of bony injuries and helps to differentiate soft tissue inflammation from bony injury.133 As the bony lesion heals, the perfusion returns to normal first, followed by normalization of the blood pool image a few weeks later. Focal increased uptake on the delayed scan resolves last because of ongoing bony remodeling and generally lags well behind the disappearance of pain. As healing continues, the intensity of the uptake diminishes gradually during a 3- to 6-month period following an uncomplicated stress fracture, with a minimal degree of uptake persisting for up to 10 months132 or even longer. Changes on bone scan may be seen as early at 48 to 72 hours after the commencement of symptoms. The radionuclide scan may be positive as early as 7 hours after bone injury.134 The bone scan is virtually 100% sensitive, at least twice as sensitive as x-ray,135 and consistently more sensitive that ultrasound,136 thermography,137 and computerized tomography (CT).138 In several studies, only 10% to 25% of bone–scan-positive stress fractures had radiographic evidence of stress fracture.139-142 In the appropriate clinical setting, the scintigraphic diagnosis of a stress fracture is defined as focal increased uptake in the third phase of the bone scan. However, bone scintigraphy lacks specificity because other nontraumatic lesions, such as tumor (especially osteoid osteoma), osteomyelitis, bony infarct, and bony dysplasias also can produce localized increased uptake. Therefore it is vitally important to correlate the bone scan appearance with the clinical features. The radionuclide scan will detect evolving stress fractures at the stage of accelerated remodeling. At that stage, which may be asymptomatic, the uptake usually is of mild intensity, progressing to more intense and better defined uptake as microfractures develop.13,143 In stress fractures all three phases of the triple-phase bone scan are positive.133,144 Other bony abnormalities, such as periostitis (shin splints), are positive only on delayed images,133,145 whereas certain other overuse soft-tissue injuries would be positive only in the angiogram and blood pool phase, thus allowing one to differentiate between bony and soft-tissue pathology. The characteristic bone scan appearance of a stress fracture is of a sharply marginated or fusiform area of increased uptake involving one cortex or occasionally extending the width of the bone13 (Fig. 3-3). Increased radionuclide uptake often is found in asymptomatic sites.108,146,147 Originally the presence of increased tracer uptake at nonpainful sites in athletes was interpreted as unrecognized stress fractures.13,148,149 Other
CHAPTER 3
Stress fractures: their causes and principles of treatment
occur. It is not clear what percentage of these cases progress to symptomatic bone stress and ultimately to stress fracture if exercise is continued. It also is not clear what treatment is appropriate in these cases of asymptomatic bone stress. Many athletes and dancers in hard training show numerous areas of bone stress on an isotope bone scan. These are indicators of active remodeling and are not necessarily bone at risk for the development of stress fracture. Attempts have been made to classify the bony continuum into ‘‘bone strain’’ or ‘‘asymptomatic stress reaction’’ and stress fracture. A summary of these features may be seen in Table 3-8. A scheme for grading bone scan appearance on the basis of severity has been proposed by Zwas et al.141 This is shown in Table 3-9.
Computerized tomography CT may be useful in differentiating those conditions with increased uptake on bone scan that may mimic stress fracture. These include osteoid osteoma, osteomyelitis with a Brodie’s abscess, and other malignancies. CT scans also are particularly valuable in imaging fractures in which this may be important in treatment. CT scanning of the navicular bone is particularly helpful.153,154 CT scanning also may be valuable in detecting fracture lines as evidence of stress fracture in long bones (e.g., metatarsal and tibia) in which plain radiography is normal and isotope bone scan shows increased uptake (see Fig. 3-3). CT scanning will enable the clinician to differentiate between a stress fracture, which will be visible on CT scan, and a stress reaction (Fig. 3-4). Particularly
Table 3-8
in the elite athlete, this may considerably affect his or her rehabilitation program and forthcoming competition program.
Magnetic resonance imaging Magnetic resonance imaging (MRI), although not imaging cortical bone as well as CT scan, has certain advantages in the imaging of stress fractures. Specific MRI characteristics of stress fracture include new bone formation and fracture lines appearing as very low signal medullary bands that are contiguous with the cortex; surrounding marrow hemorrhage and edema seen as low signal intensity on T1-W images (Fig. 3-5) and as high-signal on T2-W and short T1 inversion and recovery (STIR) images; and periosteal edema and hemorrhage appearing as high signal intensity on T2-W and STIR images.155 These changes are seen best if the MRI is performed within 3 weeks of symptoms.156 MRI is thought to be more sensitive than conventional radiography. MRI visualizes marrow hemorrhage and edema well, a characteristically difficult finding with CT. Although CT scan visualizes bone detail, another advantage of MR imaging is in distinguishing stress fractures from a suspected bone tumor or infectious process.155 Stafford et al.157 reported findings of stress fractures in MRI. Zones of decreased signal of T1 images are seen in the affected region, whereas T2-weighted images show increased signal. A low signal line may be seen running through the medullary cavity, presumably corresponding
Continuum of bony changes with overuse
From Brukner PD, Khan KM: Clinical sports medicine, rev ed 2, Sydney, 2002, McGraw-Hill Book Company. CT, Computed tomography; MR, magnetic resonance.
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Diagnosis
Table 3-9
Grading of tibial or long bone stress fractures by bone scan or magnetic resonance imaging (MRI) appearance
Grade
Bone scan appearance
MRI appearance
Grade I
Small, ill-defined cortical area of mildly increased activity
Periosteal edema: mild to moderate on T2-weighted images. Marrow edema: normal on T1- and T2-weighted images.
Grade II
Better defined cortical area of moderately increased activity
Periosteal edema: moderate to severe on T2-weighted images. Marrow edema on T2-weighted images.
Grade III
Wide, fusiform cortical-medullary area of highly increased activity
Periosteal edema: moderate to severe on T2-weighted images. Marrow edema on T1- and T2-weighted images.
Grade IV
Transcortical area of increased activity
Periosteal edema: moderate to severe on T2-weighted images. Marrow edema on T1- and T2-weighted images. Fracture line clearly visible.
Figure 3-4 Computed tomography (CT) appearance of stress fracture of navicular.
Figure 3-5 Magnetic resonance imaging (MRI) appearance of stress fracture.
edema, as well as bone marrow edema on T2-weighted images only. Grade III showed moderate to severe edema of both the periosteum and marrow on both T1- and T2-weighted images. Grade IV demonstrated a low signal fracture line on all sequences with changes of severe marrow edema on both T1- and T2-weighted images. Grade IV also may show severe periosteal and moderate muscle edema. The comparison of grading of stress fractures between bone scan141 and MRI159 is shown in Table 3-9. Steinbronn et al.158 advocated the use of MRI in patients who have negative radiographs, a positive bone scan, and a diagnosis still not firmly established. 67
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to the zone of localized fracture. Further advances in marrow imaging have occurred, such as STIR sequences that help to better identify such marrow pathology. The appearance of a stress fracture on MRI is characteristic with intraosseous bands of very low signal intensity that are continuous with the cortex and surrounding areas of decreased signal intensity of the marrow space on T1-weighted images. T2 images show prominent intramedullary areas of high signal intensity and juxtacortical and/or subperiosteal areas of high signal intensity.156,158 Fredericson et al.159 proposed a grading scheme for MRI appearances of stress fractures using STIR images. The authors felt that their grades I to IV were equivalent to the bone scan grading described by Zwas et al.,141 mentioned in the previous section. In this grading system, grade I indicated mild to moderate periosteal edema on T2-weighted images, only with no focal bone marrow abnormality. Grade II showed more severe periosteal
CHAPTER 3
Stress fractures: their causes and principles of treatment
DIFFERENTIAL DIAGNOSIS The differential diagnosis of stress fracture can be divided into nonbony causes or bony causes. Nonbony causes, in particular, relate to muscle or tendon injury; either muscle strain, hematoma or delayed-onset muscle soreness, or tendon inflammation or degenerative change. Bony pathologies that can mimic stress fracture include tumor and infection. Osteoid osteoma commonly is mistaken for a stress fracture because it presents with pain and a discrete focal area of increased uptake on isotope bone scan. Two distinguishing features of osteoid osteoma are the presence of night pain and the relief of pain with the use of aspirin. In addition, a CT scan or MRI can clearly distinguish the nidus of an osteoid osteoma from the cortical abnormality of a stress fracture.
TREATMENT The basis of treatment of stress fractures involves rest from the aggravating activity, a concept known as ‘‘relative rest.’’ The amount of time from a diagnosis of a stress fracture to full return to sport depends on a number of factors, including the site of the fracture, the length of the symptoms, and the stage in the spectrum of bone strain. Most stress fractures with a relatively brief history of symptoms will heal in a straightforward manner, and return to sport should occur within 6 to 8 weeks. However, there is a group of stress fractures that require additional treatment to relative rest, and these are considered later. The primary aim of initial management of stress fracture is pain relief. This may involve the use of mild analgesics or nonsteroidal anti-inflammatory drugs (NSAIDs). In some cases in which activities of daily living are painful, it may be necessary for the patient with a stress fracture to be nonweight bearing or partial weight bearing on crutches for a period of up to 7 to 10 days. In the majority of cases this is not necessary, and mere avoidance of the aggravating activity will be sufficient. The rate of resumption of activity should be modified according to symptoms and physical findings. At all time, activity should be pain free; and, if any bony pain occurs, then activity should be ceased for 1 to 2 days and then resumed at a lower level. The patient should be clinically reassessed at regular intervals, in particular looking for bony tenderness. When activities of daily living are pain free and there is no focal tenderness, then resumption of the aggravating activity can occur on a graduated basis. For lower limb stress fractures in which running is the aggravating activity, we recommend a program that involves initial brisk walking increased by 5 to 10 minutes per day, up to a length
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of 45 minutes. Once this is achieved without pain, we then recommend introducing initially a period of 5 minutes of slow jogging within the 45-minute walk. Assuming that this increase in activity does not reproduce the patient’s symptoms, then the amount of jogging can be increased on a daily basis until the whole 45 minutes is completed at jogging pace. Once this is achieved, then strides can be introduced, initially half-pace and then gradually increasing to full-pace striding. Once full sprinting is pain free, then gradual functional activities, such as hopping, skipping and jumping, twisting, and turning can be introduced gradually. It is important that this process is a graduated one, and it is important to err on the side of caution rather than try to be too hasty. A typical program for an uncomplicated lower limb stress fracture resuming activity after a period of initial rest and activities of daily living is shown in Figure 3-6. Progress should be monitored clinically by the presence or absence of symptoms and local signs. It usually is not necessary to monitor progress by radiography, scintigraphy, CT, or MRI. Radiologic healing often lags behind clinical healing.
Fitness maintenance It is important that the athlete with a stress fracture be able to maintain strength and cardiovascular fitness while undergoing the appropriate rehabilitation program. It should be emphasized to the athlete that the rehabilitation program is not designed to maintain or improve the patient’s fitness but rather to allow the damaged bone time to heal and gradually develop or regain full strength. Fitness should be maintained in other ways. The most common ways are biking, swimming, water running, and using upper body weights. These workouts should mimic the athlete’s normal training program as much as possible in both duration and intensity. Water running is particularly attractive to runners for this reason. Water running involves the use of a buoyancy vest as a flotation device. Stretching should be performed to maintain flexibility during the rehabilitation process. Muscle strengthening also is an important component of the rehabilitation phase. In addition to maintaining these parameters of physiologic fitness, it is possible in most cases for the athlete to maintain specific sports skills. In ball sports these can involve activities either seated or standing still. This active rest approach also greatly assists the athlete psychologically. Modified risk factors As with any overuse injury, it is not sufficient merely to treat the stress fracture itself. An essential component of the management of an athlete with an overuse injury involves identification of the factors that have contributed to the injury and, when possible, correction or
Treatment
Day 1 (mins)
Day 2 (mins)
Day 3 (mins)
Day 4 (mins)
Day 5 (mins)
Day 6 (mins)
Day 7 (mins)
Week 1
Walk 5
Walk 20
Walk 25
Walk 30
Walk 35
Walk 40
Walk 45
Week 2
Walk 20 Jog 5 Walk 15
Walk 15 Jog 15 Walk 15
Walk 15 Jog 20 Walk 15
Walk 10 Jog 25 Walk 10
Walk 5 Jog 30 Walk 10
Walk 5 Jog 35 Walk 5
Jog 45
Week 3
Jog 45 Sprint 10
Jog 45 Sprint 10
Jog 45 Sprint 15
Jog 45 Sprint 15
Jog 45 Sprint 10
Jog 45 Sprint 10
Jog 45 Sprint 15
Week 4
Add functional activities
Week 5
Gradually increase all week
RESUME FULL TRAINING
Figure 3-6 Activity program following uncomplicated lower limb stress fracture following period of rest and activity of daily living (ADL).
on the previously injured area and reduce the likelihood of a recurrence.
Stress fractures requiring specific treatment Although the majority of stress fractures of the foot and ankle will heal without complications in a relatively short time frame, there are a number of stress fractures that require specific additional treatment. These are as follows: Medial malleolus Navicular Base of second metatarsal Proximal fifth metatarsal Sesamoids These ‘‘difficult stress’’ fractures are covered in Chapter 4.
4 PEARL Stress fractures of the second, third, or fourth metatarsals swell and the pain is dorsal, whereas neuromas of the forefoot do not swell and the pain typically is plantar. Most stress fractures of the foot and ankle heal with relative rest. Navicular, fifth metatarsal Jones, base of second, medial malleolus, sesamoid, and lateral process of the talus require more involved care for healing. Stress fractures are fatigue fractures and result from repeated overuse, and they are common in the athlete. For stress fractures, always investigate for eating abnormalities, and in females ask about their menstrual history. Bone scans and MRI are helpful to diagnose a stress fracture early in its presentation (<3 weeks of symptoms).
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modification of some of these factors to reduce the risk of the injury’s recurring. The fact that stress fractures have a high rate of recurrence is an indication that this part of the management program often is neglected. The risk factors for the development of stress fractures have been discussed at length in a previous section. Although not yet supported by rigorous scientific evidence, one possible precipitating factor is training errors. Therefore it is important to identify these and to discuss them with the athlete and his or her coach when appropriate. Another important contributing factor may be inadequate equipment, especially running shoes. These shoes may be inappropriate for the particular foot type of the athlete, may have general inadequate support, or may be worn out (see Chapter 26). Biomechanical abnormalities also are thought to be an important factor contributing to the development of overuse injuries in general and stress fractures in particular. Both excessively supinated and excessively pronated feet can be contributing factors in the development of stress fractures. Excessively supinated feet generally give poor absorption and require footwear that gives good absorption. Excessively pronated feet will require appropriate footwear for their foot type and also may require the use of custom-made orthotics (see Chapter 27). It is important that these risk factors are corrected by the time the athlete resumes training. When training resumes, it is important to allow adequate recovery time after hard sessions or hard weeks of training. In view of the history of stress fracture, it is advisable that some form of cross training, for example, swimming and cycling for a runner, be introduced to reduce the stress
CHAPTER 3
Stress fractures: their causes and principles of treatment
CONCLUSION Stress fractures are a common injury, particularly in runners and in sports that involve a large amount of running. Various risk factors for the development of stress fractures have been proposed; however, the relative importance of these is still uncertain. The diagnosis is primarily on clinical grounds, but imaging can be used to confirm the diagnosis or to assess the extent of the injury. The treatment is straightforward in most cases, but there is a small group of stress fractures that require more specific management.
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23. Bennell KL, et al: Risk factors for stress fractures in female trackand-field athletes, a retrospective analysis, Clin J Sport Med 5:229, 1995. 24. Bennell KL, et al: The incidence and distribution of stress fractures in competitive track and field athletes, Am J Sports Med 26:211, 1996. 25. Warren MP, et al: Scoliosis and fractures in young ballet dancers: relation to delayed menarche and secondary amenorrhea, N Engl J Med 314:1348, 1986. 26. Frusztajer NT, et al: Nutrition and the incidence of stress fractures in ballet dancers, Am J Clin Nutr 51:779, 1990. 27. Kadel NJ, Teitz CC, Kronmal RA: Stress fractures in ballet dancers, Am J Sports Med 20:445, 1992. 28. Johnson AW, Weiss CB, Wheeler DL: Stress fractures of the femoral shaft in athletes—more common than expected. A new clinical test, Am J Sports Med 22:248, 1994. 29. Goldberg B, Pecora C: Stress fractures. A risk of increased training in freshmen, Phys Sportsmed 22:68, 1994. 30. Pecina M, Bojanic I, Dubravcic S: Stress fractures in figure skaters, Am J Sports Med 18:277, 1990. 31. Dixon M, Fricker P: Injuries to elite gymnasts over 10 yr, Med Sci Sport Exerc 25:1322, 1993. 32. Protzman RR, Griffis CG: Stress fractures in men and women undergoing military training, J Bone Joint Surg 59-A:825, 1977. 33. Reinker KA, Ozburne S: A comparison of male and female orthopaedic pathology in basic training, Milit Med 144(8):532-536, 1979. 34. Scully TJ, Besterman G: Stress fracture—a preventable training injury, Milit Med 147:285, 1982. 35. Brudvig TJS, Gudger TD, Oberinger L: Stress fractures in 295 trainees: a one-year study of incidence as related to age, sex, and race, Milit Med 148:666, 1983. 36. Gardner LI, et al: Prevention of lower extremity stress fractures: a controlled trial of a shock absorbent insole, Am J Public Health 78:1563, 1988. 37. Pester S, Smith PC: Stress fractures in the lower extremities of soldiers in basic training, Orthop Rev 21:297, 1992. 38. Taimela S, et al: Risk factors for stress fractures during physical training programs, Clin J Sport Med 2:105, 1992. 39. Jones BH, et al: Intrinsic risk factors for exercise-related injuries among male and female army trainees, Am J Sports Med 21:705, 1993. 40. Beck TJ, et al: Dual-energy x-ray absorptiomety derived structural geometry for stress fracture prediction in male U.S. Marine Corps recruits, J Bone Miner Res 11:645, 1996. 41. Milgrom C, et al: Stress fractures in military recruits. A prospective study showing an unusually high incidence, J Bone Joint Surg 67-B:732, 1985. 42. Milgrom C, et al: Youth is a risk factor for stress fracture. A study of 783 infantry recruits, J Bone Joint Surg 76-B:20, 1994. 43. Jones H, et al: Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology, and classification, Exerc Sports Sci Rev 17:379, 1989. 44. Milgrom C, et al: The long-term followup of soldiers with stress fractures, Am J Sports Med 13:398, 1985. 45. Carter DR, Hayes WC: Fatigue life of compact bone-1. Effects of stress amplitude, temperature and density, J Biomech 9:27, 1976. 46. Keller TS, et al: Fatigue of immature baboon cortical bone, J Biomech 18:297, 1985. 47. Matheson GO, et al: Musculoskeletal injuries associated with physical activity in older adults, Med Sci Sport Exerc 21:379, 1989. 48. Cohn SH, et al: Comparative skeletal mass and radial bone mineral content in black and white women, Metabolism 26:171, 1977. 49. Giladi M, et al: The low arch, a protective factor in stress fractures. A prospective study of 295 military recruits, Orthop Rev 14:709, 1985.
References 80. Grimston SK, et al: Menstrual, calcium, and training history: relationship to bone health in female runners, Clin Sport Med 2:119, 1990. 81. Kaiserauer S, et al: Nutritional, physiological, and menstrual status of distance runners, Med Sci Sport Exerc 21:120, 1989. 82. Guler F, Hascelik Z: Menstrual dysfunction rate and delayed menarche in top athletes of team games, Sports Med Training Rehabil 4:99, 1993. 83. Wolman RL, Harries MG: Menstrual abnormalities in elite athletes, Clin Sport Med 1:95, 1989. 84. Warren MP, et al: Lack of bone accretion and amenorrhea: evidence for a relative osteopenia in weight bearing bones, J Clin Endocrinol Metab 72:847, 1991. 85. Carbon R, et al: Bone density of elite female athletes with stress fractures, Med J Aust 153:373, 1990. 86. Frisch RE, et al: Delayed menarche and amenorrhea of college athletes in relation to age of onset of training, JAMA 246:1559, 1981. 87. Moisan J, Meyer F, Gingras S: A nested case-control study of the correlates of early menarche, Am J Epidemiol 132:953, 1990. 88. Carter DR, et al: Fatigue behaviour of adult cortical bone: the influence of mean strain and strain range, Acta Orthop Scand 52:481, 1981. 89. Pouilles JM, et al: Femoral bone density in young male adults with stress fractures, Bone 10:105, 1989. 90. Giladi M, et al: Stress fractures: identifiable risk factors, Am J Sports Med 19:647, 1991. 91. Milgrom C, et al: The area moment of inertia of the tibia: a risk factor for stress fractures, J Biomech 22:1243, 1989. 92. Giladi M, et al: Stress fractures and tibial bone width. A risk factor, J Bone Joint Surg 69-B:326, 1987. 93. Zernicke R, et al: In Stress fracture risk assessment among elite collegiate women runners, International Society of Biomechanics XIVth Congress, 1993, 1012, 1993. 94. Myburgh KH, Grobler N, Noakes TD: Factors associated with shin soreness in athletes, Phys Sportsmed 16:129-134, 1988. 95. Grimston SK, et al: The application of historical data for evaluation of osteopenia in female runners: the menstrual index, Clin Sports Med 2:108, 1990. 96. Matkovic V, Heaney RP: Calcium balance during human growth: evidence for threshold behaviour, Am J Clin Nutr 55:992, 1992. 97. Schwellnus MP, Jordaan G: Does calcium supplementation prevent bone stress injuries? A clinical trial, Int J Sport Nutr 2:165, 1992. 98. Frederick EC, Hagy JL: Factors affecting peak vertical ground reaction forces in running, Int J Sport Biomech 2:41, 1986. 99. Lindsay R, et al: Bone mass and body composition in normal women, J Bone Miner Res 7:55, 1992. 100. Elliot JR, et al: Historical assessment of risk factors in screening for osteopenia in a normal Caucasian population, Austr New Z J Med 23:458, 1993. 101. Meyer SA, Saltzman CL, Albright JP: Stress fractures of the foot and leg, Clin Sports Med 12:395, 1993. 102. Stanitski CL, McMaster JH, Scranton PE: On the nature of stress fractures, Am J Sports Med 6:391, 1978. 103. Voloshin A, Wosk J: An in vivo study of low back pain and shock absorption in the human locomotor system, J Biomech 15:21, 1982. 104. Clement DB: Tibial stress syndrome in athletes, J Sports Med 2:81, 1974. 105. Scott SH, Winter DA: Internal forces at chronic running injury sites, Med Sci Sport Exerc 22:357, 1990. 106. Grimston SK, et al: External loads throughout a 45 minute run in stress fracture and non-stress fracture runners, J Biomech 27:668, 1994.
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50. Brubaker CE, James SL: Injuries to runners, J Sports Med 2:189, 1974. 51. James SL, Bates BT, Osternig LR: Injuries to runners, Am J Sports Med 6:40, 1978. 52. Orava S: Stress fractures, Br J Sports Med 14:40, 1980. 53. Pagliano J, Jackson D: The ultimate study of running injuries, Runners World November: 42, 1980. 54. Witman PA, Melvin M, Nicholas JA: Common problems seen in a metropolitan sports injury clinic, Phys Sportsmed 9:105, 1981. 55. Taunton JE, Clement DB, Webber D: Lower extremity stress fractures in athletes, Phys Sportsmed 9:77, 1981. 56. Clement DB, et al: A survey of overuse running injuries, Phys Sportsmed 9:47, 1981. 57. Sullivan D, et al: Stress fractures in 51 runners, Clin Orthop Rel Res 187:188, 1984. 58. Hulkko A, Orava S: Stress fractures in athletes, Int J Sports Med 8:221, 1987. 59. Matheson GO, et al: Stress fractures in athletes. A study of 320 cases, Am J Sports Med 15:46, 1987. 60. Courtenay BG, Bowers DM: Stress fractures: clinical features and investigation, Med J Aust 153:155, 1990. 61. Ha KI, et al: A clinical study of stress fractures in sports activities, Orthopaedics 14:1089, 1991. 62. Benazzo F, et al: Stress fractures in track and field athletes, J Sports Traumatol Rel Res 14:51, 1992. 63. Brukner P, et al: Stress fractures: a series of 180 cases, Clin J Sport Med 6:85, 1996. 64. Brukner P, Khan K: Clinical sports medicine, Sydney, 1993, McGraw Hill. 65. Carlson GD, Wertz RF: March fracture, including others than those of the foot, J Bone Joint Surg 43:48, 1944. 66. Pocock NA, et al: Genetic determinants of bone mass in adults, J Clin Invest 80:706, 1987. 67. Soroko SB, et al: Family history of osteoporosis and bone mineral density at the axial skeleton: the Rancho Bernardo study, J Bone Miner Res 9:761, 1994. 68. Seeman E, et al: Reduced bone mass in daughters of women with osteoporosis, N Engl J Med 320:554, 1989. 69. Prior JC, et al: Spinal bone loss and ovulatory disturbances, N Engl J Med 323:1221, 1990. 70. Singer A, et al: Multiple identical stress fractures in monozygotic twins, J Bone Joint Surg 72-A:444, 1990. 71. Myburgh KH, et al: Low bone density is an etiologic factor for stress fractures in athletes, Ann Intern Med 113:754, 1990. 72. Snow GR, Anderson C: The effects of continuous progestogen treatment on cortical bone remodelling activity in beagles, Calcif Tiss Int 37:282, 1985. 73. Lindberg JS, et al: Exercise-induced amenorrhea and bone density, Ann Intern Med 101:647, 1984. 74. Marcus R, et al: Menstrual function and bone mass in elite women distance runners, Ann Intern Med 102:158, 1985. 75. Lloyd T, et al: Women athletes with menstrual irregularity have increased musculoskeletal injuries, Med Sci Sport Exerc 18:374, 1986. 76. Nelson ME, et al: Elite women runners: association between menstrual status, weight history and stress fractures, Med Sci Sport Exerc 19:S13, 1987. 77. Grimston SK, et al: Bone mass, external loads, and stress fractures in female runners, Int J Sport Biomech 7:293, 1991. 78. Bennell KL, et al: Risk factors for stress fractures in track and field athletes: a 12 month prospective study, Am J Sports Med 24:810, 1996. 79. Clark N, Nelson M, Evans W: Nutrition education for elite female runners, Phys Sports Med 16:124, 1988.
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Stress fractures: their causes and principles of treatment
107. Worthen BM, Yanklowitz BAD: The pathophysiology and treatment of stress fractures in military personnel, J Am Podiatr Med Assoc 68:317, 1978. 108. Greaney RB, et al: Distribution and natural history of stress fractures in U.S. marine recruits, Radiology 146:339, 1983. 109. McBryde AM: Stress fractures in runners, Clin Sports Med 4:737, 1985. 110. McMahon TA, Greene PR: The influence of track compliance on running, J Biomech 12:893, 1979. 111. Steele JR, Milburn PD: Effect of different synthetic sport surfaces on ground reactions forces at landing in netball, Int J Sport Biomech 4:130, 1988. 112. Cook SD, Brinker MR, Poche M: Running shoes, Sports Med 10:1, 1990. 113. Milgrom C, et al: The effect of a viscoelastic orthotic on the incidence of tibial stress fractures in an animal model, Foot Ankle 10:276, 1990. 114. Schwellnus MP, Jordaan G, Noakes TD: Prevention of common overuse injuries by the use of shock absorbing insoles, Am J Sports Med 18:636, 1990. 115. Simkin A, et al: Combined effect of foot arch structure and an orthotic device on stress fractures, Foot Ankle 10:25, 1989. 116. Giladi M, et al: The low arch, a protective factor in stress fractures. A prospective study of 295 military recruits, Orthop Rev 14:709-712, 1985. 117. Brosh T, Arcan M: Toward early detection of the tendency to stress fractures, Clin Biomech 9:111, 1994. 118. D’Amico JC, Dinowitz HD, Polchaninoff M: Limb length discrepancy: an electrodynographic analysis, J Am Podiatr Med Assoc 75:639, 1985. 119. Friberg O: Leg length asymmetry in stress fractures. A clinical and radiological study, J Sports Med 22:485, 1982. 120. Milgrom C, et al: Stress fractures in military recruits. A prospective study showing an unusually high incidence, J Bone Joint Surg 67-B:732, 1985. 121. Montgomery LC, et al: Orthopedic history and examination in the etiology of overuse injuries, Med Sci Sport Ex 21:237-243, 1989. 122. Hughes LY: Biomechanical analysis of the foot and ankle for predisposition to developing stress fractures, J Orthop Sports Phys Ther 7:96, 1985. 123. Hamill J, et al: Relationship between selected static and dynamic lower extremity measures, Clin Biomech 4:217, 1989. 124. Cole JP, Gossman D: Ultrasonic stimulation of low lumbar nerve roots as a diagnostic procedure: a preliminary report, Clin Orthop 153:126, 1979. 125. Delacerda FG: A case study: application of ultrasound to determine a stress fracture of the fibula, J Orthop Sports Phys Ther 2:134, 1981. 126. Moss A, Mowat AG: Ultrasonic assessment of stress fractures, Br Med J 286:1478, 1983. 127. Prather JL, et al: Scintigraphic findings in stress fractures, J Bone Joint Surg 59-A:869, 1977. 128. Milgrom C, et al: Negative bone scan and impending tibial stress fractures. A report of three cases, Am J Sports Med 12:488, 1984. 129. Keene JS, Lash EG: Negative bone scan in a femoral neck stress fracture, Am J Sports Med 20:234, 1992. 130. Monteleone G: Stress fractures in the athlete, Orthop Clin North Am 26:423, 1995. 131. Batillas J, Vasilas A, Pizzi WF: Bone scanning in the detection of occult fractures, J Trauma 21:564, 1981. 132. Ammann W, Matheson GO: Radionuclide bone imaging in the detection of stress fractures, Clin J Sports Med 1:115, 1991. 133. Rupani HD, et al: Three-phase radionuclide bone imaging in sports medicine, Radiology 156:187, 1985.
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134. Rosenthall L, Hill RO, Chuang S: Observation on the use of 99 mTc-phosphate imaging in peripheral bone trauma, Radiology 119:637, 1976. 135. Saunders AJS, et al: Stress lesions of the lower leg and foot, Clin Radiol 30:649, 1979. 136. Giladi M, Ziv Y, Aharonson Z: Comparison between radiography, bone scan and ultrasound in the diagnosis of stress fractures, Milit Med 149:459, 1984. 137. Devereaux MD, et al: The diagnosis of the stress fractures in athletes, JAMA 252:531, 1984. 138. Somer K, Meurman KOA: Computed tomography of stress fractures, J Comp Assoc Tomogr 6:109, 1982. 139. Prather JL, et al: Scintigraphic findings in stress fractures, J Bone Joint Surg 59-A:869, 1974. 140. Matheson GO, et al: Scintigraphic uptake of 99 mTc at nonpainful sites in athletes with stress fractures. The concept of bone strain, Sports Med 4:65, 1987. 141. Zwas ST, Elkanovitch R, Frank G: Interpretation and classification of bone scintigraphic findings in stress fractures, J Nucl Med 28:452, 1987. 142. Clement DB, et al: Exercise-induced stress injuries to the femur, Int J Sports Med 14:347, 1993. 143. Wilcox JR, Moniot AL, Green JP: Bone scanning in the evaluation of exercise-related stress injuries, Radiology 123:699, 1977. 144. Martire JR: The role of nuclear medicine bone scan in evaluating pain in athletic injuries, Clin Sports Med 6:13, 1987. 145. Sterling JC, et al: Stress fractures in the athlete. Diagnosis and management, Sports Med 14:336, 1992. 146. Meurman KOA, Elfving S: Stress fracture of the cuneiform bones, Br J Radiol 53:157, 1980. 147. Lombardo SJ, Benson DW: Stress fractures of the femur in runners, Am J Sports Med 10:219, 1982. 148. Rosen PR, Micheli LJ, Treves S: Early scintigraphic diagnosis of bone stress and fractures in athletic adolescents, Pediatrics 70:11, 1982. 149. Daffner RH, Martinez S, Gehweiler JA: Stress fractures in runners, JAMA 247:1039, 1982. 150. Geslien GE, et al: Early detection of stress fractures using 99 m Tc-polyphosphate, Radiology 121:683, 1976. 151. Butler JE, Brown SL, McConnell BG: Subtrochanteric stress fractures in runners, Am J Sports Med 10:228, 1982. 152. Matheson GO, et al: Scintigraphic uptake of 99 m Tc at nonpainful sites in athletes with stress fractures, Sports Med 4:65, 1987. 153. Khan KM, et al: Outcome of conservative and surgical management of navicular stress fracture in athletes, Am J Sports Med 20:657, 1992. 154. Kiss ZA, Khan KM, Fuller PJ: Stress fractures of the tarsal navicular bone: CT findings in 55 cases, Am J Roentgenol 160:111, 1993. 155. Terrell PN, Davies AM: Magnetic resonance appearances of fatigue fractures of the long bones of the lower limb, Br J Radiol 67:332, 1994. 156. Lee JK, Yao L: Stress fractures: MR imaging, Radiology 169:217, 1988. 157. Stafford SA, et al: MRI in stress fractures, Am J Roentgenol 147:553, 1986. 158. Steinbronn DJ, Bennett GL, Kay DB: The use of magnetic resonance imaging in the diagnosis of stress fractures of the foot and ankle: four case reports, Foot Ankle 15:80, 1994. 159. Fredericson M, et al: Tibial stress reaction in runners. Correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system, Am J Sports Med 23:472, 1995.
........................................... C H A P T E R 4 Problematic stress fractures of the foot and ankle James A. Nunley and Anthony S. Rhorer CHAPTER CONTENTS ...................... Introduction
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Stress fracture of the fifth metatarsal
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Stress fracture of the tarsal navicular
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Summary
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Stress fracture of the base of second metatarsal
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References
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Stress fracture of the medial malleolus
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4 PEARL 1. Subtle, unexplained pain in the foot or ankle in an athlete often is a stress fracture. The best screening examination is a bone scan.
2. Stress fractures of the medial malleolus may be associated with pathologic varus coming from the knee, ankle, or hindfoot. One should search for this because treatment without addressing biomechanics is not always successful. 3. Navicular stress fractures are becoming more recognized; they occur only in the competitive athlete, and surgical intervention often is required in the professional athlete. 4. Second metatarsal base stress fractures in elite dancers must be treated aggressively because they put the dancers’ careers at risk.
INTRODUCTION The insidious onset of ill-defined foot and ankle pain in the athlete is a confusing problem for trainers, physicians, and patients. As Americans become more interested in recreational sports and the number of professional and collegelevel athletes continues to grow, stress fractures of the foot and ankle will continue to become more prominent in the training room, the primary care setting, and the orthopaedic surgeon’s office. Understanding the predispositions to such injuries, the various themes common to them, and
the mechanisms of diagnosis therefore should be requisite in the armamentarium of physicians treating athletes. A stress fracture is a complete or incomplete fracture of bone secondary to failure over a prolonged period and marked by repeated stress in a rhythmic, reproducible fashion. Stress fractures differ from acute fractures in that their course generally is more gradual and their radiographic appearance can be elusive.1 Stress fractures of the foot and ankle are most common in running athletes, especially those who jump. For example, track athletes, ballet dancers, and basketball players have a high incidence of stress injury. Many studies have implicated biomechanical factors, such as leg-length discrepancies, cavus foot deformities, and limb malalignment. Women have a higher incidence of stress fractures, and amenorrhea often is a concomitant finding in female athletes with these injuries.2 Several stress fractures are treated easily with cessation of activity, orthoses, and modification in training. However, there exists in the foot and ankle a subset of stress fractures that are difficult to diagnose and treacherous to treat. These are truly the problematic stress fractures of the foot and ankle.
STRESS FRACTURE OF THE TARSAL NAVICULAR Unexplained pain of the midfoot in the everyday and high-performance athlete can be a conundrum for both the patient and treating physician. The diagnosis of stress
CHAPTER 4
Problematic stress fractures of the foot and ankle
fracture of the tarsal navicular remains an elusive and poorly understood facet of midfoot pain in sports. Treatment of this unusual stress fracture requires an understanding of its presentation, anatomy, imaging, and response to conservative and surgical management. The proper diagnosis of this unusual condition portends an excellent prognosis for the athlete and a rapid return to sport. Therefore it should be part of the repertoire for any physician treating conditions of the foot and ankle in athletes.
Anatomy and presentation The tarsal navicular serves as a keystone in the medial longitudinal arch and consequently is subjected to tremendous forces through the foot. Moreover, nutrient arteries arising from both the anterior and posterior tibial arteries create a generous supply of blood to the medial and lateral thirds of the navicular. The result is a poorly vascularized zone in the middle third of the bone.2 Incredible stresses and decreased nutrition make the middle third of the navicular the most common location for stress fracture. Misdiagnosis of stress fracture of the tarsal navicular generally is the rule rather than the exception. There are several sources of midfoot pain that are more common, including plantar fasciitis, anterior tibial and posterior tibial tendinitis, spring ligament injury, Lisfranc sprain, and degenerative joint disease.3 Therefore unrelenting symptoms in the seemingly normal midfoot merit further diagnostic workup and probably referral. Towne et al.4 first reported stress fracture of the tarsal navicular in 1970. In this series of two patients, each was a distance runner who had experienced midfoot pain with swelling and failure to respond to conservative therapy. Plain radiographs were negative, and only specialized studies were able to reveal the occult fracture. Subsequent reports have corroborated a history of insidious pain in the midfoot that is relieved by rest and exacerbated by forceful striking of the forefoot and with direct palpation of the navicular.5-7 A common thread in these reports is the normal appearance of plain radiographs. In most cases the diagnosis must be confirmed by computed tomography (CT), magnetic resonance imaging (MRI), or bone scan. Imaging Stress fracture of the tarsal navicular often is overlooked secondary to the low sensitivity of plain radiographs in diagnosing this condition. Some characteristics appreciated on anteroposterior views of the foot have been shown to correlate with navicular stress fractures. These include sclerosis of the proximal border of the navicular; a short first metatarsal; metatarsus adductus and hyperostosis; and stress fracture of the second, third, and fourth metatarsals. Improved imaging techniques have demonstrated that most fractures are linear, lie in the middle third of the navicular, and can be complete or partial.8 Oblique or supinated radiographs can be useful (Fig. 4-1).
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Radionuclide bone scanning always demonstrates increased isotope uptake and can be a useful adjunct in the diagnosis of ill-defined midfoot pain. Views should include a medial, lateral, and plantar view. Uptake generally will appear in the shape of the navicular on the plantar view.5 Although radionuclide scanning can assist in localizing the area of concern to the navicular, definitive diagnosis and definition of the fracture pattern require tomography or computer-aided tomography. The majority of fractures occur in the middle third of the navicular. An anatomic anteroposterior (AP) tomogram views the middle third of the navicular en face and therefore is more likely to identify fractures.5 However, modern computer-aided tomography has supplanted the use of tomography and is essential in the delineation of fracture pattern. Fine, 1.5-mm cuts are necessary in the axial plain to ensure that small incomplete fractures on the dorsal surface of the bone are not ‘‘skipped.’’ The role of MRI has not been clearly defined but likely will prove useful in the early diagnosis of this condition. Successful identification of the injury and its anatomy is crucial to effective management of the fracture.
Treatment Complete elucidation of the fracture pattern is important in dictating management of the athlete. Patients with incomplete and nondisplaced complete fractures can respond well to conservative management. When treated in a nonweight-bearing cast for at least 6 weeks, 86% to 100% of patients will go on to union.2-4
Figure 4-1 An oblique radiograph of the tarsal navicular demonstrates a stress fracture.
Stress fracture of the base of second metatarsal
STRESS FRACTURE OF THE BASE OF SECOND METATARSAL Stress fracture of the base of the second metatarsal is an often-misdiagnosed condition that seemingly is exclusive to elite-level ballet dancers. However, fractures of the other metatarsals also are seen in new military recruits and running athletes.9 These stress metatarsal fractures tend to be more diaphyseal and behave somewhat differently from the base of the second metatarsal. The unique biomechanics of ballet dancing, coupled with the high incidence of hypoestrogenism among female performers, generates an environment conducive to stress fracture of the base of the second metatarsal. High-level ballerinas generally have a narrow window of opportunity and short-lived careers. Therefore rapid diagnosis and treatment of conditions in this population is essential. Outcomes from treatment of second metatarsal fractures are excellent, and this injury usually is not considered to be a career-threatening disability.
Anatomy and presentation The most common presentation of stress fracture of the second metatarsal is the insidious onset of midfoot pain. However, ballerinas intermittently will report sudden onset of pain after an increase in training or after a jumping maneuver. Many performers will be able to ‘‘dance through’’ the pain and often do not present until 2 to 6 weeks after the onset of symptoms.10 Hamilton11 reported five risk factors for stress fracture in the ballet dancer. They include amenorrhea, anorexia nervosa, cavus foot, anterior ankle impingement, and a Morton’s foot (short first metatarsal). Delayed menarche or abnormally long intervals between menses should motivate the clinician to suspect a stress fracture in the presence of pain. Examination of the foot often is more obfuscating than revealing because patients will exhibit generalized tenderness of the midfoot with palpation and motion. Occasionally tenderness can be localized to the base of the second metatarsal; however, this does not differentiate metatarsal stress fracture from synovitis of the Lisfranc joint.12 The nature of this injury is due primarily to the interesting biomechanics of ballet and specifically to the incredible
stresses placed on the midfoot when the dancer is in the en pointe position. When en pointe, the ballerina (male dancers dance only on demi-pointe) stands on the tips of her toes with the foot in maximal plantarflexion.13 Consequently the mechanical axis of the lower extremity is directed straight through the plantarflexed foot. The middle cuneiform serves as a keystone in an arch-type configuration reminiscent of the sturdy arch first introduced in Roman architecture. The base of the second metatarsal is countersunk into this keystone. Furthermore, the plantar ligaments of the second metatarsal base are powerful, owing to the tensile forces experienced from push-off during normal gait. This fortified anchor of the proximal second metatarsal generates a substantial stress riser at the junction of the metaphysis and diaphysis when the dancer is en pointe. Understanding this relationship is important because treatment can be as simple as restricted dance with a moratorium on en pointe maneuvers until union is achieved.
Imaging The evaluation of the painful foot in a ballerina must include clear weight-bearing views of the foot and ankle. O’Malley et al.10 recommended a specialized view called the posteroanterior (PA) dancer’s view. The dancer’s foot is placed with the dorsum on the cassette to eliminate overlap of metatarsals. Approximately 30% of plain films will demonstrate a stress fracture. Bone scintigraphy is positive in 100% of second metatarsal stress fractures; yet Harrington et al.12 reported positive bone scans in two of their patients diagnosed with synovitis of the second tarsometatarsal joint. In this series, T1-weighted and short tau inversion recovery (STIR) MRI images were used to differentiate stress reaction, fracture, and synovitis. CT with fine cuts also is an effective method to demonstrate a stress fracture of the base of the second metatarsal. The role of MRI has not been clearly defined, but eventually it may supplant scintigraphy as a more effective method for defining pathology at the base of the second metatarsal. Differentiation can help to direct a less disruptive management routine for professional dancers. For example, nonsteroidal treatment and dance modifications for traumatic synovitis may seem more attractive to a professional dancer than 6 weeks of rest. Treatment The timing of this injury, in concert with the goals and aspirations of the dancer, should lead the clinician in treatment. Patients usually can expect a full recovery in approximately 6 to 8 weeks. Initial management should include cessation of all dance activity and application of a hard-soled shoe. Pain at the base of the second metatarsal then serves as a barometer for return to activity. The dancer may begin working out but should delay return to 75
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Patients with displaced fractures or those who have failed nonoperative management benefit from bone grafting with or without open reduction and internal fixation. Most of these athletes will return to sport within 5 to 7 months.2-4 High-performance career athletes and the treating surgeon may elect a more aggressive approach to nondisplaced fractures. Theoretically, surgical management of the injury could expedite the return to sport.
CHAPTER 4
Problematic stress fractures of the foot and ankle
jumping and en pointe maneuvers. The rate of recurrence can be as high as 12%. Ballerinas should be reassured that this is rarely if ever a career-ending injury.
C A S E S T U D Y
An 18-year-old, college-level, female basketball player presented to the sports medicine clinic with a longstanding history of left midfoot pain that had gotten acutely worse. The pain was exacerbated by play and persisted the majority of the season. She had a history of a similar injury that was treated successfully in high school. Examination demonstrated bilateral pes planovalgus deformities with tenderness over the base of the second metatarsal. Pain was reproduced with motion of the second, third, and fourth tarsometatarsal joints. Plain radiographs and a CT scan (Figs. 4-2, 4-3, and 4-4) showed a chronic stress fracture at the base of the second metatarsal. She was given a walker boot for daily activity and a rigid shank for her shoe to wear during play. The boot was worn during off times, and the shank was worn during games. She successfully completed the season without limitations. Follow-up images showed a nonunion of the second metatarsal and a healed third metatarsal fracture. At last follow-up, she continued to play at the collegiate level asymptomatically.
Figure 4-3 An oblique radiograph shows a chronic stress fracture of the base of the second metatarsal.
Figure 4-4 A sagittal computed tomogram (CT) shows a chronic stress fracture of the base of the second metatarsal.
STRESS FRACTURE OF THE MEDIAL MALLEOLUS
Figure 4-2 An anteroposterior (AP) oblique radiograph shows a chronic stress fracture of the base of the second metatarsal.
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Stress fracture of the medial malleolus is a rare yet consternating condition of the medial ankle often experienced by running and jumping athletes. Although there is a paucity of literature regarding this unusual injury, there are similarities among the patients reported with this condition. In some of the series, patients went on to develop an acute fracture of the medial malleolus.14
Stress fracture of the medial malleolus
Anatomy and presentation The majority of patients with stress fracture of the medial malleolus are running and jumping athletes who present with gradual onset of pain over the medial ankle. Pain is exacerbated by activity and is localized to the medial malleolus.15-18 The ratio of male to female occurrence is 3:1, and the mean age of injury is 24 years. Most case reports represent high-performance athletes, of which several are professional.11 Commensurate with the complete history involving any stress fracture, the treating physician should identify risk factors such as amenorrhea, nutritional deficiency, changes in footwear, and changes in training. Shelbourne et al.18 identified three criteria for the evaluation of medial malleolar stress fracture. They include tenderness over the medial malleolus with an ankle effusion, pain during activity preceding an acute episode, and a vertical line from the tibial plafond proximally. Physical examination often demonstrates edema of the medial malleolus with bony tenderness. Patients often will have normal motion in the ankle and subtalar joints and should not have tenderness of the lateral ankle or posterior tibial tendon. Analysis of hindfoot alignment is critical to assess any varus deformity that may exacerbate stresses on the medial malleolus. A true biomechanical explanation for medial malleolar stress fracture is not described. However, the tensile forces of the medial ankle ligamentous structures ostensibly generate significant stress on the posteromedial concave side of the tibia. The majority of these fractures are vertical. This concept becomes important when one considers proper screw placement for internal fixation. Imaging Plain film radiography is requisite in the diagnosis of medial malleolar stress fractures and can be more useful with other problematic stress fractures of the foot. Roentgenograms often show a small area of fissuring at the junction of the tibial plafond and the medial malleolus. Infrequently, this fissure will be accompanied by radiolucent cysts along the fracture line.12 When one has normal radiographs, bone scintigraphy can be extremely useful. Increased uptake in the area of the medial malleolus is seen uniformly in the presence of a stress fracture. The cases reported in the literature also have used CT and MRI. Although the role of these modalities has not been clearly defined, in isolated cases they have proven useful in defining the anatomy of a fracture or in confirming the diagnosis. Perhaps modern MRI will supplant the use of scintigraphy, given its ability to clearly delineate bony and ligamentous anatomy while defining inflammatory or reactive pathology.
Treatment Initial management of stress fracture of the medial malleolus should include cessation of sport, with nutritional and endocrine interventions when appropriate. Recreational athletes with small fracture lines can be treated nonoperatively in a short-leg cast or removable boot. Disabling rotation about the ankle and dorsiflexion are key factors in neutralizing the tensile forces that can lead to displacement and delayed union of the injury. Patients treated conservatively should not return to sport until they are asymptomatic, a period of time that averages 6 weeks. Furthermore, patients treated nonoperatively will go on to complete union in about 6.7 months.11 Conversely, many authors prefer operative management of this injury, citing the possibility of nonunion and faster return to sport as incentives. The objective of operative management is to create a construct that counters the tensile forces of the medial malleolus and allows quick rehabilitation. Standard AO technique should be used with either cancellous or cortical lag screws positioned perpendicular to the fracture line. Some surgeons advocate the use of lag screws through a buttress plate. Patients treated with internal fixation return to sport on average at 4.5 weeks and have evidence of union by 4.2 months.11 The elite or professional athlete may prefer this option because it portends a faster return to activity and theoretically reduces the risk of nonunion or complete fracture. Reider et al.19 reported a nonunion in a college-level football player who was misdiagnosed and managed conservatively for several months. This athlete went on to heal after operative intervention. Although such reports are seemingly anecdotal, they highlight the importance of diagnosing and aggressively treating this injury in the high-performance athlete. A malleolar nonunion can lead to significant lost playtime and potentially can be career ending. Isolated medial ankle pain with normal radiographs merits further workup with either bone scintigraphy or MRI, followed by an appropriate scheme of management tailored to the athlete’s goals and aspirations.
C A S E S T U D Y
An elite-level, male, college basketball player began to note pain in the anteromedial distal ankle early in the season. As the season progressed, he had to stop playing because of recalcitrant pain. Physical examination demonstrated tenderness along the anteromedial aspect of the tibia and pain with dorsiflexion. Plain films (Figs. 4-5 and 4-6) showed a small lucency in the anteromedial plafond that may have been consistent with
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This point underscores the necessity of making the appropriate diagnosis in the avid athlete before a simple injury progresses to a more complex and debilitating injury.
CHAPTER 4
Problematic stress fractures of the foot and ankle
an osteochondral defect. An MRI (Figs. 4-7 and 4-8) did not show a definitive chondral lesion; however, there was high signal in the anterior and medial tibial plafond, suggesting a stress fracture of the medial malleolus. The patient was treated conservatively, and he sat out the remainder of the season. He returned the following year and played successfully without incident.
Figure 4-7 T2 coronal images show increased signal in the anterior medial malleolus. Note that this area appears normal on the initial plain radiographs.
Figure 4-5 An anteroposterior (AP) radiograph in an elite college athlete does not show obvious fracture of the medial malleolus.
Figure 4-8 T2 sagittal images show increased signal in the anterior medial malleolus. Note that this area appears normal on the initial plain radiographs.
C A S E S T U D Y
Figure 4-6 A lateral radiograph in an elite college athlete does not show obvious fracture of the medial malleolus.
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An elite-level, male athlete experienced debilitating pain in the ankle. Examination and imaging were consistent with a stress fracture of the medial malleolus. Axial CT
Stress fracture of the medial malleolus
Figure 4-9 Axial computed tomography (CT) scan showing stress fracture of the anteromedial tibial plafond.
Figure 4-10 Internal repair of vertical stress fracture of the medial malleolus.
Stress fracture of the hallucal sesamoids Clandestinely located on the plantar surface of the great toe metatarsophalangeal (MTP) joint, the hallucal sesamoids are an often neglected and inadequately respected pair of tiny bones. They are capable of causing an enormous amount of pain, discomfort, and disability in the running and jumping athlete. Stress fracture of the sesamoid is an unusual and rare diagnosis that requires clinical and radiographic perseverance on the part of the treating clinician.
Anatomy and presentation Rarely will a patient report focal pain of his sesamoid bones. Rather, he or she often describes a gradual onset of pain about the plantar surface of the great toe. This pain often is exacerbated by dorsiflexion of the hallux. In some instances, pain may be replaced by paresthesia of the great toe. Conversely, the patient may recall a specific incident in which he or she experienced a loud pop or snap on toe-off. Key features of the history should include changes in activity level, adequacy of footwear, and other important risk factors for stress fracture previously described.20 Physical examination should include a detailed, segmental analysis of the hindfoot, midfoot, and forefoot. Cavus feet have a penchant for sesamoid injury because of the increased load placed on the first metatarsal head. Direct palpation of the sesamoid will elicit pain. The tibial or medial sesamoid is most commonly involved. Furthermore, one may note decreased dorsiflexion of the first MTP joint and pain with range of motion. The corollary to this finding may be decreased strength of plantarflexion of the first toe.17 The hallucal sesamoids increase the mechanical advantage of the flexor hallucis brevis by acting in a mechanism similar to that of the patella; they are intrinsically located at the level of the MTP joint within the substance of the short flexor tendon. This location affords them an articulation with the metatarsal head and subjects them to enormous amounts of force when the phalanx is dorsiflexed and planted. The medial sesamoid is injured more often, owing to its larger size and more demanding role in weight bearing. Approximately 10% of patients have a bipartite sesamoid. This fact becomes important when interpreting plain radiographs of the sesamoid.17 Imaging Plain radiographs of the foot can be more perplexing than useful in the diagnosis of sesamoid stress fracture. The clinician first must understand that a standard lateral view is essentially useless, and an AP of the foot is infrequently revealing. Medial and lateral oblique views of the sesamoids will more clearly visualize the tibial and fibular sesamoids, respectively. Several patients will have normal radiographs or the appearance of a bipartite sesamoid. The role of scintigraphy, CT, and MRI continues to evolve. Many authors have recommended the use of bone scintigraphy in the evaluation of sesamoid pain. However, the ordering physician must communicate the need to perform oblique scans because a traditional anteroposterior bone scan of the foot can reveal first MTP activity that can obscure the sesamoids. A study of army recruits found no difference in sesamoid bone 79
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images clearly demonstrated involvement of the anteromedial tibial plafond (Fig. 4-9). The player was not able to return to preinjury performance after nonoperative management. Therefore he was treated with internal repair of the vertical fracture fragment (Fig. 4-10).
CHAPTER 4
Problematic stress fractures of the foot and ankle
scan activity between soldiers in basic training for several weeks in comparison with sedentary adults. They cautioned readers about the interpretation of increased uptake in the sesamoid, warning that this may be normal physiologic activity for this bone.21 Perhaps axial imaging serves a more important role to the surgeon who potentially will treat the patient with excision of one of the sesamoid fragments. CT is an excellent modality for detection of sesamoid stress fractures. However, obtaining only axial images of the sesamoid can result in a false negative by ‘‘skipping’’ the fracture line. This error can be prevented by supplementing axial CT images with longitudinal cuts through the sesamoid.22 Improved availability of high-quality MRI may supplant the use of CT and bone scan because it enables the treating physician to obtain axial and longitudinal images, as well as indicators of stress fracture such as edema. Imaging facilities must use the appropriately sized coil for imaging of the sesamoids to ensure the proper resolution. High-resolution MRI of the sesamoid will show fragmentation and marrow changes in the face of acute stress fracture. Although MRI may not clearly define stress fracture versus avascular necrosis or chronic nonunion, this point is moot because treatment ultimately will be the same.23
Treatment Treatment of this relatively debilitating condition can be rewarding yet frustrating. Most clinicians favor a conservative approach consisting of a nonweight-bearing, short-leg cast for 6 to 8 weeks.17 Return to jumping and running activity should be graded on the basis of symptomatology. Furthermore, custom orthoses designed to unload the first MTP joint, such as a dancer’s pad or a metatarsal bar, can be instituted after completing a course of casting. Because of the obscure diagnosis and the vulnerable physiologic location of the injury, nonunion and delayed union of the hallucal sesamoids is a common occurrence. Management of the recalcitrant sesamoid fracture is surgeon specific and may include bone grafting or excision of the sesamoid. Authors have reported excellent results for all types of procedures. Potential pitfalls of operative intervention include digital nerve injury and weakness of the great toe flexor. A recent study reported good or excellent outcomes in dancers and in a long jumper treated with a partial excision of the medial sesamoid.24 Athletes should expect a full recovery but should remain nonweight bearing for 4 to 6 weeks in the postoperative setting, followed by protection of the first MTP joint for another 4 to 6 weeks and a gradual return to activity by 3 to 4 months. Stress fracture of the hallucal sesamoid should be suspected in the jumping or running athlete with first MTP
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pain that is refractory to initial conservative management. Notwithstanding that the diagnosis largely is clinical, axial imaging is extremely useful. Longitudinal CT is recommended for definitive revelation of fracture lines and surgical planning. Surgeons and patients will find that diligent treatment of these seemingly diminutive and insignificant bones can lead to a full recovery and return to competitive sport.
C A S E S T U D Y
A 30-year-old, recreational athlete presented to a foot and ankle surgeon after a several-day history of right forefoot pain. The pain was associated with a long walk and progressed significantly in the week before the office visit. Examination demonstrated edema of the first MTP joint and pain with dorsiflexion. The patient was exquisitely tender over the tibial sesamoid. Plain x-rays showed a fracture of the tibial sesamoid (Fig. 4-11). This was confirmed with CT. She was placed in a compressive boot with no weight bearing on the forefoot for 6 weeks. She was progressively weaned out of the boot and back to full weight bearing. At last follow-up she had full return to activity and radiographic evidence of callous formation.
Figure 4-11 A plain radiograph demonstrates stress fracture of the hallucal sesamoid.
Stress fracture of the fifth metatarsal
No stress fracture of the foot and ankle has received more discussion and enamored more orthopaedic surgeons than the often-misunderstood stress fracture of the fifth metatarsal. A constant stream of dialogue exists in the literature regarding the history and treatment of fracture disorders of the proximal fifth metatarsal. Accordingly, misuse of the eponym ‘‘Jones fracture’’ is both propagated and defied. True stress fractures in this anatomic location in fact represent an entirely different injury, with its own mechanism and behavior, and should not be confused with the traditional Jones fracture or an avulsion fracture of the tuberosity (Fig. 4-12). This point becomes critical because there are nuances in the treatment of these three distinct injuries.
Anatomy and presentation The history and presentation of this injury is useful in discerning the diagnosis of stress fracture over an acute Jones fracture. DeLee et al.25 defined stress fractures in the metatarsal as spontaneous fractures of normal bone that result from the summation of stresses, any of which by themselves would be harmless. They also reported on a series of patients who met three criteria. These include a prodrome of pain in the lateral foot, ultimately leading to debilitating pain; radiographic evidence of stress fracture; and no history of previous fracture and treatment of the fifth metatarsal. Consequently, patients often report a prolonged period of pain on the lateral border of the foot that may be exacerbated by a jumping or running maneuver. This final event generally is the impetus for a visit to a health care provider. Understanding the diagnosis of fifth metatarsal stress fracture necessitates a thorough understanding of the anatomy of the lateral border of the foot. The fifth metatarsal itself consists of a head, neck, shaft, base, and tuberosity. The base of the metatarsal has three articulations. They are the cuboid-fourth metatarsal
2
3
Shaft
1
Figure 4-12 The three zones of injury at the base of the fifth metatarsal. Modified from: Lawrence ST, Botte MJ: Foot Ankle Int 4:358, 1993.
joint, the cuboid-fifth metatarsal joint, and the fourth and fifth intermetatarsal articulation. The peroneus brevis has a broad, fan-like insertion on the dorsal surface of the tuberosity, whereas the peroneus tertius inserts on the diaphysis of the bone slightly more distally. A styloid on the plantar surface of the tuberosity receives the fibers of the lateral band of the plantar aponeurosis.26 Variations in the anatomy of the proximal fifth metatarsal are described and can be misleading clues for diagnosing fracture of the tuberosity. These variations include the os peroneus, the os vesalianum, and the secondary ossification center of the tuberosity. The os peroneum is a sesamoid bone located in the tendon of the peroneus longus that may occur in up to 15% of normal feet. The os vesalianum is a similar sesamoid, with a less regular shape, occurring only 0.1% of the time. The secondary ossification center or apophysis of the fifth metatarsal does not appear until after age 8 in females and age 11 in males. The apophysis may be present only in up to 50% of feet. This structure can be differentiated from a fracture because the physeal line runs parallel to the shaft of the bone. Conversely, a fracture in this anatomic location generally is in a plane orthogonal to the diaphysis of the bone.27 Although the task seems daunting, organization and diagnosis of the myriad fractures of the fifth metatarsal can be simplified by applying a classification scheme. Fractures of the base of the fifth metatarsal are subdivided into three types. They include type I tuberosity avulsion fractures, type II Jones fractures, and type III stress fractures of the diaphysis.28 Stress fractures are subdivided further into types A, B, and C, which correspond to early stress fracture, delayed union, and nonunion.24 This classification scheme is useful because it is anatomically based and describes separate fractures with differing mechanisms. The scope of this topic is large, and therefore we discuss here treatment of stress fracture of the fifth metatarsal.
Imaging Radiographic diagnosis of fifth metatarsal stress fracture typically is not as elusive as the other bones of the foot and ankle. However, clear interpretation of roentgenograms is critical in defining the type of fracture. Patients who present early in the course of their lateral foot pain may have normal radiographs. The first feature to appear is thickening of the cortex and a small periosteal reaction.29 The three subtypes of stress fractures can be differentiated radiographically. Type I, or acute or chronic fractures, are characterized by a straight line at the junction of the proximal and middle third of the diaphysis. The bone ends are sclerotic, there is minimal periosteal reaction, and there is no widening. Type II fractures, or delayed unions, will demonstrate 81
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STRESS FRACTURE OF THE FIFTH METATARSAL
CHAPTER 4
Problematic stress fractures of the foot and ankle
widening with hypertrophic periosteum and a wide band of radiolucency across the diaphysis. The medullary canal may be sclerotic. The type III fracture, or nonunion, differs in that the bone ends will appear to be entirely sclerotic, as though the medullary canal were nonexistent.23 The clinical and plain radiograph diagnosis of fifth metatarsal stress fractures rarely requires the use of bone scan or MRI. Scintigraphy will demonstrate increased uptake within 72 hours of acute injury but is less specific. As in other stress fractures, MRI will clearly demonstrate a fracture line with surrounding edema and signal change.26
Treatment Management of fifth metatarsal stress fractures is determined on the basis of the needs and goals of the athlete, as well as the radiographic classification of the injury. Surgeons may opt to be more aggressive in professional athletes, who are dependent on a rapid return to play. Conversely, patients may advocate a less invasive approach to initial management. All athletes with this injury should be counseled on the pitfalls that may be encountered, including nonunion and temporary disability. Authors favoring conservative management have reported lackluster results. Specifically, patients are prone to prolonged immobilization and nonunion.25 Improved results have been demonstrated with surgical intervention, and as such this modality is advocated in most athletes who desire early definitive treatment. Torg et al.30 have demonstrated that acute, nondisplaced stress fractures of the fifth metatarsal can be treated successfully with nonweight-bearing immobilization. The importance of compliance with nonweight-bearing status should be emphasized for the first 6 to 8 weeks, as weight bearing has been shown to diminish healing. The management of type II delayed unions is less clear. Nonweight-bearing immobilization is effective but prolonged, and the specter of nonunion is not unreal. Athletes with a strong penchant for an expedited recovery may opt for intramedullary fixation.31 Nonunions, or type III stress fractures, have been treated with pulse electromagnetic fields and bone grafting. However, most surgeons now agree that intramedullary fixation promises the most success. Although the type of fixation varies among surgeons, the common theme is a minimally invasive procedure in which the base of the fifth is exposed and a screw is inserted through the canal under fluoroscopic guidance. Drilling of the canal in preparation for the fixation creates an autogenous intramedullary bone graft and stimulates healing at the fracture site. Initial reports of this treatment demonstrated 100% union in
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less than 8 weeks, with return to sport averaging less than 9 weeks.22 However, patients should be aware that nonunion is a potential complication and possibly is related to screw diameter.32 Stress fracture of the base of the fifth metatarsal is a debilitating injury that requires expertise in diagnosis on behalf of the treating surgeon. Mistaking this injury for a less benign fracture, such as a tuberosity avulsion, can result in painful nonunion and significant loss of playing time. Therefore commensurate management demands a thorough understanding of the anatomy of the fifth metatarsal and the variable fracture patterns existing in this location. Athletes treated correctly can often expect an excellent prognosis.
C A S E S T U D Y
A 22-year-old, college-level, female soccer goalie noted lateral border of the foot pain after kicking a soccer ball. Physical examination was consistent with fifth and fourth metatarsal tenderness. Plain films demonstrated a fracture at the base of the fifth metatarsal (Fig. 4-13). She underwent percutaneous screw fixation with a 4.5-mm shaft screw (Figs. 4-14 and 4-15) and had full return to sport 6 weeks postoperatively.
Figure 4-13 Stress fracture of the base of the fifth metatarsal in a female soccer player.
References
Therefore a global approach to care of the athlete is advised. This should involve activity modification, improvements in training, nutritional and psychological counseling, as indicated, and definitive orthopaedic intervention. Athletics are an important facet of life, and disability related to sports can be devastating. Accurate diagnosis and successful treatment of problematic stress fractures of the foot and ankle is a rewarding and attainable goal for all trainers and physicians.
REFERENCES
Figure 4-15 Lateral radiograph after percutaneous fixation with a 4.5-mm shaft screw.
SUMMARY Poorly defined foot and ankle pain in the athlete can be a consternating and often frustrating condition for athletes, trainers, and physicians. Stress fractures represent a subset of maladies of the foot and ankle that require diligence on behalf of the diagnostician. Careful history and physical examination will illuminate mechanisms of injury specific to each fracture type and risk factor, such as weight loss, amenorrhea, and eating disorders. Moreover, the clandestine fracture often will require advanced imaging modalities, such as CT, bone scintigraphy, and MRI.
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Figure 4-14 Anteroposterior (AP) radiograph after percutaneous fixation with a 4.5-mm shaft screw.
1. McBryde AM: Stress fractures. In Baxter DE, editor: Foot and Ankle in Sport, St. Louis, 1995, Mosby. 2. Korpelainen R, et al: Risk factors for recurrent stress fractures in athletes, Am J Sports Med 29:304, 2001. 3. Nunley JA, Vertullo CJ: Classification, investigation and management of midfoot sprains: Lis Franc injuries in the athlete, Am J Sports Med 30:871, 2002. 4. Towne LC, Blazina ME, Cozen LN: Fatigue fracture of the tarsal navicular, J Bone Joint Surg 52-A:376, 1970. 5. Torg JS, et al: Stress fracture of the tarsal navicular, J Bone Joint Surg 64-A:700, 1982. 6. Fitch KD, Blackwell JB, Gilmour WN: Operation for non-union of stress fracture of the tarsal navicular, J Bone Joint Surg 71-B:105, 1989. 7. Kahn KM, et al: Outcome of conservative and surgical management of navicular stress fracture in athletes, Am J Sports Med 20:657, 1992. 8. Pavlov H, Torg JS, Freiberger RH: Tarsal navicular stress fractures: radiographic evaluation, Radiology 148:641, 1993. 9. Weinfeld SB, Haddad SL, Myerson MS: Metatarsal stress fractures, Clin Sports Med 16:319, 1997. 10. O’Malley MJ, et al: Stress fractures at the base of the second metatarsal in ballet dancers, Foot Ankle Int 17:89, 1996. 11. Hamilton WG: Physical prerequisites for ballet dancers, J Musculoskel Med 10:61, 1986. 12. Harrington T, Crichton JK, Anderson IF: Overuse ballet injury of the base of the second metatarsal, Am J Sport Med 21:591, 1993. 13. Hardaker WT: Foot and ankle injuries in classical ballet dancers, Orthop Clin North Am 20:621, 1989. 14. Shabat S, et al: Stress fractures of the medial malleolus—review of the literature and report of a 15 year old elite gymnast, Foot Ankle Int 23:647, 2002. 15. Schils J, et al: Medial malleolar stress fractures in seven patients: review of the clinical and imaging features, Radiology 185:219, 1992. 16. Orava S, et al: Stress fracture of the medial malleolus, J Bone Joint Surg 77A:362, 1995. 17. Okada K, et al: Stress fracture of the medial malleolus: a case report, Foot Ankle Int 16:49, 1995. 18. Shelbourne KD, et al: Stress fractures of the medial malleolus, Am J Sports Med 16:60, 1988. 19. Reider B, Falconeiro R, Yurkofsky J: Nonunion of a medial malleolus stress fracture, Am J Sports Med 21:478, 1993. 20. Richardson GE: Hallucal sesamoid pain: causes and surgical treatment, JAAOS 7:270, 1999. 21. Chisin R, Peyser A, Milgrom C: Bone scintigraphy in the assessment of the hallucal sesamoids, Foot Ankle Int 16:291, 1995. 22. Biedert R: Which investigations are required in stress fracture of the great toe sesamoids? Arch Orthop Tr Surg 112:94, 1993. 23. Burton EM, Amaker BH: Stress fracture appearance of the great toe sesamoid in a ballerina: MRI appearance, Pediatr Radiol 24:37, 1994.
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24. Biedert R, Hinterman B: Stress fractures of the medial great toe sesamoids in athletes, Foot Ankle Int 24:137, 2003. 25. DeLee JD, Evans P, Julian J: Stress fracture of the fifth metatarsal, Am J Sport Med 11:349, 1983. 26. Rosenberg GA, Sferra JJ: Treatment strategies for acute fractures and nonunions of the proximal fifth metatarsal, JAAOS 8:332, 2000. 27. Quill GE: Fractures of the proximal fifth metatarsal, Orthop Clin North Am 26:353, 1995. 28. Lawrence SJ, Botte MJ: Jone’s fracture and related fractures of the proximal fifth metatarsal, Foot Ankle 14:358, 1993.
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29. Harmath C, et al: Radiologic case study: stress fracture of the fifth metatarsal, Orthopedics 24:204, 2001. 30. Torg JS, et al: Fractures of the base of the fifth metatarsal distal to the tuberosity: classification and guidelines for non-surgical and surgical management, J Bone Joint Surg 66:209, 1984. 31. Nunley JA: Fractures of the base of the fifth metatarsal, Orthop Clin North Am 32:171, 2001. 32. Nunley JA: Jones fracture technique, Tech Foot Ankle Surg 1(2):1, 2002.
........................................... C H A P T E R 5 Ankle and midfoot fractures and dislocations William C. McGarvey CHAPTER CONTENTS ...................... Introduction
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Anterior process calcaneal fracture
100
Clinical diagnosis
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Tarsometatarsal dislocations
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Treatment
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Tarsal bone fractures
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Ankle fractures
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Fractures of the base of the fifth metatarsal
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Lateral process talar fractures
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References
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INTRODUCTION Fractures and dislocations of the foot are among the most common injuries in the musculoskeletal system. With the recent explosion of interest in athletic activity, the foot and ankle have been exposed to a variety of new stresses. The disability and time away from sports resulting from these injuries warrant close attention to diagnosis and management (Figs. 5-1, 5-2, 5-3, and 5-4).
CLINICAL DIAGNOSIS In evaluating patients with trauma to the foot, it is essential to obtain a thorough, detailed history to direct the examiner in physical and radiographic examination. In addition, it will provide a clue to the associated degree of soft tissue injury. Physical examination should be meticulous and systematic. It is recognized that although most forefoot injuries are easily diagnosed, midfoot injuries often go undetected. Because of the high incidence of multiple fractures or fracture/dislocations in the injured foot, careful examination and palpation of points of tenderness should be performed to detect evidence of occult injury. Evaluation of range of motion of the ankle, subtalar midtarsal, and metatarsophalangeal joints is incorporated into every routine examination. A careful motor examination, both intrinsic and extrinsic, as well
as a sensory examination, is performed. Vascular examination, including Doppler studies, is essential. Radiographs are guided by the examiner’s history and physical examinations. Standard views of the foot include anteroposterior (AP), lateral, and oblique views. The oblique view, for example, is particularly useful for evaluating joints, such as the calcaneal cuboid joint, that typically are hidden or poorly examined in AP view. Specialty views, such as axial views of the heel, Broden’s view of the subtalar joint, and stress views of the foot also are helpful in certain circumstances. Because of the complexity of the anatomy and lack of uniform appreciation or interpretation of the foot radiographs, adjunctive studies, such as computed tomography (CT), bone scan, and magnetic resonance imaging (MRI), can be of tremendous value. These also are particularly useful because of the subtle nature of many foot and ankle injuries. Standard radiographic examination of the ankle includes three views: AP, lateral, and mortise. From these, a remarkable amount of information may be obtained, not only about fracture patterns but, more importantly, about the relationship of the three bones that comprise the ankle mortise—tibia, fibula, and talus. Use of measurements of mortise width; medial or tibiofibular clear space; talocrural angle; ‘‘Shenton’s’’ line of the ankle (that space that demonstrates a mirrored congruity between the lateral talar wall and the corresponding curvature of the distal medial fibula); and talar tilt all are helpful in determining the subtle abnormalities of the ankle mortise (Fig. 5-5).
CHAPTER 5
Figure 5-1
Ankle and midfoot fractures and dislocations
Conservative modalities for managing acute injuries.
Figure 5-3 Athletes often will find ways to return to sport earlier than expected.
Figure 5-4
Inset from Figure 5-3.
Figure 5-2 Rehabilitation methods involve patient participation.
When in doubt, the clinician also may obtain contralateral views to determine that which constitutes normal anatomy for that particular patient, because there tends to be a high degree of variability in what is considered normal from patient to patient. Medial clear space is as viewed in anterior/posterior radiographs. It is the measure of distance between the medial talar wall and lateral portion of medial malleolus. Although this is a linear measure, it reflects a rotational (external) abnormality of the talus with respect to the tibia. Injury leading to abnormality of this relationship with measurements of less than 1 mm or greater than 4 mm has been shown to correlate with poor outcomes, including chronic pain, instability, and arthrosis.1-3 Mortise views should demonstrate relative congruity of the joint space circumferentially—medial tibiotalar,
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dorsal tibiotalar, and lateral fibulotalar. The distance between these bone margins should be equivalent. In addition, a congruous relationship should exist between lateral talus and medial fibula, the so-called Shenton’s line of the ankle. Abnormalities, as evidenced by incongruity, provide clues to malalignment resulting from bony or soft tissue injury. The talocrural angle helps to define the appropriate fibular length. This is measured as the angle between the line parallel to the distal tibial joint surface and another line drawn between tips of the medial and lateral malleoli. Normal values average 83 4 degrees. Differences of more than 2 degrees to the contralateral normal side suggest fibular shortening. Talar tilt is measured by determining the angle between articular surface lines drawn parallel to the distal tibia and
Treatment
B
D
C
E
Figure 5-5 A to F, Schematic representation of radiographic parameters. (A) Medial clear space should equal the articular distance at any point around the mortise. (B) Talo-crural angle. (C) Talar tilt. (D) ‘‘Shenton’s line’’ of the ankle. (E) Tibio-fibular clear space. (F) Tibio-fibular overlap. (From Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
proximal talus. Although uniform agreement on what is considered normal does not exist, a side-to-side difference of more than 5 degrees (or 2 mm) is considered pathologic. Syndesmotic space probably is the most confounding of all radiologic measures. Measurements should be performed to account for the space existing between the medial edge of the fibula and the lateral edge of the tibial incisura, determined at 1 cm proximal to the joint line to ensure reproducibility. Average distance should be less than 5 mm but may vary up to 6 mm in larger individuals. Another measure of syndesmotic integrity is the tibiofibular overlap. The distance between the medial fibula and the lateral edge of the anterior tibia should be 10 mm (see Fig. 5-5). Ancillary studies, such as stress radiographs, CT scanning, and MRI are used liberally to provide more information regarding ankle relationships and stability.
TREATMENT Generic goals in the treatment of fractures and dislocations of the foot are as follows: Avoiding stiffness and loss of mobility. Removing bony prominences, which may result in pressure phenomena. Restoring the articular surfaces.
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A
Any fracture or dislocation of the foot or ankle that results in focal skin pressure or evidence of neurovascular compromise must be addressed immediately. Manipulation or even open reduction must be carried out to reduce the potential sequelae, including skin necrosis, neuropraxia, ischemia, and/or pressure-induced necrosis of articular surfaces, because of abnormal loading secondary to malpositioning after fracture or dislocation. Even anatomic restoration does not guarantee optimal functional outcome, but it certainly provides the athlete with a significantly reduced risk of morbidity associated with sequelae of delayed or untreated injury. However, injuries that present without gross distortion of anatomy or imminent threat to the viability of the limb may be treated better after an appropriate ‘‘cooling down’’ period. This is not to say that they should be splinted and ignored, but a short period should be devoted to rest, ice, compression, and elevation (RICE) to allow the soft tissue integrity and oxygenation to reestablish itself, particularly before the clinician embarks on any invasive procedures. The evolution of treatment of the traumatized foot and ankle of the athlete has directed more attention to aggressive intervention than to ‘‘benign neglect.’’ Recognition of the fact that long periods of immobilization after trauma may lead to muscular atrophy, myostatic contracture, reduction of joint mobility, associated connective tissue proliferation leading to scarring, synovial adhesion, and cartilage degeneration has prompted a more aggressive approach to foot and ankle injuries, using appropriate surgical intervention to stabilize injuries and institute earlier range of motion and weight bearing when possible. These tenets provide for the ability to institute potential prevention against previously disabling factors such as disuse osteopenia, limb atrophy, proprioceptive losses, and chronic, persistent pain.4-8 Introduction of early range of motion, physical therapy modalities, appropriate splinting, and bracing, as opposed to casting, allows for the earlier restoration of function and avoidance of complications. The static accumulation of hematoma, fluid extravasation, and resultant articular and tendinous adhesions is far less with treatment that promotes earlier rehabilitation.4 This type treatment also helps to prevent disabling sequelae, such as arthrofibrosis and regional pain syndromes.7 Although the realm of athletically related foot and ankle injuries is too vast to be encompassed in this chapter, the more common injury patterns encountered are addressed. Diagnostic and management controversies are discussed and elucidated for the reader. Rather than a trauma compendium, this is meant to be a guide for the treatment of frequently occurring sports and athletic injuries to the foot and ankle for one’s reference and perusal.
CHAPTER 5
Ankle and midfoot fractures and dislocations
ANKLE FRACTURES Medial fractures Isolated medial fractures are unusual but not rare (Fig. 5-6, A and B). One must have suspicion for a ‘‘bimalleolar variant’’ in which lateral ligamentous injury has occurred in deference to bony injury. Generally, medial malleolar fractures indicate loss of stability of the ankle. Anywhere from 5% to 15% of untreated fractures may go on to nonunion (Fig. 5-7, A through D). Fracture patterns may vary from vertical, oblique, or horizontal, depending on the mechanism of injury. However, because of the risk of sequelae and potential for instability and abnormal mechanics, all but those that are nondisplaced should be repaired. Even those demonstrating minimal (<2 mm) displacement carry some advantage to stabilization, such as reliable fixation, early range of motion, lack of immobilization, and potentially early return to activity. As evidenced by Ramsey and Hamilton,9 as well as Yablon,10 ankle stability is dependent on medial integrity. Michelson and others1,11-20 have shown that the
talus will not shift abnormally with integrity of medial structures. Therefore attention should be directed to anatomic restoration of the medial ankle if it is disrupted. Repair may be performed percutaneously with cannulated screw fixation but should be reserved for absolutely anatomic reductions. Any incongruity, as evidenced by articular irregularity, necessitates open repair with restitution of the articular surfaces. I prefer open techniques because radiographs often may disguise an occult malreduction. Often, anterior/posterior reduction appears anatomic, but evaluation via live fluoroscopy will demonstrate some degree of articular step-off with internal rotation toward a mortise view. I prefer an open reversed J incision with attention to interposed periosteum and unrecognized comminution at the fracture site. Additionally, open reduction affords the opportunity to inspect the articular surface, which provides useful prognostic information. Fixation is dictated by fracture pattern. Most often, one or two partially threaded cancellous screws are sufficient; however, with a more vertical fracture pattern, several screws with washers or even a small one-third tubular anti-glide plate will be indicated.
Figure 5-6 (A and B) Medial malleolar fracture in a 16-year-old basketball player. The athlete elected to undergo nonoperative treatment and healed uneventfully in 6 weeks.
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Ankle fractures
Figure 5-7 (A and B) Computed tomography images of a 17-year-old offensive lineman with delayed union of repaired medial malleolar fracture. (C and D) Union was achieved with local bone grafting from the calcaneus and revision internal fixation.
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Ankle and midfoot fractures and dislocations
Once wound healing is stable, range of motion and resistance exercises are instituted. Weight bearing is restricted until 4 weeks and is advanced on the basis of symptoms. Results generally are good.
Lateral fractures Isolated lateral malleolar fractures present one of the most challenging management dilemmas in the realm of sports injuries. Associated syndesmosis widening or medial injury, bony or ligamentous, make the choice of treatment fairly simple and obvious.15,21,22,23 However, fibular fractures at any level without concomitant injury or significant radiographic displacement generate varied and controversial opinions as to what is considered appropriate intervention. On one hand, arguments may be made that surgery is unnecessary because, even though the lateral stability is compromised, it is not completely diminished. Intact medial structures, specifically the malleolus and deltoid ligament, provide primary resistance to lateral talar translation, thus limiting or preventing abnormal ankle mechanics. Several studies support displacement, lateral or posterior, of up to 5 mm without significant
Figure 5-8
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compromise in clinical outcomes.22-25,26 Physiologic loading studies of the normal and compromised ankle suggest that the medial structures are, in fact, most important for stability.1,10-19,26,27 It also has been shown by CT analysis that fibular displacement occurring as a result of an external rotation force with intact medial structures (Lauge-Hansen SER2) is the result of internal rotation of the proximal fragment.18 This implies that the distal fibula maintains its relationship with the mortise and that no functional incongruity is present (Fig. 5-8, A through D). Clinical studies have supported this notion, demonstrating good results with up to 30-year follow-up on nonoperative treatment of isolated lateral malleolar fractures.24,28-30 Alternatively, an argument may be made for repairing all but nondisplaced fibular fractures, the rationale being that even small increments of displacement may lead to fibular shortening or mortise widening.4,10 Early mechanical testing suggested that the lateral talar displacement of as little as 1 mm would significantly increase contact pressures in the tibiotalar joint, thus creating a potential predisposition to early arthritic changes.9 In addition, it was shown that the talus would routinely
(A and B) Nondisplaced distal fibula fracture that this athlete elected to treat without surgery.
Ankle fractures
Figure 5-8 cont’d. (C and D) Note that, despite clinical healing, radiographs still disclose fracture line at 4 months. The athlete was asymptomatic and back to full activity.
earlier return to weight-bearing; and stabilizing weight bearing; rehabilitation; and shorter duration of pain. All are anecdotal, and none have been demonstrated in a prospective comparison study of operative versus nonoperative treatment specific to this injury pattern. Controversy persists surrounding the process of decision making. Despite evidence to the contrary, many surgeons perform, and athletes elect to undergo, repair of the injured lateral malleolus, presumably for fear of abnormal and untoward results of pathologic mechanics and to resume activity as quickly as possible. A large body of clinical evidence favoring this faction is the demonstrated lack of reliability of reproducible medial tenderness on clinical examination in disclosing the presence or absence of deltoid ligament injury.31 It is unclear as to what degree of deltoid injury in the face of the fibular fracture will allow for clinical instability.10 Therefore many surgeons ascribe to the philosophy that it is better to be aggressive, especially in someone whose livelihood may depend on the anatomic function of an ankle or lower extremity. Again, the perspective is anecdotal but reasonable. Surgical treatment often is pursued, as detailed later. 91
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follow the displacement of the fibula, thus lending itself to anatomic malpositioning and subsequent abnormal loading stresses10 (Fig. 5-9, A through F). However, these studies9,10 are some of the most often misquoted or misinterpreted in the literature. These analyses were performed in vitro and, as such, focused specifically on the relationship between the fibula and talus after eliminating all other attachments. There was no medial restraint to motion; thus, even though the results can be viewed as reliable and truthful, they bear limited clinical applicability because the contribution of the medial osseous and ligamentous structures was ignored. Appropriate interpretation of these studies suggests that abnormal ankle mechanics may be encountered when a fibular fracture exists in the face of medial deficiency. In these cases, operative treatment should be used.15 However, these studies fail to speak to the longterm, clinical consequences of a truly isolated lateral malleolar fracture. More practical arguments for operative fixation in the athlete are more reliable reduction in the face of unclear medial injury; anatomic bone-to-bone contact, facilitating primary bone healing, faster recovery times, and
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Ankle and midfoot fractures and dislocations
Nonoperative management consists of immobilization until swelling and pain allow motion, usually about 10 to 14 days. Subsequent weight bearing ensues in a walking boot, again, when symptoms abate. In most instances, athletes are back to protected weight bearing somewhere between 3 and 4 weeks. The walking boot is maintained until full weight bearing and nearly normal range of motion are restored. Physical therapy focuses on maintaining muscle tone, joint mobility, and proprioception during the healing phase. Return to activity is dictated by relief of pain, normal symmetric joint range, and strength equal to 75% of that in the normal, unaffected side. Sports-specific activities are resumed with protective taping or bracing as necessary. Radiographs are monitored frequently in the first month to ensure no displacement, but after 4 weeks these typically are not helpful as long as no changes are noted, specifically no mortise widening. Should one embark on the surgical management of the isolated lateral malleolus fracture, operative principles of anatomic restoration and rigid fixation apply. The goal is to allow early mobilization and quick
recovery. Debate still exists regarding the use of interfragmentary fixation combined with lateral buttress plating versus posteriorly placed, anti-glide fixation. Lateral plating is technically easier, whereas posterior plating theoretically provides greater mechanical stability.32,33 Both seem to perform well clinically. No current consensus exists, and the method remains the preference and comfort level of the surgeon. A recent resurgence of interest has been noticed in an older technique of fibular fixation—intramedullary nailing. This method of fixation has some limited application in the treatment of fibular fractures but really has no place in the operative fixation of a high-demand individual or high-performance athlete. What little advantage one can gain from biomechanical stability of an intramedullary device quickly is counteracted by the notorious inability to correct or control rotation and length. In fact, my experience suggests that the insertion of the device often will alter or displace a previously anatomic reduction because of the force required to install it, as well as the angled flange on the interlocking nails. These are not recommended when one is in need of an
Figure 5-9 (A and B) Displaced fractures of the fibula with mortise widening require open reduction and internal fixation, with possible attention to the deltoid ligament if the mortise remains widened.
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Figure 5-9 cont’d. (C and D) Even after anatomy is restored through closed reduction, stability is in question. (E and F) Open reduction and internal fixation (ORIF) ensures anatomic restoration of the joint and allows early institution of joint motion and therapy.
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Ankle and midfoot fractures and dislocations
anatomic restoration of the joint and should be reserved for lower-demand, medically compromised patients in need of surgical stabilization. One indication for this type of fixation would be in the athlete with a displaced, low (Weber A) fibula fracture. In this instance, an intramedullary, 4.0-mm, cancellous screw would be reasonable, provided that an anatomic reduction can be achieved.
Bimalleolar/trimalleolar fractures Little debate exists regarding treatment of bimalleolar/ trimalleolar ankle fractures. In an athletic population, uniform agreement exists regarding the need for operative intervention21,22 (Fig. 5-10, A through D). Some caveats do exist, however. Particularly attention should be paid to the fibular length and rotation. Any degree of malreduction may lead to abnormal mechanics and possibly could hasten the advance of degenerative arthritis. High fibular fractures associated with bimalleolar fracture patterns should be stabilized rigidly and anatomically. All injuries should be tested for syndesmotic stability, but especially those demonstrating a medial soft tissue injury. This test can be done by directly visualizing
Figure 5-10
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the syndesmotic ligaments while applying a laterally directed pull on the fibula with a towel clamp, reduction tool, or other grasping object. Any laxity in tibiofibular stability associated with a fibular fracture more than 3.5 to 4.0 cm from the joint should be stabilized with syndesmotic fixation11 (Fig. 5-11, A through D). I prefer to use a 3.5-mm screw with three cortex fixation and a plate long enough to incorporate the screw proximally to the distal-most hole (see Fig. 5-11, D). Routine screw removal is performed after 12 weeks on the basis of biomechanical evidence of abnormal ankle mechanics in the face of restricted talofibular motion.34 This reduces the risk of a free-standing screw hole as a stress riser and theoretically allows quicker, safer, and more reliable return to activity. Trimalleolar fractures at least should have the medial and lateral components repaired. Fixation of the posterior fragment of tibia is performed on the basis of size of the segment and, more importantly, percentage of articular surface involved. Those with more than 25% to 30% of the joint involved in the fracture should undergo stabilization with at least one anterior to posterior screw (see Fig. 5-10, C and D).
(A through D) Bimalleolar and trimalleolar fractures require open treatment.
Ankle fractures
Figure 5-10 cont’d.
(continued)
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Figure 5-11 (A through D) Syndesmosis repairs should be performed at the level of injury occurrence and be based on the stability of the joint after malleolar repair. (A and B) Displaced bimalleolar fracture in an adolescent wrestler. Note the avulsion of the anterior inferior tibiofibular (AITF) ligament from the distal tibia.
CHAPTER 5
Ankle and midfoot fractures and dislocations
Figure 5-11 cont’d. (C) Malleolar repair with a screw in the syndesmotic fragment. (D) More traditional fixation for a higher level fibula fracture and persistent tibio-fibular widening.
Pediatric ankle fractures Pediatric ankle fractures constitute a wide variety of patterns and complexity. However, these often are encountered in the growing population of high school, junior high, and primary school athletes. Salter-Harris (S-H) fractures not involving the joint adhere to principles of all generic, pediatric fracture management protocols (Fig. 5-12). Closed anatomic reduction often is successful simply by reversing the mechanism of injury. Cast immobilization typically is effective for management, and bony remodeling usually compensates for any minor malalignments. Immobilization usually is required for 6 to 8 weeks, at which point gradual weight bearing and range of motion may be advanced as tolerated. Any articular incongruity necessitates open management (Fig. 5-13, A and B). Complexity increases in the diagnosis and management of the adolescent variants of the Tillaux (S-H III) and triplane (S-H IV) fractures. These typically occur in the 12- to 14-year age range as the medial tibial physis begins to close, creating an irregular stress distribution and resistance to forces applied across the ankle (Fig. 5-14).
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Tillaux and triplane fractures are considered adult, and issues regarding treatment should be viewed as such (Fig. 5-15). The focus of treatment should be based on congruity of articular reduction because the complications surrounding these injuries arise from nonanatomic incongruous relationships, leading to early degenerative changes rather than the more popular but erroneous presumption of growth arrest. Abnormalities or asymmetry in growth actually are rare and not terribly consequential in these scenarios. Any question of articular irregularity should be settled by obtaining advanced imaging studies, specifically CT scanning, to eliminate the possibility of articular step-off. Separations of more than 2 mm in distance along the joint surface, regardless of congruity, should be repaired. No compromise should be accepted at the articular surface for fear of early degenerative changes. Percutaneous techniques using large reduction clamps or devices and cannulated screw fixation are acceptable, but the surgeon must be certain of anatomic restoration and no interposed tissue. If there is any question regarding adequacy of reduction, open treatment is required. Once stability is ensured, motion may be introduced;
Lateral process talar fractures
A
B
C D Figure 5-12 Dias, Tachdjian modification of Salter-Harris’ classification of ankle fractures in the immature skeleton. (From Green NE, Swiontkowski MF: Skeletal trauma in children, Philadelphia, 2002, WB Saunders.)
LATERAL PROCESS TALAR FRACTURES Fractures of the lateral process of the talus previously have been considered an uncommon injury. Historically, this injury was thought to occur as the result of highenergy trauma and would result from a peritalar dislocation that caused avulsion of the subtalar ligamentous attachments on loading. More recently, however, this injury has gained notoriety because of its strong predilection for presentation after snowboarding injuries. Before the advent of this relatively new winter sport, reports were infrequent. However, with the explosion of attention to this activity by a predominantly young, risk-taking population, the incidence and recognition have risen dramatically—so much so that this injury has been deemed by some as the ‘‘snowboarder’s ankle.’’35,36
One review demonstrates 74 lateral process fractures of the talus that occurred as the result specifically of snowboarding, accounting for 2.3% of all snowboard injuries. This is, to date, the largest series reported.36 Lateral process fractures often are missed, commonly masquerading as chronic ankle sprains. It is easy to understand why this happens because of the relative anatomic proximity of this injury to the anterior talofibular ligament, as well as the lack of reliability of reproducible evidence of fracture on standard radiographic studies. Early diagnosis and treatment, however, are important because studies have suggested that late recognition and failure to implement treatment routinely lead to poor outcomes, such as chronic pain, stiffness, instability, and arthritis.37-44 Traditionally, lateral process fractures were purported to arise from a sudden dorsiflexion inversion force on a fixed foot. However, mechanical loading studies have demonstrated that an acute external rotation or shear force is a key element in reproducing this fracture pattern in a cadaveric model.35 97
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however, weight bearing should be withheld for 6 to 8 weeks until healing is confirmed.
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Ankle and midfoot fractures and dislocations
Figure 5-13 (A and B) Supination-inversion injury of the ankle. (B) With repair. Care is taken to avoid the tibial physis and articular surface. The fibular pin is removed after 4 to 6 weeks.
Hawkins39 has classified these fractures into three subcategories (Fig. 5-16). Type I is a simple fracture of the lateral process extending from the tibiofibular articulation down to the posterior talocalcaneal articular surface of the subtalar joint, with or without displacement of the fragment. Type II fractures involve comminution of the fibular and posterior calcaneal articular surfaces, as well as the lateral process. Type III is an avulsion or chip fracture off the anterior and inferior part of the posterior articular processes of the talus. Another classification system has been proposed by Fjeldborg,38 who described stages of injury with type I fissuring, type II lateral process fracture with displacement, and type III lateral process fracture with subtalar dislocation. Diagnostically, this fracture pattern presents a dilemma, and a high index of suspicion is needed by the clinician. Injury pattern reports by the patient often are unreliable and inaccurate. Physical examination findings often are similar to those found with an acute, severe ankle sprain with tenderness just anterior and inferior to the tip of the fibula, along with swelling and ecchymosis. Radiographs sometimes are helpful when large fragments or significant comminution are present but, again,
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are not reproducibly diagnostic because of the irregular anatomy and overlap of joints in this area.37,45 Special radiographic views have been proposed to help elucidate these fractures, including a 20-degree internal rotation view with the foot in neutral dorsiflexion.46 Alternatively, Dimon37 has suggested that the ankle be placed in 45degree internal rotation and the foot plantarflexed at 30 degrees to show the posterior facet in profile. If the diagnosis is entertained, the best and most reliable study remains CT scanning. This not only provides the examiner with diagnostic evidence but also demonstrates the degree of displacement and comminution of fragments. Because of the poor outcomes obtained, all fractures must be sought and treated aggressively. Nondisplaced fractures should not be ignored but immobilized in a cast for 6 to 8 weeks with no weight bearing and then reevaluated at that time for bony union. Failure to aggressively treat larger displaced fracture fragments or comminuted fractures may and often does result in malunion, nonunion, heterotopic overgrowth, subtalar instability, and, ultimately, disabling arthritis.39,40,42,43,47-53 Late symptoms have been shown often to not respond to excision of the offending fragments.37,47,51
Lateral process talar fractures
Epiphyseal plate
Anterior Lateral
Posterior Medial
A
12.5 yr.
13 yr.
13.5 yr.
14 yr.
Figure 5-14 Demonstrating the unusual closure of the distal tibial physis. First, it starts in the middle of the growth plate, then moves anteromedially and finally laterally. (From Green NE, Swiontkowski MF: Skeletal trauma in children, Philadelphia, 2002, WB Saunders.)
B Figure 5-15 (A and B) Tillaux and triplane ankle fracture variants in the adolescent athlete. (From Green NE, Swiontkowski MF: Skeletal trauma in children, Philadelphia, 2002, WB Saunders.) Superior
Anterior
Posterior
A
B
C Figure 5-16 (A through C) Hawkins classification of lateral talar process fractures. (From: Boon AJ, Smith J, Zobitz ME, Amrami KM, et al: Am J Sports Med, 29(3):333, 2001.)
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Treatment is fracture type dependent. Large displaced fractures are managed with anatomic restoration of the articular surface with internal fixation (Fig. 5-17, A through E). These often are large enough to accept at least one small fragment screw for fixation (2.7 or 3.0 mm usually will suffice). This most often can be done through a typical Ollier approach to the sinus tarsi and subtalar joint region. Comminuted fracture patterns are more ominous and carry a more unpredictable outcome. These often are refractory to repair and necessitate excision for all fragments. This at least removes any potentially abrasive surfaces and areas of future impingement. If repaired, early range of motion, focusing on inversion/eversion, will promote restoration of subtalar mechanics. Sequelae of untreated or missed fractures are well documented. Malunion, nonunion, instability, overgrowth, and/or arthritis of the subtalar joint can be debilitating. Missed fractures that present late often are refractory to repair or remove fragments and will necessitate subtalar arthrodesis.37,47,51 Therefore it is critical that awareness of this injury pattern remains prevalent and a high index of suspicion be maintained for any patient presenting with atypical or persistently painful ankle sprains.35,36,47
CHAPTER 5
Ankle and midfoot fractures and dislocations
Figure 5-17 (A) Schematic of a lateral process talus fracture. (B and C) Direct visualization of the lateral process fragment before (B) and after (C) reduction.
ANTERIOR PROCESS CALCANEAL FRACTURE Anterior process calcaneal fractures often are missed in the acute setting. This fracture must be sought in anyone with recalcitrant lateral foot pain or ankle sprain; if untreated, it will lead to problematic sequelae. There are two types of anterior process fractures, and they occur by opposing mechanisms of injury: avulsion and compression.50,54 Avulsion injuries occur as a result of a plantarflexion, inversion force (Fig. 5-18). As such, these often are misrepresented as lateral ankle sprains.55-57 The overall
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presentation is similar with respect to mechanism in the onset of lateral foot or ankle pain, ecchymosis, and swelling. However, tenderness typically occurs 1 to 2 cm more distally in the region of the sinus tarsi. The fracture fragment often is small and extra-articular, occurring as a plantarflexion and inversion force tensions the bifurcate ligament, which overcomes the attachment of the distal-most calcaneus. Alternatively, compressive injuries occur with sudden abduction forces across the foot and are much more ominous. These often will be intra-articular and involve variably sized fragments of joint surface, as well as causing displacement of the fragments posterior, dorsal, or lateral, sometimes leading to substantial incongruity.
Anterior process calcaneal fracture
Figure 5-17 cont’d. (D and E) Fixation is achieved with a posteromedially directed screw. A talar neck fracture is fixed here, as well. (A from Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
Figure 5-18 Anterior process fracture of the calcaneus. (From Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
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Ankle and midfoot fractures and dislocations
Because of the similarity in presentation to lateral ankle sprain, a high index of suspicion should be maintained and careful clinical inspection performed. Radiographs are helpful, but a clear and obvious fragment is not always visible. Because these often are confused with ankle sprains, it is not uncommon that only ankle x-rays are obtained. Suspicion should prompt the clinician to obtain foot radiographs, particularly obliques, to verify the diagnosis.58 Occasionally, a small fragment or ossicle, the calcaneus secondarium, will be noted on a lateral ankle or oblique foot radiograph. This is smooth and regular in its contours and should be differentiated from the rough, irregular edges of an acute anterior process fracture. CT may be helpful to determine specific characteristics of acute fracture versus ossicle presence.50,58 Additionally, this is recommended for those patients presenting with compressive injuries to determine the degree of articular involvement. Early diagnosis aids in the quality of treatment for this injury. Healing, particularly of the avulsion type of fracture, is reliable if identified early. Typically, immobilization in a walking boot or a cast for 4 weeks is sufficient. Delay in diagnosis and lack of immobilization can lead to persistent symptoms and affect the ultimate outcome. Occasionally, excision will be required to remove a nonunited fragment after delayed or missed diagnosis. Compressive injuries, especially those with displacement, are more complex and carry less-predictable outcomes because of the articular damage sustained at the time of the injury. Displacement of the fragments requires early reduction and fixation to restore congruity. Still, these patients may develop degenerative disease at the calcaneal cuboid articulation, depending on the energy of the injury. Results of treatment for any form of these fractures are few and anecdotal. Degan et al.59 reported on surgical treatment of seven patients who developed symptomatic nonunions after anterior process fractures. Late excision provided pain relief in five of six. Surgical treatment may involve a need to osteotomize the calcaneus just below the area of nonunion to excise the entire affected area. Care should be taken to immobilize the foot for 6 weeks after this procedure, because destabilization may occur as a result of removing the bifurcate ligament, which connects the hind foot to the midfoot at the navicula and cuboid, respectively. Resumption of full athletic activity after surgical treatment may take up to 6 months; and rarely, in some patients, persistent residual degenerative joint disease symptoms may persist and limit return to sport.50,59
TARSOMETATARSAL DISLOCATIONS The tarsometatarsal joint, consisting of the bases of the five metatarsals and their articulation with the three
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cuneiforms and the cuboid, is named after Lisfranc, a French surgeon in the army of Napoleon, who originally described an amputation through that joint.4,50,54,60 The dislocations or fracture/dislocations of the tarsometatarsal joint are reported to occur at the rate of one injury per 55,000 people per year.50,60 These are recognized more commonly in a polytrauma patient because of the severity,61-63 but also are increasingly recognized to occur in the athletic population. Faciszewski et al.64 have reported on patients with ‘‘subtle’’ injuries to the Lisfranc joint, defined as diastasis of 2 to 5 mm between the bases of the first two metatarsals. A third of their patients’ injuries were sports related. Other reports support the increasing frequency of occurrence of Lisfranc injuries in athletic events.65-68 Any patient diagnosed with a midfoot sprain should arouse suspicion for an undiagnosed tarsometatarsal ligament disruption. In the athletic population, the occurrence and severity varies by sport. Lisfranc injuries are reported to be the second most common athletic injury to the foot, after metatarsophalangeal joint injuries, presenting in 4% of football players per year, with a preponderance occurring in linemen (29.2%).67 Although complete injuries resulting in diastasis of more than 5 mm are easier diagnostically and more dogmatic in treatment plan, more subtle injuries (1 to 5 mm) often are overlooked and, even when diagnosed, may lead to therapeutic dilemmas for the surgeon, as well as frustration for the injured athlete. Partial capsule tears with no diastasis, for instance, can be a compounding problem resulting in prolonged disability for the elite performer. The tarsometatarsal joint really is more of an articulating complex providing both motion and stability— much more so the latter. The osseous anatomy reveals multiple, wedge-shaped bones coalescing to form an arch in the transverse plane. The second metatarsal often has been referred to as the keystone of this Roman arch analogy, reflecting its overall importance to the integrity of the maintenance of this structure. Structural rigidity of the shape of the foot is dependent on the stability of this relationship of the midfoot bones. Because the bases of the metatarsals are wider dorsally, collapse of the arch in any plane is prevented in the face of weight-bearing load. The 2nd through 5th metatarsals are interconnected by a dense weave of short, broad-based ligaments and capsular ligamentous structures. These tend to be bundled together and often will move as one unit. However, there is a notorious absence of ligamentous connection between the bases of the first and second metatarsals. This is thought to account for the predominance of diastasis in this interval. Instead, there exists a dense, plantar-based, oblique ligament extending from the base of the second metatarsal to the lateral portion of the
Tarsometatarsal dislocations
as may be seen in ballet dancers en pointe.70-72 Alternatively, supination or inversion of the hindfoot on a fixed plantarflexed forefoot will result in a more dissociative pattern of injury because the medial column is disrupted, followed by the lateral dislocation of the lesser metatarsal and associated tarsal cuneiforms.73 A third type of injury occurs when the fixed plantarflexed foot is forced into extreme equinus as a result of being struck from behind.60 This is more common in turf sports such as football. Elements of torque, rotation, and compression are all present and cumulatively lead to a dorsal capsule ligamentous disruption. Many classification systems have been proposed to describe the multitude of injury patterns that may occur.60,61,63,69,74,75 Because of the tremendous variation, no one system has been universally accepted. These classification systems usually apply to high-energy injuries and are based on segmental patterns of metatarsal-tarsal bone displacement. Recently a useful classification has been proposed specifically for the athletic midfoot injury, including undisplaced sprains, and is based on clinical findings, weight bearing, x-rays, and bone scan results67 (Fig. 5-19). Stage I patients were found to have pain at the midfoot and were unable to play sports but had no radiographically visible changes. Bone scan results did demonstrate increased uptake in the area of Lisfranc joint. Pathoanatomy is thought to include dorsal capsular tear without elongation of Lisfranc’s ligament. Stage II is described as clinical findings similar to those in stage I, but with diastasis of 1 to 5 mm between the bases of the medial two metatarsals present on plain AP radiographs. No loss of longitudinal arch was noted on weight-bearing lateral x-rays. Pathoanatomy here differs from stage I in that the Lisfranc ligament is elongated, but the plantar structures remain stable and prevent arch collapse. Stage III was defined as diastasis greater than 5 mm and loss of lateral arch height, defined by loss of space between the fifth metatarsal and the medial cuneiform on lateral radiograph.38,67,75 All capsuloligamentous structures are thought to be injured in stage III. Other forms of injury, such as gross disruption with fracture and/or dislocation, were defined by these authors in the method originally proposed by Myerson,76 which was based on segmental instability (Fig. 5-20). The advantage of such a classification is that treatment may be predicated on the level of injury. Up to one in five Lisfranc injuries are missed or improperly diagnosed on initial screening, whether it be in the emergency department or at practitioner’s office. This often can be ascribed to the presentation of these injuries as part of a polytrauma, with other, more severe and more obvious injuries demanding the bulk of attention.77-79 103
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medial cuneiform—Lisfranc’s ligament. This ligament anchors the lesser metatarsal complex to the medial column of the foot. The tibialis anterior, with its insertion on the medial aspect of the proximal first metatarsal and the peroneus longus, which inserts into the lateral proximal first metatarsal, also contributes to the stability of the Lisfranc articulation. In certain phases of gait, these two tendons provide dynamic restraint. Plantar fascia, intrinsic musculature, and plantar tarsometatarsal ligaments provide additional structural support against arch collapse and plantarward dislocation. The midfoot articulation may be divided mechanically by columns. The medial column includes the first metatarsal and medial cuneiform. The middle column consists of the second and third metatarsals, as well as the middle and lateral cuneiforms. The lateral column is formed with the fourth and fifth metatarsals, along with the cuboid bone. This column provides the greatest motion throughout the tarsometatarsal joint. Vascular structures in this region deserve mention because of their proximity to the area of potential injury. The dorsalis pedis artery and the plantar arterial arch are structures at risk, particularly when the dorsalis pedis dives down between the bases of first and second metatarsals. Disruptions here, especially with a tethered vessel, can result in kinking, vasospasm, and, ultimately, ischemia. Lisfranc dislocation derives its name, in fact, as previously stated, from the Napoleonic surgeon who so definitely amputated cavalrymen after midfoot injuries resulting in vascular catastrophes.50,60-63 Although less common compared with the high-energy version of this injury, anecdotal reports of associated vascular injuries abound and should be sought for fear of missing an ischemic sequela. Patterns of injury to the tarsometatarsal joint have been described as a result of both direct trauma to the foot and indirect violence. The majority of nonathletic traumatic midfoot injuries can occur as a result of significant direct force, usually applied to a foot in plantarflexion or abduction, and typically will accompany highvelocity or high-energy trauma, such as motor vehicle accidents or falls from heights.60,61,63,69 These can result in significant soft-tissue compromise, neurovascular injury, and compartment syndrome.62 Indirect injury is more relevant to this discussion. Athletes may sustain direct violence to the foot as the result of an awkward collision or in the melee of a collision in certain sports. However, more commonly the athlete is injured because of low-velocity, indirect energy imparted to the foot. Most will describe some sort of axial longitudinal force while the foot is plantarflexed and, often, slightly rotated.67 Two specific patterns have been described. Simple lateral dislocations result from eversion of the hind foot on a fixed plantarflexed foot,
CHAPTER 5
Ankle and midfoot fractures and dislocations
Lisfranc ligament sprain
Ruptured Lisfranc ligament
2–5 mm diastasis
No diastasis Stage I
Ruptured Lisfranc ligament
Stage II
2–5 mm diastasis
Diastasis and loss of longitudinal arch height
Stage III
Figure 5-19 Figure 1.)
Nunley classification of athletic Lisfranc injuries. (From: Nunley JA, Vertullo CJ: Am J Sports Med, 30:6, 2002, p.872,
In the athlete, however, it is the subtle or complete absence of radiographic diastasis that may occur that confounds the examiner.64,67,77,80 A high index of suspicion must be maintained for athletes presenting with midfoot pain after athletic contact or activity, even without radiographic evidence of injury. Consideration should be given to stress radiographs as a means of furthering diagnostic abilities. Physical examination is especially important with subtle injury. Gross distortion of the bony architecture of the foot is readily identified. Clinical and radiographic findings of fractures and dislocations are relatively simple to determine. The patient presenting with no overt disruption or equivocal radiographic divergence becomes a diagnostic dilemma. Examination typically demonstrates tenderness at the midfoot that is worsened by provocative maneuvers such as pronation or abduction of the foot. Swelling is often significant, and ecchymosis is variably present. Neurovascular injuries are unusual in the lower energy traumas, but the possibility of impending compartment syndrome always should be considered, because there often is tremendous edema accompanying these injuries. Classic radiograph findings and markers have been well established. A minimum of three radiographic views
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of the foot (AP, lateral, and oblique) should be obtained. Assessment in suspicious injuries should be made of all of the following relationships: 1. Diastasis of metatarsals 1 and 2. 2. Cuneiform diastasis, especially medial and middle. 3. Widening between the second and third metatarsals. 4. Widening between middle and lateral cuneiforms. 5. Small fracture, ‘‘fleck sign’’ at the medial base of the second metatarsal or medial cuneiform, representing an avulsion of Lisfranc’s ligament. 6. Horizontal plane malalignment of metatarsals on lateral x-ray. 7. Relationship of medial border of the second metatarsal should be parallel to the medial edge of the middle cuneiform. 8. Relationship of the medial fourth metatarsal should be parallel to the medial edge of the cuboid. 9. General loss of parallelism of metatarsal bases with respect to one another. 10. A small compression fracture at the lateral edge of the cuboid.45,52,74,76,77,80-85 Even after perusing the radiographs with these parameters in mind, the clinician may find it difficult to make a diagnosis. Weight-bearing, contralateral radiographs often are helpful in discerning any asymmetry.
Tarsometatarsal dislocations
A
B
C
D
E
F
Myerson classification of Lisfranc injuries. (From Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
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Figure 5-20
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Ankle and midfoot fractures and dislocations
In more subtle and problematic cases, multiple advanced imaging studies have been suggested, including CT, MRI, static stress radiographs, and stress fluoroscopy under anesthesia.54,63,65,86-88 However, the best and most reliable studies seem to be a set of standing radiographs (Fig. 5-21, A through E) and bone scan, if necessary, in the completely undisplaced metatarsal that manifests persistent pain.67,68 There are two advantages to weight-bearing radiographs. First, the dynamic nature of the injury can be determined in a more appropriate physiologic and mechanical state, thus determining the need for treatment. Second, prognostic value exists in determining the presence of collapse or instability.64 Principles of treatment of Lisfranc injuries are universal and include providing an anatomic reduction in stabilization. Care must be taken to observe and manage the soft tissue and neurovascular consequences, as well. Debate still exists as to how much diastasis is acceptable in the injured athlete. The literature is heavily weighted toward high-energy trauma management, and little has been proposed regarding management of the athletic midfoot sprain. Most recent literature suggests that residual diastasis may result in a poor outcome, such as persistent pain, deformity, and arthrosis.45,60,65,67,76,81,87-92 Nonanatomic reductions have been shown to be inferior with respect to outcome and the need for secondary procedures, such as revision repairs or fusions. Athletic injuries are sparsely documented, but the evidence that is available seems to support the conclusion that injuries resulting in diastasis will lead to poor outcomes. Curtis, et al.65 reviewed 19 athletes with varying degrees of tarsometatarsal (TMT) injury, citing poor functional results despite ‘‘relatively nondisplaced injuries’’ in patients with delays in diagnosis and those not treated adequately, with three failing to return to sport. Meyer et al.66 reported on nonoperative management of 23 collegiate football players with good outcomes after nonoperative treatment of midfoot injuries. In this study, 20 of 23 had no diastasis, but of those that did, one of three had significant pain with high-demand activity. Nunley and Vertullo67 showed that 14 of 15 patients had good results when treated within the algorithm based on a classification they proposed that guided treatment on the basis of displacement. Patients were assessed on the basis of plain x-rays and bone–scan-documented injury. Only completely nondisplaced injuries (seven patients) were treated nonoperatively. All others were treated by open reduction with internal fixation. The only patient with residual pain was one treated by open reduction and internal fixation after 10 months of failed conservative treatment. Return to sport in the operative group averaged 14.4 weeks, which was comparable to nonoperative results.
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Only one study demonstrates reasonable results with nonanatomic reductions. Shapiro et al.68 reported on nine athletes with diastasis between 2 to 5 mm. Eight elected for nonoperative treatment and returned to sport within 3 months, with good results reported in an average of 33 months after the injury. On the basis of these reports and personal experience, my recommendation is for operative treatment in all but nondisplaced injuries of the tarsometatarsal joint. Although percutaneous techniques have been proposed, an open approach is more reliable and eliminates the possibility of retained or interposed tissue, as well as allowing direct visualization of the joint for an anatomic reduction (Fig. 5-22). Closed or percutaneous techniques using the large Weber reduction clamp carry the risk of malreduction, especially in a horizontal plane, even in the face of an anatomic appearing anterior/posterior image (Fig. 5-23). Open treatment affords the surgeon the opportunity to extricate any incarcerated bony fragments or soft tissue that may have been interposed, including the Lisfranc’s ligament itself or, in high-energy injuries, the tibialis anterior tendon. Anatomic restoration of the arch is achieved and verified, as well as providing direct visualization for hardware placement. Screw fixation is preferable because K-wire fixation is tenuous, at best, and not as reliable in maintaining an anatomic reduction. In addition, especially in unstable injuries, the motion at the joint surfaces will induce pin loosening and migration with predictable loss of stability, thus requiring concurrent cast immobilization, which prevents early rehabilitation. Conversely, screw fixation is reliable and allows for early mobilization of the foot and ankle, as well as edema control after wound healing has been achieved. Screw configuration is dependent on injury pattern and extent of ligamentous disruption. My preference is to use fully threaded, 4.0 mm or larger screws. Partially threaded screws are acceptable, but because this is a ‘‘position screw’’ to maintain reduction, the surgeon must guard against the tendency to compress across the TMT joints. Typically, the first screw is placed on the orientation of the disrupted Lisfranc’s ligament, that is, from medial cuneiform to second metatarsal base. Additional screws are placed as needed across the base of the first and third TMT joints from distal to proximal (Fig. 5-24, A through C). Should the injury extend through the medial and middle cuneiforms, an intercuneiform screw should be placed first. The patient is kept on weight bearing for 6 to 8 weeks. Early motion and therapy modalities such as muscle stimulation can begin as soon as soft tissue healing allows. Partial weight bearing in a boot begins at 6 to 8 weeks and is advanced until 12 weeks. Screws are maintained for no fewer than 16 weeks and often,
Tarsometatarsal dislocations
Figure 5-21 (A) Radiograph of a 34-year-old professional waterski jumper with acute midfoot pain after a fall. There is a suggestion of subtle intermetatarsal diastasis. (B through D) Various advanced imaging studies confirm the Lisfranc ligament disruption by avulsion of the base of the second metatarsal. (B) Bone scan shows increased uptake about the midfoot. (C) Computed tomography demonstrates the avulsed fragment. (D) Magnetic resonance imaging reveals edema in the region of the ligament with suggestion of bony injury. (E) Plain anteroposterior weight-bearing x-rays of the injured and comparative contralateral side clearly disclose the diastasis.
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but not routinely, are removed. The athlete is returned to athletic activity with a molded, semirigid insole and a semirigid extended steel shank device. Frank disruptions are treated in the way that trauma guidelines dictate and uniformly are managed with open reduction and internal fixation. Postoperative protocols are similar to those described previously, but usually require larger periods of rehabilitation, and return to activity is less predictable in these patients.
TARSAL BONE FRACTURES
Figure 5-22 Planned incision for approach to the diastasis of Lisfranc’s joint. (From Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
Figure 5-23 Percutaneous reduction technique with a large Weber clamp. Surgeons must be aware of the tendency for dorsal plane malalignment as a result of overtightening or improper clamp placement. Lateral fluoroscopy should always be employed to verify anatomic reduction. (From Myerson MS: Foot and ankle disorders, St Louis, 1999, Mosby.)
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Anatomic variants of Lisfranc’s injuries do exist. There have been reports citing evidence of bipartite cuneiforms and anatomic variations in anatomy throughout the midfoot bones (Fig. 5-25, A through F). These should be encountered but pursued and treated aggressively, with the same guidelines as those for the previously described injuries.93-95 Fractures or dislocations exclusive to the cuneiforms or cuboid area are unusual. These often are present in conjunction with a tarsometatarsal joint injury, in which the force of the injury has disrupted further proximally through the navicula, cuneiform, or talonavicular joints, or even through the body of the cuboid. Although rare, these injuries have been identified.96,97 Because cuneiform fractures and dislocations often occur as part of a midfoot dislocation, treatment principles should follow those of the injured tarsometatarsal joint. Isolated cuboid injuries most often present as insignificant ‘‘chip’’ fractures along the lateral side. Typically, these occur as a result of an inversion injury and often are seen secondarily after the patient has been diagnosed with ‘‘sprain.’’ Treatment requires supportive immobilization in either a walking cast or hard-soled shoe for approximately 4 weeks or until symptoms allow resumption of activity. A rigid orthosis may allow earlier return to sport. Fracture instability is not usually a concern. Compressive cuboid injuries can occur with a sudden abduction force. So-called nutcracker injuries are far more severe. Again, this is considered a variant of the mechanism for Lisfranc injuries, and the same principles are applied. Early anatomic reduction is necessary (Fig. 5-26, A through E). Manipulation alone is often unsuccessful in restoring the length of the lateral column. Open treatment frequently is required. Placing a small plate to span the collapsed intercalary segment is necessary on occasion. Often, there is poor-quality bone fixation in the subarticular cuboid; therefore a spanning plate to the distal calcaneus represents a good alternative. For severe comminution, I prefer structural tricortical graft to reestablish the length. This may be interposed between subchondral bone proximally and distally, because the articular surfaces often are not
Fractures of the base of the fifth metatarsal
Figure 5-24 (A and B) Repair of injury seen in Figure 5-19 performed through dorsal incision. (C) Patient returned to sport in 6 months.
FRACTURES OF THE BASE OF THE FIFTH METATARSAL Fractures of the base of the fifth metatarsal are the most common metatarsal fracture. However, there are many misconceptions regarding the description, the understanding, and thus the treatment of these injuries throughout the literature. The classic Jones fracture was named after Sir Robert Jones,98 who originally described the fracture in his own foot in 1902. He sustained the fracture ‘‘Whilst dancing, I trod on the outer side of my foot, my heel at the moment being off the ground.
Something gave way midway down my foot. . .the 5th metatarsal was found fractured about 3/4 inch from its base.’’ Jones originally described the fracture of the metaphyseal diaphyseal junction without extension distal to the anterior metatarsal (4-5 intermetatarsal) junction. Currently, a Jones fracture is recognized as any fracture involving the fifth metatarsal metaphyseal-diaphyseal junction. This fracture often is confused with, although less commonly encountered than, its cohort, the avulsion of the tuberosity encountered more proximally. The significance of the true Jones fracture is that it can develop delayed or nonunion. Zelko et al.,99 Kavanaugh et al.,100 and DeLee101 have reported difficulty treating the fractures of this region in which diagnoses initially were missed or that, in reality, were stress fractures. Stewart102 originally introduced a classification to help clarify fractures in this region. Type I fractures are at the junction of the base and shaft of the metatarsal. Subgroups include noncomminuted (IA) and 109
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severely comminuted. If necessary, fixation can be applied as previously stated, or a spanning external fixator from distal calcaneus to proximal metatarsals may be used to distract the lateral column.
CHAPTER 5
Ankle and midfoot fractures and dislocations
Figure 5-25 (A) Weight-bearing anteroposterior radiograph, with comparison, of a high school quarterback with acute midfoot injury. (B) Close-up suggests unusual arrangement in the area of medial cuneiform. (C) Lateral radiograph demonstrates separation of dorsal and plantar halves of medial cuneiform. (D) Computed tomography confirms bipartite tarsal bone. (continued)
comminuted (IB) variants. Type II fractures involve only the styloid process. Again, these are subdivided into extra-articular (IIA) and intra-articular (IIB). Stewart established a treatment plan that is based on his classification system. Zelko et al.99 tried to define fractures on the basis of clinical history and initial radiographic findings. Group 1 patients reported an acute injury with no previous
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symptoms. Radiographs demonstrated what appeared to be acute fracture line and no evidence of any chronic change, defined as periosteal reaction or intramedullary sclerosis. Group 2 demonstrated an acute injury but also reported a prodrome of mild lateral foot pain. Radiographs in these patients evidenced a clear fracture pattern. However, there also was demonstration of some periosteal reaction. Group 3 patients were categorized
Fractures of the base of the fifth metatarsal
Figure 5-25 cont’d. (E and F) Open repair requires attention to both the separated bipartite cuneiform with removal of synchondrosis and closure of the intermetatarsal diastasis, as well.
Figure 5-26 (A through C) Radiographs of an 18-year-old female athlete with acute injury after awkward landing. Note the homolateral metatarsal displacement pattern and the cuboid compression injury.
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Ankle and midfoot fractures and dislocations
Figure 5-26 cont’d. (D and E) Open repair addresses the metatarsal displacement but also distracts the cuboid to buttress the lateral column of the foot.
as a reinjury after one or more previous injuries. Radiographs of these patients demonstrate lucent fracture line, periosteal reaction, and intramedullary sclerosis, and this group presented with chronic pain or multiple recurrent injuries with sclerotic margins bordering a lucent fracture line.
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DeLee and colleagues50,101have attempted to combine classifications and divides these into multiple fracture types. Type I fractures are those at the junction of the base of the shaft and the base and are subcategorized into Type A for nondisplaced and Type B for comminuted fractures in this area. Type II fractures occurred
Fractures of the base of the fifth metatarsal
current management protocols use some form of zone concept in classifying and reporting fractures. Therefore the bulk of the discussion regarding treatment will reflect this trend and be focused on management of fractures by type and location. An alternative classification system also exists that defines fractures on the basis of chronicity of symptoms, presence of stress fracture, and recurrence of injury.103 Again, these are poorly defined and not terribly useful from a management standpoint. Stress fractures involving the proximal shaft of the fifth metatarsal differ in their behavior and somewhat in their treatment, and therefore are not discussed in this section on acute injuries. The fifth metatarsal itself has been subdivided into main segments, including the head, neck, shaft, base, and tuberosity or styloid process. The metaphyseal portion of the bone tapers into a tubular diaphyseal segment. The size and the shape of this bone vary somewhat but typically demonstrate that a larger, wider, more triangular proximal portion becomes a fairly narrow tubular structure that has a slightly lateral curve as it traverses distally. The radius of curvature as the bone proceeds distally is highly variable and can lead to tremendous distortions in the shape and stress applied to the distal end of this structure.104 The proximal end of the fifth metatarsal not only articulates with the cuboid at the tarsometatarsal joint but also has an intermetatarsal articulation with the base of the fourth metatarsal. This is a true joint. The bases of the fourth and fifth metatarsals are bound closely to the cuboid by dense, ligamentous structures on every side. The stability of the tarsometatarsal complex is provided by capsular ligamentous structures, the dorsal and plantar cubometatarsal ligaments, the lateral band of the plantar aponeurosis, and the broad insertion of the peroneus brevis tendon (Fig. 5-28). It is believed that these capsular ligamentous structures contribute greatly to the genesis of a true Jones fracture45,100 because the proximal portion of the fifth metatarsal and its articulation
Figure 5-27 Fracture zone classification at the base of the fifth metatarsal. (From Lawrence SJ, Botte M: Foot Ankle 14:360, 1993.)
Figure 5-28 Anatomy of tendon attachments at the base of the fifth metatarsal. (From Lawrence SJ, Botte M: Foot Ankle 14:360, 1993.)
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again at the junction of the shaft and the base but carried clinical and radiographic evidence of prior injury. To fall into this category, patients had to report prior lateral foot pain and/or an established radiographic periosteal stress reaction or frank fracture line. Type III fractures included those of the styloid process or tuberosity and again were classified into subcategories A, nonarticular, and B, articular. The recommended current classification includes a combination of all the classifications discussed and divides the metatarsal injuries into classification that correlates to zones of vascular anatomy (Fig. 5-27). Currently, preferred classification uses three separate zones. Zone 1, or the most proximal zone, includes the cancellous fifth metatarsal, the so-called tuberosity fragment. It includes the insertion of the peroneus brevis tendon and calcaneometatarsal ligamentous branch of the plantar fascia. Fractures in this zone typically extend into the fifth metatarsal cuboid joint but may be extra-articular. Zone 2 injuries involve the metaphyseal-diaphyseal junction. This encompasses the articulation of the proximal fourth and fifth metatarsals. The ligaments holding the fourth and fifth metatarsals together proximally are secure both dorsally and plantarly and provide tremendous stability. Finally, zone 3 injuries are fractures of the fifth metatarsal shaft. This zone begins just distal to the fourth and fifth intermetatarsal ligaments and extends distally into the tubular portion of the diaphysis approximately 1.5 to 2.0 cm. Most
CHAPTER 5
Ankle and midfoot fractures and dislocations
with the cuboid is held fast while torsional forces produce stress that is relieved through the fracture line just distal to these structures, approximately 0.5 cm distal to the insertion of the peroneus brevis and just distal to the joint between the fifth and fourth metatarsals. The base of the fifth metatarsal proceeds laterally and inferiorly beneath the inferior edge of the cuboid on the lateral radiograph. There is a tremendous variability in size and shape of this prominence, accounting for its variable susceptibility to injury. The vascular anatomy in this region also is relatively important (Fig. 5-29). This has been thought to be a fairly tenuous vascular supply, particularly at the proximal diaphysis. The arterial plexus at this level has been well established by Shereff et al.105 and Smith et al.,106 demonstrating only a small nutrient vessel in the so-called watershed area. This is unique contradistinction to the fairly abundant blood supply more proximal to this watershed area. Direct and indirect mechanisms have been implicated in the genesis of the fifth metatarsal fracture.45 Certainly, the prominence of the tuberosity makes it particularly at risk to a more direct mechanism of injury when discussing this version of the fracture.104 Jones himself alluded to the indirect nature of injuries, describing a ‘‘cross-breaking strain directed anteriorly to the metatarsal base and caused by body pressure on an inverted foot while the heel is raised.’’98 Presumably, he is describing the commonly accepted foot in fixed equinus sustaining rotatory and/or tensile forces overcoming the thinning cortical bone in the proximal metaphyseal-diaphyseal junction. Fractures of the tuberosity occurring indirectly are more common because of the number of structures that attach to the prominence.104 These structures have been identified previously. The importance of the pull of the peroneus brevis has been emphasized in the creation of a separation stress that forces the proximal fragment of the metatarsal away from the shaft. Because of the strong peroneus brevis contraction in stance phase, the tendon already is contracted when an inversion stress is applied to a weight-bearing, plantarflexed foot. This tendon holds fast while the force causes the shaft to be pulled away from it. Avulsion of the base away from
Figure 5-29
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the shaft is the result.45 Kavanaugh et al.100 used highspeed cinematography and force platform analysis in an attempt to recreate the position of the foot at the time of the index injury. Conclusions of this study suggested either an axial or mediolateral force or a combination of these acting on the fixed base of the fifth metatarsal. This would bring the patient up on the metatarsal heads, concentrating the axial and mediolateral forces on the lateral metatarsal. It was postulated that failure to invert the foot would produce a tremendous axial and mediolateral ground force culminating in fracture. Other factors also have been implicated in the genesis of the injury here, including repetitive use, such as prolonged running or jumping activities; vascular contribution, particularly at the avascular or watershed zone; and certain morphologies of foot shape. Individuals with more cavus foot alignment have been shown to be more likely to develop this injury pattern because of the increased rigidity of the foot, as well as the propensity to have a stress transfer to the lateral foot.50,99-101,103,105-107 Individuals with planovalgus foot also have been suggested to be predisposed to this injury because of increased loads forced along the lateral border of the foot during the latter part of stance, phase, and gait. These relationships have not been demonstrated in any formal mechanical studies. Clinical diagnosis of the Jones fracture is dependent on making an appropriate diagnosis and localizing the specific type of injury with respect to zone as well as acuity. History may be vague, but typically involves an aching sensation on the lateral aspect of the foot related to some sort of push-off or inversion-type injury. Prodromal symptoms may be reported for up to several weeks before any evidence of the actual documented injury suggestive of a prefracture state or impending fracture.99,101,103 Physical examination findings are fairly reproducible and include an improved tenderness, specifically over the base of the fifth metatarsal. Ecchymosis and swelling are present to variable degrees and, again, depend on the acuity of the injury. There is typically an accentuation of pain by inversion of the foot. However, there is little motion at the fracture site, and therefore no crepitus or palpable mobility of the fracture site on manipulation.
Vascularity of the fifth metatarsal. (From Smith J, Arnoczky SP, Hersh A: Foot Ankle 13:144, 1992.)
Fractures of the base of the fifth metatarsal
oversized, yielding a tight fit. The postoperative protocol includes nonweight-bearing cast applied for 6 weeks, with gradual resumption of activities determined on the basis of pain tolerance after that. Percutaneous intramedullary screw fixation also has been described.50,54,101,108-120 This is performed through a small incision initially at the base of the fifth metatarsal between the peroneus brevis tendon and the lateral band of the plantar fascia. The interval is developed, and a guidewire for a cannulated screw is inserted under fluoroscopic guidance. The key point to remember about placement of the screw is that, on the basis of the anatomy, the wire should be initiated ‘‘high and inside.’’ Theis suggests that the guidepin should be started on the dorsal and medial aspect of the bone just inside and superior to the edge of the tuberosity. Once the guidepin is positioned appropriately and verified under fluoroscopic guidance, a canal is drilled and an appropriate length screw is placed. Choices for the size of the screw typically are based on the size of the bone, and it is well accepted that the largest screw that the canal can accommodate should be placed. One technique tip is to overdrill using the cannulated guidepin system and then to remove the guidepin and place a solid screw to provide greater tensile strength to the bone. It is crucial to avoid fracturing the metatarsal, and thus maintenance of the intramedullary position is of utmost importance. No cortex should be violated on passage of the screw. Postoperatively, the patient is placed in a splint for approximately 1 week, and a short-leg, nonweight-bearing cast is applied for an additional 2 to 3 weeks. At 3 weeks, stationary bicycling, swimming, and stair climbing are allowed in a protective boot, with weight bearing progressed as tolerated, depending on pain. Running is encouraged only when evidence of significant fracture healing is present radiographically, and typically this takes 5 to 7 weeks. Return to sports-specific activity is prohibited until the patient can run and cut painlessly. Caveats with respect to this procedure involve injury to the sural nerve, which is as close as 2 to 3 mm from the position of the screw head.109 Lastly, a combination of the previous two procedures mentioned has been applied.54 The technique for screw placement is as previously stated. However, this is done with a larger incision, and access is gained through the canal before placement of the screw. Bone graft should be placed dorsally, medially, and plantarly before insertion of the screw. Once bone graft is placed, the screw is inserted and the wound is closed. An alternative to this method is a so-called strain-relieving cancellous bone graft, which can be placed in similar fashion, but specifically in a dorsomedial trough spanning the fracture site. Once the screw has been placed, additional bone graft can be packed in and around the fracture site. Return to activity is similar to that as previously stated for screw fixation alone. 115
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Radiographs often will confirm the diagnosis, although in some instances some fractures may present as occult or incomplete. Careful radiographic assessment is important to determine the presence of a fracture line because this may be particularly subtle. If the diagnosis is in question, studies such as MRI or bone scintigraphy tend to be particularly helpful.45,102 Diagnosis of fractures can be especially confounding in the adolescent athlete because secondary centers of ossification at the base of the fifth metatarsal are present and sometimes are confused with acute fractures. The ossification center typically occurs between 8 and 12 years of age and usually is united by 12 years in girls and by 15 years in boys. A secondary ossification center occurs in approximately one-fourth of all children.104 Distinction between these secondary centers of ossification and acute fracture is relatively straightforward. Distinguishing characteristics include the orientation of the apophyseal line, which reproducibly traverses the tubercle parallel to the long axis of the shaft. Additionally, the apophysis occurs lateral to and does not extend into the tarsometatarsal joint.104 Ossification centers also tend to have smooth, regular edges, as opposed to a more irregular appearance of fracture. Two other ossicles often will occur in this region. The os peroneum is present in approximately 10% to 15% of all radiographs. The os vesalianum is variably present as well. Again, a smooth, sclerotic, appositional surface often is present and differentiates this from fracture. These ossicles, which are independent, sesamoidal-type bones, should be distinguished easily from acute fracture situations. Treatment is injury specific and fracture type dependent. Treatments vary and range from weight bearing in a protective shoe as soon as pain allows to various forms of open reduction and internal fixation and, sometimes, bone grafting. The literature is replete with information to support just about any stance one may want to take. It is crucial that a clear understanding of the injury pattern, the outcomes of nonoperative versus operative treatment, and the potential complications be understood by the surgeon before embarking on a treatment plan. Various forms of surgical treatment have been described and are addressed independently by procedure. First, the technique of medullary curettage and inlay bone grafting has been well established.103,107 The base of the fifth is approached via a curvilinear dorsolateral incision. The fracture site is exposed subperiosteally. A rectangular section of bone measuring 0.7 2.0 cm centered over the fracture is outlined by four drill holes and removed with a sharp osteotome. The medullary canal is curetted free of all sclerotic bone, and the continuity of this cavity is reestablished. The original description includes a tibial corticocancellous graft that is fashioned and replaced into the fracture defect. No fixation typically is applied because the graft often is slightly
CHAPTER 5
Ankle and midfoot fractures and dislocations
As previously stated, literature abounds regarding multiple forms of fractures. It is somewhat confusing because, in some of the earlier literature, either specific type of fracture is not specified or uniform treatment is applied to all fracture types. An attempt will be made to dissect the literature and apply it in a relatively simple yet appropriate fashion.50,54,99,103,107-122 Extra-articular tuberosity fractures typically require no more than supportive therapy and weight bearing as tolerated as soon as the patient is able to manage pain and swelling appropriately. Multiple forms of ‘‘benign neglect’’ have been described, including suggestions for compressive dressings, adhesive taping, supportive footwear with padding around the prominence, and even short-leg casting.45,102 There has been no consensus on the type of protective device necessary. However, it has been reported that even short-leg walking casts probably are overprotective in the management of this fracture.45,83 The pain usually has subsided significantly by the second week to allow reasonably functional walking and transition into a more sports-specific shoe and resumption of activity, again, as pain would allow. It also is important to note that radiographic union may not be present for a minimum of 4 to 6 weeks, and often longer. However, this should not preclude an athlete’s returning to sport should symptoms subside appropriately. It also has been suggested that, on occasion, the fracture will heal with fibrous union, and that typically this also is not symptomatic and, again, will allow the athlete to return to activity appropriately.123 Indications for surgery in this region are reserved for those patients that have either significantly displaced tuberosity fractures or intra-articular involvement with displacement.102,123 Open reduction need not require an intramedullary screw as previously described, but only a small interfragmentary screw. Recognition and treatment after delayed presentation may require that excision of the fragment be performed, as opposed to standard open reduction. My experience with this fracture, even with intra-articular, nondisplaced varieties, suggests that the nonoperative treatment is and continues to be the standard of care. However, if there is any question regarding management, a more aggressive approach should be instituted. Poor results with tuberosity fractures are largely anecdotal124,125 and may be a result of a painful fibrous union, because lack of bony consolidation can approach 19%.126 Other factors involved in poor outcomes would be articular incongruity or sural nerve entrapment in the fracture after healing ensues, necessitating surgical management. Treatment of the true acute Jones fracture has evolved. Initially, universal treatment was considered to be the application of short-leg walking cast.45,122 However, even in reports advocating this form of treatment, there were found to be nonunions occurring that required subsequent surgical treatment. Review
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116
of the literature demonstrates a rate of delayed union as high as 38% and a definite nonunion rate of 14% with nonoperative treatment of these fractures.127 It was additionally noted by Zelko et al. that, even after an extended period of nonweight-bearing, short-leg casting for a period of 10 to 12 weeks, refracture was possible, and surgical treatment would be indicated for these patients.99 Still, there exists a fairly large and reputable group of surgeons who suggest that only in circumstances in which previous conservative treatment has failed should surgical treatment be implemented. These authors suggest that fractures that occur with no intramedullary sclerosis or no prior attempts at treatment not only will heal, but will allow athletes to return to weight bearing within 6 weeks and to activity by 12 weeks122,128,129 (Fig. 5-30, A through D). In general, however, most authors agree that because of the potential for refracture, the cited delayed union rate, and the incapacitation required from nonweight bearing and immobilization as a result of casting, highperformance athletes and high-demand individuals be given the option for and be treated with some form surgical management.99,101,115 Paired comparisons of operative versus nonoperative treatments have been analyzed. Josefsson et al.113 described 63 patients in which one third of the patients were treated operatively and two thirds conservatively. Average follow-up was 5 years, and, on the basis of delayed union or refracture, in almost 25% of the nonsurgically treated patients subsequent surgical treatment was required. Late surgery was required in 12% of the acute fractures and 50% of chronic fractures. Clapper indirectly supported operative intervention, based on a review of 100 patients treated for acute Jones fractures with 8 weeks of nonweight-bearing casting. Results demonstrated only a 72% success rate with this form of treatment and average time to union of 21 weeks.121 On the basis of the historical literature and currently available techniques and prevailing opinions, a protocol has been established that is my preference for the approach to the fifth metatarsal-based fracture. This should be fractures of zone 1, acute fractures of the tuberosity portion that are nondisplaced, typically are treated with a removable boot, and typically require 6 to 8 weeks for full healing. Surgery virtually is never indicated in this type of patient unless a painful nonunion develops. Should the fracture be displaced or comminuted, the activity level of the patient must be assessed. In a younger, high-performance athlete, surgical management certainly is offered and may be helpful to reduce the risk of late complications and speed to recovery. In zone 2 injuries, the classic acute Jones-type fracture, completely nondisplaced fractures may be treated in a nonweight-bearing cast for 6 to 8 weeks in a moderate-demand to low-demand type of patient. High-
Fractures of the base of the fifth metatarsal
Figure 5-30 (A and B) Acute fifth metatarsal or ‘‘Jones fracture.’’ (C and D) The patient elected for conservative treatment and healed uneventfully after 6 weeks of nonweight-bearing casting.
bone grafting or possibly even a minifragment plate and screw fixation. A zone 3 injury, a true shaft fracture, usually involves a distraction-type force and typically behaves differently from a Jones fracture. These injuries often will present in a delayed fashion and may in fact even be stress fractures. An acute fracture in this region typically will heal with a nonweight-bearing cast in a lower-demand 117
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performance athletes should be offered intramedullary percutaneous screw fixation in a technique as previously described (Fig. 5-31, A and B). Displaced fractures as a result of higher-energy trauma actually may require a true open reduction. Fixation is performed in similar fashion as that described for nondisplaced fractures. An exception to this would be an excessively comminuted metaphyseal-diaphyseal junction, which might require
CHAPTER 5
Figure 5-31
Ankle and midfoot fractures and dislocations
(A and B) Percutaneous fracture reduction and treatment with intramedullary screw fixation.
individual, but again, operative treatment as described for the Jones fracture should be offered to a highdemand or high-performance athlete. In a more delayed or recurrent injury at this level with prodromal symptoms, these patients should be treated with surgical management with intramedullary screw, with or without application of bone graft. Frank nonunions and chronic injuries should be treated with internal fixation and bone grafting. My preference here is for the large intramedullary screw fixation and concomitant bone grafting as described.
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CHAPTER 5
Ankle and midfoot fractures and dislocations
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........................................... C H A P T E R 6 Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes Vincent James Sammarco and G. James Sammarco CHAPTER CONTENTS ...................... Introduction
121
Tibialis anterior
126
Flexor hallucis longus
121
Peroneal tendons
131
Flexor digitorum longus
126
References
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INTRODUCTION The extrinsic muscles of the anterior, lateral, and deep posterior compartments of the leg play an important part in both static and dynamic body support. Actions of these muscles serve to stabilize the body during stance, as well as provide power and stability during all lower-extremity motion. They are of particular importance because they provide balance and power during push-off, as well as decelerating the body while stopping, turning, and cutting. They also stabilize the foot on both even and uneven surfaces. The muscles of the anterior compartment, the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius, are important because of their location, functioning to dorsiflex the ankle and toes and to control the forefoot during the swing phase of gait. Injuries to nerve, muscle, or tendon may lead to pain, weakness, and dropfoot. Muscles of the lateral compartment include the peroneus longus, an important lateral foot stabilizer that also controls pressure beneath the first metatarsal head, which is so important in jumping activities, cutting, and turning as in skiing. The peroneus brevis is the strongest abductor of the foot, and both peroneal muscles act as accessory flexors of the ankle and foot. Muscles of the deep posterior compartment of the leg, the posterior tibialis, flexor digitorum longus, and flexor hallucis longus, likewise serve important functions by stabilizing the longitudinal arch of the foot. They also provide additional power during running, cutting, turning, and stopping. The flexor digitorum longus and flexor hallucis longus are of particular
importance because of their attachments to other muscles and tendons within the foot itself. Injury to these muscles and tendons, whether partial or complete, can compromise a sports career. This is particularly true with respect to the flexor hallucis longus in the classical ballet dancer. Injury to the nerves that innervate the deep flexors of the leg result in weak push-off and decreased stability. This chapter deals with injuries to muscles and tendons in the anterior compartment, the tibialis anterior, extensor hallucis, and extensor digitorum longus, as well as those in the lateral compartment, the peroneus brevis, and peroneus longus, and the deep posterior compartment, the flexor hallucis longus and flexor digitorum longus. Conditions of the tibialis posterior and Achilles tendons are presented elsewhere. Early diagnosis is emphasized. Special diagnostic studies, including magnetic resonance imaging (MRI) computed tomography (CT), and electrodiagnostic testing, are useful, special diagnostic studies that help to confirm a diagnosis. Surgical intervention often is necessary to correct these problems, and rehabilitation ultimately is required to return the athlete to preinjury status.
FLEXOR HALLUCIS LONGUS The flexor hallucis longus muscle arises in the deep posterior compartment of the calf. From its attachment on the interosseus membrane, lower two thirds of the fibula and intermuscular septa, it passes from the deep compartment into its own tunnel at the posterior aspect of the talus, lateral to the flexor digitorum longus tendon
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Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes
and deep to the posterior tibial artery and nerve. It then passes beneath the sustentaculum tali of the calcaneus in a fibro-osseous tunnel from the posterior talus to the master knot of Henry, where it lies beneath the flexor digitorum longus tendon. Here it gives a slip of tendon that inserts on the medial fibers of the flexor digitorum longus tendon. It then passes beneath the first metatarsal between the sesamoids to insert onto the distal phalanx of the hallux. A sesamoid may be present within the tendon at the metatarsophalangeal joint. Like all polyarthrodial muscles, the extrinsic muscles of the foot in the anterior, lateral, and posterior compartments of the leg have a complex function. The flexor hallucis longus muscle functions as a flexor of the distal and proximal phalanges of the hallux; aids in flexion of the midtarsal joints and supination of the foot, as well as plantarflexion of the ankle; and also supports the longitudinal arch during ambulation, particularly in the latter part of the stance phase of gait.
Tendinitis Acute tendinitis occurs most commonly at the posterior ankle.1 This injury is common in dancers and has been termed ‘‘dancer’s tendinitis.’’2-4 It is less common than Achilles tendinitis and occurs in inexperienced dancers and in athletes who are not conditioned. Tendinitis also develops when athletes change sports without proper conditioning for the new activity. Symptoms begin within a few days following a change of technique or at the beginning of the season. When the dancer rises on the ball of the foot, pain occurs in the posterior aspect of the ankle. The pain initially is vague and occurs with flexion of the ankle and foot. Passive dorsiflexion of the ankle with deep palpation 1 cm anterior and medial to the Achilles tendon at the ankle joint elicits tenderness and crepitus.2 Radiographs exclude bony abnormalities such as os trigonum and posterior talar fracture. Treatment includes improving dance technique or reducing running in the athlete. Noninflammatory medication is prescribed, and a program of flexibility and power-building exercises is instituted. Chronic tendinitis produces symptoms of tenderness in the same region with active flexion and also on deep palpation of the tendon during flexion and extension.5 Crepitus is present over the tendon. Radiographs differentiate this from os trigonum syndrome and arthritis of the subtalar joint. Symptoms of os trigonum syndrome include pain in the posterior ankle when the patient actively rises on the ball of the foot. The provocative test is reproduction of pain with passive forced plantarflexion of the foot and ankle. The differential diagnosis includes pseudocyst of the flexor hallucis longus tendon, symptomatic subtalar cyst, posterior impingement syndrome, and insertional Achilles tendinitis.
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MRI helps to rule out a mass but may show a ‘‘dumbbell’’-shaped configuration of fluid in the tendon sheath around the ankle, narrowing beneath the sustentaculum and enlarged distal to the sustentaculum tali (Fig. 6-1). In the well-conditioned athlete, the muscles of the calf are hypertrophied. Because of the low insertion of the fibers of the flexor hallucis longus muscle onto its tendon, dorsiflexion of the ankle draws the enlarged lower muscle fibers into the fibro-osseous tunnel through which the tendon passes behind the ankle. This causes inflammation at the musculotendinous junction, the stopper bottle sign, and symptoms of posterior ankle pain. Treatment includes anti-inflammatory medication and a flexibility program including gentle stretching.6 If symptoms do not abate, surgical intervention with release of the pulley and tenosynovectomy may be necessary. In cases in which significant hypertrophy of the muscle is present, a myoplasty, excision of impinging muscle fibers, may be necessary. The tendon is debrided, and fibrosed muscle fibers that attach on the tendon just above the pulley also are excised to permit smooth passage of the tendon in the tunnel throughout its full excursion. Other areas of chronic tenosynovitis of the tendon include the midfoot and metatarsophalangeal joint.7 Symptoms of pain with tenderness usually occur in the specific area of stenosis. To relieve symptoms, the pulleys
Figure 6-1 Magnetic resonance imaging (T2-weighted sagittal cut) of a patient with symptomatic tendinitis of the flexor hallucis longus tendon. There is significant swelling of the tendon sheath (arrows) starting at the musculotendinous junction above the ankle joint, narrowing as the tendon sheath is compressed beneath the sustentaculum, and then ballooning out again as the tendon passes into the midfoot, ‘‘dumbbell sign.’’
Flexor hallucis longus
in either of these areas are released surgically, and a tenosynovectomy is performed. Injections of corticosteroids should be avoided because inadvertent injection directly into the tendon may cause it to rupture.2
4 PEARL Flexor Hallucis Longus Tendinitis (1) Crepitus on deep palpation of the tendon behind the medial malleolus during active plantarflexion and dorsiflexion of the ankle and foot. (2) Pain posterior to the ankle when rising on toes or on dorsiflexion of the ankle against resistance. (3) No pain with passive plantarflexion of the ankle.
Trigger toe Partial rupture of the flexor hallucis longus tendon consists of a longitudinal tear in the tendon and a fusiform thickening at the distal end of the tendon tear beneath the sustentaculum tali.4,8,9 Occasionally the tendon may be trapped in a fracture.10-12 When the nodule on the tendon lies distal to the sustentaculum, the narrow tunnel through which the tendon passes restricts motion in a manner similar to that of the flexor pulley of trigger finger. The result is triggering of the great toe. The condition occurs commonly in ballet dancers and is more common in females in their second to fourth decades. As the dancer begins to rise (releve´) on the ball of the foot (demipointe), the great toe dorsiflexes and remains in contact with the floor (Fig. 6-2: photos of toe flexed and extended). The flexor hallucis longus contracts, but the
tendon excursion is limited by the nodule’s position at the distal end of the tarsal canal. Once the dancer has achieved demi-pointe, pain may occur in the posterior ankle. As the dancer further rises onto her toes (sur les pointes), the great toe plantarflexes from 90 degrees dorsiflexion to neutral position to support the body. The pull of the flexor hallucis longus muscle is strong enough to force the nodule proximally through the stenotic tunnel, triggering the great toe into flexion. While the dancer is en pointe, the nodule lies proximal to the tunnel. As the dancer returns from pointe to flat foot, the tendon is passively pulled distal, and the fuseform thickening in the tendon snaps forward distally through the stenotic tunnel again. As the great toe snaps straight, it produces pain and may alter the dancer’s appearance in the dance step. The longitudinal tendon tear usually is single, but it may be multiple, and measures from 3 to 5 cm in length. Radiographs exclude bony abnormalities. MRI reveals a tear with degeneration of the tendon. A pseudocyst of the tendon may be present.13 The differential diagnosis includes a posterior impingement syndrome of the ankle, os trigonum syndrome, retrocalcaneal bursitis, and Achilles tendinitis. Conservative therapy consisting of gentle stretching exercises, and antiinflammatory medication to reduce swelling may be effective. Patients with compromised performance who fail to respond to conservative measures are surgical candidates. Surgical approach consists of a 5-cm incision on the posteromedial aspect of the ankle. The posterior tibial neurovascular structures are retracted medially. The tendon is delivered through the wound with a tendon hook, and the pulley is released at its lateral attachment to the talus and calcaneus distally. The nodular swelling
Figure 6-2 Left and right, Clinical appearance of the trigger toe sign. Left, With ankle and foot actively flexed, the interphalangeal joint of the hallux snaps into flexion. Right, When the ankle and foot are actively extended, the interphalangeal joint of the Hallux remains locked in flexion (left) or snaps straight.
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Figure 6-3 Left, Operative photograph of a ballet dancer with trigger toe. The flexor hallucis longus tendon is exposed and delivered into the wound. A longitudinal tear is visible distally (at the right). The thickening of the tendon seen in the region of the tear is causing triggering as the ankle and foot are flexed and extended. Right, The tendon is repaired using a 4-0 nonabsorbable Dacron running suture.
present at the distal end of the tear is trimmed to conform to the uniform diameter of the tendon throughout its length (Fig. 6-3). The tear is repaired with a running 4-0 braided nonabsorbable suture. The tendon must be trimmed to slide easily in the canal throughout full flexion and extension. Following closure, a splint is applied until two weeks postoperatively. A gentle active range of motion (ROM) program is begun 3 weeks following surgery. The foot and ankle are protected for 3 additional weeks in a splint, and the patient then is transitioned to an ankle stirrup brace. Dancing en pointe may take up to 4 months, whereas return to full athletic routine usually occurs by 3 months. Full recovery may take 6 months.
4 PEARL Trigger Toe (1) A snap noted on palpation of the tendon behind the medial malleolus with active flexion, and extension of the ankle and hallux with patient in sitting position. (2) Toe snaps backward and forward with flexion and extension of the ankle and hallux. (3) Dancer complains of pain in the posterior ankle region and a snapping sensation of the great toe when rising up (releve ´) or landing from a leap. (4) Occurs most commonly in female, classical ballet dancers who dance on their pointes.
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C A S E S T U D Y 1
A 28-year-old, female, classical ballet dancer noticed increasing pain in her posterior ankle following dance class for 2 months. She then developed a snapping of her great toe when rising from the demi-pointe position (on the ball of the foot) to en pointe position (on her toes). A triggering sensation was felt behind the ankle. When descending from en pointe position to a flat foot, the great toe snapped again as the toe dorsiflexed. Pain was felt behind the ankle. The snapping of the foot was visible and became unaesthetic as well as disabling. Physical examination revealed a palpable popping sensation felt posteriorly at the ankle as the foot, ankle, and great toe were moved repeatedly from dorsiflexion to plantarflexion. At surgery, a 5-cm incision was made at the posteromedial aspect of the ankle, and the flexor hallucis longus muscle and tendon were identified. Traction with a tendon hook revealed a 5-cm longitudinal tear in the tendon beginning at the musculotendinous junction and extending distally (see Fig. 6-3, A and B). The fibro-osseous canal through which the tendon passed was noted to be tight. A fusiform thickening of the tendon was present at the distal end of the tear. The thickened tendon was trimmed sharply so that the width of the tendon was uniform throughout, and the tendon sheath was carefully released, allowing the tendon to slide its length unimpeded through a full ROM of the ankle and foot. The
Flexor hallucis longus
Complete rupture Complete rupture of the flexor hallucis longus is uncommon but can occur in several areas. Iatrogenic surgical laceration has been described.14 Avulsion fracture from the hallux distal phalanx is caused by great resistance to flexion on the distal phalanx as the foot is forcibly plantarflexed. If the avulsed tendon contains a fragment of bone, anatomic open reduction is recommended. Tear of the tendon at its insertion without a bony fragment permits the tendon to retract proximally, allowing the great toe to dorsiflex. Surgical repair is performed through a medial incision along the proximal phalanx of the hallux above the neurocirculatory bundle. The tendon sheath is exposed at or just proximal to the metatarsophalangeal joint with a direct repair of the tendon to the distal phalanx. Tendon rupture also can result following corticosteroid injection into the tendon at the metatarsophalangeal joint (Fig. 6-4). Symptoms include pain, sudden loss of active flexion at the interphalangeal joint, and weakness in flexion at the metatarsophalangeal joint. This is accompanied by a dramatic change in athletic performance. Chronic, complete, spontaneous rupture
Figure 6-4 An operative photograph taken through a medial incision at the level of the metatarsophalangeal joint. The two ends of the ruptured flexor hallucis longus tendon are visible held by two Adson forceps. The athlete received several injections of corticosteroids beneath the first metatarsal head for ‘‘metatarsalgia.’’ Following debridement the tendon was reconstructed using a plantaris tendon graft.
also has been reported in basketball players and aerobic walkers at the sustentaculum tali. Symptoms occur over a 6-week period. Treatment in the high-performance athlete consists of surgical repair. If the tendon has retracted proximally and cannot be reapproximated, a tendon graft using plantaris tendon may be necessary to reestablish continuity. Reconstruction returns strength to flexion of the metatarsophalangeal joint, although a flexion lag at the interphalangeal joint commonly results.2,4 Complete rupture of the flexor hallucis longus tendon within the tarsal tunnel and beneath the sustentaculum tali may be treated by transfer of the flexor digitorum longus to the stump of the flexor hallucis longus.15,16 Resection of the degenerated portion of the flexor hallucis longus tendon also is performed. The flexor digitorum longus tendon lies adjacent to the flexor hallucis longus beneath the sustentaculum tali. Suturing of the flexor hallucis longus tendon stump to the flexor digitorum longus tendon proximal to the master knot of Henry permits good function, if not complete return of strength. An alternative method of treatment for complete rupture is to use a tendon graft. The graft is sutured proximally and distally following resection of the diseased portion of the flexor hallucis longus tendon. The foot and ankle are immobilized for 6 weeks.17 Both methods provide good function of the flexor hallucis longus but do not necessarily return normal flexion to the hallux interphalangeal joint. In some patients with low demands on the foot, complaints of a hyperextended distal phalanx rubbing on top of the shoe persist. Arthrodesis of the hallux interphalangeal joint in 20 degrees of flexion provides relief of symptoms without altering performance.
Tumor masses The most common mass of the flexor hallucis longus tendon is a pseudocyst located at the posterior ankle. It may extend distally into the foot along the tendon sheath and is associated with degeneration or tears of the tendon. Symptoms of fullness and achiness along with decreased performance are common. Symptoms of tarsal tunnel syndrome also have been reported. An MRI reveals a cystic mass, often bilobed, with one end at the posterior ankle and the other end distal to the tarsal tunnel in the midfoot (Fig. 6-1). If symptoms warrant, excision of the cyst and tenosynovectomy are performed through a posteromedial ankle incision. Associated tendon tears are repaired as described previously. Postoperatively, the ankle is protected in a splint for 3 weeks, followed by initiation of a flexibility and power-building program. Return to play is permitted when postoperative pain subsides and foot function approaches the level of the normal, contralateral side. 125
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tear was repaired with 4-0 braided Ethibond suture. A splint was applied for 3 weeks, followed by gentle active ROM and a supervised physical therapy program. Three months later, the dancer was able to resume dance. She returned to dancing sur les pointes 4 months after surgery. Six months following surgery, she was asymptomatic.
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FLEXOR DIGITORUM LONGUS Isolated injury to the flexor digitorum longus tendon is uncommon. This muscle takes origin deep in the posterior calf on the tibia and distal one-third of the fibula and passes medial to the flexor hallucis longus tendon posterior to the ankle in its own tunnel. It lies close to the tibialis posterior tendon at the sustentaculum tali, then crosses superficially to the flexor hallucis longus at the master knot of Henry distally. The tendon receives the insertion of the quadratus plantae muscle as it divides into four slips, one to each of the toes. A slip of the flexor hallucis longus tendon also inserts on its medial fibers. Each of the four lumbricals originates on the individual tendon slips. The lumbricals pass forward to insert on the extensor hoods of their respective toes. The tendon then passes through the distal split in the flexor digitorum brevis of each of the toes to insert on its respective distal phalanx. This muscle functions primarily to flex the toes. Accessory functions include foot and ankle flexion, as well as a stabilization of the foot during the stance phase of gait.
Tendinitis Tendinitis often is associated with tendinitis of associated flexor tendons, including the flexor hallucis longus and posterior tibialis. Isolated lesions of the tendon are rare and are associated with penetrating injuries, most commonly in the forefoot. Generalized disease such as gout can result in tophus deposition within the tendon at the ankle. Small longitudinal rents have been noted. Symptoms consist of tenderness deep beneath the medial malleolus of the ankle in the region of the sustentaculum tali. An MRI reveals fluid in the sheath about the tendon. Treatment primarily is nonoperative and consists of anti-inflammatory medication and stretching exercises. In recalcitrant cases that compromise athletic performance, surgical debridement and repair are recommended.
TIBIALIS ANTERIOR Anatomy The tibialis anterior muscle lies in the anterior compartment of the leg and originates from the proximal lateral tibial metaphysis and proximal two thirds of the tibial shaft and interosseous membrane. The tendon twists and crosses the extensor hallucis longus tendon at the level of the ankle at which it enters a synovial tendon sheath. The tendon courses dorsomedially across the foot and rotates 90 degrees from the myotendinous junction to the broad insertion.18 The majority of tendons insert at the plantar medial border of the
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first metatarsal and medial cuneiform. Approximately 10% of tendons have variations to the insertion, the most common being a bifid insertion to the cuneiform and first metatarsal, or insertions reaching proximally or distally along the medial column of the foot.19,20 Accessory tibialis anterior tendons have been reported, but are rare and have not been reported to cause pathology. The tibialis anterior is bounded proximally to the ankle by the superior extensor retinaculum, and variably may enter a synovial tendon sheath within the retinacular fibers at this level. More distally, the tibialis anterior tendon predictably enters a synovial sheath as it passes into the inferior extensor retinaculum complex. An early study using a modified Spaltehoz technique failed to reveal any zones of hypovascularity within the tendon,21 but a later study using immunohistochemical methods suggests that such a zone exists within the inferior retinacular system where tendon rupture is most likely to occur.22,23 The tibialis anterior acts primarily in dorsiflexion of the ankle and also as a strong inverter of the subtalar joint. It is active during the first phase of gait and contracts eccentrically from heel strike to toe-off. Its primary function is to decelerate the foot during the initial plantarflexion that occurs immediately following heel strike, and to clear the foot during toe-off. Absence of this muscle in active individuals is poorly tolerated, causing a slapping of the foot during heel strike and a steppage gait, with difficulty clearing the foot during swing.
Tibialis anterior tendinitis Tendinitis of the tibialis anterior is an uncommon entity that may be caused by overuse of the tendon or poor conditioning. It is seen most commonly in runners and usually accompanies a rapid increase in mileage or change in training techniques. Both uphill and downhill running significantly increase demands on the tibialis anterior, as does the practice of running stairs. A tight gastrocsoleus muscle also contributes to increased strain in the myotendinous unit. Symptoms include anterior ankle pain with activity that often continues for a few hours after exercise. Other diagnoses that must be considered are exertional compartment syndrome, tibial stress fracture, intra-articular ankle pathology, and tibial periostitis. The diagnosis is readily appreciated on physical examination. Physical findings include pain with palpation of the tendon and pain with resisted dorsiflexion. The tendon may be tender, particularly as it passes under the superior extensor retinaculum. Palpable synovitis, swelling, and crepitance are variably present. In cases in which weakness in dorsiflexion is present, or when swelling and tenderness exist more distally within the
Tibialis anterior
inferior extensor retinaculum or at the tendon insertion, a more aggressive workup is required to rule out intrasubstance degeneration or impending rupture. In these instances, MRI or ultrasound are useful tools for evaluating tendon continuity and tendonosis24-26 (Fig. 6-5). In younger, athletic individuals, the area of inflammation usually involves the superior extensor retinaculum and responds well to conservative management. A three-phase rehabilitation protocol is used to resolve the tendinitis.6,27 Phase I involves limiting the extent of injury and diminishing inflammation. An oral antiinflammatory is initiated, and the area may be iced and wrapped with an ACE bandage to diminish pain and swelling. Immobilization is rarely indicated, but discontinuation of the exacerbating activity is required for 10 to 14 days. Phase II is started after pain and swelling have diminished and involves guided rehabilitation. Equinus contracture must be addressed with frequent stretching exercises. Resistive exercises with elastic tubing can isolate the tibialis anterior for pliability and strengthening. Therapeutic modalities also
can be helpful because of the subcutaneous positioning of the tendon. Phase III involves return to activity. Running should be initiated on a flat surface such as a track or treadmill, with gradual advance of mileage and hilly terrain as tolerated. We avoid the use of steroid injections around the tendon sheath because of the risk of rupture.28,29 Rarely, proximal degeneration of the tendon occurs that does not resolve with appropriate rehabilitation techniques. In these recalcitrant cases, surgical exploration and tenosynovectomy may be required to resolve symptoms. Pain and swelling of the tendon at or near its insertion represents a different disease process and may represent significant degeneration and impending rupture, as discussed in the next section.
4 PEARL Tibialis Anterior Tendinitis Tenderness and often crepitus on palpation over the tendon at the superior extensor retinaculum, a ‘‘leather bottle sign.’’
Figure 6-5 Magnetic resonance imaging demonstrating distal avulsion of tibialis anterior tendon. (A) The tendon usually retracts proximally to the level of the inferior extensor retinaculum. (B) Axial cuts demonstrate intrasubstance degeneration of the tendon.
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Tibialis anterior rupture and laceration The tibialis anterior tendon is vulnerable to laceration because of its subcutaneous position over the anterior aspect of the foot and ankle.30 The tendon may be cut in a ‘‘boot top’’ laceration when a sharp object such as a skate, ski edge, or sharp cleat cuts the skin and underlying structures.31,32 Dropping a sharp object onto the dorsum of the foot also can result in laceration. A high index of suspicion is required to make the diagnosis because these lacerations typically look benign, with minimal bleeding or pain. Dorsiflexion of the ankle will be weakened and lack full extension but will be intact because of the secondary action of the extensor hallucis longus (EHL) and extensor digitorum longus (EDL). Routine exploration of all dorsal foot and ankle lacerations should be performed if there is suspicion of partial or complete tendon laceration. These structures heal well and have minimal dysfunction when repaired acutely. Traumatic rupture may occur because of higher energy blunt trauma and is associated with anterior compartment syndrome.33-38 Spontaneous rupture of the tendon at or near its insertion is the more common presentation of tibialis anterior deficiency. It typically occurs in middle-aged athletes and often accompanies other comorbid conditions, such as diabetes, inflammatory arthritis, gout, obesity, and steroid use.24,39-42 The tendon in this location may demonstrate a zone of relative hypovascularity near its insertion that may predispose it to tendinosis and rupture in this area. A prodrome of pain and swelling along the medial arch variably precedes rupture. Pain and tenderness at the insertion of the tibialis anterior tendon should be treated as an impending rupture. The patient is immobilized in an ROM boot unlocked in dorsiflexion but locked at 0 degrees of plantarflexion. This allows active tendon remodeling and motion while protecting the tendon from further degeneration. Physical therapy is initiated with the goals of decreasing inflammation and encouraging tendon remodeling through therapeutic exercises and modalities. The ROM boot is unlocked gradually to allow more plantarflexion as symptoms permit. The boot may be discontinued after 4 to 6 weeks. In recalcitrant cases or elderly individuals, a hinged ankle foot orthosis (AFO) with a plantarflexion stop may be necessary to control symptoms and prevent tendon rupture. Rupture of the tibialis anterior in the middle-aged athlete often is the result of a minor trauma. The mechanism of injury involves a strong contraction of the muscle with the ankle in plantarflexion. The rupture may be painless, but dysfunction is noted immediately by the patient, who develops a slapping gait and experiences tripping on his or her toes. Medical attention may not be sought for weeks, and the diagnosis often is missed at the initial evaluation.5,43 The
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diagnosis can mimic peroneal nerve or L5 nerve root dysfunction.40,44,45 Diagnosis may be made by physical examination and presents as the classic triad of ankle dorsiflexion by hyperextension of the toes, a slapping gait, and a mass over the anterior ankle (pseudotumor) (Fig. 6-6). Weakness in ankle dorsiflexion occurs because the tibialis anterior function is lost, but ankle dorsiflexion is still present because of the secondary function of the digital extensors. The patient complains of a slapping gait and has notable difficulty clearing his or her toes during swing phase. The mass over the anterior ankle, or pseudotumor, is the avulsed tibialis anterior tendon stump, which becomes entrapped at the inferior border of the superior extensor retinaculum. Repair may be performed early or late, but the results of surgery are better if repair is performed within the first 3 to 6 weeks. Nonoperative treatment is acceptable for elderly, inactive patients, but primary or delayed repair is preferred for active individuals regardless of age.46-49
4 PEARL Tibialis Anterior Rupture and Laceration The triad of (1) pseudotumor anterior to the ankle; (2) loss of normal anatomy of the tibialis anterior tendon at the medial aspect of the ankle and foot when compared with the contralateral normal side; and (3) the use of accessory dorsiflexors, extensor digitorum longus, and extensor hallucis longus, to dorsiflex in the ankle. A less consistent finding is a slapping gait on the affected side.
Surgical treatment of tibialis anterior tendon rupture In rupture of the tibialis anterior tendon, the ruptured tendon end often becomes caught at one of the extensor retinacular layers and easily may be palpated beneath the skin. The skin incision is made in line with the axis of the tendon from 1 to 2 cm proximal to the palpable tendon end and carried distally to the terminal insertion at the plantar medial aspect of the first tarsometatarsal joint (Fig. 6-7). Deeper dissection involves incision of the inferior extensor retinacular sheath for the tibialis anterior tendon, which usually is well defined. If the delay to surgery has been greater than 3 or 4 weeks, the tendon sheath will have filled with fibrous tissue, which must be excised sharply or removed with a small rongeur. In more acute cases, the sheath may be filled with fluid or hematoma. Atraumatic tendon rupture usually occurs by partial avulsion from the insertion and elongation of the degenerative tendon within the inferior extensor retinaculum. Twenty percent to 30% of the distal tendon stump may remain in continuity
Tibialis anterior
Figure 6-6 Physical findings with tibialis anterior avulsion. (A) Absence of the usually pronounced tibialis anterior tendon is appreciated with compared active dorsiflexion of both ankles. (B) The affected ankle demonstrates a pseudotumor, which represents the proximally migrated tendon stump at the level of the ankle. Ankle dorsiflexion is incomplete and weak and occurs by hyperextension of the hallux and lesser digits.
Figure 6-7 Surgical technique of repair of the tibialis anterior. (A) The tendon end usually can be teased distally without violating the inferior edge of the superior extensor retinaculum. Avoiding incision of the latter helps to prevent tendon adhesions and wound problems. (B) Once the tendon is pulled distally, it can be grasped with a Krackow-style suture and pulled to full excursion. Adhesions are disrupted to free the tendon by gently passing a freer around the tendon and muscle belly.
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Figure 6-7 cont’d. (C) Repair is accomplished by pulling the tendon distally to its insertion. One or two suture anchors usually are needed to secure the repair.
with the anatomic insertion and, if present, should be preserved for use in the repair. In exposing the proximal tendon stump, consideration should be given to the superior extensor retinaculum. When possible, the superior extensor retinaculum should be left intact during exposure of the tendon. The retinaculum at the level of the ankle often is thin, and repair can be difficult. Adhesions of the repaired tendon to the retinaculum are common and difficult to avoid because of the immobilization required in the postoperative protocol. In patients with comorbid conditions, the retinaculum may not be repairable, possibly leading to subcutaneous adhesions, bowstringing of the tendon, and wound healing problems. Often retraction of the tendon will stop at the inferior margin of the superior extensor retinaculum, either because the tendon end has formed a pseudotumor that becomes entrapped here or because some of the more proximally inserting fibers are still in continuity.
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If the tendon is at the inferior edge of the retinaculum or just under it, it can be grasped with an Alice clamp and teased distally, then secured with a Krackow-type, locking suture. Once the tendon has been secured, tension is applied, and a blunt elevator such as a small Cobb or Freer is passed proximally within the retinaculum and used to break up adhesions and gain excursion of the tendon. In delayed cases in which adequate tendon excursion cannot be gained by blunt dissection, or when more significant tendon retraction has occurred, the superior retinaculum must be divided for exposure. Once the tendon end has been recovered and adequate excursion obtained, the tendon end must be debulked of fibrous material and degenerative tendon. Dissection of the scarred end usually will reveal intact tendon fibrils mixed with degenerative tendon and a mass of scar tissue. Degenerative tendon and scar tissue must be excised before repair, but maximal length of the tendon must be maintained.
Peroneal tendons
PERONEAL TENDONS Anatomy The lateral or peroneal compartment of the leg houses the peroneus longus and brevis tendons. The peroneus
longus originates in the head of the fibula and the proximal two thirds of the shaft and interosseous membrane. The peroneus brevis originates more distally from the lateral shaft of the fibula and intermuscular septum. The superficial peroneal nerve innervates the lateral compartment, and its sensory branches exit the compartment proximal to the ankle and divide to become the medial and lateral dorsal cutaneus nerves of the foot. The peroneus longus and brevis become synovial tendons at the level of the ankle joint, with the longus becoming completely tendinous 2 to 3 cm proximal to the ankle and the brevis usually retaining some muscle fibers to the level of the ankle joint. Both tendons enter a series of fibro-osseous tunnels as they approach their insertion points. The retromalleolar tunnel is bounded anteriorly by the fibula, which usually has a natural concavity to hold the tendons, and posterolaterally by the superior peroneal retinaculum. The peroneus brevis sits anterior to the longus as the muscles enters the retromalleolar tunnel, and at this level is flat or cupped around the longus tendon. Both tendons course around the distal fibula, passing superficial to the calcaneofibular ligament, and enter separate tunnels along the anterior process of the calcaneus. These tunnels are parallel and divided by the peroneal tubercle, with the peroneus brevis passing dorsal to the tubercle and the longus tendon passing plantar to the tubercle. The peroneus brevis proceeds over the cuboid and then fans out to its broad insertion on the lateral styloid of the fifth metatarsal. The peroneus longus tendon continues plantarly and enters an osseous groove at the lateral cuboid, where it is redirected medially across the midfoot to its main insertion at the plantar lateral tubercle of the first metatarsal. Variable lesser insertions usually are present at the medial cuneiform, second metatarsal base, and fibrous septae of the medial interossei. An osseous (approximately 20%) or fibrocartilaginous sesamoid is present as the peroneus longus tendon changes directions at the cuboid laterally.20,51 Stenosing tenosynovitis can occur at any of the fibro-osseous tunnels in either or both tendons.52 Accessory muscles and tendons are common, particularly tendinous slips from the peroneus brevis to the fifth toe.20 Complete accessory muscles may originate from the distal fibula, the lateral calcaneus, or the peroneal muscles and tendons themselves.53,54 Welldeveloped accessory muscles can cause impingement, particularly if the muscle enters the fibro-osseous tunnel system distal to the fibula. The peroneus brevis tendon is the primary everter of the subtalar joint and acts to balance the forces of the foot against inversion during weight acceptance and to stabilize the subtalar joint during stance phase and push-off. The peroneus longus tendon acts to plantarflex the first metatarsal and aids in eversion of the subtalar joint. Loss of function of either of these 131
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Lacerated tendons may be sutured primarily if repaired within 2 or 3 days using a Krackow, Kessler, or Bunnell suturing method. In cases of delayed treatment, reattachment of the tendon to its anatomic insertion is ideal but not always possible. For cases in which the repair is under tension, we reconstruct the insertion of the tendon and augment fixation with one or more suture anchors. The distal tendon tract overlying the medial cuneiform is incised before repair, and a curette is used to roughen the underlying medial cuneiform to encourage attachment of the tendon. The tendon is pulled distally, using the previously applied suture, and is sewn to the distal tendon stump or attached to a suture anchor at the insertion. An anchor also is applied dorsally along the course of the tendon, usually in the medial cuneiform, and is used to suture the tendon tightly down to the curetted tendon tract. In cases in which repair is delayed more than 6 weeks, successful results can still be achieved but may require a free tendon graft, either as a reinforcement of the primary repair or as an intercalated graft if adequate length cannot be obtained.50 The extensor hallucis longus tendon also may be used as a transfer in chronic cases because it is easily accessible. After the tendon has been repaired or reconstructed, the overlying extensor retinaculum is repaired with absorbable suture. Meticulous repair of the retinaculum is important to prevent tendon adhesions, bowstringing or wound dehiscence. If 5 to 10 degrees of ankle dorsiflexion is not present with the patient under anesthetic, we perform a gastroc-soleus recession to lengthen the tendo-Achilles complex. Layered closure of the skin and subcutaneous tissue is performed, and the extremity is splinted in neutral dorsiflexion. This is changed to a shortleg walking cast at 10 days. Cast immobilization is discontinued at 3 to 4 weeks, depending on the quality of the tendon repair, at which time an ROM boot is applied. This device is left unlocked in dorsiflexion and locked to prevent plantarflexion beyond 0 degrees, thereby allowing active motion of the tendon during walking but protecting the repair. Physical therapy is initiated after casting is discontinued and begins with gentle, passive ankle dorsiflexion and plantarflexion. Active strengthening may be started at 6 weeks with elastic tubing. The ROM boot is discontinued at 6 to 8 weeks. Activities are progressed as tolerated.
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tendons may result in varus of the hindfoot because of loss of opposition to the posterior tibialis, and loss of the peroneus longus may cause cavus of the midfoot because of lack of opposition to the tibialis anterior and posterior.
Tendinitis Tendon injury occurs through one of three mechanisms. Direct injury occurs primarily with laceration. Indirect injury occurs when a musculotendinous unit is loaded beyond its ultimate strength and fails primarily. This occurs most often as an avulsion fracture at the tendon insertion or as a tear at the myotendinous junction. The peroneus longus tendon may avulse from its insertion at the base of the first metatarsal,55 or the os peroneum may fracture and be pulled proximally.56,57 Acute injuries usually are incomplete, but if the myotendinous unit loses continuity, prompt surgical repair is recommended. Tendon overuse and entrapment is seen more commonly. Repetitive microtrauma may lead to small tears of the collagen fibrils. Localized hemorrhage and infiltration of inflammatory cells result in pain and edema. If the condition becomes chronic, the paratenon and synovial lining will hypertrophy and scar. Hypertrophy of the synovium causes further entrapment of the tendon at the fibro-osseous tunnels, further impairing healing by compromising blood flow. As microtears develop in the tendon, the resultant load on the remaining intact fibrils increases, potentially causing further tears and elongation of the structure. Calcification of the peroneus longus tendon is associated with chronic tendinitis and may complicate treatment.58,59 Tendinitis of the peroneal tendons is encountered most commonly as an overuse phenomenon and typically responds well to conservative treatment.6 Lateral ankle pain after vigorous exercise is the usual presenting complaint and often occurs early in the athlete’s season or during a period of increased intensity in training. Downhill skiing, basketball, skating sports, ballet, running, and soccer are the sports at highest risk. Poorly fitting footwear, particularly ski boots and hockey skates, often is an inciting factor. Tendinitis may be present at the myotendinous junction or in the fibro-osseous tunnel system beginning at the distal fibula. Tendinitis in the synovial sheath may progress to the stenosing condition that often requires surgery. Pain proximal to the myotendinous junction that worsens with exercise may represent an exertional compartment syndrome or superficial peroneal nerve entrapment and warrants investigation.60-62 A stress fracture of the fibula, particularly in dancers, also may create pain at the distal one-third of the fibula and can be difficult to differentiate from tendinitis.
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Varus alignment of the hindfoot predisposes to both lateral ankle instability and peroneal tendon pathology.56,57,63-66 Initiation of a nonsteroidal anti-inflammatory drug (NSAID), a brief period of immobilization, and avoidance of exacerbating activities usually are effective in diminishing acute pain and inflammation. Cross training with swimming, biking, a cushioned treadmill, or other low-impact activities can be used to maintain aerobic conditioning. A stirrup ankle brace usually is effective in diminishing tendon demands and may diminish pain and inflammation, although if subluxation at the distal fibula is present, the pressure from the brace may worsen the symptoms. If boggy synovitis, crepitance, or significant weakness is present, a short period of immobilization in a ROM boot is indicated. Weight bearing is allowed as tolerated, and active ranges of motion exercises are initiated. Active eversion uses both the peroneus longus and brevis muscles. The muscles are isolated best when eversion exercises are performed in plantarflexion. Stretching of the peroneal tendons occurs as the ankle is brought into maximal inversion and dorsiflexion. Graduated peroneal strengthening and open-chain exercises are advanced as tolerated. Therapeutic ultrasound is helpful and may improve the quality of the tendon as it remodels. Cryotherapy, particularly ice massage, is effective for the peroneal tendons because of their subcutaneous position. Underlying hindfoot varus should be addressed with a laterally posted orthotic. Shoewear must be examined because the heel counter may impinge directly on the tendons, or a laterally worn running shoe may cause a slight varus thrust at heel strike. Chronic or recurrent tenosynovitis reflects a more difficult entity to treat. Once secondary changes in the tendon occur, surgery often is required to resolve symptoms. Attritional tears of the peroneus brevis tendon; stenosing tenosynovitis or peroneal entrapment; chronic or acute peroneal dislocation; accessory peroneal muscles; traumatic rupture; or posttraumatic sequelae represent the spectrum of entities that may require surgical intervention.
Peroneus brevis entrapment and attritional tendinitis The peroneus brevis tendon is subject to both tension and significant compression during standing and the weight-bearing portion of gait. As it passes around the distal fibula, it lies between the peroneus longus tendon and the fibula and takes on a flattened or semilunar shape. The tendon is tightly constrained at this level, and similarly as it passes superior to the lateral process of the calcaneus. Entrapment can occur because of synovial swelling with overuse or inflammatory conditions.
Peroneal tendons
It has been theorized that hypovascularity may occur in pathologic states and may be responsible for impaired tendon repair, although there does not appear to be a distinct hypovascular zone.67 Certain anatomic features, such as low-lying muscle fibers on the peroneus brevis, anomalous tendons or muscles, or bony irregularities can initiate and exacerbate entrapment. In an anatomic study, Sobel noted an 11.3% incidence of attritional tears of the peroneus brevis tendon in cadavers.68 Histologic examination of the attritional tears showed minimal inflammatory response, suggesting that these tears are mechanical in nature.69 The peroneus longus muscle acts as a wedge against the tendon, and even small tears are propagated proximally and distally as the ankle moves in dorsiflexion and plantarflexion.
Hypertrophy of the synovium may stretch the peroneal retinaculum, allowing subluxation over the lateral fibula, and this may initiate and propagate tears (Fig. 6-8). Complete rupture of the tendon is unusual in the athletic population but can occur, particularly in the middle-aged athlete. More distally, the peroneus brevis can become entrapped along the lateral border of the anterior process of the calcaneus. An accessory muscle can act as a space-occupying lesion in this area, causing entrapment. The peroneus brevis tendon passes superior to the peroneal tubercle, where it can become entrapped and undergo degeneration. A large, peroneal tubercle may predispose to entrapment at this level.70 As the tendon courses distally, anomalous slips of the tendon passing
Figure 6-8 Peroneal tendinitis with synovitis at the superior retinaculum. (A) Physical examination demonstrates tenderness and a boggy synovitis posterior to the fibula. (B) Surgical exploration shows the stretched tendon sheath. (C) Hypertrophied synovium requiring excision. (D) Attritional tears of the brevis tendon at the level of the fibula. Excision of the degenerative tendon and side-to-side repair is performed.
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Figure 6-9 Accessory peroneal tendons. (A) Most commonly, these exist as an accessory muscle that lies within the peroneal compartment. Mass effect can cause tendinitis and impingement as the tendons enter the superior peroneal retinaculum. (B) Distally, accessory tendon slips may branch from the brevis and extend to various insertions along the fifth metatarsal or toe. In this instance, a large accessory muscle was present beneath the inferior extensor retinaculum, causing pain and impingement.
distally to the fifth digit are common and can be a source of pain and entrapment, particularly if a muscle belly arises in this area (Fig. 6-9). Diagnosis can be determined on the basis of history and physical examination. Lateral ankle pain, weakness, and episodes of giving way are typical complaints. Pain, tenderness, and swelling posterior to the distal fibula or pain with palpation of the tendon during resisted eversion are diagnostic. Swelling and palpable synovitis of the sheath often are present once secondary changes begin to occur. Weakness and pain with resisted eversion are present. An MRI can be helpful in defining the extent of involvement and the presence of accessory muscles. We prefer not to inject corticosteroids into the tendon sheath because this may impair the recovery process and can lead to tendon rupture. Injection of local anesthetic into the peroneal tendon sheath has been described as a method of verifying the diagnosis, although communication of the tendon sheaths with the ankle or subtalar joint may make it less specific.71 Early in the disease course, oral anti-inflammatory medication, a short period of immobilization with a boot walker, or bracing with a stirrup ankle brace can help to diminish acute inflammation. Functional rehabilitation as outlined above should be initiated. Once secondary changes occur in the tendon, conservative treatment usually is ineffective. If symptoms are not controlled after 4 to 6 weeks, surgical exploration, debridement, and repair should be considered to prevent further progression and possible tendon rupture.
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4 PEARL Peroneus Brevis Tendon Tear (1) Tenderness over the peroneus brevis tendon behind and inferior to the lateral malleolus. (2) Pain in the same area on active flexion and abduction of the foot and ankle against resistance.
Peroneus longus entrapment and tendinitis The peroneus longus tendon also is subject to a combination of tensile and compressive forces as it enters the fibro-osseous tunnels of the ankle and foot. Like the peroneus brevis tendon, the peroneus longus can become entrapped as it enters the synovial sheath posterior to the fibula, although pathology of the peroneus brevis is much more common at this level. The tendon courses inferior to the peroneal tubercle and can develop stenosing tenosynovitis at this level, particularly in the presence of a large peroneal tubercle.56,70,72,73 The most common site of pathology in the peroneus longus tendon is at the osseous groove beneath the cuboid. It is here that the tendon sharply changes direction, resulting in a combination of tensile and compressive forces within the tendon fibers. A bony sesamoid or cartilaginous thickening is variably present at this level and often is the site of rupture in advanced cases.55,57,74 More distal avulsion from the medial cuneiform may occur, but this is rare because of the multiple attachments in the
Peroneal tendons
4 PEARL Peroneus Longus Tendinitis (1) Tenderness over the peroneus longus tendon at the inferior calcaneus laterally and distally and at the calcaneocuboid joint inferiorly. (2) Pain in the same area on active ankle flexion and with depression of the first metatarsal head.
4 PEARL Peroneus Longus Entrapment and Rupture (1) Tenderness over the peroneus longus tendon along the lateral distal calcaneus. (2) A mass may be present on the lateral calcaneus. Palpable os perineum noted on the lateral calcaneus with complete rupture and proximal migration of the sesamoid. Lateral x-ray of the foot reveals proximal migration of the os perineum (when ossified).
Surgical treatment of stenosing tenosynovitis, attritional tendinitis, rupture, and laceration In addressing pathology of the peroneal tendons, it is helpful to divide the course of the tendons into anatomic zones. Brandes and Smith divided the areas of pathology into three zones for the peroneus longus tendon, but this same system can be useful in evaluating the peroneus brevis tendon, as well56 (Fig. 6-10). Zone A includes the superior peroneal retinaculum and distal fibula. Zone B is the inferior peroneal retinaculum at the level of the peroneal tubercle of the calcaneus. Zone C is the cuboid notch where the peroneus longus turns and enters the osseous groove. We have added an additional zone D to this classification that involves avulsion of the tendons from their insertion at the respective metatarsal base. If the tendons are diffusely involved, the entire tendon sheath may need to be explored; however, if the pathology is limited to one or two zones, surgery often can be limited to the affected zone. Attritional tears of the peroneus brevis tendon are most commonly affected in zone A, although both tendons often have an associated hypertrophic synovitis. During exploration, it is important to evaluate the stability of the tendons, and, if instability is present, this should be addressed. Attritional tears of the brevis typically are longitudinal, and complete rupture is infrequent. After the retinaculum is incised, the tendons are inspected, and any redundant synovium is excised. If an accessory peroneal muscle or tendon is present, this also is excised. Degenerative and frayed tendon edges are debrided. If a thickening of the tendon is present, this represents an area of intrasubstance tendinopathy, and an incision is made in the tendon overlying the affected area in line with its fibers. Any central fibrosed or degenerative tendon is sharply excised, taking care not to transect the normal peripheral tendon fascicles. A side-to-side repair of the tear then is performed with 2-O nonabsorbable suture. Deepening of the fibular groove and repair of the superficial peroneal retinaculum should be performed if necessary, as discussed in the section on tendon dislocation. 135
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plantar midfoot. Rupture can occur as the result of a sudden inversion injury and usually occurs at the level of the cuboid.52,57,75-77 Fracture of the os peroneum also can occur and will result in proximal migration of part or all of the ossicle.78-82 Stenosing tendinitis occurs with chronic overuse in athletes. Calcification of the peroneus longus tendon and its synovium is associated with inflammatory arthropathy, and if present it warrants rheumatologic workup.58,59,83,84 Diagnosis of the condition is similar to peroneus brevis tendinitis. Pain, swelling, and tenderness along the course of the tendon and pain with resisted eversion are the hallmarks of diagnosis. Sammarco noted that 8 of 14 cases had no prodrome before peroneus longus rupture, whereas 6 of 14 patients had a prodrome of increasing pain and discomfort during activity.57 In this series, diagnosis was delayed more than 6 months in all cases but one. Brandes and Smith noted a cavovarus position of the foot in 82% of patients, although it is not clear whether this was secondary to chronic tendon insufficiency or the inciting event in tendonopathy.56 Plain x-rays of the foot may demonstrate a fractured os peroneus. If the tendon is no longer in continuity, the proximal fragment will migrate proximally and become entrapped just distal to the peroneal tubercle, where it can be palpated and is typically exquisitely tender. Unusually, the tendon will avulse from its insertion at the medial cuneiform and first metatarsal base and present with longitudinal arch pain with progressive cavus of the midfoot. Early MRI is useful in the diagnosis and may demonstrate attritional tears or complete rupture.85 Tendon rupture is poorly tolerated and results in muscular imbalance of the foot and development of pes cavovarus.56,86 Early repair results in better outcome; therefore a high index of suspicion is necessary, and early diagnostic studies are indicated. Fracture of the os peroneum with even a small separation of the fragments should be treated as a complete rupture and warrants exploration and repair. As noted previously, early tenosynovitis can be treated conservatively, but once attritional changes in the tendon occur, surgery often is necessary to alleviate symptoms and restore function.
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Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes
Figure 6-10 Zones of entrapment of the peroneal tendons. (A) Zones A, B, and C. (B) Zone D: Rarely, avulsion may occur at the insertion of the peroneus brevis at the base of the fifth metatarsal or the peroneus longus distal to the os peroneus. (A, modified and reprinted from Brandes CB, Smith RW: Foot Ankle Int 21:462, 2000.)
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Tendon pathology in zone B may involve both the longus and brevis tendons. The primary site of entrapment is the peroneal tubercle, where the inferior peroneal retinaculum attaches to the peroneal tubercle and divides the peroneal tendons into two separate tendon sheaths. The peroneus brevis tendon courses superior to the tubercle and the longus inferiorly. Entrapment of the longus or brevis tendons can result from a large or hypertrophic peroneal tubercle or, alternatively, from an accessory muscle or tendon (Fig. 6-11). Chronic tenosynovitis can result in fusiform swelling of the tendon that worsens the entrapment phenomenon and may result in longitudinal tears. The surgical incision for lesions isolated to zone B is directly over the peroneal tubercle, in line with the axis of the tendons. Care must be taken to identify and protect the sural nerve in this area, because it usually lies directly in the surgical field and may have branches that cross dorsally over the tendons. The tendon sheath must be incised in a way that it can be closed without tension over the tendons. The retinaculum is incised just inferior to the tubercle and split from proximal to distal over the peroneus longus tendon. The superior portion of the sheath then is elevated subperiosteally from its insertion on the lateral wall of the calcaneus and peroneal tubercle, and the central coalescence of fibers that insert on the tubercle then can be split to add length to the retinaculum (Fig. 6-12). The entire peroneal tubercle should be excised with an osteotome or chisel so that the area is flush with the lateral wall of the calcaneus.
Figure 6-11
Case Study: Entrapment of the peroneus longus (continued)
Peroneal tendons
Figure 6-11 cont’d. at the peroneal tubercle. A 13-year-old girl with pain over the lateral ankle and peroneal tubercle. (A) Anteroposterior ankle radiograph demonstrating enlarged peroneal tubercle. (B) Peroneal tubercle is best visualized with oblique foot film, which demonstrates the tubercle in profile. (C) Coronal magnetic resonance imaging demonstrates synovitis of peroneus longus and brevis and the large peroneal tubercle. (D) Operative findings: The peroneus longus tendon was subluxing over the enlarged tubercle. Excision of the tubercle, localized tenosynovectomy, and reconstruction of the inferior peroneal retinaculum resolved the patient’s symptoms.
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Inferior peroneal retinaculum
PB
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Peroneal Tubercle
3 1 PL
B
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C
Figure 6-12 Excision of the peroneal tubercle and reconstruction of the inferior peroneal retinaculum. (A) The peroneal tubercle lies between the peroneus brevis and longus tendons and can be a source of impingement. (1) The tubercle is approached through the longus sheath, inferior to the coalescence of fibers that insert onto the tubercle. (B) (2) The dorsal portion of the inferior retinaculum is elevated subperiosteally, exposing the peroneal process. (3) A sharp chisel is used to excise the process. (C) (4) The bony process is removed flush with the lateral wall of the calcaneus. (5) The retinaculum is carefully split with a sharp scalpel to add length, and (6) repaired with suture.
Peroneal tendons
The longus and brevis tendons are inspected for intrasubstance degeneration or gross attritional tears, debrided, and repaired side to side as described previously. Any anomalous muscles or tendons or hypertrophic synovium should be excised. The peroneal sheath then is closed, and the surgeon must make certain that there is adequate room for the tendons to glide. If not enough length has been gained during the approach for a loose closure of the retinaculum, a Z-lengthening of the inferior retinaculum can be performed. Zone C involves the peroneus longus tendon where it changes course abruptly to enter the osseous groove on the plantar surface of the cuboid. Tendon pathology at this level often presents as complete rupture of the peroneus longus tendon. Fracture of the os peroneus may be complete with retraction of the proximal fragment or incomplete with some separation of the fragments (Fig. 6-13). Complete or partial rupture of the tendon requires repair. An incision is made overlying the peroneus longus tendon, and dissection is carried distally, extending from the peroneal tubercle to the osseous groove of the cuboid. If the tendon is ruptured, the proximal end must be sought, and dissection proximal
to the fibula may be required. An os peroneum that has fractured or avulsed may require excision of the fragment, and direct repair of the tendon should be accomplished with at least a four-strand repair of 2-O nonabsorbable braided suture. If the fragments are large or the tendon has avulsed from the proximal pole, direct repair may be accomplished, retaining the os peroneum by freshening the osseous surface, drilling through the ossicle with a K-wire, and locking the suture into the adjacent tendon. Zone D injuries involve avulsion of the insertion of the tendon. Peroneus brevis tendon avulsion usually is traumatic and incomplete. Avulsion may accompany a fracture of the metaphyseal area of the fifth metatarsal and usually carries a small piece of bone. Most avulsions heal with a short period of immobilization and limited weight bearing. Chronic avulsions can be painful and may require surgical repair by fixation and bone grafting of the avulsed fragment or by excision of smaller fragments with direct repair to the metatarsal. Avulsion of the distal insertion of the peroneus longus tendon is rare because of its multipenate insertion. Clinical diagnosis is difficult, and early diagnosis is required if reattachment
Figure 6-13 (A) A fractured os peroneus following inversion injury in a 35-year-old man. This was treated with casting. (B) Repeat radiographs 2 weeks later revealed proximal migration of the fragment to the peroneal tubercle. Surgical repair was accomplished with good functional results.
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is to be successful. Surgical repair may be accomplished using medial and lateral incisions, avoiding incision of the plantar aspect of the foot. If diagnosis or treatment is delayed, transfer of the longus to the brevis at the lateral ankle is preferred over delayed reconstruction because the tendon tract will obliterate with fibrous tissue. Laceration of the peroneal tendons may occur in sport because of sharp penetration by cleats or skates or by direct injury from a fixed object, such as the metal supports of gymnastic equipment. Any laceration directly overlying the course of the tendons must be treated with a high index of suspicion because substitution by the uninvolved peroneal may mask injury. Surgical repair usually is successful with limited morbidity. Absence of either of the peroneals is poorly tolerated. Surgical repair is always indicated.30 Delayed diagnosis of rupture or laceration of the peroneal tendons presents a challenging problem. The resultant muscular imbalance may cause varying degrees of midfoot cavus and hindfoot varus deformity. Most neglected ruptures still can be repaired if they are treated within 4 to 6 months, although surgical results are not as good as those repaired primarily.57 Typically, the entire tendinous portion must be exposed laterally, and the lateral muscular compartment of the leg also must be entered so the muscular unit can be freed up. The proximal portion of the tendon is grasped with a running locked suture, and tension is pulled distally while a medium-sized Cobb or other blunt elevator is used to free the muscle belly from any surrounding adhesions. Approximately 3 to 4 cm of excursion is necessary for delayed repair to be successful. If the muscle is fibrosed and no meaningful excursion can be regained, transfer of the distal stump of the tendon to the uninvolved tendon should be performed. If good excursion can be obtained but primary repair of the tendon ends still cannot be accomplished, a bridging tendon graft can be harvested from the Achilles or the plantaris. Longer standing cases tend to develop inflexible deformity that may require calcaneal and metatarsal osteotomies or arthrodesis to achieve a plantigrade foot.64
Peroneal tendon dislocation Acute dislocation of the peroneal tendons is an uncommon injury that results from forceful contraction of the peroneal tendons with the ankle in a position of risk. The exact mechanism has not been demonstrated; however, it has been our experience that traumatic dislocation can accompany both eversion and inversion sprains. Fracture of the calcaneus also is associated with dislocation of the tendons. Dislocation occurs at the level of the fibula and is accompanied by avulsion of the superficial peroneal retinaculum; this in turn may avulse the distal lateral rim of the peroneal groove in the fibula. The anatomy of the distal fibula has been
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inferred to predispose some individuals to dislocation. Edwards described anatomic variations of the distal fibula in relation to the peroneal tendons (Fig. 6-14).87 In an anatomic study of 178 fibulas, 82% of specimens had a definite sulcus posteriorly, whereas 11% were flat and 7% were convex. At the posterolateral edge of the fibula, a bony or cartilaginous flange88 often is present that helps to contain the peroneal tendons. Absence of a lateral bony ridge was noted to be 30% in Edwards’ series. The presence of a distinct sulcus and lateral ridge give bony support to the peroneal tendons and is protective for dislocation. Absence of these anatomic features may predispose to acute dislocation and often accompanies chronic subluxation, which can lead to tendon degeneration.65,89-91 Classification of these injuries was first proposed by Eckert and Davis88 and modified by Oden.92 In Type 1, the osseous attachments of the retinaculum to the fibula are disrupted, whereas the attachment to the periosteal sleeve remains intact. The tendons dislocate to a subperiosteal location at the lateral fibula, and the periosteal sleeve remains intact with the superficial peroneal retinaculum. Type 2 represents a rupture of the retinaculum at the fibular insertion. Type 3 represents an avulsion fracture of the posterolateral fibula at the insertion of the retinaculum, and type 4 represents an avulsion of the retinaculum from the posterior origin at the Achilles fascia (Fig. 6-15). Diagnosis of acute peroneal tendon dislocation often is delayed because the tendons often spontaneously relocate following the injury. Pain and tenderness at the insertion of the peroneal retinaculum is the hallmark of the injury. Swelling and ecchymosis over the lateral fibula often is present. If the tendons remain dislocated, more commonly in type 3 and type 4 injuries, they can be palpated along the lateral edge of the fibula. Resisted eversion with the ankle in plantarflexion may cause the tendons to redislocate or sublux. Ankle radiographs may reveal an avulsion fracture in type 3 injuries but usually are not diagnostic.93 If the diagnosis is in question, CT or MRI can be helpful and may demonstrate dislocated tendons, avulsion of the retinaculum, or a fluid collection laterally over the fibula.73,94-96 Treatment is controversial. Some authors recommend treatment for 6 weeks in a short leg cast with the ankle in slight plantarflexion if the tendons are reducible and stable.88,92 Recurrent dislocation can be problematic with nonoperative treatment even if reduction is accomplished in a timely manner. Recurrent tendon instability following closed treatment of acute tendon dislocation may be as high as 50%.91,97-99 A high recurrence rate and the extended cast immobilization required for nonoperative treatment has led to the recommendation for surgical repair as the primary treatment recommendation in active and athletic
Peroneal tendons
Figure 6-14 Edward’s anatomic observations of the distal fibula. (A) In 82% there is a distinct concave groove for peroneal containment. (B) In 11% the posterior fibula is flat with no groove. (C) In 11% the posterior fibula is convex, which predisposes the tendons to subluxation and dislocation.
effective in the presence of gross instability, and surgical reconstruction should be considered in symptomatic individuals to prevent progressive degeneration of the tendons.52,89,90,99,102-106
4 PEARL Acute Peroneal Tendon Dislocation (1) Tenderness and swelling at the lateral malleolus with the tendons easily subluxing on flexion of the ankle with rotation of the foot internally and/or externally. (2) AP and oblique x-rays of the ankle may reveal a ‘‘flake’’ fracture at the lateral malleolus.
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individuals.52,97,99-102 Type III dislocations represent a disruption of the osseous fibular groove and are inherently unstable. These injuries are best treated surgically. In type IV dislocations, the peroneal retinaculum itself may become entrapped behind the tendons, preventing reduction and necessitating surgery.92 Chronic subluxation of the peroneal tendons is a common cause of lateral ankle pain and peroneal tendinitis. Recurrent sprains and chronic ankle instability are associated with chronic subluxation of the tendons because of progressive incompetence of the peroneal retinaculum.66 As discussed previously, some individuals without an adequate osseous groove at the posterior fibula are anatomically predisposed to tendon subluxation even without trauma. Conservative treatment is rarely
CHAPTER 6
Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes
Figure 6-15 Classification of peroneal tendon dislocation. I, Superior peroneal retinaculum remains in continuity with fibular periosteum. II, Avulsion of retinaculum from fibula. III, Avulsion fracture of distal fibula. IV, Avulsion of the retinaculum from posterior origin. Retinaculum becomes interposed between tendons and osseous groove in fibula.
4 PEARL Chronic Peroneal Tendon Dislocation (1) The tendons are palpable lateral or anterior to the lateral malleolus at the ankle. (2) Weakness is noted with gait and tenderness over the dislocated tendons.
Surgical management of peroneal tendon subluxation and dislocation The surgical approach to acute and chronic dislocation of the peroneal tendons is similar. The goals of surgery are to repair the injured structures, which may include tears of the peroneal tendons, avulsion of the retinaculum,
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142
and fracture of the fibula. It also is important to address any anatomic features that increase the risk of dislocation or subluxation. An incision is made posterior to the fibula directly over the peroneal tendon sheath and extends proximal to the tip of the fibula 4 or 5 cm. This approach lies distinctly between the sural nerve and superficial peroneal nerve. Care must be taken during the dissection to avoid aberrant branches that may lie in the field of dissection because injury to a branch may lead to painful neuroma formation. Inspection of the sheath at this point will determine the deeper approach. Incision of the retinaculum is dependent on the pathology at hand and is extremely important for successful reconstruction. For type 1 dislocations, in which the retinaculum remains in
Peroneal tendons
recovery, particularly if the ankle is immobilized for a significant period of time (>2 weeks). We prefer a modification of the method described by Zoellner and Clancy.107 The posterolateral edge of the fibula is incised with a sharp chisel or thin oscillating saw from the inferior tip of the fibula 3 or 4 cm proximally. The medial cortex is left intact, and the posterior fibular cortex, with its cartilaginous lining, is hinged open to expose the cancellous bone of the distal fibula. Three or 4 mm of the underlying cancellous bone are removed with a curette or burr, and the cortical flap in hinged back into place, then impacted into the defect with a bone tamp to create an osseous groove. This effectively deepens the groove and creates a lateral ridge of fibular cortex, preventing recurrence of the subluxation. The tendons are allowed to relocate, and the ankle and subtalar joints are brought through a full ROM. The tendons should remain reduced in all positions, even without repair of the superior peroneal retinaculum. The avulsed retinaculum then can be repaired directly to the lateral cortical ridge with nonabsorbable suture during closure. In acute dislocations, direct repair of the retinaculum is accomplished with multiple nonabsorbable sutures that are passed and tied directly through drill holes in the lateral fibula. If a large piece of bone is avulsed, this may be reduced and sutured into place or fixed with 3.0-mm compression screws. In type 4 dislocations, the tendons are reduced, and the posterior torn edge of the peroneal retinaculum must be sutured to its posterior insertion. Proximally, this is the deep posterior compartment fascia overlying the distal aponeurosis of the Achilles tendon, and distally the retinaculum is repaired to the periosteum of the lateral calcaneus.20 In chronic dislocations, the superficial peroneal retinaculum often is attenuated, if not entirely absent. This is particularly problematic when the dislocation was unrecognized following surgical treatment of severe ankle trauma or following closed or open treatment of calcaneus fracture. In these instances, secondary reconstruction can be accomplished with a tendon graft104,108-110 or in conjunction with reconstruction of the calcaneofibular ligament.102,107,111-113 If ankle instability is not an issue, the retinaculum can be reconstructed with a split graft from the peroneus brevis or Achilles tendon, or with an accessory tendon if one is present. A 5-cm slip of tendon is harvested as a free graft and sutured to the deep fascia overlying the Achilles complex. The graft then is attached to the fibula 3 cm proximal to the tip of the fibula either by suturing it to the periosteum of the fibula or attaching it directly to bone. The graft then is attached distally to the tip of the fibula in a similar fashion and sutured to the calcaneofibular ligament near its calcaneal insertion or attached directly to the calcaneus with a suture anchor. 143
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continuity with the periosteum, it is helpful to incise anterior to the fibular border and harvest 3 or 4 mm of periosteum in continuity with the retinacular sleeve. This will ensure that enough tissue is present for adequate repair of the retinaculum during closure. Chronic or congenital subluxation mimics the anatomy of a type 1 dislocation, in which the retinaculum is in continuity with avulsed periosteum, and incision of the retinaculum should similarly harvest a slip of contiguous periosteum for aid in later repair. In types 2 and 3 dislocations, the retinaculum is avulsed from the fibula, either with or without a small piece of bone. The tendons overlie the fibula in the subcutaneous tissue, and the peroneal retinaculum must be dissected posteriorly so that it can be repaired later. Large avulsion fractures should be left in continuity with the retinaculum and repaired directly to the fibula, whereas the typical small fleck fracture should be excised. It is important to recognize type 4 dislocations because the retinaculum should not be incised. The retinaculum is avulsed from the deep posterior tissues, and this torn edge must be identified with the anterior retinaculum left intact. In the type 4 dislocations, the avulsed retinaculum may lie within the peroneal groove posterior to the fibula holding the tendons displaced. Direct inspection of the tendons is performed after adequate exposure has been obtained. Traumatic dislocations are associated with tendon pathology infrequently, whereas chronic subluxation or acute or chronic dislocation often are associated with attritional tears of the peroneus brevis. Redundant synovium should be excised. Attritional tears are debrided and repaired side to side with 2–0 or 3–0 nonabsorbable suture. If the peroneus brevis muscle belly extends distal to the tip of the fibula, the muscle fibers should be excised to diminish impingement within the fibroosseous tunnel. Similarly, accessory muscles may cause impingement and lend to instability because of mass effect and should be excised. It is important to assess the anatomy of the distal fibula because a flat or convex fibula lends to instability of the tendons that must be addressed at the time of repair. Multiple procedures have been described to assess this problem.98,100 We have found that deepening of the fibular groove is highly effective in preventing recurrent subluxation or dislocation.52,89,107 The peroneal tendons are pulled anteriorly with a tendon hook, and the distal fibula inspected. A shallow or absent sulcus necessitates deepening of the groove. We do not recommend deepening the groove by burring or rasping a trough in the posterior aspect of the fibula because this removes the cortical bone and cartilaginous surface necessary for the smooth tendon glide. If the posterior surface is simply burred or rasped, adhesions between the tendon and rough cancellous surface may impede
CHAPTER 6
Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes
If lateral ankle instability is surgically addressed in conjunction with the repair, the retinaculum can be reconstructed successfully by passing the tendons deep to the calcaneofibular ligament during its reconstruction. Postoperatively, the patient is placed in a well-padded splint with the ankle in neutral dorsiflexion. The splint is discontinued at 8 to 10 days following suture removal, and the patient is allowed to bear weight in a ROM boot. Passive and active motion exercises of the ankle and subtalar joint are permitted in a controlled setting. Peroneal strengthening exercises with an elastic band can be initiated at 3 or 4 weeks, depending on the quality of the reconstruction. Weight-bearing, proprioceptive exercises are allowed after 5 to 6 weeks, and activities are advanced as tolerated.
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15. Krakow KA: Acute traumatic rupture of a flexor hallucis longus tendon: a case report, Clin Orthop 261, 1980. 16. Rasmussen RB, Thyssen EP: Rupture of the flexor hallucis longus tendon: a case report, Foot Ankle 10:288, 1990. 17. Stark HH, et al: Bridge flexor tendon grafts, Clin Orthop 242:51, 1989. 18. Fennell CW, Phillips P 3rd: Redefining the anatomy of the anterior tibialis tendon, Foot Ankle Int 15:396, 1994. 19. Luchansky E, Paz Z: Variations in the insertion of tibialis anterior muscle, Anat Anz 162:129, 1986. 20. Sarrafian SK: Anatomy of the foot and ankle: descriptive, topographic, functional, ed 2, Philadelphia, 1993, JB Lippincott. 21. Geppert MJ, Sobel M, Hannafin JA: Microvasculature of the tibialis anterior tendon, Foot Ankle 14:261–4, 1993. 22. Petersen W, Stein V, Bobka T: Structure of the human tibialis anterior tendon, J Anat 197(Pt 4):617, 2000. 23. Petersen W, Stein V, Tillmann B: Blood supply of the tibialis anterior tendon, Arch Orthop Trauma Surg 119:371, 1999. 24. Aydingoz U, Aydingoz O: Spontaneous rupture of the tibialis anterior tendon in a patient with psoriasis, Clin Imaging 26:209, 2002. 25. Bianchi S, et al: Evaluation of tibialis anterior tendon rupture by ultrasonography, J Clin Ultrasound 22:564, 1994. 26. Otte S, et al: Operative treatment in case of a closed rupture of the anterior tibial tendon, Arch Orthop Trauma Surg 122:188, 2002. 27. Sammarco V, Sammarco G: Principles and techniques in rehabilitation of the athlete’s foot: part I—introduction of concepts and Achilles tendon rehabilitation, Tech Foot Ankle Surg 2:50, 2003. 28. Richter R, Schlitt R: [Subcutaneous rupture of the tibialis anteriortendon. (Report of 3 cases) (author’s transl)], Z Orthop Ihre Grenzgeb 113:271, 1975. 29. Velan GJ, Hendel D: Degenerative tear of the tibialis anterior tendon after corticosteroid injection—augmentation with the extensor hallucis longus tendon, case report, Acta Orthop Scand 68:308, 1997. 30. Myerson MS, Sammarco VJ: Penetrating and lacerating injuries of the foot, Foot Ankle Clin 4:647, 1999. 31. Griffiths JC: Tendon injuries around the ankle, J Bone Joint Surg Br 47:686, 1965. 32. Stuart MJ: Traumatic disruption of the anterior tibial tendon while cross-country skiing. A case report, Clin Orthop 193, 1992. 33. Church JS, Radford WJ: Isolated compartment syndrome of the tibialis anterior muscle, Injury 32:170, 2001. 34. Din R, Therkilsden L: Rupture of tibialis anterior associated with a closed midshaft tibial fracture, J Accid Emerg Med 16:459, 1999. 35. Freundlich BD, Dashiff JE: Avulsion of tibialis anticus and peronei muscles resulting in acute anterior and lateral compartment syndrome, J Trauma 27:453, 1987. 36. Hovelius L, Palmgren H: Laceration of tibial tendons and vessels in ice hockey players. Three case histories of a skate boot top injury, Am J Sports Med 7:297, 1979. 37. Machani B, Narayan B, Casserly HB: Closed avulsion of the tibialis anterior: an unusual cause of compartment syndrome, Injury 31:738, 2000. 38. Simonet WT, Sim L: Boot-top tendon lacerations in ice hockey, J Trauma 38:30, 1995. 39. Bernstein RM: Spontaneous rupture of the tibialis anterior tendon, Am J Orthop 24:354, 1995. 40. Kashyap S, Prince R: Spontaneous rupture of the tibialis anterior tendon. A case report, Clin Orthop 159, 1987.
References 66. Sobel M, Geppert MJ, Warren RF: Chronic ankle instability as a cause of peroneal tendon injury, Clin Orthop 187, 1993. 67. Sobel M, et al: Microvascular anatomy of the peroneal tendons, Foot Ankle 13:469, 1992. 68. Sobel M, Bohne WH, Levy ME: Longitudinal attrition of the peroneus brevis tendon in the fibular groove: an anatomic study, Foot Ankle 11:124, 1990. 69. Sobel M, et al: Longitudinal splitting of the peroneus brevis tendon: an anatomic and histologic study of cadaveric material, Foot Ankle 12:165, 1991. 70. Boles MA, et al: Enlarged peroneal process with peroneus longus tendon entrapment, Skeletal Radiol 26:313, 1997. 71. Mizel MS, Michelson JD, Newberg A: Peroneal tendon bupivacaine injection: utility of concomitant injection of contrast material, Foot Ankle Int 17:566, 1996. 72. Pierson JL, Inglis AE: Stenosing tenosynovitis of the peroneus longus tendon associated with hypertrophy of the peroneal tubercle and an os peroneum. A case report, J Bone Joint Surg Am 74:440, 1992. 73. Rademaker J, et al: Tear of the peroneus longus tendon: MR imaging features in nine patients, Radiology 214:700, 2000. 74. Evans JD: Subcutaneous rupture of the tendon of peroneus longus. Report of a case, J Bone Joint Surg Br 48:507, 1966. 75. Ross G, et al: Rupture of the peroneus longus tendon in a military athlete, Am J Orthop 28:657, 1999. 76. Thompson FM, Patterson AH: Rupture of the peroneus longus tendon. Report of three cases, J Bone Joint Surg Am 71:293, 1989. 77. Wind WM, Rohrbacher BJ: Peroneus longus and brevis rupture in a collegiate athlete, Foot Ankle Int 22:140, 2001. 78. Bianchi S, Abdelwahab IF, Tegaldo G: Fracture and posterior dislocation of the os peroneum associated with rupture of the peroneus longus tendon, Can Assoc Radiol J 42:340, 1991. 79. Kilkelly FX, McHale KA: Acute rupture of the peroneal longus tendon in a runner: a case report and review of the literature, Foot Ankle Int 15:567, 1994. 80. Peacock KC, Resnick EJ, Thoder JJ: Fracture of the os peroneum with rupture of the peroneus longus tendon. A case report and review of the literature, Clin Orthop 223, 1986. 81. Peterson JJ, Bancroft LW: Os peroneal fracture with associated peroneus longus tendinopathy, AJR Am J Roentgenol 177:257, 2001. 82. Tehranzadeh J, Stoll DA, Gabriele OM: Case report 271. Posterior migration of the os peroneum of the left foot, indicating a tear of the peroneal tendon, Skeletal Radiol 12:44, 1984. 83. Geppert MJ, Sobel M, Thompson FM: Peroneus longus tendon calcification, J Bone Joint Surg Br 74:163, 1992. 84. Malhotra CM, Lally EV, Buckley WM: Ossification of the plantar fascia and peroneus longus tendons in diffuse idiopathic skeletal hyperostosis (DISH), J Rheumatol 13:215, 1986. 85. Khoury NJ, et al: Peroneus longus and brevis tendon tears: MR imaging evaluation, Radiology 200:833, 1996. 86. DeLuca PA, Banta JV: Pes cavovarus as a late consequence of peroneus longus tendon laceration, J Pediatr Orthop 5:582, 1985. 87. Edwards M: The relations of the peroneal tendons to the fibula, calcaneum and cuboideum, Am J Anat 42:213, 1928. 88. Eckert WR, Davis EA Jr: Acute rupture of the peroneal retinaculum, J Bone Joint Surg Am 58:670, 1976. 89. Kollias SL, Ferkel RD: Fibular grooving for recurrent peroneal tendon subluxation, Am J Sports Med 25:329, 1997. 90. Krause JO, Brodsky JW: Peroneus brevis tendon tears: pathophysiology, surgical reconstruction, and clinical results, Foot Ankle Int 19:271, 1998. 91. Stover DN, Bryan DR: Traumatic dislocation of the peroneal tendons, Am J Surg 103:108, 1962. 92. Oden RR: Tendon injuries about the ankle resulting from skiing, Clin Orthop 63, 1987.
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41. Kausch T, Rutt J: Subcutaneous rupture of the tibialis anterior tendon: review of the literature and a case report, Arch Orthop Trauma Surg 117:290, 1998. 42. Patten A, Pun WK: Spontaneous rupture of the tibialis anterior tendon: a case report and literature review, Foot Ankle Int 21:697, 2000. 43. Dooley BJ, Kudelka P, Menelaus MB: Subcutaneous rupture of the tendon of tibialis anterior, J Bone Joint Surg Br 62-B:471, 1980. 44. Meyn MA Jr: Closed rupture of the anterior tibial tendon. A case report and review of the literature, Clin Orthop 154, 1975. 45. Moskowitz E: Rupture of the tibialis anterior tendon simulating peroneal nerve palsy, Arch Phys Med Rehabil 52:431, 1971. 46. Markarian GG, et al: Anterior tibialis tendon ruptures: an outcome analysis of operative versus nonoperative treatment, Foot Ankle Int 19:792, 1998. 47. Ouzounian TJ, Anderson R: Anterior tibial tendon rupture, Foot Ankle Int 16:406, 1995. 48. Rimoldi RL, et al: Acute rupture of the tibialis anterior tendon: a case report, Foot Ankle 12:176, 1991. 49. Weissinger M, Landsiedl F: [Bilateral subcutaneous rupture of the tendon of the anterior tibial muscle and its differential diagnosis], Z Orthop Ihre Grenzgeb 122:659, 1984. 50. Forst R, Forst J, Heller KD: Ipsilateral peroneus brevis tendon grafting in a complicated case of traumatic rupture of tibialis anterior tendon, Foot Ankle Int 16:440, 1995. 51. Le Minor JM: Comparative anatomy and significance of the sesamoid bone of the peroneus longus muscle (os peroneum), J Anat 151:85, 1987. 52. Sammarco GJ: Peroneal tendon injuries, Orthop Clin North Am 25:135, 1994. 53. Sobel M, Bohne WH, O’Brien SJ: Peroneal tendon subluxation in a case of anomalous peroneus brevis muscle, Acta Orthop Scand 63:682, 1992. 54. Sobel M, Levy ME, Bohne WH: Congenital variations of the peroneus quartus muscle: an anatomic study, Foot Ankle 11:81, 1990. 55. Cooper ME, Selesnick FH, Murphy BJ: Partial peroneus longus tendon rupture in professional basketball players: a report of 2 cases, Am J Orthop 31:691, 2002. 56. Brandes CB, Smith RW: Characterization of patients with primary peroneus longus tendinopathy: a review of twenty-two cases, Foot Ankle Int 21:462, 2000. 57. Sammarco GJ: Peroneus longus tendon tears: acute and chronic, Foot Ankle Int 16:245, 1995. 58. Cox D, Paterson FW: Acute calcific tendinitis of peroneus longus, J Bone Joint Surg Br 73:342, 1991. 59. Roggatz J, Urban A: The calcareous peritendinitis of the long peroneal tendon, Arch Orthop Trauma Surg 96:161, 1980. 60. Eisele SA, Sammarco GJ: Chronic exertional compartment syndrome, Instr Course Lect 42:213, 1993. 61. Fronek J, et al: Management of chronic exertional anterior compartment syndrome of the lower extremity, Clin Orthop 217, 1987. 62. Rorabeck CH, Bourne RB, Fowler PJ: The surgical treatment of exertional compartment syndrome in athletes, J Bone Joint Surg Am 65:1245, 1983. 63. Harris N, Stevens M: A cavovarus foot is a predisposing factor for rather than a result of peroneus longus tendinopathy, Foot Ankle Int 22:525, 2001. 64. Sammarco GJ, Taylor R: Cavovarus foot treated with combined calcaneus and metatarsal osteotomies, Foot Ankle Int 22:19, 2001. 65. Sobel M, et al: The dynamics of peroneus brevis tendon splits: a proposed mechanism, technique of diagnosis, and classification of injury, Foot Ankle 13:413, 1992.
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93. Church CC: Radiographic diagnosis of acute peroneal tendon dislocation, AJR Am J Roentgenol 129:1065, 1977. 94. Rosenberg ZS, et al: MR features of longitudinal tears of the peroneus brevis tendon, AJR Am J Roentgenol 168:141, 1997. 95. Rosenberg ZS, Feldman F, Singson RD: Peroneal tendon injuries: CT analysis, Radiology 161:743, 1986. 96. Rosenberg ZS, et al: Peroneus brevis tendon in normal subjects: MR morphology and its relationship to longitudinal tears, J Comput Assist Tomogr 22:262, 1998. 97. Alanen J, et al: Peroneal tendon injuries. Report of thirty-eight operated cases, Ann Chir Gynaecol 90:43, 2001. 98. Clarke HD, Kitaoka HB, Ehman RL: Peroneal tendon injuries, Foot Ankle Int 19:280, 1998. 99. Safran MR, O’Malley D Jr, Fu FH: Peroneal tendon subluxation in athletes: new exam technique, case reports, and review, Med Sci Sports Exerc 31:S487, 1999. 100. Mason RB, Henderson JP: Traumatic peroneal tendon instability, Am J Sports Med 24:652, 1996. 101. McLennan JG: Treatment of acute and chronic luxations of the peroneal tendons, Am J Sports Med 8:432, 1980. 102. Steinbock G, Pinsger M: Treatment of peroneal tendon dislocation by transposition under the calcaneofibular ligament, Foot Ankle Int 15:107, 1994. 103. Hammerschlag WA, Goldner JL: Chronic peroneal tendon subluxation produced by an anomalous peroneus brevis: case report and literature review, Foot Ankle 10:45, 1989.
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104. Hansen BH: Reconstruction of the peroneal retinaculum using the plantaris tendon: a case report, Scand J Med Sci Sports 6:355, 1996. 105. Karlsson J, et al: Surgical treatment of concomitant chronic ankle instability and longitudinal rupture of the peroneus brevis tendon, Scand J Med Sci Sports 8:42, 1998. 106. Sammarco GJ, Diraimondo CV: Chronic peroneus brevis tendon lesions, Foot Ankle 9:163, 1989. 107. Zoellner G, Clancy W Jr: Recurrent dislocation of the peroneal tendon, J Bone Joint Surg Am 61:292, 1979. 108. Jones E: Operative treatment of chronic dislocation of the peroneal tendons, J Bone Joint Surg Am 14:574, 1932. 109. Mick CA, Lynch F: Reconstruction of the peroneal retinaculum using the peroneus quartus. A case report, J Bone Joint Surg Am 69:296, 1987. 110. Stein RE: Reconstruction of the superior peroneal retinaculum using a portion of the peroneus brevis tendon. A case report, J Bone Joint Surg Am 69:298, 1987. 111. Acevedo JI, Myerson MS: Modification of the Chrisman-Snook technique, Foot Ankle Int 21:154, 2000. 112. Platzgummer H: [On a simple procedure for the operative therapy of habitual peroneal tendon luxation], Arch Orthop Unfallchir 61:144, 1967. 113. Sobel M, Geppert MJ: Repair of concomitant lateral ankle ligament instability and peroneus brevis splits through a posteriorly modified Brostrom Gould, Foot Ankle 13:224, 1992.
........................................... C H A P T E R 7 Achilles tendon disorders including tendinosis and tears Craig I. Title and Lew C. Schon CHAPTER CONTENTS ...................... Introduction
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Acute Achilles tendon rupture
173
Achilles tendinitis
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Chronic Achilles tendon rupture
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Treatment of Achilles tendinitis
151
Conclusion
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Role of ultrasound and shock wave therapy
173
References
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INTRODUCTION The Achilles tendon is formed by a coalescence of fibers from the gastrocnemius and soleus muscles. This complex spans both the knee and ankle joints, making it more susceptible to injury than muscles that span a single joint. The Achilles tendon is notably susceptible to injury with concomitant knee extension and ankle dorsiflexion. The medial and lateral heads of the gastrocnemius originate from the medial and lateral femoral condyles, respectively. The soleus muscle originates from the posterior proximal tibia and fibula. More distally, the medial and lateral gastrocnemius and soleus tendons coalesce to form the triceps surae complex. The Achilles tendon then rotates 90 degrees such that the medial gastrocnemius position is more posterior and superficial. This rotation may result in torque stresses that can increase the risk of tendinitis.1After passing distal to the posterior superior calcaneal tuberosity, the Achilles tendon inserts into the posterior and plantar calcaneal tuberosity about halfway between the dorsal and plantar aspects of the calcaneus. The retrocalcaneal bursa lies between the distal Achilles tendon and the posterior superior calcaneal tuberosity. It is horseshoe shaped and sits around the insertion of the Achilles, which has more fibers centrally and proximally. Anteriorly it is composed of fibrocartilage, whereas posteriorly it blends with the paratenon and commonly connects to the posterior Achilles tendon. The pre-Achilles bursa lies superficial to the Achilles between the Achilles and the skin. These bursae,
composed of synovium, provide lubrication to assist with tendon gliding and to minimize tendon irritation. A large, sometimes abnormal prominence of the posterior superior calcaneus, Haglund’s deformity,2 may create repetitive frictional irritation on the Achilles tendon that can lead to tendinitis (Fig. 7-1, A and B). The Achilles tendon is the strongest and longest tendon in the body, measuring approximately 12 to 15 cm in length. Although it is the main plantarflexor of the ankle, it also functions to invert the heel during late stance phase and thereby locks the transverse tarsal joint for push-off along with the posterior tibial tendon. It is subject to forces up to 10 times body weight during running, experiencing up to 7000 N of force.1,3,4 The blood supply to the Achilles tendon is segmental and is predominantly derived from anterior branches of the paratenon. Additional sources include intratendinous vessels, the posterior tibial artery, and distal osseous and periosteal branches. A relative zone of hypovascularity exists within 2 to 6 cm proximal to the calcaneal insertion, corresponding to the site of most Achilles tendon ruptures and noninsertional tendinitis.5,6 Similar to other tendons, the Achilles is composed of predominantly type I collagen. Collagen fibrils are bundled into fascicles, held together by the endotenon, which contain elastin, lymphatics, and neurovascular structures. The epitenon surrounds the group of fascicles, forming the structural unit of the tendon. The paratenon further surrounds the epitenon and consists of an inner parietal layer, lying directly on the epitenon,
CHAPTER 7
Achilles tendon disorders including tendinosis and tears
Figure 7-1 (A) Lateral radiograph of calcaneus demonstrating Haglund’s deformity. (B) Sagittal magnetic resonance imaging of the same patient showing changes at Achilles tendon from bony prominence and its effect on Achilles tendon, with thickening and fibrosis as it passes by the bone and more proximally.
and an outer, visceral layer. The paratenon, containing a small amount of fluid between its layers, facilitates glide and minimizes posterior adhesion formation.
ACHILLES TENDINITIS Achilles tendinitis is common among athletes, affecting nearly 18% of runners.7-9 Repetitive impact-loading activities (overuse) such as jumping are responsible for the majority of cases.1 Other predisposing factors include poor extremity biomechanics (foot pronation, cavus foot, genu varum), improper training techniques (excessive running, sudden increase in intensity, uphill running), and poor shoewear.8 Another potential risk factor includes the previous use of fluoroquinolone antibiotics. Athletes commonly affected by tendinitis are involved in running, dancing, tennis, racquetball, basketball, and soccer (unnumbered box 7-1). Puddu et al.10 classified Achilles tendinitis into three categories. Peritendinitis is characterized by inflammation affecting only the paratenon. Peritendinitis with tendinosis refers to inflammation involving both the Achilles tendinitis risk factors Repetitive impact-loading activities Abnormal lower-extremity biomechanics (foot prona-
tion/supination, stiff joints, genu varum) Improper training techniques (intensity, frequency,
duration, speed, terrain) Poor shoewear selection Fluoroquinolone antibiotics
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paratenon and Achilles tendon. Tendinosis reflects isolated Achilles degeneration. Clain and Baxter1 later created an anatomic classification, separating tendinitis into insertional disorders, affecting the area of the enthesis, and noninsertional disorders, commonly affecting the tendon 2 to 6 cm proximal to the calcaneus. Whereas noninsertional tendinitis occurs more often in younger, more active athletes, insertional Achilles tendinitis develops more often in those athletes who are older, less active, and sometimes overweight. Additionally, the presentation of bilateral insertional tendinitis typically occurs in young athletic men and is commonly associated with inflammatory disorders, including seronegative spondyloarthopathies.11,12
Noninsertional tendinitis Peritendinitis is inflammation affecting only the paratenon. The Achilles tendon itself is uninvolved. In chronic cases, adhesions may form between the paratenon and tendon, leading to more profound pain and tenderness. Pain is noted most often at the initiation of activity (start-up pain) and improves with continued exercise. Acute pain typically resolves with rest. In chronic cases, however, the pain may persist and significantly impair further athletic participation. On examination, a localized, increased diameter that more commonly affects the medial side is appreciated with palpation of the tendon. Tenderness, and at times crepitus, is noted throughout all ankle range of motion (Fig. 7-2). Radiographs generally are unremarkable. Peritendinitis with tendinosis represents further inflammation with associated intratendinous degeneration. Pain is more marked and constant. The tendon is thickened and infrequently has palpable intrasubstance calcifications (Fig. 7-3). The painful arc sign may help
Achilles tendinitis
Figure 7-2 Tenderness with squeezing the Achilles and crepitance with range of motion are hallmarks of peritendinitis. The discomfort related to peritendinitis will be constant in location as the ankle is brought through a range of motion. With Achilles tendinosis the tenderness moves with the thickened tendon during range of motion.
Figure 7-3 (A) Noninsertional Achilles tendinitis with characteristic swelling 2 to 5 cm above dorsal aspect of calcaneus. (B) Magnetic resonance imaging shows thickened Achilles tendon. A Haglund’s deformity also is noted. (continued)
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CHAPTER 7
Achilles tendon disorders including tendinosis and tears
Peritendinitis affects the paratenon; the Achilles tendon is not involved: Overuse etiology Tends to be in younger athletes Pain at the initiation of activity (start-up pain) Improves with continued exercise A localized increased diameter Tenderness, and sometimes crepitus, throughout all ankle range of motion Tendinosis, noninflammatory, atrophic degeneration of the Achilles: Associated with normal aging Accelerated by overuse Pain and weakness in push-off Tender thickening 2 to 5 cm proximal to calcaneus Ankle dorsiflexion commonly is limited Less typically, tendon elongation may develop Palpation during range of motion reveals tenderness that moves with movement of the tendon Calcific deposits may be present
Figure 7-3 cont’d. (C) Technetium bone scan demonstrating increased uptake in the Achilles tendon; the third phase of the scan, indicative of advanced intrasubstance degeneration.
to distinguish between tenderness associated with peritendinitis and that associated with tendinosis. Tenderness related to peritendinitis will be constant in location as the ankle is brought through a range of motion, whereas tenderness associated with tendinosis will change position with ankle motion.13 Isolated tendinosis, or noninflammatory atrophic degeneration, is associated with normal aging and typically is accelerated by overuse. Most affected are middle-aged, recreational athletes. With repetitive trauma, microtears develop within the tendon, mostly in the hypovascular zone, leading to further fibrosis and degeneration.14 These athletes complain of weakness in push-off, with pain localized to the area approximately 2 to 5 cm proximal to calcaneus. Whereas ankle dorsiflexion commonly is limited, tendon elongation may develop with an associated increase in passive ankle dorsiflexion. Pathologic examination reveals fatty degeneration with disorganized collagen. Calcific deposits may be present (unnumbered box 7-2).
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Insertional achilles tendinitis Insertional tendinitis is an inflammatory reaction within the Achilles tendon affecting the enthesis, or tendon insertion onto the calcaneus. This disorder more commonly affects older, heavier, and less active athletes but can be seen in competitive athletes as well.12 An abnormally enlarged, bony prominence may aggravate this condition. There is a high association with Haglund’s deformity and retrocalcaneal bursitis, but unlike these disorders, insertional tendinitis involves the tendon itself. This most often results from chronic overuse and poor training habits. Improper techniques include inadequate stretching, rapid increase in training, running on harder surfaces, and heel running. Although pain initially follows exercise, particularly uphill running, symptoms may become continuous over time. Pain, swelling, and warmth are noted specifically at the tendon-bone junction, the enthesis. In athletes, there often is a localized area of pain with a small spur. Ankle range of motion is painful, with dorsiflexion typically limited because of a tight Achilles tendon. External irritation from a shoe’s heel counter plays less of a role in provoking symptoms in athletes with Achilles tendinitis than in retrocalcaneal bursitis and Haglund’s deformity. Radiographs generally reveal calcifications or a bony spur at the most distal aspect of the Achilles insertion (Fig. 7-4, A). Magnetic resonance imaging (MRI) will show degeneration where the tendon attaches to the calcaneus (Fig. 7-4, B). Haglund’s deformity Haglund is credited with first describing the presence of a prominent posterolateral superior calcaneal tuberosity
Treatment of Achilles tendinitis
Retrocalcaneal bursitis Retrocalcaneal bursitis refers to inflammation affecting the bursa immediately anterior to the Achilles tendon. As with Haglund’s deformity and Achilles tendinitis, this condition is common in running athletes, including long-distance runners. In the general population, as with insertional tendinitis, those most commonly affected are older, less active recreational athletes. As the disorder becomes chronic, the bursa enlarges and may become adherent to the Achilles tendon. A prominent posterosuperior bony projection may be present. Athletes typically complain of pain with activities that force the ankle into dorsiflexion, particularly uphill running, and thereby compress the inflamed bursa between the posterosuperior calcaneus and the Achilles tendon. Schepsis et al.14 described the two-finger squeeze test, in which pain is noted when two fingers compress medially and laterally immediately superior and anterior to Achilles insertion. This area will be warm with a notable soft-tissue bulge. Pain is elicited with passive dorsiflexion. Radiographs often are not useful but may demonstrate loss of the retrocalcaneal soft-tissue shadow, as well as the presence of a posterosuperior bony prominence. MRI demonstrates soft-tissue changes anterior
to the Achilles tendon above its insertion in the retrocalcaneal region (Fig. 7-6).
TREATMENT OF ACHILLES TENDINITIS Nonsurgical treatment The initial treatment for Achilles tendinitis is nonoperative. The majority of symptoms respond to rest; activity modification; improved training techniques; stretching; and, at times, shoe modifications and heel lifts. Surgical intervention should be considered only for recalcitrant cases. Initial treatment should include anti-inflammatory medications and a supervised program of Achilles stretching. At times, a heel lift (one-fourth to three-eighths inch), night splint, or temporary immobilization in slight plantarflexion with a removable walking boot or cast may be required. Relative rest with limitations on intensity, duration, or frequency of training and concomitant institution of nonstressful cross training
Figure 7-4 A lateral x-ray (A) and a series of sagittal magnetic resonance imagings (B, p. 152) of the same patient with insertional degeneration of the Achilles tendon with tendon thickening and fibrosis from about 2 cm proximal to its insertion on the calcaneus. (continued)
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in 1927.2 This enlarged superolateral tuberosity predisposes the precalcaneal bursa to be compressed between it and any tightly fitting shoe heel counter, possibly leading to skin irritation and inflammation. Because of the association of shoewear, this disorder also has been referred to as a ‘‘pump bump’’ and ‘‘winter heel.’’ Although there is a frequent association with retrocalcaneal bursitis and insertional Achilles tendinitis, Haglund’s deformity generally does not involve the Achilles tendon. Poorly fitting shoes generally are responsible for the development of symptoms of Haglund’s disorder. Other predisposing risk factors include the presence of a cavus foot and hindfoot varus. In rare cases, childhood apophyseal trauma may be a cause. In the nonathletic population, repetitive injury or trauma may result in bone overgrowth. Most affected are young women who wear fashionable high-heeled shoes. In the athletic population, we have observed this condition more commonly in males who participate in running sports. Longdistance runners are susceptible to this condition, as well as to the other Achilles tendon disorders (see Figs. 7-1 and 7-5). On examination, the affected heel has a swollen, red, and tender posterior prominence, predominantly on the lateral side of the calcaneus. The Achilles tendon itself is not tender. Numerous radiographic measurements have been used to quantify the size of the posterosuperior prominence. These techniques generally are not used by orthopaedists because they do not always correlate with the clinical findings.
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Figure 7-4 cont’d.
(exercise bike, pool running, elliptical trainer) also should be helpful. If the athlete has notable foot pronation, a semirigid orthotic may improve overall foot biomechanics by supporting the medial arch. An
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open-back shoe may benefit those with Haglund’s or retrocalcaneal bursitis (Fig. 7-7). Additionally, deepening the heel counter or use of a heel pad or sleeve may be considered.
Treatment of Achilles tendinitis
Figure 7-5
Clinical photograph of Haglund’s deformity.
we advise against corticosteroid injections and use them only in very limited and specific circumstances. For refractory peritendinitis, we have found that brisement may provide symptomatic relief in a third to half of total cases.18 Brisement consists of injecting 5 to 10 ml of sterile saline or local anesthetic agents into the Achilles tendon sheath; this may forcibly disrupt any adhesions between the paratenon and Achilles tendon. Repeating the injections two to three times over several weeks may be necessary to achieve success.14,18 After initial symptoms resolve, it is imperative to correct predisposing factors, including improper technique, excessive training, inappropriate shoewear, and poor flexibility. In addition, it may be critical to temporarily or permanently eliminate provocative, more rigid, and less compliant surfaces and terrain. Reported results of nonoperative treatment of insertional and noninsertional Achilles tendinitis have been generally successful. Studies have found that 70% to 90% of patients have found symptomatic improvement after corrections in their shoewear, training habits, and mechanics.8,18-22 There are, however, fewer predictable results with nonsurgical management in those with chronic tendinopathy and in the older athlete, as a result of greater degenerative tendon involvement.21 In our experience, athletes with isolated Haglund’s deformity can be managed with shoewear modification about 50% of the time. We have seen improvement in about 30% of patients with retrocalcaneal bursitis and in about 25% of those with insertional tendinitis. The presence of a prominence does not mandate surgery. One should not perform prophylactic resection because the degenerative process may be improved with mechanical means, rest, and other modalities, as described above.
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Intratendinous corticosteroid injections should be avoided because local use of these injections has been associated with tendon attrition and potential rupture. Although there is no strong evidence of similar deleterious effects after peritendinous corticosteroid injections, there are similar worries with an injection in the bursa. It would be advisable to immobilize the ankle temporarily after a retrocalcaneal injection because the retrocalcaneal bursa has a direct communication to the Achilles and may injure the Achilles tendon.12,15-17 In general,
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Figure 7-6 Magnetic resonance imaging demonstrates Haglund’s deformity with enlarged posterior superior aspect of the calcaneus.
Surgical intervention is considered only after approximately 3 months of good, nonoperative treatment measures. The surgical technique is chosen on the basis of location of pathology. For a symptomatic athlete with a normal tendon, determined by physical examination and possibly by MRI, we generally try to avoid a procedure that may irritate or traumatize the tendon. A medial or lateral approach 5 to 10 mm anterior to the Achilles tendon and paralleling its course is best in these cases because it runs through thicker skin with more substantial subcutaneous tissues. If the tendon is involved, an approach directly through the posterior aspect of the tendon is possible. This approach has the additional benefit of obtaining even greater exposure and improved debridement of bone and tendon. Other issues must be taken into consideration to help guide the surgical approach and choice of technique,
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Figure 7-7 Shoe alternatives and modifications for patients with Achilles tendinitis. Clockwise from the top left: (A) A higher-heeled, backless shoe, ‘‘a mule.’’ (B) A completely removed heel counter. (C) A partial heel counter cut to relieve external pressure. (D) A backless sneaker.
such as identifying whether Haglund’s deformity, retrocalcaneal bursitis, or insertional tendinitis is involved and determining the extent of tendon involvement (length, width, and depth of pathology). Any prominence of the bone, as well as the location of the prominence relative to the insertion of the tendon (above, at, or below the insertion of the tendon), should be noted, and the surgeon should determine whether the bursa is inflamed and how much additional debridement is necessary. In general, the points of tenderness dictate where the exposure must occur. Thus if there is more medial and central Achilles tendinitis versus lateral, the tendon in the medial and central aspect has to be elevated off the calcaneus, the tendon must be debrided there, and the underlying bone must be resected and recontoured.
Noninsertional tendinitis For noninsertional tendinitis, the choice of procedure is based on whether the disease involves the paratenon, tendon, or both. In peritendinitis, all adhesions are excised, and the surgeon also performs a limited resection of any thickened paratenon. The extremity is immobilized for 3 to 5 days, followed by a range of motion program to limit the recurrence of scar formation (Fig. 7-8). When there is tendinitis and peritendinitis, elliptical excision of the tendon and longitudinal paratenon release is performed. Maffulli et al.23 have reported a success rate of approximately 70% after percutaneous longitudinal tenotomy of the middle third of the Achilles tendon.
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Figure 7-8 Release of the paratenon. Note that the incision is made 1 cm anterior to the margin of the Achilles tendon. The incision can be made much smaller than shown in this case.
In this technique a no. 11 or no. 15 blade is introduced posteriorly through the skin and tendon. With the blade held stationary, the ankle is dorsiflexed and the tendon is cut longitudinally. Next the blade direction is reversed 180 degrees and the ankle is plantarflexed. The process is repeated through four additional incisions in the zone of the degenerative tendon (Fig. 7-9).
Treatment of Achilles tendinitis
Figure 7-9 The Maffulli technique: an incision is made with a no. 11 or no. 15 blade. The blade is held stationary and the ankle is dorsiflexed creating a longitudinal cut in the tendon. The blade then is turned 180 degrees, and the ankle is plantarflexed. The process is repeated until there are five longitudinal cuts.
Tendinosis The type of procedure chosen for treatment of tendinosis depends on many factors, the largest, in our experience, being the extent of tendon involvement, determined by clinical findings, ultrasound, or MRI. When less than 50% of the tendon is involved, we longitudinally ellipse the diseased tendon; and when more than 80% of the tendon is involved, a debridement and tendon augmentation (e.g., turndown) or transfer is recommended (Fig. 7-10). When there is between 50% and 80% involvement, the decision is determined by the patient, the sport, and the surgeon’s preference. Debridement of tendon. For tendinosis, typically the degenerative portion of the Achilles tendon is debrided and the paratenon is released. If less than 50% of the tendon width is debrided, then the remaining section of intact longitudinal tendon should be strong enough to withstand stresses.
Figure 7-10 Magnetic resonance imaging cross section of the Achilles tendon demonstrating more than 80% tendon involvement. This would indicate the need for tendon augmentation or transfer following debridement.
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Figure 7-11 Intraoperative photo of debridement of the Achilles tendon. Once the degenerative tissue is ellipsed from within the substance of the tendon, buried sutures are used to close the defect.
Typically a medial incision is made just anterior and parallel to the border of the tendon that is thickened, and the paratenon is entered. On the basis of maximal tenderness, MRI, or ultrasound localization of the degenerative zone of the tendon, an elliptical longitudinal excision of the diseased tendon is performed, leaving intact the anterior and posterior surfaces of the tendon. Essentially the zone of ellipsed tissue should include the degenerative fibers and the thickened tendon (Fig. 7-11). The tendon then is repaired with internally placed, nonabsorbable sutures with buried knots. The subcutaneous tissues are apposed, followed by closure of the skin. The leg is immobilized for 3 to 5 days in a splint, followed by range of motion exercise, strengthening, and nonimpact activities. A boot brace is worn for 6 to 12 weeks during ambulation to unload the healing tendon. Jogging and running may be introduced at 3 months, depending on the extent of involvement and the nature of the patient’s athletics. Tendon transfer. If more than 50% of the tendon width is involved, then one must consider the risks and benefits of either longitudinal tenotomy, debridement, or tendon transfer. The decision to consider tendon transfer is determined by the structural weakening of the tendon that may result from a large debridement. Because most athletes use all their tendons for ultimate, lower-extremity performance, it is difficult to justify harvesting a working structure to improve the function of the Achilles. Thus depending on the demands of the athlete and nature of his or her skills, we have to balance the pros and cons of using the tendon transfer. If 50% to 80% of the width of the tendon is resected, we consider these factors. However, if 80% or more of the tendon is involved, our experience has
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been that the transfer becomes more critical to restore function. Alternative procedures in this latter scenario include a turndown procedure, tendon allograft, and V-Y advancement. The flexor hallucis longus (FHL), flexor digitorum longus (FDL), or, less commonly, the peroneal tendons can be transferred. We prefer to use the FHL tendon in a nonsprinting athlete, nondancer, or rock climber. Transferring the FHL or any other tendon in a sprinting athlete or ballet dancer could lead to loss of agility, power, or balance. In these athletes, it is better to consider performing a turndown procedure, a V-Y advancement, or an allograft if a wide area of tendon is involved. The patient is positioned prone and both legs are prepped for any tendon transfer, turndown procedure, or V-Y advancement because it usually is necessary to compare resting tensions with those of the contralateral side. In a tendon transfer, our preferred technique is to use a medial approach to the Achilles tendon, typically staying 1 cm anterior to the medial edge of the tendon. The incision is extended more inferiorly. The paratenon is opened, the degenerative tendon is excised, and the deep fascia between the superficial and deep compartment is released. It is felt that, by opening the fascia and exposing the deeper FHL muscle belly, there is an improved vascular bed for the Achilles. Ranging the big toe should facilitate identification of the moving FHL muscle belly and tendon. The FHL tendon may have a more distal origin and may not be viewed readily in the wound. Care should be taken while dissecting along the course of the muscle because the tibial nerve runs immediately medial to the tendon (Fig. 7-12, A through E). Follow and release the FHL tendon from the sheath (fibroosseous tunnel) as it travels between the medial and lateral tubercles of the posterior talus. Continue to release the tendon for as much length as possible from the posterior approach, dissecting toward the underside of the sustentaculum tali. Cut the tendon as distally as possible, again avoiding the tibial nerve. The FHL tendon then is either sewn to the Achilles repair or inserted into the calcaneus or its periosteum, depending on tendon length. A useful technique involves drilling a hole the width of the tendon (typically 5 mm) through the calcaneus from dorsal to plantar (Fig. 7-13). A small incision made over a K-wire passed through this tunnel can facilitate placement of a small-bore suction tip over the wire from plantar to dorsal and out the planned entry point for the tendon. The whip suture in the FHL tendon then can be passed through the suction tip and pulled plantarly to permit tensioning. An interference screw can be inserted through the tunnel. Alternatively, an anchor can be placed obliquely in the tunnel wall just distal to the opening but not obscuring the passageway. After the proper tension has been determined,
Treatment of Achilles tendinitis
Figure 7-12 (A) A medial approach 1 cm anterior to the medial edge of the Achilles tendon. (B) The deep fascia between the superficial and deep compartment is released. Ranging the big toe should allow palpation and identification of the moving flexor hallucis longus (FHL) (marked with two arrows). The tibial nerve runs immediately medial to the tendon, therefore dissection of the tendon must be carefully performed. (C) The tendon is released distally and secured with a whipstitch. The degenerative Achilles tendon is excised. (D) 4-0 or 2-0, nonabsorbable suture is buried within the tendon. (E) The defect is closed and the FHL tendon is sewn to an anchor into the calcaneus. This area of the calcaneus is prepared by locally elevating the periosteum. In this case the Achilles tendon length was normal, so the FHL was tensioned to permit full dorsiflexion.
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Figure 7-13 (A) Following debridement of the Achilles and harvest of the flexor hallucis longus (FHL), the thickness of the FHL is determined to properly select the drill size. (B) A guidewire is passed through the calcaneus and then is advanced to pierce the plantar soft tissues. The exit point plantarly is just anterior to the fat pad of the heel. (C) A drill matching the width of the FHL is used to create a channel in the calcaneus but should not penetrate the soft tissues. (D) A small incision is made and a small-bore suction tip is placed over the wire from plantar to dorsal and out the planned entry point for the tendon. (E) The whip suture in the FHL tendon then can be passed through the suction tip and pulled plantarly to permit tensioning. (F) An interference screw is inserted through the tunnel. As an alternative, an anchor can be placed obliquely in the tunnel wall just distal to the opening but not obscuring the passageway.
Treatment of Achilles tendinitis
Figure 7-14 The V-Y advancement. (A) The section of the diseased Achilles is debrided, and the new edges are sutured with a whipstitch for anastomosis. (B) A V-shaped fascial incision is made with the apex proximal. With traction on the tendon distally, an advancement of 2 to 3 cm can then be achieved. (C) The final tendon tensioning is performed by checking the resting posture of the ankle and testing the ‘‘springiness’’ of the foot as it sits in the normal slightly plantarflexed position. A comparison with the other side is helpful. The V-Y is then sutured. If it appears that there is too large a gap to close, a turndown or a tendon transfer may span the defect.
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Figure 7-13 cont’d. (G) A corkscrew anchor is inserted to repair the Achilles tendon onto bone.
the tendon is secured. Occasionally there is a need to resect the posterior superior calcaneus; this procedure is determined by the presence of Haglund’s deformity and bursitis. We do not close the deep fascia between the compartments because the FHL muscle belly may provide for improved healing following the Achilles repair. V-Y advancement. A V-Y advancement may be required if more than 80% of the tendon width and 2 to 3 cm in length is involved. With this large amount of tendon involvement, the remaining normal tendon may not be thick or wide enough to safely flap. The V-Y advancement is accomplished by extending the initial posterior incision more proximally toward the musculotendinous junction (Fig. 7-14, A through C). A V-shaped fascial incision is made with the apex proximal. With traction on the tendon distally, an advancement of 2 to 3 cm then can be achieved; this should close the distal gap sufficiently. The distal repair
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can be performed with a modified Krackow or whipstitch, and then balancing of the tendon tension is performed by checking for the resting posture of the foot and testing the ‘‘springiness’’ of the foot as it sits in the normal, slightly plantarflexed position. The V-Y advancement is performed with the patient prone. Because it usually is necessary to compare resting tensions with those of the contralateral side, both legs are prepped as for any tendon transfer or turndown procedure. However, the tendon may begin to tear and pull off the muscle base beyond an advancement of 3 to 5 cm. If it appears that there is not enough fascia/tendon substrate or if too large a defect exists for advancement, then a turndown or an allograft tendon transfer
such as with a semitendinosus tendon may be used as a connecting bridge. Turndown procedure. A turndown procedure provides substrate for healing and may limit the possibility of rerupture when there is between 50% and 80% of tendon width involvement. The patient is positioned prone with both legs prepped to compare the two and re-create normal resting tension. A medial incision is used, with care taken on deeper exposure to avoid branches of the sural nerve. After the rupture or degeneration site is exposed, the end of the proximal tendon is mobilized, then grasped with Alice clamps and gently distracted by pulling distally on the Alice clamps for 5 to 10 minutes (Fig. 7-15, A).
Figure 7-15 The turndown procedure. (A) After the rupture or degeneration site is exposed, the end of the proximal tendon is mobilized and then grasped with Alice clamps, and tension is pulled. (B) The size of the gap is measured while the foot is maintained in a neutral position. (C) An additional 4 cm then are added to the tendon defect (a 2-cm distal hinge that is overlapped by the turned-down flap, or 2 cm plus 2 cm). Another 1 cm is added to account for the intended 1-cm overlap of the tendon ends distally. Thus the flap begins proximally at a point 5 cm more than the size of the gap. (D) A strip of tendon 1 cm wide is harvested centrally.
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Treatment of Achilles tendinitis
Figure 7-15 cont’d. (E and F) The tendon graft now can be turned distally to span the void. (G) Two no. 1 Ethibond sutures are used to anchor the corner of the turned-down graft (arrows) reinforcing the high stress junction. The central slip typically is passed anteriorly deep to the tendon to decrease the bulk. The distal tendon end then is secured to the remaining viable Achilles or to the bone. Comparison with the nonoperative side facilitates tensioning of the graft.
used to anchor the corner of the turned-down graft, reinforcing the high stress junction so there is no propagation of the split between the strip and the main body of the tendon (Fig. 7-15, G). To decrease the bulk created by this method, the tendon then is passed anteriorly deep to the tendon instead of posteriorly. The distal tendon end then is secured to the remaining viable Achilles or to the bone. Tensioning of the graft requires checking the range of motion and the springiness of the operative side versus the normal side. Usually, the foot should have a resting position of 15 degrees of plantarflexion. The graft and the turneddown flap are held in place by hand or by suture. Once the appropriate tension and position are established, 161
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The size of the gap is measured while the foot is maintained in a neutral position (Fig. 7-15, B). An additional 4 cm then is added to the tendon defect (a 2-cm distal hinge that is overlapped by the turned-down flap, or 2 cm plus 2 cm). Another 1 cm is added to account for the intended 1-cm overlap of the tendon ends distally (Fig. 7-15, C). Thus the flap begins proximally at a point 5 cm more than the size of the gap. For example, if the gap is 6 cm, then a flap is initiated 11 cm proximal to the gap (Fig. 7-15, D). A strip of tendon approximately 1 cm wide and 1 cm thick is harvested centrally. The tendon graft now can be turned distally to span the void (Fig. 7-15, E and F). At approximately 2 cm proximal to the defect, two no. 1 Ethibond sutures are
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whipstitches are used for final anastomosis. The resting tension and springiness are checked once again at the end of the procedure (unnumbered box 7-3). Noninsertional tendinitis surgical alternatives Paratendinitis: release paratenon Tendinosis: degree of width involved <50% ellipse and repair >80% ellipse and augment Tendinosis: degree of length involved 1-3 cm V-Y 3-5 cm turndown >5 cm turndown with consideration for FHL
or FDL tendon transfer
Insertional tendinitis Insertional tendinitis is surgically treated by excising the retrocalcaneal bursa and any prominent posterosuperior bone. Additionally, the Achilles tendon is debrided of any intratendinous calcifications and degenerated tissue, including detachment of part of the tendon’s insertion. Achilles tendon reattachment through calcaneal bone tunnels or with suture anchor is advised. A central splitting or paralateral Achilles approach both have been advocated.12 Our preference is a central approach for optimal visualization (Fig. 7-16, A through H). The direct posterior central approach for the distal Achilles tendonopathies requires an incision through thick, well-vascularized skin. This is distinct from the thinner skin found proximal to the calcaneus that is
Figure 7-16 Insertional Achilles tendinitis. (A) Sagittal magnetic resonance imaging of a patient with insertional Achilles tendinitis and retrocalcaneal bursitis. Note the bony prominence, the fluid in the bursa anterior to the tendon, and the abnormal signal at the insertion consistent with degeneration at the interface. (continued)
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Treatment of Achilles tendinitis
Figure 7-16 cont’d. (B) A central incision is made through the site of maximal tenderness through the tendon down to the bone. (C) The tendon is released from its insertion posteriorly and the posterior superior calcaneus is exposed. (D) Two human retractors are placed, and the chisel is used to resect the insertion site and the posterior superior bony prominence. (E) A side view of the chisel angle to resect the bony prominence. Care is taken not to inadvertently penetrate too anteriorly and end up in the subtalar joint. The medial lateral and dorsal edges are checked for remaining bone. (F) The bone has been resected and the suture anchor is placed centrally into the calcaneus about 5 to 8 mm proximal to the previous insertion site. (continued)
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Figure 7-16 cont’d. (G) An intraoperative image demonstrating the anchor placement. (H) The sutures are placed close to the midline, penetrating the tendon directly over the anchor with very minimal divergence to maximize tendon apposition to the bone. The knots should be buried so that postoperative irritation is avoided.
potentially more problematic with delayed healing of a wound. Through the central incision, we debride both the bone and the tendon at the junction and resect the posterior superior process. Tendon augmentation may be required, depending on the extent of debridement. When more than 80% of the tendon is involved or when the Achilles is degenerative at the insertion and proximally, an FHL graft should be considered (Fig. 7-17, A through C). The FHL can be harvested in the arch of the foot or, as we prefer, behind the ankle. After the FHL is attached to the bone through a tunnel or into a trough, the Achilles tendon is reattached with one or two suture anchors. A biomechanical study by Kolodziej et al.24 demonstrated that as much as 50% of the Achilles tendon may be safely resected through this approach. Despite this study, we still recommend placing suture anchors to optimize tendon bone contact and healing. When reattaching the tendon, it is important to restore normal resting tension, using the remaining intact portions of medial and lateral slips of tendon as a guide. Inadvertent overtensioning of the repair when using anchors could cause an equinus contracture or difficulty squatting or lunging.
Haglund’s deformity Surgical treatment for Haglund’s deformity and retrocalcaneal bursitis focuses on resecting the enlarged posterior bony prominence, including the attached
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precalcaneal bursal projection. Any inflamed retrocalcaneal bursa also is excised. Because the lateral side is more commonly affected, it is easier to approach through a lateral incision (Fig. 7-18, A). A medial approach is warranted when the bony prominence is found medially (Fig. 7-18, B). When the tendon is not involved, the insertion can be avoided through the lateral or medial approaches. Either way, it is critical to resect a sufficient amount of bone to prevent impingement on the tendon and avoid creating a sharp edge after resection that may irritate the tendon (Fig. 7-18, C and D). Too much resection can weaken the tendon insertion, and the subtalar joint may be penetrated if the surgeon is not careful. Jones and James25 advocated a combined medial and lateral approach to ensure a thorough bony resection (Fig. 7-18, E). This exposure helps to avoid inadvertent creation of a sharp, bony edge. We recommend a lateral approach or the combined medial and lateral exposure. The central posterior approach for Haglund’s deformity should not be used because it is better to avoid disrupting the insertion of the tendon unless there is a clinically relevant component of insertional tendinitis (Fig. 7-19, A through D). Bone resection should be performed just proximal to the insertion of the tendon (Fig. 7-19, E). A power reciprocating rasp should be used to help contour the cut edges by the tendon (Fig. 7-19, F). A mini-C arm should be used to help identify any remaining prominences (Fig. 7-19, G).
Treatment of Achilles tendinitis
Figure 7-17 When the Achilles is degenerative at the insertion and proximally or when more than 80% of the tendon is involved a flexor hallucis longus (FHL) graft should be considered. (A) The central approach is used to detach the Achilles posteriorly, and the prominent bone is resected. (B) The degenerative tendon is debrided. (C) The FHL tendon is harvested from behind the ankle and will be reattached through a tunnel or into a trough before repairing the Achilles tendon.
Figure 7-18 The incisions for treatment of the Haglund’s deformity. (A) A lateral incision is more common because the prominence is usually more pronounced on this side. (B) A medial approach is warranted for a medial bony prominence. (continued)
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Figure 7-18 cont’d. (C and D) Radiographs preoperatively and postoperatively show sufficient bone resection without impingement at the tendon insertion. (E) A combined medial and lateral approach ensures a thorough bony resection and edge contouring.
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Treatment of Achilles tendinitis
(continued)
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Figure 7-19 (A) through (C) This athlete’s x-rays and sagittal magnetic resonance imagings demonstrate a Haglund’s deformity, retrocalcaneal bursitis, posterior calcaneal bony edema, and some insertional Achilles tendon changes.
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Figure 7-19 cont’d. (D and E) Because all the tenderness and prominence were lateral and there was no tenderness at the Achilles insertion, a lateral approach was chosen, with the intraoperative option of an additional medial incision to contour the sides.
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Treatment of Achilles tendinitis
Figure 7-19 cont’d. (F) Bone resection should be performed just proximal to the insertion of the tendon. A power reciprocating rasp should be used to help contour all edges by the tendon. (G) A mini-C arm should be used to help identify any remaining prominences.
(Fig. 7-21). It should be reserved for atypical cases (unnumbered box 7-4).
Postoperative management Our postoperative management for the athlete is determined on the basis of the extent of tendon involvement. If there is no tendon repair or reconstruction, a nonweight-bearing posterior and U-splint is applied in mild plantarflexion for the first 10 days. The sutures then are removed, and progressive, full weight bearing is permitted with a boot brace in neutral position. Between 6 and 12 weeks, the athlete is weaned out of the boot as tolerated. Early range of motion and strengthening exercises are encouraged. Impact activities are avoided for about 8 to 12 weeks. Swimming and exercise bicycling are encouraged by 3 weeks, followed by the elliptical trainer by 4 weeks. Beyond 12 weeks, the athlete may progress to sports-specific activities. Our average time for athletes to return to sports has been 3 to 6 months. If the tendon was repaired or reconstructed or if a tendon was transferred, a postoperative splint is applied in a relaxed resting position (25 to 45 degrees of equinus). At 10 days, the sutures are removed, and a boot brace is applied in 20 degrees of plantarflexion. We permit active dorsiflexion progressively up toward the neutral point but recommend reaching the neutral point at 6 weeks. Exercises are encouraged with the knee flexed to eliminate extra pulling of the gastrocnemius muscle during dorsiflexion. Ankle inversion and eversion strengthening may be performed. Flexing the toes 169
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Endoscopic Haglund’s resection as presented by Niek van Dijk (see Chapter 16) recently has gained popularity. In this technique, the patient is placed in a prone position, and a lateral incision is made just dorsal to the calcaneus and anterior to the tendon (Fig. 7-20). A 4.5-mm, 30-degree arthroscope is introduced. A spinal needle then is introduced medially just dorsal to the calcaneus, and the 5.0-mm full-radius resector is inserted. With the shaver on the superior surface of the bone, the periosteum is removed. In plantarflexion the Haglund’s prominence can be resected with the shaver. A burr may be needed to remove bone at and near the insertion point of the tendon. The site of the burr placement should be confirmed with fluoroscopy. Adequate decompression is achieved at the posterior medial and lateral edges by alternating portals. The portals are sutured after the bursa and Haglund’s prominence have been removed with fluoroscopic assistance. This technique avoids the creation of tender scars in this region, has low morbidity, and may shorten recovery relative to the open procedures. Alternatively, some authors have advocated a dorsal closing wedge osteotomy of the posterior tuberosity of the calcaneus. It is rarely used in athletes because of inherent complications with this procedure, including nonunion or malunion, potentially longer recovery times, difficult fixation, painful prominent hardware, broken hardware, and altered mechanics. This procedure may have a role if an athlete has a noticeably deformed posterior and superior calcaneal prominence, which we call the ‘‘pregnant heel’’
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Figure 7-20 Endoscopic portal landmarks. With the patient in a prone position, the lateral incision is made just dorsal to the calcaneus and anterior to the tendon. (A) The posterior view demonstrating the lateral portal (black arrow) and the medial portal (white arrow). The area of pain is marked on the patient’s skin. A dotted line is marked at the superior site of the Achilles insertion below the area of pain. (B) The lateral perspective of the portal site. (C) The medial perspective of the portal. A 4.5-mm, 30-degree arthroscope is introduced laterally. A spinal needle is introduced medially just dorsal to the calcaneus. The 5.0-mm. full-radius resector then is inserted.
against resistance is avoided if a tendon transfer was performed but encouraged if no transfer was done. Partial weight bearing in a boot is allowed while maintaining the ‘‘triple flex walk’’ (Fig. 7-22) (flexion
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of hip, knee, ankle). With the ankle in plantarflexion and the ipsilateral leg remaining anterior to the body at all times, the patient leads with that leg in gait and keeps the sole of the foot in contact with the
Treatment of Achilles tendinitis
Figure 7-21 Top left corner shows the preoperative appearance of this large posterior prominence. It is uncharacteristically inferior, although the patient did not have insertional tendinitis. Title calls this the ‘‘pregnant heel.’’ This is a rare exception to consider, a dorsal closing wedge osteotomy of the posterior tuberosity of the calcaneus. Top left shows the lateral approach anterior to the Achilles tendon. Bottom left shows the preoperative radiograph. The bottom right demonstrates the calcaneus following the resection of the dorsally based closing wedge and fixation with a screw. The technique is used rarely because of inherent complications with this procedure, including nonunion or malunion, potentially longer recovery times, difficult fixation, painful prominent hardware, broken hardware, and altered mechanics.
Symptoms and surgery Haglund’s/retrocalcaneal bursitis Tender over posterior superior bony prominence and/or anteromedial and anterolateral Achilles Surgery: resect bone through medial and/or lateral incision over prominence Insertional Achilles tendinitis Tender at the insertion of the Achilles halfway between the dorsal and plantar aspect of the calcaneus Surgery: central posterior Achilles splitting incision, debride tendon and bone
9 months, depending on the extent of the tendon disease and the integrity of the repair. 171
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ground by flexing the knee and hip, similar to a fencer’s advance. Although the appearance is awkward, this method permits ambulation without crutches. Ankle neutral position is achieved by 6 weeks, permitting full weight bearing with the boot adjusted at a right angle to the leg. Then progressive dorsiflexion exercises beyond neutral are performed, with caution not to overstretch. Dorsiflexion is progressed slowly, depending on the integrity of the repair. Swimming, bicycling, and other nonimpact activities are commenced at 6 weeks. At 12 weeks, the boot is discontinued, and lower-impact activities such as the elliptical trainer are instituted and increased. The patient then is progressed to jogging and then running. It may take 4 to 6 months to return to play, or perhaps more than
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Figure 7-22 Partial weight bearing in a boot in plantarflexion is allowed while maintaining the ‘‘triple flex walk’’ (flexion of hip, knee, ankle). (A) With the ankle and the ipsilateral leg remaining anterior to the body at all times, the patient leads with that leg in gait and keeps the sole of the foot in contact with the ground by flexing the knee and hip, similar to a fencer’s advance. (B) The back leg is now brought forward but does not advance beyond the front healing leg so that the Achilles can be kept unloaded. Next the braced leg is advanced again as in A. This method permits ambulation without crutches.
Surgical results typically correspond to the athlete’s age, with patients younger than 50 years generally having less tendon involvement, more rapid return to work and sports, and fewer postoperative problems. Patients older than 50 years typically have more tendon involvement, require greater debridement, and have longer postoperative recovery.18,21
Expected success rates and return to sport Success rates have ranged from 50% to 90%, depending on the extent and location of tendon involvement. Surgical debridement for Haglund’s syndrome and chronic tendinosis generally has less favorable results.26,27 Watson et al.28 reported that those with insertional tendinosis are older athletes, have greater tendon involvement, take a longer time to recover, and often do not achieve results as satisfying as those with isolated
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retrocalcaneal bursitis. Leach et al.29 reported in a small series of athletes that the long-term success rate was 85% following surgical treatment. However, the authors noted that symptoms recurred in two patients and required reoperation. A study by Schepsis et al.26 also demonstrated initially high satisfactory results, mostly in athletes with paratendinitis, although longterm results deteriorated with time. In a recent study by Saxena,30 return to activity was fastest in elite athletes requiring only soft tissue procedures, particularly peritenolysis. Return to competition was approximately 6 months. Although many studies in the literature have quoted high success rates, this optimism for surgical treatment must be tempered by the fact that these were retrospective analyses that often did not differentiate among the various Achilles tendon disorders.14,18,21,25-27,29,31,32
Acute Achilles tendon rupture
The use of extracorporeal shock wave therapy (ESWT) for the treatment of Achilles tendinitis has not been widely studied. Most information on shock wave therapy comes from research on kidney stone lithotripsy, upper extremity tendinitis, and plantar fasciitis. Shock wave therapy works by creating a pressure change that propagates rapidly through a medium. When transmitted through a water medium, it can either directly create high tension at a given structure or indirectly create microcavitations. Theories behind its analgesic effect in orthopedic applications include an alteration of the permeability of neuron cell membranes and induction of an inflammatory-mediated healing response by increasing local blood flow.33 Studies on ESWT on Achilles tendinitis have shown a success rate of approximately 30% to 40%.34,35 In our experience, we have found a similar success rate of approximately 30% in athletes, although more severe cases are indicated for surgery. Even with this lower success rate, we try ESWT for 3 months on all patients before surgery because this treatment has minimal side effects. Depending on the immediate results, we may allow sports play with only 1 or 2 weeks off. If the athlete is in midseason, then this modality is his or her best chance to resume play. If the athlete is at the end of the season, then we may try shock wave therapy and a boot brace for 2 to 6 weeks and then allow the athlete to resume impact activities. After the season, when there is more time for recovery, decisions regarding further treatment can be made. Contraindications to ESWT quoted in the literature include pregnancy, coagulopathies, bone tumors, bone infection, and skeletal immaturity.33 Saggini et al.36 noted successful outcomes after two treatments with no complications using shock wave therapy on Achilles tendinitis. Several later studies reported promising results after ESWT with those affected with chronic Achilles tendinitis.37-39 The cost of shock wave treatment can be an important consideration because the therapy may not be covered by insurance. With lower-energy shock wave machines, three treatments are used, at a cost of $500 to $800 each. One treatment (at a cost of about $1500) is the norm for the higherenergy machines. The temporary pain with this procedure is considerable and requires an ankle block or general anesthesia, which increases both the risk and the cost.
ACUTE ACHILLES TENDON RUPTURE Although the incidence of Achilles tendon ruptures has increased over the past few decades, many still are
missed on initial presentation. Achilles tendon ruptures typically occur in men in their 30s and 40s, with more than 75% of these injuries occurring during athletic participation. Most of these patients are recreational athletes. Those engaged in abrupt repetitive jumping or sprinting sports, such as basketball, football, and soccer, are particularly at risk.40 Sports-related injuries are most often the result of a rapid eccentric load that is applied to a tensioned tendon with ankle dorsiflexion and simultaneous knee extension. This occurs during the loading phase of a rapid push-off or sudden jump. Most ruptures occur in an area of relative hypovascularity of the Achilles tendon, 2 to 4 cm proximal to the superior aspect of the calcaneus.41 Additional risk factors include intratendinous degeneration, vascular impairment, corticosteroid or fluoroquinolone use, mechanical malalignment, and systemic disorders such as gout, hyperthyroidism, and renal insufficiency.40,41 An athlete typically reports an audible snap and a sensation of being struck or shot from behind following a misstep or sudden jump. The player will note significant loss of push-off strength and normally will be unable to continue sports participation. Diffuse swelling, ecchymosis, and residual strength from remaining ankle plantarflexors can make diagnosing an initial injury difficult. However, findings consistent with an acute Achilles tendon rupture include a palpable tendon gap (Fig. 7-23), positive Thompson test (absence of passive ankle plantarflexion with calf squeeze in prone position; Fig. 7-24), loss of the normal plantarflexion resting tone while prone in comparison with the unaffected side, inability to perform a single toe heel rise, and weak active plantarflexion. Although imaging generally is unnecessary in acute cases, lateral radiographs may show an avulsion fracture (Fig. 7-25). MRI and ultrasound are useful in equivocal or late cases (Fig. 7-26).
Nonsurgical treatment Although the treatment of choice for most athletes with an acute Achilles tendon rupture is surgical repair followed by early, protected range of motion and weight bearing, nonoperative treatment of Achilles ruptures using cast immobilization has some advocates. The ill effects of ‘‘cast disease’’42,43 include calf atrophy and resultant muscle weakness, as well as the consequences of immobilizing joints, ligaments, and uninvolved muscles and tendons. Furthermore, nonoperative management of an Achilles tendon rupture typically does not restore the normal functional length of the tendon, and the athlete will note significant muscle weakness. Although operative management is associated with inherently potential surgical risks, including poor wound healing, infection, and nerve injury, the risks are balanced by a lower incidence of tendon rerupture rates, less 173
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ROLE OF ULTRASOUND AND SHOCK WAVE THERAPY
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Achilles tendon disorders including tendinosis and tears
Figure 7-23 (A) The side with the Achilles rupture has a visible indentation (white arrow). (B) The normal side. (C) The ruptured side has a palpable defect.
than 2%, compared with 13% to 35% after nonoperative care.42 Further, studies have demonstrated improved strength and ankle motion with a greater potential of sports resumption following surgical repair.42,44 Nonoperative management generally is better than operative management in those with systemic disorders, such as diabetes, peripheral vascular disease, lower-extremity edema, or overlying skin conditions. However, these comorbidities are not often found in the athletic population. Following nonoperative management, a short-leg, nonweight-bearing cast in slight equinus is used for 6 weeks. This is followed by a weight-bearing cast or walking boot with progressively increased dorsiflexion. Results similar to those of operative management have been reported for nonoperative treatment with a functional boot brace guided by ultrasound.45 Ultrasound is used to ensure that the ends of the torn tendon remain apposed as the ankle is progressively dorsiflexed during the first 6 weeks. Additionally a successful nonoperative protocol has been reported using a functional brace to minimize the ill effects of immobilization and
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to shorten the time needed for rehabilitation and return to activities.46 A more recent study found similar success with operative and nonoperative treatment in the athlete.47 More recent postoperative trends have focused on a functional rehabilitation program with early controlled range of motion and strengthening exercises.48-50 Early mobilization limits the dystrophic effects of prolonged cast use and has been shown to reduce tendon adhesion, improve healing, and maximize tendon strength without increasing the risk of rerupture or infection. We favor operative repair unless contraindicated.
Surgical treatment ............................................................. Athletes with well-controlled systemic disorders, such as diabetes, should be considered for operative treatment. This higher-risk situation requires close attention to wound closure and postoperative management, including meticulous and frequent follow-up.
Acute Achilles tendon rupture
Standard technique Acute Achilles tendon ruptures in an athlete should be treated operatively with the goal of recreating normal tendon length and tension. After positioning the patient prone, the contralateral leg is additionally prepped to help match resting ankle tension. A medial approach 1 cm anterior to the Achilles tendon border avoids injury to the sural nerve and is located in relatively thick tissues, which are biomechanically better suited to provide a healthy closure farther away from the tendon (Fig. 7-27). Care is taken to minimize soft-tissue handling. A Krackow-type stitch technique with nonabsorbable, no. 2 sutures is used to reapproximate the ‘‘mop end’’ rupture (Fig. 7-28). Whenever possible, the paratenon is reapproximated to minimize scar formation and improve tendon glide. Additionally, reapproximation of the fat pad anterior to the tendon can be performed. Initially, we immobilize the leg for 10 days until the wounds have healed. The same postoperative protocol described above for tendon reconstructions is used. Return to sport for the athlete after repair is 4 to 6 months. Mini-open technique To minimize the possibility of injury to the sural nerve inherent in a purely percutaneous suture technique, a mini-open approach can be used. A small stab incision
Figure 7-25 A lateral radiograph shows an avulsion fracture in a patient with a history of retrocalcaneal bursitis. There was no history of steroid injection.
is made, and then the subcutaneous soft tissue is spread bluntly before passing the suture/wire. A miniopen technique using a new instrument, the Achillon (Newdeal SA, Vienne, France), or Giannini’s device (Citieffe, Calderara di Reno, Bologna, Italy), combines the advantage of direct visual repair with minimizing potential complications of wound and nerve problems. A small skin incision is made, and the Achillon or Giannini’s device is introduced under the paratenon. A needle with suture is passed from the external guide through the skin into the tendon and out the opposite side. Three sutures are passed through the proximal tendon end, and three are used in the distal tendon end. The device and the suture ends are pulled out from under the paratenon and incision such that the ends of the sutures grasping the tendon now rest entirely within the paratenon. The tendon ends are reapproximated, and the sutures are tied. Assal et al.51 reported their experience using the Achillon device in 82 patients, noting that all patients who were elite athletes were able to return to their same level of competition.
Expected results of acute surgical repair One may expect return to sports generally at 4 to 6 months after acute repair and a program of early 175
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Figure 7-24 A positive Thompson test in the near leg with the Achilles tendon rupture. The calf muscles are squeezed and there is an absence of passive ankle plantarflexion in the prone position.
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Figure 7-26
Achilles tendon disorders including tendinosis and tears
The sagittal magnetic resonance imaging shows a long, complex Achilles tear (white arrows).
;
Figure 7-27 (A) An acute Achilles tendon rupture repair is performed with the patient in a prone position. (B) A medial approach made 1 cm anterior to the Achilles tendon border avoids injury to the sural nerve.
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Acute Achilles tendon rupture
Figure 7-27 cont’d. (C) The approach is with the scalpel, avoiding blunt dissection. (D) The exposure is through relatively thick tissues, which are biomechanically better suited to provide a closure that provides a barrier to the tendon, which is 1 to 1.5 cm away from the incision. (E) The exposed mop ends of the tendon.
Figure 7-28 (A) Another acute Achilles repair with exposure of the frayed tendon ends. (B) Care is taken to minimize soft-tissue handling. A Krackow-type stitch technique with nonabsorbable, no. 2 sutures is used to reapproximate the ‘‘mop end’’ rupture. (continued)
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Figure 7-28 cont’d. (C) The edges of the anastomosis should be made neat with a 2-0 or 4-0, absorbable suture. The resting tension should be restored.
protected weight bearing.14,44,52,53 Cetti et al.42 previously showed less calf atrophy and improved ability to resume preinjury level of athletic play after surgical repair as compared with nonoperative treatment.42,44,48-50,52 In a meta-analysis of acute Achilles tendon treatment, Bhandari et al.54 confirmed a statistically significant reduction in rerupture rates after surgical repair (3.1%) as compared with nonoperative treatment (13%). However, infections occurred only in the surgically treated group (infection rates ranging from 4% to 20%). The proportion of patients who regained normal function was similar in the operative and nonoperative treatment groups. In another meta-analysis, Kahn et al.55 identified 12 suitable papers for inclusion. They found that the relative risk of rerupture was 0.27 with operative versus nonoperative treatment. Complications including infection, adhesions, and altered skin sensitivity had a relative risk of 10.6 (operative vs. nonoperative). Functional bracing postoperatively had lower complications than casting postoperatively (relative risk 1.88). They concluded that operative treatment significantly reduced the risk of rerupture but significantly increased the risk of complications.
CHRONIC ACHILLES TENDON RUPTURE More than 20% of patients with an Achilles tendon rupture are missed on initial examination,14 and it therefore is not uncommon to diagnose a late injury. Chronic Achilles tendon ruptures generally present for delayed
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diagnosis or after a failed acute repair. Chronic ruptures typically are defined as those diagnosed more than 4 to 6 weeks after initial injury.53 After this period, the gap between the separated tendon ends fills with fibrinous material. This scar tissue contains disorganized fibroblasts and does not possess the same biomechanical strength as normal tendon. Over time, the tissue will elongate and lead to further functional weakness.14 Typically, a patient will complain of loss in push-off strength and be unable to perform toe walking and repetitive heel rise. When the patient lies prone, the injured extremity will demonstrate less resting plantarflexion tone as compared with the contralateral ankle. The involved ankle will display a relative increase in passive dorsiflexion and significantly less plantarflexion with calf squeeze. A palpable tendon gap is not typically evident, but the contour of the tissues will be altered, with thickening and loss of defined margins. The appearance of the affected calf muscle can be different from the contralateral side. Often the muscle belly is more proximally situated (‘‘balled up’’) as a result of its detachment distally. MRI and possibly ultrasound evaluation are useful in evaluating the size of the tendon gap and assist in surgical planning.
Nonsurgical treatment Nonoperative management may be considered in those without functional deficits or potentially high-risk patients, but surgical management is the treatment of choice for the athlete.
Surgical treatment ............................................................. Operative reconstruction generally will restore optimal musculotendinous length and improve strength and endurance. Direct repair often is not possible because of the relative immobility of the separated tendon ends with associated muscular retraction and atrophy. The size of the gap after debridement of interposed scar tissue determines whether a repair or reconstruction should be done and also determines which type of reconstruction should be done. If the delayed diagnosis is made within 4 to 6 weeks of injury, we perform tendon end debridement. We then mobilize the tendon by applying tension, holding the tendon in a stretched position for 10 minutes, and attempt a direct repair. After the tendon apposition, if it appears that the repair is too tight, we do a V-Y lengthening proximally to adjust the tension. After 6 to 12 weeks postinjury, it is not likely that the tendon ends can be mobilized sufficiently for direct repair with proper tension. If the gap is between 1 and 3 cm after debridement and mobilization, a V-Y
Chronic Achilles tendon rupture
For those cases with preoperative atrophy of the gastrocnemius/soleus muscle, an FHL tendon transfer may be considered (see Figs. 7-12 and 7-13). The FHL can be harvested from the posterior ankle in the depths of the posterior approach (Fig. 7-29, A) to the Achilles, or, if a longer graft is felt to be advantageous, from the arch of the foot. The graft harvest can be performed through a medial approach just plantar to the posterior tibial tendon and the talonavicular joint (Fig. 7-29, B) or through the plantar aspect through the plantar fascia (Fig. 7-29, C). For the latter approach, once the incision is made through the plantar fascia, care is taken to avoid the medial plantar nerve. The FHL and FDL tendons can be found in the depth of the wound next to the first metatarsal and medial cuneiform. Once the tendons have been identified, the FHL is sutured to the FDL distal to the point at which the tendon will be transected (at or near the knot of Henry). A suture placed in the
Figure 7-29 (A) The flexor hallucis longus (FHL) can be harvested from the posterior ankle in the depths of the posterior approach to the Achilles. (B) The graft harvest through a medial approach just plantar to the posterior tibial tendon and the talonavicular joint. (C) The graft harvest through the plantar aspect of the foot. After incising the plantar fascia and reflecting the medial plantar nerve, the FHL and flexor digitorum longus (FDL) tendons can be found next to the bones. The FHL is sutured to the FDL distal to where the tendon will be transected. Next, the FHL is cut proximal to the tenodesis and withdrawn out the proximal ankle incision.
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procedure can be performed (see Fig. 7-14). To perform the V-Y advancement, a direct reapproximation is performed using a no. 2, nonabsorbable suture in a Krackow or whipstitch. This allows further ability to stretch out the tendon. If reapproximating the tendon ends results in too much tension, we then proceed with the V-Y advancement. We allow the V-Y gap distance to reduce the contraction and restore proper tension as compared with the contralateral side. For more chronic cases seen more than 12 weeks after a missed rupture or after a previous completely failed repair, a V-Y advancement or turndown likely will be required, depending on the size of the defect after repair. For defects between 2 and 3 cm, a V-Y advancement is possible, as mentioned previously. For defects longer than 3 to 5 cm, a turndown procedure with possible tendon augmentation is required, as discussed earlier (see Fig. 7-15).
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FHL proximal to the transection is helpful in case the tendon does not pull through into the proximal wound. Den Hartog56 described a technique of harvesting the FHL tendon near the tip of the medial malleolus for chronic Achilles tendinosis. Good to excellent results were reported in 23 of 26 treated patients without any deficit to first-toe function. A recent biomechanical study showed little pressure change under the first or second metatarsophalangeal (MTP) joint and no clinical functional deficit after FHL harvesting.57 Prior studies also showed promising clinical results.58,59
CONCLUSION Achilles tendon disorders are common in the athlete. If diagnosed early, the process usually is a tendinitis and is amenable to nonoperative treatment such as intermittent immobilization, stretching, modalities such as ultrasound and iontophoresis, and use of antiinflammatoriy medication. More chronic cases take longer to treat and have a higher risk of requiring operative intervention. Operative treatment typically is 70% to 90% successful but requires 3 to 6 months for return to athletic participation. Achilles rupture typically will require operative treatment in the athlete, and 6 to 9 months can be a typical recovery period.
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References 49. Solveborn SA, Moberg A: Immediate free ankle motion after surgical repair of acute Achilles tendon ruptures, Am J Sports Med 22:607, 1994. 50. Speck M, Klaue K: Early full weightbearing and functional treatment after surgical repair of acute Achilles tendon rupture, Am J Sports Med 26:789, 1998. 51. Assal M, et al: Limited open repair of Achilles tendon ruptures: a technique with a new instrument and findings of a prospective multicenter study, J Bone Joint Surg Am 84-A:161, 2002. 52. Maffulli N: Rupture of the Achilles tendon. Current concepts review, J Bone Joint Surg 81A:1019, 1999. 53. Myerson MS: Achilles tendon ruptures, Instructional Course Lectures 48:219, 1999. 54. Bhandari M, et al: Treatment of acute Achilles tendon ruptures: a systematic overview and metaanalysis, Clin Orthop 400:190, 2002Jul. 55. Kahn RJ, et al: Treatment of acute Achilles tendon ruptures: a meta-analysis of randomized, controlled trials, J Bone Joint Surg Am 87-A:2202, 2005. 56. Den Hartog BD: Flexor hallucis longus transfer for chronic Achilles tendinosis, Foot Ankle Int 24:233, 2003. 57. Coull R, Flavin R, Stephens MM: Flexor hallucis longus tendon transfer: evaluation of postoperative morbidity, Foot Ankle Int 24:931, 2003. 58. Wapner KL, et al: Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer, Foot Ankle 14:443, 1993. 59. Wilcox DK, Bohay DR, Anderson JG: Treatment of chronic Achilles tendon disorders with flexor hallucis longus tendon transfer/augmentation, Foot Ankle Int 21:1004, 2000.
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38. Galasso O, et al: Chronic achillodynia. Treatment with extracorporeal shock wave. Presented at the 3rd International Congress of the ISMST, Naples, Italy, 2000. 39. Ogden JA, Cross GL: Application of electrohydraulic orthotripsy for chronic Achilles tendinopathy. Presented at the 5th International Congress of the ISMST, Orlando, Florida, 2003. 40. Title CI, Katchis SD: Traumatic foot and ankle injuries in the athlete, Orthop Clin North Am 33:587, 2002. 41. Thermann H: Treatment of Achilles’ tendon ruptures, Foot Ankle Clin 4:773, 1999. 42. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature, Am J Sports Med 21:791, 1993. 43. Soma CA, Mandelbaum BR: Achilles tendon disorders, Clin Sports Med 13:811, 1994. 44. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation, Am J Sports Med 23:392, 1995. 45. Thermann H, Zwipp H, Tscherne H: [Functional treatment concept of acute rupture of the Achilles tendon. 2 years results of a prospective randomized study], Unfallchirurg 98(1):21, 1995. 46. McComis GP, Nawoczenski DA, DeHaven KE: Functional bracing for rupture of the Achilles tendon. Clinical results and analysis of ground-reaction forces and temporal data, J Bone Joint Surg 79-A:1799, 1997. 47. Weber M, et al: Nonoperative treatment of acute rupture of the Achilles tendon: results of a new protocol and comparison with operative treatment, Am J Sports Med 31:685, 2003. 48. Mortensen HM, Skov O, Jensen PE: Early motion of the ankle after operative treatment of a rupture of the Achilles tendon. A prospective, randomized clinical and radiographic study, J Bone Joint Surg Am 81:983, 1999.
........................................... C H A P T E R 8 Posterior tibialis tendon dysfunction W. Grant Braly CHAPTER CONTENTS ...................... Introduction
183
Treatment
191
Anatomy and biomechanics
183
Perils and pitfalls (with illustrative case reports)
200
Diagnosis
185
Summary
202
Disease staging
190
References
202
INTRODUCTION Acute posterior tibialis tendon injury in the athlete is rare1,2 but must be considered in the differential diagnosis of a patient who presents primarily with tenderness, swelling, and pain over the medial ankle or plantar medial midfoot. Antecedent to the acute presentation, there often is a history of less severe prodromal symptoms more consistent with a chronic interstitial rupture with tendinosis. The chronic picture is seen more often in the middle-aged to elderly patient, athlete or not, that was especially popularized by the late Kenneth A. Johnson, MD,3-5 with whom I had the honor of fellowship training. Others,1,2,6-9 of course, also have contributed to a further understanding of the diagnosis and treatment of this condition. Although most of the literature emphasizes chronic posterior tibialis tendon disease, the ultimate presentation of the acutely injured athlete may be very similar to the chronic form. Therefore given the rarity of acute injury versus the more commonly seen chronic presentation, posterior tibialis tendon ‘‘dysfunction,’’ rather than ‘‘injury,’’ probably is a more accurate description and title for this chapter.
ANATOMY AND BIOMECHANICS The posterior tibialis muscle is a resident of the deep posterior compartment of the leg, originating along
the proximal one third of the tibia and intraosseous membrane. Distally, its tendon travels posterior, then inferior, through the medial malleolar groove, changing direction abruptly almost 90 degrees. The stout retinaculum of the long flexors prevents the tendon from subluxating over the medial malleolus.10 Because the posterior tibialis tendon is without a mesotenon, there is an area of relative hypovascularity from this acute turn at the medial malleolus to the medial navicular insertion. These factors of hypovascularity and the mechanical stress of an acute turn of the tendon as part of a strong, weight-bearing leg muscle (second only to the gastrocnemius) make the tendon predisposed to injury in this area. Because the posterior tibial tendon travels posterior to the axis of the ankle and medial to the axis of the subtalar joint, it serves as an ankle plantarflexor and foot invertor via the transverse tarsal joint (talonavicular and calcaneocuboid joints).11 The tendon also has multiple slip attachments to the capsule of the naviculocuneiform joint, all three of the cuneiforms, the cuboid, and their respective metatarsal bases in the plantar arch.4,12 The posterior tibialis tendon therefore is primarily a midfoot invertor and dynamically supports and elevates the medial longitudinal arch. It also indirectly supports the hindfoot because of its medial malleolar pulley action and intimate relationship to the deep deltoid ligament, plantar medial talonavicular joint capsule, and spring ligament (calcaneonavicular ligament).13 With relatively little elongation because of rupture, the tendon becomes
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incompetent to support the medial longitudinal arch initially, resulting in the acquired adult flatfoot with forefoot pronation and abduction (Fig. 8-1). However, over time other ligamentous structures are affected, including the talonavicular joint capsule, deltoid ligament, and spring ligament. The stretching out or even
frank rupture of these structures eventually leads to a valgus inclination of the hindfoot and external rotation of the calcaneus, also resulting in contracture of the Achilles tendon as it becomes a hindfoot everter11 (Fig. 8-2). Clinically, this may result in impinging pain and swelling in the subfibular or sinus tarsi area as the
Figure 8-1 Dorsal-plantar view demonstrating the normal foot (A) and the posterior tibialis tendon incompetent foot (B). With external rotation or abduction of the forefoot, the medial talar head becomes more uncovered by the navicular as it rotates externally. The calcaneus also secondarily rotates externally and tilts into more valgus.
Figure 8-2 Posterior-anterior view of the normal (A) and posterior tibialis tendon incompetent ankle and hindfoot (B). With external calcaneal rotation, the talar head translates plantarward. This also leads to increased valgus tilting of the calcaneus and subfibular or sinus tarsi impingement.
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Diagnosis
calcaneus abuts against the lateral malleolus. In very severe or neglected cases, a valgus tilt of the ankle may be seen as the deltoid ligament becomes incompetent.
DIAGNOSIS Usually, a detailed history, conscientious physical examination, and x-rays will establish the diagnosis of a posterior tibialis tendon injury.
Physical examination and questions to be answered For comparison, both unclothed and unshod lower extremities from the midthigh distally to the toes should be carefully examined. Is there a valgus knee deformity (genu valgum) of the symptomatic side? (This may precipitate or exacerbate posterior tibialis tendon dysfunction, especially if chronic.) Is there tenderness and swelling along especially the terminal course of the tendon, generally between the medial malleolus and the navicular insertion or, less commonly, in the posterior aspect of the medial malleolus (Fig. 8-3, A and B)?
Figure 8-3 Usual area of maximal tenderness and swelling along the terminal course of the posterior tibialis tendon between the medial malleolus and medial navicular insertion. Occasionally, this can extend to the area posterior to the medial malleolus.
Figure 8-4 The positive ‘‘too many toes’’ sign in the posterior tibialis dysfunctional right foot is appreciated when examining the weight-bearing patient from behind. The forefoot is abducted/pronated and the hindfoot is in greater valgus, resulting in more toes seen laterally in the right foot when compared with the left.
Is there tenderness in the insertional area of the anterior tibialis tendon? In viewing the weight-bearing patient from behind, is there increased forefoot abduction or pronation (the so-called ‘‘too many toes sign’’) (Fig. 8-4)? Does the patient have difficulty heel rising with all of his or her weight on the injured side (‘‘single foot heel rise’’ test), or if he or she is able to heel rise, does the hindfoot fail to invert or invert less than the normal side (Fig. 8-5)? 185
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History and questions to be answered Sometimes the history alone will provide the examiner with enough information to suggest the diagnosis. What was the mechanism of injury? Specifically, did the foot sustain an eversion twisting injury, especially on impact from tripping or a fall? Or, was there a sudden increase in the level of athletic activity temporally related to the onset of symptoms? Were there prodromal symptoms of possible tendon degeneration before the acute injury? Has the athlete noticed that the arch on the involved side is ‘‘flatter,’’ the foot is ‘‘turned out,’’ the ankle ‘‘turned in,’’ or complained that the injured foot is ‘‘weaker’’? When unshod on a hard, wet floor surface, such as at bath time, does the patient notice a different footprint or a ‘‘sucking sound’’ because of a vacuum effect of the collapsed arch on the symptomatic side? Has the athlete noticed more medial shoe sole wear or ‘‘running over’’ the medial vamp? Is there any history of gout, pseudogout, or autoimmune disease? Are there sensory (dysesthesias or paresthesias) complaints? In terms of predisposing risk factors, is there a history of oral steroid use, injected steroids in the area of the tendon, diabetes, smoking, vasculopathy, obesity, or worsening of a preexisting pes planus deformity?
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Figure 8-5 Notice hindfoot inversion in the normal left foot. Although patients with posterior tibialis tendon dysfunction may be able to perform the single-foot heel-rise test, notice that the hindfoot does not invert, or inverts less, than the normal foot. This may be due to some residual function of the posterior tibialis muscle tendon unit with assistive recruitment of the long toe flexors.
Is there tenderness and swelling laterally in the sinus tarsi or subfibular area, suggesting impingement, especially in the patient with deformity (Fig. 8-6)? Is the Achilles tendon contracted? Are there abnormal sensory findings that might suggest peripheral neuropathy, especially in the diabetic patient? Is there a positive Tinel’s sign over the tibial nerve in the medial ankle or plantar foot sensory deficits that might suggest a tarsal tunnel syndrome? Is there a tender and swollen bony prominence in the area of the medial navicular, suggesting an accessory navicular or stress fracture? Is the medial malleolus itself tender, thus suggesting a stress fracture? Are there any dysvascular findings (absent posterior tibial or dorsalis pedis pulses, delayed capillary refill, cyanosis, toe hair loss, and dystrophic nail changes)?
X-rays and questions to be answered ............................................................. Ideally, weight-bearing x-rays of the symptomatic foot and ankle should be taken. Also, comparison views of the other foot and ankle often are helpful diagnostically.
Ankle x-rays Do films demonstrate a medial or valgus tilt (Fig. 8-7, A)? Are there arthritic changes with joint space narrowing, osteophytes, or loose bodies medially? Is there any evidence of a medial malleolar stress fracture or medial talar dome osteochondritis dissecans (Fig. 8-7, C)? Is there major arterial (anterior and posterior tibial) calcification?
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Figure 8-6 Zone of tenderness and swelling indicative of impingement in the subfibular or sinus tarsi area, often seen with more severe posterior tibialis tendon dysfunction with hindfoot valgus deformity.
Foot x-rays Is there an accessory navicular or possible avulsion fracture of the medial navicular (see Fig. 8-7, B)? Do the films of the foot reveal arthritic changes of the medial subtalar (additional Broden’s views may be helpful), talonavicular, naviculocuneiform, or medial tarsometatarsal joints (Fig. 8-7, D)? Is there any evidence of a tarsal coalition, especially in the periadolescent athlete? On the lateral view, is the talo-first metatarsal angle negative, especially if it is more so than a comparison view of the contralateral foot (Fig. 8-8)?
Diagnosis
Figure 8-7 Radiographs of patients with medial ankle or midfoot pain and swelling demonstrating medial talar tilt because of primary deltoid ligament incompetency (A) accessory navicular (B) medial talar dome osteochondritis dissecans with a coronal magnetic resonance imaging (MRI) view (C) and medial column arthritis. (continued)
On the anteroposterior (AP) view, is there an increased talo-first metatarsal angle or increased ‘‘uncovering’’ of medial talar head at the talonavicular joint, thus indicating forefoot abduction, again especially when compared with the contralateral foot (Fig. 8-9)?
As in the ankle, is there arterial calcification of the dorsalis pedis or posterior tibialis arteries?
Magnetic resonance imaging (MRI) Although rarely necessary, if the history, physical examination, and x-rays fail to conclusively determine the 187
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Figure 8-7 cont’d. (D) all of which can mimic to varying degrees the clinical presentation of posterior tibialis tendon dysfunction.
Figure 8-8 Lateral weight-bearing views demonstrating the midfoot sag of the posterior tibialis incompetent right foot. I prefer this more simplistic measurement of the angle between the long axis of the talus (a) and the I metatarsal (b). The resultant angle (c) is greater in the involved foot. In this case in the normal left foot, these lines are virtually parallel. Also, notice that the subtalar joint is less clearly seen in the symptomatic right foot because of superimposition of the talus and calcaneus from a hindfoot valgus deformity.
diagnosis of a posterior tibialis tendon injury, or to confirm the diagnostician’s impression, then an MRI may be indicated.14,15 An MRI also is helpful to determine the extent of acute injury or chronic tendinosis and thus guide treatment, especially if surgery is planned, and may predict the postoperative clinical outcome.15 Finally, the MRI may help to determine other conditions that may mimic, be concomitant with, or even contribute
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to posterior tibialis tendon disease8,10,13,16,17 (Table 8-1). Perhaps of historical interest, others have proposed the diagnostic use of tenography7 or ultrasound,18 but their sensitivity is significantly less than that of a highquality MRI. Generally, the MRI will reveal fibrous tendinotic longitudinal hypertrophy or bulbous enlargement of the tendon, sometimes with cystic or longitudinal voids
Diagnosis
Figure 8-9 Anteroposterior (AP) weight-bearing views demonstrating abduction deformity resulting from posterior tibialis tendon incompetency in the right foot. Again, I prefer this more simplistic measurement of the ankle between the long axis of the talus (a) and the I metatarsal (b). The resultant angle (c) is great in the involved right foot. Also, notice that the medial talar head is more uncovered by the navicular in the involved foot (d).
Differential diagnosis
Medial ankle arthritis
Medial subtalar joint or medial column arthritis
Medial ankle instability with deltoid ligament rupture/laxity
Symptomatic accessory navicular with synchondrosis disruption
Medial malleolar or talar stress fracture
Medial navicular bony avulsion or stress fracture
Medial talar dome osteochondritis dissecans
Acute injury or tendinosis of the flexor hallucis longus or flexor digitorum longus tendons
Tarsal tunnel syndrome
Peri-insertional anterior tibialis tendon rupture or tendinosis
Tarsal coalition, especially in periadolescent athletes
Medial ankle or hindfoot/midfoot crystalline or autoimmune arthritis
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Table 8-1
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Figure 8-10 Magnetic resonance imaging (MRI) findings of posterior tibialis tendon dysfunction. (A) Sagittal view at the level of the medial malleolus (MM) demonstrating longitudinal void within the tendon. (B) Transverse view at the level of the talus (T) also demonstrating intratendinous voids and increased fluid around the tendon.
(Fig. 8-10, A). Also, there usually is increased tenosynovial fluid within the sheath surrounding the tendon18,19 (Fig. 8-10, B). These findings usually are seen between the medial malleolus and navicular but also can extend proximally into the posterior medial malleolar area.
Table 8-2 Disease stages Stage I Peritendinitis and/or tendon degeneration (tendinosis) No deformity
DISEASE STAGING Once the diagnosis is firmly established, the stage of posterior tibialis tendon disease, as popularized by Kenneth A. Johnson’s seminal work, is important to determine the proper course of treatment. Johnson initially described stages I to III,5 but a stage IV11,20 has more recently been described that involves a valgus inclination of the talus with degenerative arthritis of the ankle joint (Table 8-2). This is exceedingly rare in the active athlete and will not be elaborated upon beyond its mention. Stage I is essentially peritendinitis and/or tendon degeneration (tendinosis) with a normal tendon length and no deformity. Stage II is characterized by an incompetent or lengthened tendon with a mild flexible deformity. Stage III encompasses the findings of the
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Stage II Tendon elongated/incompetent Mild flexible deformity Stage III Findings of Stage I and II Moderate-to-severe deformity that may be rigid with possible subfibular or sinus tarsi impingement Radiographic arthritic changes of triple joint complex and/or naviculocuneiform joints (Stage IV, which involves a valgus talar tilt and early ankle joint degeneration, also has been described but probably is not applicable to this discussion, given its extreme rarity in the active athlete.)
Treatment
TREATMENT Conservative In general, conservative treatment is recommended initially, especially for the stage I and II presentation in the otherwise healthy athlete. However, in the patient who has significant comorbid conditions (e.g., diabetes, smoking, vasculopathy, obesity, etc.) that makes surgical treatment ill advised, conservative treatment may be the definitive treatment. In the young, competitive athlete, these comorbidities are uncommon, but, in the middle-aged athlete, they are not rare. As with any inflammatory condition or injury, immobilization is therapeutic. Either casting or rigid bracing is recommended for several weeks, the length of immobilization depending on the response of such treatment with diminution of the associated swelling or tenderness. The cast that is well molded to support the arch or the incorporation of an arch support and/or medial wedge if a brace is chosen is further recommended. Weight bearing during the immobilization treatment period is allowed as tolerated. In the less acute or chronic presentation, or after a positive response to immobilization, custom-molded arch supports, perhaps with medial wedging incorporated either in the orthotic and/ or on a supportive shoe on the symptomatic side are advised for several months. Nonsteroidal anti-inflammatory medications also are helpful, but chronic oral steroids should be avoided. Steroid injections also should be shunned because these may lead to complete rupture7,21 or at least exacerbate a tendinotic condition, especially if an injection is inadvertently intratendinous. In terms of athletic activity during the conservative treatment period, and perhaps for several weeks after, the injured athlete also should avoid any repetitive impact-loading sports or conditioning. Cross training (e.g., bicycling, swimming, perhaps walking and/or primarily upper-extremity bench weight training) is advised. In the athlete with a tight Achilles tendon, stretching is helpful,22 especially to avoid reinjury once he or she has been successfully treated conservatively and returns to the preinjury level of activity. Also, ideal long-term
management includes supportive and often-replaced, high-quality athletic shoes. Finally, if it is an issue in the overweight athlete, weight loss obviously is recommended. Other comorbid conditions also should be addressed, for example smoking cessation and good control of diabetes and autoimmune disease.
Surgical treatment The following discussion includes surgical treatment of the stages of posterior tibial tendon rupture gleaned from the literature but also is biased by my own experience (Table 8-3). Stage I—tendon length normal Intraoperative findings include tenosynovitis, often with granulation tissue, increased tenosynovial fluid, and an interstitial longitudinal rupture, usually between the medial malleolar tip and the navicular insertion of the tendon.5,9 Fusiform hypertrophy with tendinotic ‘‘crabmeat’’ tissue often is encountered, as well as possible cystic degeneration, especially in a more chronic presentation. Surgical treatment involves opening the tendon sheath from at least the medial malleolus to the navicular insertion. If disease is noted proximal to the medial malleolus, then it is important to preserve, if possible, an approximately 1-cm section of the sheath at the medial malleolar level to prevent subluxation of the tendon. (If this is not possible because of extensive proximal disease, then that portion of the tendon should be repaired after the tendon itself is addressed.) Tenosynovitis and granulation tissue are debrided with a small rongeur. The hypertrophied portion with tendinosis within the tendon then is debrided and debulked sharply via a longitudinal incision in the tendon itself. The incision then is repaired with absorbable, interrupted suture with inverted knots. Postoperatively, cast immobilization is recommended for 3 weeks, followed by rigid bracing, stirrup bracing, or a short articulating AFO for another 3 weeks. After immobilization, supportive shoewear with a custommade arch support is recommended for 3 months. In the athlete, repetitive impact-loading sports or conditioning endeavors are avoided until at least 3 months postoperatively. Stage II—tendon elongated, deformity mild and flexible Similar, but more severe, pathologic findings as seen in stage I are encountered in stage II disease. There usually is a longer area of interstitial rupture with accompanying bulbous enlargement of the tendon that may even extend proximal to the medial malleolus. The tendon is found to be elongated, and thus incompetent, allowing excessive pronation and abduction of the forefoot. 191
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preceding stages, but with a greater degree of deformity that also may be rigid. X-rays of the stage III foot may further reveal significant arthritic changes in any or all of the triple joint complex (subtalar, talonavicular, and/or calcaneocuboid joints) or naviculo-cuneiform joints, as well as clinical signs and symptoms of subfibular or sinus tarsi impingement.
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Table 8-3
Surgical management
Postoperative regimen
Return to sports postoperative
Tenosynovectomy
Cast: 3 weeks
3 months
Repair of interstitial rupture
Rigid brace: 3 weeks
Possible medial shift calcaneal osteotomy for severe cases?
Supportive shoes with custommolded arch supports: until 3 months postoperative
Technique Stage I
Stage II Repair and advance/shorten tendon
Cast: 6 weeks
Imbricate talonavicular joint plantar medial capsule
Rigid brace: 6 weeks
Flexor digitorum longus tendon transfer
Supportive shoes with custommolded arch supports: until 6 months postoperative
6 months
Medial shift calcaneal osteotomy with flexible deformity Possible Achilles tendon lengthening or gastrocnemius recession Stage III Repair/reconstruction of tendon may not be necessary?
Cast: 9-12 weeks
Medial shift calcaneal osteotomy and/or lateral column lengthening if deformity is flexible
Rigid brace: 6-9 weeks
Arthrodesis if deformity rigid and/or arthritic changes present
Supportive shoes with custommolded arch supports?
9-12 months
Possible Achilles tendon lengthening or gastrocnemius recession
(The function of the posterior tibialis is easily compromised with even a small increase in length because the normal excursion in the healthy tendon rarely exceeds 1 to 2 cm.) The tendon is repaired as described for stage I. Also, shortening of the tendon is advised by advancing its plantar medial insertion on the navicular. It usually is necessary to detach the medial insertion and excise excess peri-insertional tendon before securing it to the decorticated plantar medial aspect of the navicular with nonabsorbable sutures incorporated in bone anchors9
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or through drill holes4,5,9,11,13,23,24 (Fig. 8-11, F, H, and I). The surgeon also may consider elliptically excising a transverse segment and imbricate the attenuated plantar medial capsule of the talonavicular joint in severe cases,11,23 or, obviously, repair it if it is torn (Fig. 8-11, B, D, and G). With extensive stage II findings, and especially if the tendon is completely torn, a tendon transfer is recommended (Fig. 8-11, A). Most surgeons harvest the flexor digitorum longus3-5,7,9-11,13,19,23,24 for this purpose, which is in close proximity to the posterior tibialis tendon (Fig. 8-11, C and E). Within the same surgical incision,
Treatment
A
B Figure 8-11 Intraperative photographs and corresponding schematic drawings demonstrating my preferred method of reconstruction of a complete rupture of the posterior tibialis tendon. This patient had a flexible deformity without degenerative triple joint arthritis. A medial shift calcaneal osteotomy was added to the medial soft-tissue reconstruction. (A) Complete rupture of the posterior tibialis tendon. The two ends could not be approximated because of proximal migration of the proximal end. (B) Subsequent to debridement of the distal end of the posterior tibialis tendon, the plantar medial talonavicular joint capsule was incised and an elliptical segment removed to later imbricate it. (continued)
the level of flexor digitorum longus cut. Other tendons have been suggested for transfer, but these transfers may be of historical interest only. Although the flexor hallucis longus has a stronger muscle than the flexor digitorum longus, its transfer is not recommended because the dissection associated with its harvesting is technically challenging and risky, given its close 193
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the flexor digitorum longus is cut sharply as distally as possible and is secured to the navicular or as a side-toside transfer to the repaired and advanced posterior tibialis tendon. It generally is not necessary to sew the distal stump of the flexor digitorum longus tendon to the flexor hallucis longus tendon because of the many soft-tissue connections between them distal to
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C
D Figure 8-11 cont’d. (C) The flexor digitorum longus tendon is harvested as distally as possible. It is not necessary to tenodese the distal end of the flexor digitorum longus to the flexor hallucis longus tendon to maintain adequate lesser toe flexor function. (D) Heavy absorbable stay sutures are placed and tagged in the plantar medial talonavicular joint capsule. (continued)
proximity to the neurovascular bundle. Also, the resultant weakness of great toe flexion may be a significant problem for a high-performance athlete. More recently, as primarily popularized by Myerson11,23 and described by others,10,19,22,26 a medial shift or slide calcaneal osteotomy has been advocated for stage II disease. (There also may be an indication for this osteotomy in severe stage I cases.11)
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The effect of this osteotomy is to translate the pull of the gastrocsoleus muscle via the Achilles tendon more medial to the axis of the subtalar joint, which enhances the varus force on the hindfoot. Another indirect, beneficial effect therefore is to decrease tension on the reconstructed posterior tibialis tendon. The medial displacement also may at least partially reestablish the height of the medial longitudinal arch.
Treatment
E
F Figure 8-11 cont’d. (E) The flexor digitorum longus tendon is passed through and tenodesed with maximal tension to the proximal end of the posterior tibialis tendon. (F) A bone anchor is placed in the decorticated medial aspect of the navicular. (continued)
the posterior plantar edge of the calcaneal body, thereby avoiding the insertion of the Achilles tendon and the plantar fascia origin.11,19,23,24 A slightly curved incision is made, and great care is taken to protect 195
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The osteotomy is a straight cut from the lateral hindfoot at an angle of approximately 45 degrees to the plantar surface of the heel roughly equidistant between the posterior facet of the subtalar joint and
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G
H Figure 8-11 cont’d. (G) The plantar medial talonavicular joint capsular stay sutures are tied. (H) The flexor digitorum longus tendon is secured to the medial navicular under tension with the nonabsorbable sutures from the bone anchor. (continued)
the sural nerve in the lateral approach to the calcaneal wall (Fig. 8-12, A). A power saw can be used until the surgeon approaches the medial calcaneal wall, but an osteotome is recommended to complete the osteotomy medially to prevent injury to the neurovascular bundle (Fig. 8-12, B and C). A medial shift of approximately 10 mm is recommended.11,19,23,24 Provisional fixation is achieved with two percutaneous pins in the sinus tarsi area until definitive internal fixation is placed (Fig. 8-12, D). A partially threaded cannulated cancellous screw via a separate plantar
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posterior heel incision can be used for internal fixation. The proper placement of this screw should be guided fluoroscopically to avoid penetration of the subtalar joint and medial or lateral calcaneal wall. Countersinking the screw head is advised to prevent symptomatic hardware. Recently I have been using two dynamic compression nitinol step staples for definitive internal fixation (Fig. 8-13, A through C). This eliminates the need for a second incision associated with the screw placement, is technically less challenging and time
Treatment
I Figure 8-11 cont’d. (I) Final appearance of the reconstruction. Heavy absorbable sutures also are used to further secure the flexor digitorum longus tendon transfer to the fibrous tissue of posterior tibialis tendon sheath and the surrounding periosteum.
consuming, and decreases the likelihood of symptomatic hardware. Also, there is potentially less fluoroscopic radiation exposure because usually only intraoperative radiographic demonstration of the final proper staple position in the axial heel and lateral planes is necessary, versus perhaps multiple fluoroscopic guidance images that may be required for screw placement. If, after the reconstruction of the posterior tibialis tendon, the foot cannot be passively dorsiflexed to at least 10 degrees with the knee fully extended, then a percutaneous Achilles tendon lengthening or gastroc-
nemius recession is indicated.22 This procedure serves to diminish the stress on the reconstruction and may help to prevent recurrent rupture and deformity postoperatively. Postoperatively, casting is advised for 6 weeks, initially with the foot in plantarflexion and inversion for the first 2 weeks. The foot is brought to a neutral position gradually by the end of the fourth week, when partial weight bearing is permitted. If a medial shift calcaneal osteotomy is performed, then serial axial and lateral x-rays of the heel are taken to monitor healing. Following casting, rigid bracing with an arch support is
Figure 8-12 Medial shift calcaneal osteotomy. (A) Recommended location of lateral hindfoot incision. (B) Power saw used initially for osteotomy. Multiple retractors are recommended to protect the surrounding soft tissues. (continued)
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Figure 8-12 cont’d. (C) Osteotomy completed through the medial calcaneal wall using an osteotome to minimize any potential damage to the neurovascular bundle. (D) Temporary percutaneous smooth pin internal fixation until definitive internal fixation is placed.
recommended for 6 weeks, with progression to full weight bearing as tolerated. The patient may remove the brace for bathing, sleeping, and active ankle range of motion exercises. Supportive shoewear with a custom-made arch support is worn until 6 months postoperatively. Return to repetitive impact-loading sports or conditioning is ill advised before 6 months postoperatively.
Stage III—Tendon Elongated, Flexible or Rigid Moderate to Severe Deformity Stage III presentation is rare, especially in the younger athlete. Intraoperative pathologic findings often eclipse those of stage II, and the tendon is grossly incompetent even if still intact or may be completely ruptured with retraction of the proximal end of the tendon in the distal medial leg. Surgical repair or reconstruction of the tendon as described in stage II disease may not be necessary when a bony stabilization procedure (fusion or opening wedge osteotomy) is performed in stage III disease. A soft-tissue reconstruction alone, even with a medial shift calcaneal osteotomy, probably will not prevent recurrent deformity and associated symptoms, especially in the heavier patient. If the deformity, although moderate to severe, is still flexible and there are no significant degenerative arthritic changes, then the surgeon may consider a medial shift calcaneal osteotomy combined with a lateral column lengthening, with either a calcaneocuboid joint distraction arthrodesis or anterior calcaneal opening wedge with bone graft proximal to the calcaneocuboid joint.20,22 However, a calcaneocuboid distraction arthrodesis usually will limit hindfoot motion significantly and unduly stress the articulations of the
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synchronous function of the talonavicular and subtalar joints, possibly leading to early degenerative arthritis, which may be the result of diminution of circulating synovial fluid delivery of nutrition to the cartilage of these unfused, but now stiffer, joints. Theoretically, an anterior calcaneal opening wedge osteotomy may have an advantage in preserving more motion and thus preventing long-term arthritic disease.22 An opening wedge plantarflexion osteotomy with bone graft of the dorsal medial cuneiform also has been described20 to further correct residual forefoot varus deformity with restoration of a more balanced, ‘‘tripod,’’ weight-bearing foot. These procedures are technically challenging,
Figure 8-13 Intraoperative photograph (A) and lateral (B) and axial (C) heel views demonstrating nitinol step staple internal fixation of the medial shift calcaneal osteotomy of approximately 10 mm for patients with primarily stage II and III posterior tibialis tendon dysfunction.
Treatment
cont’d.
and overcorrection can be a problem. Also, if autogenous iliac tricortical bone graft is chosen, the surgeon must consider the associated morbidity. Finally, as with any distraction arthrodesis or opening wedge osteotomy, the delayed or nonunion rates may be significantly higher.22 Rigid internal fixation may lessen this complication. However, if degenerative arthritis also is an issue, then an arthrodesis is indicated. There are many proponents of an arthrodesis of the subtalar5,20,25 or talonavicular joint alone, calcaneocuboid and talonavicular joint arthrodesis (double arthrodesis),9 or triple arthrodesis.26 Perhaps it may not make much difference which type of arthrodesis is chosen, because, again, the fusion of even one of these joints severely limits the motion of the other two, thus maintaining the desired correction. However, long-term pain and eventual arthritis may develop because of the limited motion in the remaining unfused joints for the same reason as an isolated calcaneocuboid distraction arthrodesis as previously described. A triple arthrodesis with deformity correction would, of course, prevent this, but over time may lead to usually valgus ankle instability and arthritis.11,22 This is the result of long-term attenuation of the deltoid ligament usually resulting from undercorrection of hindfoot valgus that is rigid and therefore incapable of inversion/eversion torque conversion, thus translating those forces to the medial ankle. On rare occasions, especially if the hindfoot is overcorrected to
varus, or in the preexisting cavovarus foot that is undercorrected, just the opposite can occur, with lateral talar tilt, instability, and arthritis. Converse to the argument against a limited versus triple arthrodesis, a case can be made, especially in the younger patient, for selected arthrodesis of one of the joints of the triple joint complex if the deformity is severe but still flexible, because limitation of motion in the other unfused joints, even if they are somewhat cartilage deficient, may prevent arthritic symptoms from developing. Based on that rationale, I prefer an isolated talonavicular joint arthrodesis with bone graft and believe that it better corrects the abduction/pronation deformity and may indirectly correct a flexible hindfoot valgus deformity. Others feel that the subtalar joint,4,5,24 and not the talonavicular, is the ‘‘keystone’’ to correction of the deformity. Rather than proceeding with a subtalar or triple arthrodesis, I feel that if hindfoot valgus still is an issue intraoperatively after a talonavicular joint arthrodesis, then a medial shift calcaneal osteotomy can be added. As with stage II cases, and regardless of the chosen arthrodesis or osteotomy for stage III disease, a percutaneous Achilles tendon lengthening or gastrocnemius resection22 is further indicated if the foot cannot be passively dorsiflexed beyond 10 degrees with the knee fully extended. Postoperatively, cast immobilization generally is in the 9- to 12-week range, depending on the progress 199
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Figure 8-13
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Posterior tibialis tendon dysfunction
of healing of the osteotomy or arthrodesis. Some limited weight bearing usually is allowed at 6 weeks postoperatively, depending on the level of healing on serial x-rays. Rigid bracing after casting is advised for 6 to 12 weeks. Supportive shoes with custom-molded arch supports may not be necessary, especially if a fusion is performed. Return to athletic activity is allowed 9 to 12 months postoperatively.
PERILS AND PITFALLS (WITH ILLUSTRATIVE CASE REPORTS) Lack of recognition or misdiagnosis of posterior tibialis tendon injury in the athlete can be avoided with a conscientious history, physical examination, and weightbearing x-rays. The differential diagnostic possibilities (see Table 8-1) also should be kept in mind when encountering the athlete with a suspected posterior tibialis tendon injury to prevent the perils and pitfalls of misdiagnosis and to aid selection of the proper treatment. If the presenting patient’s diagnosis then is still in question, then an MRI is recommended. However, even the most astute diagnostician can fail to determine the proper diagnosis.
C A S E S T U D Y 1
One dilemma of determining the correct diagnosis and treatment is especially evident in the patient who may have preexisting bilateral pes planus, because unilaterality of the traumatically acquired pes plano valgus deformity with a positive ‘‘too many toes’’ sign may not be a conclusive physical finding. Also, in the patient who has a more chronic presentation, swelling and tenderness may not be impressive. Furthermore, because of the abnormal biomechanics in the patient with bilateral pes planus, the single-foot heel-rise test (or lack of hindfoot inversion if the patient is successful in heel rise) may be positive in both feet. I recently encountered such a case in a 58-year-old healthy man who had been an active runner until he began experiencing medial right ankle and midfoot pain and swelling 1 year before presentation. Conservative treatment by the referring physician had included cessation of running and impact-loading exercise, immobilization for 6 weeks, nonsteroidal anti-inflammatory medication, physical therapy, and the use of bilateral, custom-molded, soft, longitudinal arch supports with medial posting for the involved foot in supportive shoes.
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Physical examination revealed mild tenderness and a modicum of swelling in the area of the terminal course of the posterior tibialis tendon. The ‘‘too many toes’’ sign was inconclusive, and he was able to perform the single-foot heel-rise test bilaterally, although neither hindfoot inverted. Bilateral flexible pes planus was noted. There was no clinical evidence of subfibular or sinus tarsi impingement. The Achilles tendon was not contracted with passive dorsiflexion of the foot to 20 degrees. Weight-bearing x-rays of the involved foot were essentially unremarkable, save for pes planus. There was no evidence of an accessory navicular, tarsal coalition, or triple joint degenerative arthritis. A recent MRI suggested an interstitial rupture with tendinosis of the posterior tibialis tendon and excess fluid around it but otherwise was unremarkable. Given the chronicity of the patient’s symptoms and failed response to conservative treatment, he was scheduled for surgical reconstruction for severe stage I or early stage II disease. Intraoperatively, there was indeed mild attenuation and incompetency of the posterior tibialis tendon with a small longitudinal interstitial rupture and tenosynovitis. Also, the plantar medial capsule of the talonavicular joint was completely ruptured (Fig. 8-14, A and B). This pathology had not been detected in the preoperative MRI. In addition to repair and imbrication of the capsular tear, the posterior tibialis tendon was repaired and advanced, and a medial shift calcaneal osteotomy was performed. After 6 weeks of casting and 6 weeks of bracing postoperatively, the patient was fitted with bilateral, custom-molded, soft, longitudinal arch supports, especially in his running shoes, and returned to running at 6 months. This case points out that other traumatic pathology may mimic (see Table 8-1) and other conditions (e.g., pes planus) may contribute to posterior tibialis tendon insufficiency. More specifically, the examiner and surgeon should consider diagnostically and surgically repair a ruptured plantar medial talonavicular joint capsule.
C A S E S T U D Y 2
Another case serves to illustrate the importance of the differential diagnosis (see Table 8-1). A 17-year-old presented with a several-month history of pain, swelling, and stiffness of the left foot after a twisting eversion injury was incurred while he was playing
Perils and pitfalls (with illustrative case reports)
Figure 8-15 Case 2.
A
B Figure 8-14 Intraoperative photograph (A) and schematic drawing (B) of complete rupture of the plantar medial talonavicular joint capsule as seen in Case 1. The hyperemic interstitially torn posterior tibialis tendon is retracted inferiorly.
Bony calcaneonavicular tarsal coalition in
‘‘arch supports.’’ A report of x-rays of the left foot taken recently was described as ‘‘normal.’’ Physical examination revealed normal ankle range of motion but a rigid pes plano valgus deformity with peroneal muscle spasm. The uninjured right foot was flexible, with a normal range of hindfoot motion. Tenderness and swelling was appreciated along the terminal course of the posterior tibialis tendon. The ‘‘too many toes’’ sign was positive and the hindfoot failed to invert in the left-foot single-foot heel-rise test. Save for the rigidity of the hindfoot, the physical findings and perhaps much of the history would have suggested that the patient had sustained a posterior tibialis tendon injury with dysfunction. However, x-rays taken in my office clearly were not ‘‘normal’’ and demonstrated a skeletally mature left foot with an obvious bony calcaneonavicular tarsal coalition and significant degenerative arthritis of the triple joint complex (Fig. 8-15). Given the severe rigidity of the hindfoot, pes planus deformity, triple joint degenerative arthritis, and failure of conservative treatment, the patient underwent a triple arthrodesis with corrective joint osteotomies. It was felt that a resection of the mature bony coalition, given the degree of the deformity and arthritic changes of the triple joint complex, would not have resulted in a successful outcome. One year postoperative from the triple arthrodesis, the patient was asymptomatic and had returned to some limited, repetitive, impact-loading sports.
C A S E S T U D Y 3
The final case further emphasizes the differential diagnosis and potential diagnostic pitfalls of posterior tibialis tendon injury and dysfunction.
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soccer. As reported by his mother, the patient also had recently experienced a ‘‘growth spurt’’ several months before the injury. Before referral to my office, conservative treatment had been rendered by his pediatrician that included bracing, over-the-counter nonsteroidal anti-inflammatory medication, physical therapy, and
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Posterior tibialis tendon dysfunction
A 16-year-old patient presented to my office with the recent history of an eversion injury of the right foot when she twisted it running to first base while playing softball. There were no prodromal symptoms before the injury. She complained of swelling and pain along the distal medial navicular insertional area of the posterior tibialis tendon. Physical examination confirmed tenderness, swelling, and ecchymosis in the anatomic area of her symptoms as described. The ‘‘too many toes’’ sign was negative, but she complained of pain in the plantar medial midfoot with the single-foot heel-rise test, although the injured side hindfoot inverted normally when compared with the uninjured foot. X-rays demonstrated a medial navicular avulsion-type fracture versus a small, nonunited accessory navicular with presumed synchondrosis disruption (Fig. 8-16). Comparison x-rays of the other foot also revealed a similar small, nonunited accessory navicular, thus suggesting the latter diagnosis. (Serial x-rays during the treatment period did not reveal bony healing of the possible avulsion fracture to the main body of the navicular, thus again suggesting that this was a synchondrosis disruption of a nonunited accessory navicular and not a fracture.) Treatment consisted of immobilization and a wellmolded, short-leg, nonweight-bearing cast for 3 weeks, followed by rigid bracing with an arch support with progressive weight bearing as tolerated for another 3 weeks. She returned to sports, asymptomatic, 3 months postinjury. This case also demonstrates the importance of comparison x-rays in determining the correct diagnosis and thus the appropriate treatment.
Figure 8-16 Coned down and magnified view of nonunited accessory navicular with presumed synchondrosis disruption in Case 3.
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SUMMARY Again, although rare, the acute rupture or dysfunction of the posterior tibialis tendon in the athlete demands timely diagnostic recognition and proper treatment. Conservative treatment is recommended initially, especially in the patient without deformity (stage I). Surgical treatment is advised if conservative treatment fails in any stage, but especially if there is significant deformity (stage II and III). Prompt treatment, whether conservative or surgical, may prevent the development of primarily triple joint or even ankle degenerative arthritis and resultant need for an arthrodesis, which may spell the end of an athlete’s participation in repetitive, impact-loading conditioning and sports.
REFERENCES 1. Kettelkamp DB, Alexander HH: Spontaneous rupture of the posterior tibialis tendon, J Bone Joint Surg 51A:759, 1969. 2. Mueller TJ: Ruptures and lacerations of the tibialis posterior tendon, J Am Podiatr Med Assoc 3:109, 1984. 3. Funk DA, Cass JR, Johnson KA: Acquired adult flatfoot secondary to posterior tibial-tendon pathology, J Bone Joint Surg 68 A:95, 1986. 4. Johnson KA: Tibialis posterior tendon rupture, Clin Orthop 177:140, 1982. 5. Johnson KA, Strom DE: Tibialis posterior tendon dysfunction, Clin Orthop 239:196, 1989. 6. Goldner JL, et al: Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibial tendon and medial plantar ligaments, Orthop Clin North Am 5:39, 1974. 7. Jahss MH: Spontaneous rupture of the tibialis posterior tendon: clinical findings tenographic studies, and a new technique of repair, Foot Ankle 3:158, 1982. 8. Leach RE, DiIorio E: Pathologic hindfoot condition in the athlete, Clinic Orthop 177:116, 1983. 9. Mann RA, Thompson FM: Rupture of the posterior tibialis tendon causing flatfoot, J Bone Joint Surg 67A:556, 1985. 10. Pomperoy GC, et al: Acquired flatfoot in adults due to dysfunction of the posterior tibialis tendon, J Bone Joint Surg 81A:1173, 1999. 11. Myerson MS: Adult acquired flatfoot deformity, J Bone Joint Surg 78A:780, 1996. 12. Bloome DM, Marymont JV, Varner KE: Variations in the insertion of the posterior tibialis tendon: a cadaveric study, Foot Ankle Int 24:780, 2003. 13. Gazdag AR, Cracchiolo A: Rupture of the posterior tibialis tendon, J Bone Joint Surg 79A:675, 1997. 14. Alexander IJ, Johnson KA, Berquist TH: Magnetic resonance imaging in the diagnosis of disruption of the posterior tibial tendon, Foot Ankle 8:144, 1987. 15. Conti S, Michelson J, Jahss M: Clinical significance of magnetic resonance imaging in pre-operative planning for reconstruction of posterior tibialis tendon ruptures, Foot Ankle 13:208, 1992. 16. Koff FJ, Marcus RE: Clinical outcome of surgical treatment of the symptomatic accessory navicular, Foot Ankle Int 25:27, 2004. 17. Yeap JS, Singh D, Birch R: Tibialis posterior tendon dysfunction: a primary or secondary problem? Foot Ankle Int 22:51, 2001. 18. Perry MD, et al: Ultrasound magnetic resonance imaging, and posterior tibialis dysfunction, Clin Orthop 408:225, 2003.
References 24. Wacker JT, Hennessy MS, Saxby TS: Calcaneal osteotomy and transfer of the tendon of flexor digitorum longus for stage-II dysfunction of tibialis posterior, J Bone Joint Surg 84B:54, 2002. 25. Russotti GM, Cass JR, Johnson KA: Isolated talocalcaneal arthrodesis, J Bone Joint Surg 70A:1472, 1988. 26. Coetzee JC, Hansen ST: Surgical management of severe deformity resulting from posterior tibialis tendon dysfunction, Foot Ankle Int 22:944, 2001. 27. Marks RM, Schon LC: Post-traumatic posterior tibialis tendon insertional elongation with functional incompetency: a case report, Foot Ankle Int 19:180-183, 1998.
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19. Trnka HJ: Dysfunction of the tendon of tibialis posterior, J Bone Joint Surg 86B:939, 2004. 20. Johnson JE, Yu JR: Arthrodesis techniques in the management of stage II and III acquired adult flatfoot deformity, J Bone Joint Surg 87A:1866, 2005. 21. Ford LT, DeBender J: Tendon rupture after local steroid injection, South Med J 7:827, 1979. 22. Coetzee JC, Castro MD: The indications and biomechanical rationale for various hindfoot procedures in the treatment of posterior tibialis tendon dysfunction, Foot Ankle Clin North Am 8:453, 2003. 23. Myerson MS, et al: Tendon transfer combined with calcaneal osteotomy for treatment of posterior tibialis tendon insufficiency: a radiological investigation, Foot Ankle Int 16:712, 1995.
........................................... C H A P T E R 9 Nerve disorders and plantar heel pain A. Lower-extremity nerve injuries in athletes A. Lee Dellon CHAPTER CONTENTS ...................... A. Lower-extremity nerve injuries in athletes
205
B. Plantar heel pain
226
Introduction
205
Fat pad insufficiency
226
Joint pain of neural origin
207
Insertional plantar fasciosis
227
Peroneal nerve injuries
210
Posterior tibial nerve injuries
215
Entrapment of the first branch of the lateral plantar nerve
233
Tarsal tunnel syndrome
236
Less common lower-extremity peripheral nerve problems
222
Midsubstance plantar fasciitis
236
References
224
Summary
237
Further reading
226
References
238
INTRODUCTION It is my honor to write this chapter for the current edition of the book first edited by Donald E. Baxter, MD, and now edited by David Porter, MD, PhD, and Lew C. Schon, MD. Lew Schon, MD, and Don Baxter, MD, wrote correspondingly the first two authoritative chapters on this subject in 1994.1,2 Much of what they wrote is now among the ‘‘classical’’ knowledge base of foot and ankle surgeons everywhere. Understandably, it is with trepidation that one approaches any changes in ‘‘the classics.’’ Yet, over the past decade, much has been learned related to the pathophysiology, neuroanatomy, and neurodiagnostic testing techniques that can solidify and augment our approach to that base of knowledge related to lower extremity nerve injuries in the athlete.
Language is a critical part of our ability to make a diagnosis that relates appropriately to our treatment options. In that regard, today the word ‘‘functional’’ often is used in contrast to ‘‘organic,’’ and therefore I feel it is better to describe peripheral nerve problems related to muscular activity as ‘‘exercise-induced’’ rather than ‘‘functional,’’ because ‘‘functional’’ might connote a psychogenic origin. During diagnostic testing for such an exercise-induced problem, the examiner may use techniques that ‘‘provoke’’ the symptoms by creating compression of the peripheral nerve through certain maneuvers, such as the Phalen sign, wrist flexion test for carpal tunnel syndrome, or maintaining the elbow flexed to provoke the symptoms of cubital tunnel syndrome. Therefore the young athlete who complains of dorsolateral foot pain radiating from the lower leg early
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Nerve disorders and plantar heel pain
Figure 9A-1 Neuronal swelling proximal to the site of chronic compression can cause the appearance of a neuroma, such as in the interdigital nerve to the third webspace (A), or the deep peroneal nerve over the dorsum of the foot (B). In B the extensor hallucis brevis tendon, the source of the compression, has been excised.
in the training process, whether running or dancing, should have an exercise-induced compartment syndrome included in the differential diagnosis, because the basis of that pain is acute nerve compression. Similarly, a ‘‘neuroma’’ is the pathophysiologic process of entrapment of axonal sprouts regenerating into scar tissue.3 A painful neuroma should be treated surgically by resection and implantation of the proximal end into muscle, a technique that has withstood the test of time for the past 20 years for both the upper and lower extremity.4-8 In contrast, chronic compression of a nerve will create an area of narrowing of the nerve with a swelling resulting from axoplasmic accumulation proximal to that point (Fig. 9A-1, A and B). That swelling may appear to be a neuroma but is not a true neuroma. This situation occurs distally in the foot related to the interdigital nerve and the transverse intermetatarsal ligament. The appropriate name for this painful condition should be ‘‘interdigital nerve compression’’ and not ‘‘interdigital neuroma.’’ The history of the origin of this unusual nomenclature has been reviewed recently,9 and the term ‘‘interdigital nerve compression in the (given)-interspace,’’ although cumbersome, is used in this chapter. Resection of a Morton’s neuroma (which is not a true neuroma) results in a true (painful or not) neuroma. Resection is the appropriate surgical treatment for a painful neuroma, and neurolysis is the appropriate surgical treatment for chronic nerve compression.3 The name we ascribe to a given neuropathologic condition therefore has implications for the surgeon. The mechanism of injury results in different degrees of nerve injury. Mechanisms may include direct contusion, stretch/traction, laceration, or acute or chronic compression. The pathophysiology, initially subdivided
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by Sir Herbert Seddon into three groups (neurapraxia, axonotmesis, neurotmesis), then by Sir Sydney Sunderland into five groups (I-V), and finally by Mackinnon and Dellon into six groups,3 permits diagnosis and prognostication. One could use the knee as an example. The soccer or football player who sustains sufficient force to the medial knee may have a direct contusion to the infrapatellar branch of the saphenous nerve and medial knee pain, which is independent from ligamentous or meniscal structural problems identifiable on a magnetic resonance imaging (MRI). If the infrapatellar branch is simply crushed, recovery of nerve function will be to a normal level, and this will occur within 3 weeks. In contrast, if the force was sufficient to cause disruption of the nerve, bruising, and adherence to the pes anserinus, there will be loss of sensory function and formation of a painful neuroma. If the force of impact is sufficiently great, there may be damage to the meniscus or the collateral ligament, and, in addition to those structural problems, there may be pain resulting from direct damage to the innervation of the knee joint.10 This leads to knee pain of neural origin in addition to the musculoskeletal problems. There may be sufficient lateral force exerted on the knee to cause complete loss of continuity of the common peroneal nerve in addition to the knee joint or fibular injuries (Fig. 9A-2), resulting in peroneal motor and sensory palsy. Therefore ‘‘nerve injury’’ is an insufficient term to specify the neuropathophysiologic cause of the athlete’s pain. Even the term ‘‘peroneal nerve palsy’’ creates ambiguity: Is the correct treatment a period of observation, a neurolysis, or a nerve reconstruction? In this chapter the application of computerassisted neurosensory testing is included in an attempt
Joint pain of neural origin
Figure 9A-2 During a badminton game, this woman sustained a twisting injury to the right knee and fell, fracturing the fibular head (A). There was an associated complete footdrop. Intraoperatively, at the time of fracture fixation, the common peroneal nerve was completely divided by the stretch/traction injury. The first surgeon reunited the nerve and referred the patient for peripheral nerve reconstruction. The neuroma-incontinuity is identified at the time of reconstruction (B).
to add measurements to the staging of peripheral nerve injury,11 and therefore to the decision-making process. Peripheral nerve surgery requires the use of a pneumatic thigh tourniquet, loupe magnification, and bipolar coagulation to properly identify and protect the nerves. In some cases a disposable nerve stimulator is required to identify certain motor functions of the nerve. General anesthesia is preferred. The following is a personal approach to the problems I have encountered in athletes.
JOINT PAIN OF NEURAL ORIGIN
Figure 9A-3 Partial knee denervation patient 3 months after the left and 6 months after the right knee each had a medial and lateral knee denervation. The 3-cm scars over the medial (right) and the lateral (left) knees are apparent.
have been stretched or torn and have formed a painful neuroma within the joint structures. Indeed, these nerves may have been injured by the arthroscopy itself. (Figure 9A-3 is an example of a man with bilateral knee pain after years of martial arts, for whom all of the previously mentioned treatments were ineffective and for whom partial knee denervation permitted resumption of daily activities, but not martial arts, without pain. Demonstration of neural origin for the pain is accomplished by (1) local anesthetic block of the suspected nerves, (2) the patient having a decrease in his visual 207
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Knee joint pain can be defined to be of neural origin after any musculoskeletal problems with the integrity of the knee joint have been eliminated from the differential diagnosis or have been treated. A common situation is knee pain in the athlete with an MRI that has been interpreted to be normal. Rest, nonsteroidal antiinflammatory drugs, and intraarticular steroid injections have not been successful at relieving pain. Arthritis may or may not be present radiographically, and if it is, the patient may have failed to improve with treatment designed to form new cartilage. More than likely the patient will have had one or more knee arthroscopies, at which plica has been removed, cartilage has been debrided, or a synovectomy has been performed, but there is still pain. Could this pain be of neural origin? With the description in 1994 of the innervation of the human knee,10 it becomes reasonable to consider that the medial or lateral retinacular nerves, or both,
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Nerve disorders and plantar heel pain
Figure 9A-4 Innervation of the human knee joint is illustrated for the lateral (A) and medial (B) views of the knee region. The lateral retinacular nerve originates from the sciatic nerve, crosses deep to the biceps tendon, and innervates the lateral retinacular region. The medial retinacular nerve is the continuation of the femoral nerve branch to the vastus medialis, exits distal and deep to this muscle, and innervates the medial retinacular region.
analog scale level of pain by at least 5 points, and (3) observation of improved pain after the block while walking, climbing stairs, and kneeling. If there has been previous knee surgery, a neuroma of a cutaneous nerve, like the infrapatellar branch of the saphenous nerve or the medial cutaneous nerve of the thigh, also must be considered in the examination and the nerve blocks. Figure 9A-4 illustrates the location of these nerves. The first report of partial knee denervation was for patients after total knee arthroplasty,12 but a subsequent report includes patients with knee pain after sports injuries.13 A complete description of this subject appeared in the year 2000.14 The advantage of this approach is that the surgery is performed on an outpatient basis, does not require invasion of the knee joint, and permits immediate ambulation, and rehabilitation can begin when the sutures are removed. Success rates should approach 90% with the previous criteria. Charcot joint does not occur because this is a partial knee joint denervation. The athlete must be counseled that posttraumatic arthritis and synovitis still will occur, but their pain may be significantly lessened. Lateral ankle joint (sinus tarsi) pain can be of neural origin in the athlete who has had repetitive inversion sprains or a fracture/dislocation of the lateral malleolus. Typically, the inversion sprain is treated with immobilization and anti-inflammatories, and then a progressive regimen of stretching and strengthening is begun. If pain persists and x-rays have not demonstrated a fracture, then a computed axial tomography (CAT) scan with three-dimensional reconstruction is suggested to be sure there are not occult intra-articular fractures or
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bone fragments within the joint as the source of the pain. Any athlete in any sport can suffer this type of injury. If there is a lax lateral ankle joint, surgery to correct it with ligament reconstruction or tendon transfers (Crisman-Snook, or Watson Jones-types) still may have failed to relieve the pain, although providing good stability (see Fig. 9A-12, C). If the symptoms extend to the dorsal lateral aspect of the foot, a stretch/traction injury to the peroneal nerve must be considered in the differential diagnosis, and this is considered later in this chapter. If direct pressure into the sinus tarsi reproduces the pain, a local anesthetic block and steroid injection into this region may be given for both diagnosis and for treatment. If the pain persists, then sinus tarsi syndrome is present. Traditional treatment for this disabling condition has been either a ‘‘curettage’’ (debridement) of the sinus tarsi, resection of the lateral shoulder of the talus, or a subtalar fusion. Could this pain be of neural origin? Recently, the innervation of the sinus tarsi has been demonstrated to come from the deep peroneal nerve.15 The innervation arises most commonly from the most lateral fascicle of the deep peroneal nerve, just proximal to the origin of the innervation of the extensor digitorum brevis in all patients (Fig. 9A-5). About 25% of patients have a dual innervation of the sinus tarsi from the sural nerve.15 With this knowledge, lateral ankle pain can be proven to be of neural origin by blocking the deep peroneal nerve proximal to the ankle. At this site, the nerve is lateral to the extensor hallucis longus and medial to the extensor digitorum longus (Fig. 9A-6, A). If there is not complete relief, then the sural nerve is blocked proximal to the
Joint pain of neural origin
Deep peroneal n. Nerve to tarsal sinus Extensor digitorum brevis m.
Figure 9A-5 Innervation of the sinus tarsi from the deep peroneal nerve occurs with a branch that arises proximal to the lateral malleolus. In 25% of patients, there is a second innervation from the sural nerve.
lateral malleolus (Fig. 9A-6, B). The first case of sinus tarsi denervation was reported in 2002 using the technique of resecting just the fascicle that innervates this joint, identifying this by intraoperative nerve stimulation (the most medial fascicle is to the dorsal skin of the first webspace, the central fascicle causes contraction of the extensor brevis muscle on stimulation, and the lateral fascicle is the one innervating the joint).16 In a subsequent series of 13 patients reported in 2005, there were some failures related to this partial resection of the deep peroneal nerve because of joint afferents passing also through the other fascicles.17 The current recommendation therefore is to resect the entire deep peroneal nerve. This is accomplished through an incision located 10 to 12 cm proximal to the lateral malleolus. The anterior compartment is opened with an 8-cm long fasciotomy. The deep peroneal nerve can be identified by dissecting superficial to the interosseous towards the tibia, at which point the nerve is identified with the anterior tibial vessels. A 2-cm length is resected. Immediate weight bearing is permitted. Rehabilitation is begun when the sutures are removed. In these patients, related to the initial stretch/traction injury, there already may be decreased sensibility in the dorsal first webspace and decreased bulk or weakness of the extensor brevis. These should be pointed out to the patient. The numbness present during the block should be pointed out to the patient, who must be informed that this may be permanent after the nerve is resected. The successful relief of pain should approach 90% with this approach. Examples of a patient resuming beach activities and one resuming downhill skiing after this procedure are given in Figure 9A-7.
Figure 9A-6 Local anesthetic block of the sinus tarsi is performed by first blocking the deep peroneal nerve proximal to the ankle (A), and then, if sinus tarsi pain still is present to some degree, by blocking the sural nerve proximal to the ankle (B). (Photos courtesy Stephen L. Barrett, DPM, Phoenix, AZ.)
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Figure 9A-7 Results of denervating the sinus tarsi is demonstrated in this 19-year-old who has resumed playing Frisbee on the beach (A) and in this 49-year-old who has resumed downhill skiing (B). The first patient was injured running on the beach and the second during a fall while rock climbing.
PERONEAL NERVE INJURIES The peroneal nerve arises in the popliteal fossa from the sciatic nerve and travels distally around the fibular neck. There are no sites of entrapment in the popliteal fossa, although the nerve can be injured in this location iatrogenically. Figure 9A-8 illustrates the three most common sites for injury to athletes of this nerve, which consist of sites of anatomic narrowing at which the branches of this nerve are at the risk, namely, the common peroneal nerve at the fibular neck, the superficial peroneal nerve in the distal leg, and the deep peroneal nerve in structures over the dorsal ankle and foot. The common peroneal nerve can be injured in many athletic activities. The common mechanisms for injury
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include direct trauma to the knee in contact sports, such as sliding into base in baseball, football, or soccer, and stretch/traction injuries related to inversion sprains of the ankle. Positions such as catcher in baseball put the common peroneal nerve at risk from chronic compression. The most common symptoms include paresthesias into the lateral aspect of the leg and the dorsum of the foot or the perception that the leg is going to ‘‘give out.’’ The first symptom set is related to neural ischemia, which gives rise to the paresthesias in the reversible ischemic block degree of nerve injury. The second set of symptoms, I believe, is related to a similar phenomenon in the motor innervation of the muscles that control ankle dorsiflexion and toe extension. These symptoms are transient and worsen with activity. There may be no positive physical findings with the exception of
Peroneal nerve injuries
Skin incision Head of fibula Common peroneal n.
Deep peroneal n. Peroneus longus m. Common peroneal nerve
Deep peroneal nerve
Superficial peroneal nerve
Deep peroneal n.
Extensor digitorum brevis m.
Nerve to tarsal sinus
Figure 9A-8 The peroneal nerve is at risk for injury in athletes because of stretch/traction and compression of the common peroneal nerve at the fibular neck, the superficial peroneal nerve as it exits the fascia in the distal third of the leg, and the deep peroneal nerve as it crosses the dorsum of the ankle and the foot. For the deep peroneal nerve, the most common site of entrapment is beneath the extensor hallucis longus tendon. These three sites are noted by arrows. (Courtesy www.DellonIPNS.com Web site, patient-interactive tutorial.)
persistent, the earliest sensory change will be the pressure required to distinguish one- from two-point static touch using the Pressure-Specified Sensory Device (Fig. 9A-9). Electrodiagnostic testing most likely will still be normal. The first muscle to demonstrate 211
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tenderness of the common peroneal nerve at the neck of the fibula. At this stage of treatment, awareness of this diagnosis is critical, and the treatment is related to relieving pressure on the nerve by changing the athlete’s workout regimen. As symptoms become more
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Nerve disorders and plantar heel pain
Combined Deep Peroneal 100
Left
Combined Lateral Calf
Right
Right
80 GM/SQ MM
GM/SQ MM
80 60 40 %
1 PT
2 PT Static
60 40 %
20
20
C
Left
100
1 PT
2 PT Moving
Line indicates 99% Normal Confidence Level (gm/sq mm) 9.9 26.4 1.0 5.5 mm
1 PT
2 PT
1 PT
Static 11.0 6.4 mm
2 PT Moving
Line indicates 99% Normal Confidence Level (gm/sq mm) 4.5 25.6 1.8 6.5 mm 6.2 mm
14.3
Figure 9A-9 Physical examination and neurosensory testing related to common peroneal nerve entrapment. (A) Weakness of the extensor hallucis longus is the first muscle to show physical findings related to the motor function. (B) Weakness or atrophy of the extensor digitorum brevis should be evaluated. Complete dropfoot is obvious. (C) Evaluation of the sensory component with the Pressure-Specified Sensory Device results in a computer printout in which the pressure required to discriminate one- from two-point static touch is measured. In this report the left, blue bars are above the 99% confidence limit for pressure for age (the horizontal black bar), indicating abnormal function for the left side, whereas the right side, in red, is below the bar. The asterisk denotes abnormal distance for the measurement, indicating axonal loss. The sensibility is abnormal for both the deep and superficial peroneal nerve, indicating either that both of these nerves are abnormal or that the location of the problem is proximal, at the fibular neck.
weakness usually is the extensor hallucis longus (see Figure 9A-9). With the onset of muscle weakness or the increase in distance required for two-point discrimination, the degree of compression is sufficiently chronic and severe to justify neurolysis of the common peroneal nerve. This is illustrated in Figure 9A-10. The incision is
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oblique at the fibular neck. Care is taken not to injure the occasionally present lateral cutaneous nerve of the calf. The fascia is opened and the common peroneal nerve identified. The nerve is followed distally to the entrapment site at the peroneus longus muscle. If there has been direct knee trauma, the fascia will be adherent
Peroneal nerve injuries
to the nerve, and the neurolysis then is continued proximally into the popliteal fossa. Recent observations have made the following modifications to the procedure as previously described18: 20% of cadavers but 80% of
Figure 9A-10 Intraoperative view follows neurolysis of the common peroneal nerve. Note that the fascia superficial to the peroneus longus has been divided and is held by two clamps. The muscle has not been divided. Fascial bands deep to the peroneus longus often are present and must be divided. Similar structures deep to the nerve may be present on the lateral gastrocnemius muscle belly and should be divided. Finally, the entrance of the nerve into the anterolateral compartments must be widened. The blue vessel loop is on the sural nerve, which can be identified through this incision for the treatment of a painful sural neuroma.
patients will have a fibrous band deep to the peroneus longus muscle. This must be searched for and divided if present, and there often will be a notch at this location in the nerve (Fig. 9A-11). A smaller percentage of patients also will have fibrous bands on the surface of the lateral head of the gastrocnemius muscle, deep to the nerve, and these must be released. Finally, a high origin of the soleus muscle may narrow the entrance of the nerve into the anterolateral compartment, and this origin must be released from the fibula.19 The superficial peroneal nerve has a variable anatomy in the leg. Up to 40% of cadavers have the superficial peroneal nerve either completely in the anterior compartment (Fig. 9A-12) or a branch in the anterior and a branch in the lateral compartment (Fig. 9A-13).20,21 The superficial peroneal nerve exits from beneath the deep fascia to become subcutaneous in the distal third of the leg. This site is quite variable but is most commonly located 10 to 12 cm proximal to the lateral malleolus (see Fig. 9A-8). In young athletes, such as runners or dancers, this site can be compressed because the muscles of the anterior and lateral compartment bulge during exercise, creating ischemic neuralgia. This pain goes away with cessation of the physical activity. The diagnosis should be made with compartment pressure measurements while the patient is in a controlled exercise environment, such as on a treadmill. Elevation of pressure to greater than 30 mm Hg coinciding with the pain is an indication for fasciotomy. Although the fasciotomy incision does not need to be long, the fasciotomy should be extensive to prevent a small muscle herniation, which itself can be painful. The fascia is well
Figure 9A-11 Intraoperative view of common peroneal nerve being compressed by a fibrous band beneath the peroneus longus muscle. (A) The muscle is retracted. The white fibrous edge of the band is apparent, and it extends deep to the muscle. (B) After the band is resected, the indentation or notch in the common peroneal nerve is evident.
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Figure 9A-12 A female catcher injured her right leg sliding into base and ultimately required a lateral ankle stabilization (A). At 3 years after her injury, and with her no longer able to play softball, she was found to have a painful sinus tarsi, a nonpainful scar, and a positive Tinel sign over both the superficial and common peroneal nerve. A block was administered to the deep peroneal above the ankle, relieving her of her sinus tarsi (lateral ankle) pain. (B) In surgery, the superficial peroneal nerve was found to be completely within the anterior compartment. This view demonstrates the fasciotomy of this compartment and complete neurolysis. (C) This view demonstrates the fascia separating the two compartments, attached to the fibular, and the small retractor lies beneath the deep peroneal nerve, to denervate the sinus tarsi.
vascularized, and its edges should be cauterized to minimize postoperative bruising or hematoma. Care is taken to not injure the nerve, and the neurolysis must be extended proximally until the nerve is surrounded by muscle and distally until the nerve enters the subcutaneous tissue (see Fig. 9A-12). For soccer players, this nerve can be injured directly by the ball or by being kicked. Similar injuries can occur in field hockey and lacrosse. Symptoms of chronic compression of the superficial
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peroneal nerve are paresthesias from the distal leg into the top of the foot, without motor symptoms. There will be a positive Tinel sign at the site of compression. Sensory testing will demonstrate normal sensibility in the dorsal first webspace and abnormal sensibility over the dorsolateral foot. Results of neurolysis of this nerve are good to excellent in 85% of patients.21,22 Surgery is performed on an outpatient basis, and immediate ambulation is encouraged to permit gliding of the nerve
Posterior tibial nerve injuries
spins. Loosening the laces on her skates did not help. There was a positive Tinel sign at this location. Radiographic evaluation, including MRI, had been normal. Her electrodiagnostic studies had been normal (with the more proximal anterior tarsal tunnel location, electromyogram [EMG] of the extensor brevis digitorum brevis muscle can help in the diagnosis), but her neurosensory testing with the Pressure-Specified Sensory Device demonstrated increased pressure threshold and abnormal two-point static threshold for distance. At surgery, her deep peroneal nerve clearly was indented by the extensor hallucis brevis tendon (see Fig. 9A-1, A), and this tendon was removed. She was able to resume ice skating at 10 days and return to doing jumps and spins without pain.
through the surgical site. Rehabilitation begins when the sutures are removed. The deep peroneal nerve has been described classically as being entrapped beneath the extensor retinaculum in front of the ankle, with this location being called the anterior tarsal tunnel, and the clinical symptoms being termed the anterior tarsal tunnel syndrome.23-25 In my experience, this is a capacious region, with the deep peroneal nerve between tendons, bone, extensor retinaculum, and fat and little chance for compression unless there has been a crush, a burn, an ankle fusion, or previous surgery (see Fig. 9A-8). In contrast, just distal to the inferior crus of the extensor retinaculum the extensor hallucis longus tendon crosses the deep peroneal nerve in close proximity to the base of the first metatarsal and the cuneiform. This is the area in which ganglions arise, and a dorsal exostosis forms. This exact site was described as a location of chronic nerve compression in 1990.26 The deep peroneal nerve at this location innervates the joints of the first and second metatarsals and the cuneiform bones, and therefore symptoms of pain from the dorsum of the foot through to the plantar surface, like a ‘‘knife stabbing’’ this location, can occur, in addition to the aching in the forefoot and paresthesia in the webspace. This is a site that has been illustrated by Schon2 to be a risk for ballet dancers in the pointe position and can be directly injured and the source of persistent pain following metatarsal stress fractures or Lisfranc fracture/dislocations. Tightly fitting athletic shoes have been reported to cause compression of the deep peroneal nerve,23-25 including by ski boots. 27 I have seen this to be the problem in an ice skater who had pain in this area on the take-off and landing of her
POSTERIOR TIBIAL NERVE INJURIES There is no ‘‘anterior tibial nerve,’’ and therefore some writers use the term ‘‘tibial nerve’’ instead of ‘‘posterior tibial nerve.’’ An informal survey of anatomy texts and recent publications continues to demonstrate that the most common usage is ‘‘posterior tibial nerve.’’ This nerve is in close proximity to the posterior tibial artery and vein, and therefore this is the name used in this chapter. The proximal posterior tibial nerve arises from the sciatic nerve in the popliteal fossa, and there is no anatomic site of entrapment in that location, although the nerve can be injured iatrogenically here. For example, a 21-year-old college student injured her knee skiing. During her arthroscopy, the scope perforated the posterior capsule of the knee and avulsed the popliteal artery and vein and the posterior tibial nerve. After her emergent vascular reconstruction, she was referred at 3 months for nerve reconstruction. This required direct neurotization of the gastrocnemius muscles because their motor branches were avulsed, and nerve grafting to provide distal sensation to the plantar aspect of her foot. By 2 years after this reconstruction, she had active plantarflexion of the ankle and protective sensation to the plantar aspect of her foot.28 The posterior tibial nerve continues distally to enter the distal leg by passing between a fibrous arcade formed between the two heads of the gastrocnemius and the soleus muscle. Theoretically, this can be a site of compression, and decompression at this level has been described by Baxter1 as the ‘‘high tarsal tunnel.’’ I have had occasion to decompress the nerve in this region in two patients who had chronic compartment syndrome, and one of these was related to a sports injury. That patient developed an acute compartment syndrome related to a tight ski boot, which went without a proper diagnosis. When the leg was decompressed, about 48 hours later, the fasciotomy 215
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Figure 9A-13 Intraoperative view of neurolysis of superficial peroneal nerve. In this patient, there was a branch of the nerve in both the anterior and the lateral compartment, emphasizing, as in Figure 9A-12, the need to release both compartments.
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Nerve disorders and plantar heel pain
was proximal and inadequate. Muscle was debrided, and the wound skin grafted secondarily. By the time the patient was referred to me 3 years later, there was a chronic compartment syndrome associated with severe pain from the knee to the toes. There was inability to flex or extend the toes or ankle. The patient required a wheelchair and was under pain management, requiring a Duragesic patch, methadone, Neurontin, and fentanyl
lollipops. The pain was relieved and all motor function recovered by carrying out a neurolysis of the tibial nerve in the calf, along with a four-compartment fasciotomy and a neurolysis of the common peroneal nerve at the knee. The superficial peroneal nerve had been divided during the original fasciotomy, requiring for the neuroma now to be resected and implanted into muscle (Fig. 9A-14). However, the term ‘‘tarsal tunnel’’ should
Fig. 9A-14 Neurolysis of the tibial nerve in the leg and the peroneal nerve from the knee to the ankle in a patient who had a chronic compartment syndrome. The acute compartment syndrome 3 years earlier was related to a tight ski boot (A). The initial fasciotomy was proximal and divided the superficial peroneal nerve. The extreme swelling of the common peroneal nerve proximal to the site of compression is noted in B, with the nerve encircled by the vessel loop. In C, the four compartment fasciotomy is noted, and the extensive release required to decompress the tibial nerve compression in the leg.
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Posterior tibial nerve injuries
Table 9A-1
Relationship between the four medial ankle tunnels and the nerve compression sites in the upper extremity
Sites of nerve compression Lower extremity
Upper extremity
Tarsal tunnel
Forearm
Medial plantar tunnel
Carpal tunnel
Lateral plantar tunnel
Guyon’s canal
Calcaneal tunnel
Palmar cutaneous branch of median nerve tunnel33
paresthesias progress to constant numbness. Electrodiagnostic testing can document this problem but has a high false-negative rate. Neurosensory testing with the Pressure-Specified Sensory Device (NK Biotechnical, Minneapolis, MN) can document this problem at an earlier stage than electrodiagnostic testing.30-32 An example of the documentation of tarsal tunnel syndrome with neurosensory testing is given in Figure 9A16, B. Rehabilitation after decompression of the four medial ankle tunnels is critical to the success of the surgery. It should be clear that if a nerve is permitted to remain immobilized during the wound healing process, the formation of collagen in that process will result in scarring of the nerve into the surgical field, causing failure of the original neurolysis.34 Early if not immediate mobilization of the nerve must be part of the postoperative regimen for the tibial nerve at the ankle as it is for the ulnar nerve at the elbow.35 Although there are many reviews of tarsal tunnel syndrome, for example the one by Lau and Daniels,36 there are no reported series larger than 68 patients, and their reported surgical results vary considerably. For example, an often-quoted study, in which long-term follow-up was obtained, reported just 44% of the patients with excellent outcomes and a 13% complication rate,37 whereas a more recent report indicated 72% of the patients with satisfactory results but a 30% complication rate.38 The most recent report, using outcome assessment, found 51% of the patients having a marked improvement in the quality or their life despite 85% of the patients stating they had excellent relief of their pain, with a 7% rate of complications.39 Using the technique I described previously, a consecutive series of 87 legs in 77 patients had the four medial ankle tunnels decompressed between January of 1987 and December of 1994. The follow-up was a mean of 3.6 years. The results were 82% excellent, 11% good, 5% fair, and 2% failure.40 Using a numerical grading scale,41 there was a statistically significant improvement at the p < .001 level for each preoperative grade of impairment with the exception of level 10, intrinsic contracture. My experience has grown considerably in posterior tibial nerve 217
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be reserved for a compression site in relation to the tarsal bones and not in the midcalf. Tarsal tunnel syndrome was described in 1962 but remains relatively misunderstood. It is often referred to as the ‘‘carpal tunnel syndrome of the foot.’’ When my first patient was referred to me in about 1980, and I studied this statement, I realized that in fact the tarsal tunnel region was analogous to the forearm and not the carpal tunnel. Subsequently the appropriate relationships were published and are given in Table 9A-1.29 The patient with carpal tunnel syndrome would not be relieved by a forearm fasciotomy, and so an operation was designed to decompress the four medial ankle tunnels (Fig. 9A-15). It is not appropriate to call this operation ‘‘tarsal tunnel decompression’’ alone because four separate tunnels are decompressed. It is confusing to speak of the tarsal tunnel as the ‘‘upper tarsal tunnel’’ and the medial and lateral plantar tunnels as the ‘‘distal’’ or ‘‘lower tarsal tunnel.’’ In this chapter, each tunnel is called by its correct anatomic name. Compression of the nerves in the four medial ankle tunnels can occur in an athlete through several different mechanisms. The medial ankle may be injured directly. Inversion sprains may create sufficient bruising and swelling so that the posterior tibial nerve and its branches become adherent during the immobilization of the ankle for 3 weeks, subsequently giving rise to chronic compression. Repetitive trauma can occur in runners, cyclers, those who do step aerobics, and so forth. The pronated foot theoretically is more likely to have pressure applied to the posterior tibial nerve branches, although this remains to be proven. A fracture/dislocation of the ankle or severe inversion sprain may directly contuse the tibial nerve and its branches. Swelling or blood products related to posterior tibial nerve tears or avulsion of a portion of the navicular may cause compression of the medial plantar nerve. Symptoms of tarsal tunnel syndrome include aching, paresthesias, or numbness in the heel, arch, forefoot, or toes. Nighttime discomfort is common. In time, muscle weakness and clawing of the intrinsic muscles occur (Fig. 9A-16, A) and the
CHAPTER 9
Nerve disorders and plantar heel pain
Post. tibial n. Flexor rectinaculum
Medial plantar n.
Looped: calcaneal br. of med. plantar n.
Med. plantar vess. and n.
Abd. hallucis m. retracted to expose fascia Lat. plantar vesws. and n. Fascial roof of medial and lateral tunnels divided Calcaneal tunnel
Septum divided at origin; roof of calcaneal tunnel opened Septum removed; vessels and nerves shared a common tunnel
Figure 9A-15 Illustration of the four medial ankle tunnels and the surgical approach for decompression. (A) The traditional tarsal tunnel is almost never the site of compression, but opening it permits neurolysis of the posterior tibial nerve, identification of any mass lesion that might be present, and identification of anomalies. (B) The fascia superficial to the abductor hallucis brevis is divided, and the branch of the medial plantar nerve that innervates the skin of the arch in this region in 50% of patients is identified and preserved. The muscle is retracted to reveal the fascial roof of the medial and lateral plantar tunnels. (C-D) Each of these tunnels is opened, and the septum between them is removed to create one large tunnel. (Courtesy www.DellonIPNS.com Web site, patient-interactive tutorial.)
decompression, with more than 600 procedures being listed in my computer between January 2000 and June 2005. This large experience is due, in part, to the application of this technique to relief of pain and restoration of sensation to patients with neuropathy resulting from diabetes,42-44 chemotherapy,45 or idiopathic causes.46 None of the patients have required repeat surgery with the previously mentioned operative and postoperative regimen. Results of an ongoing, multicenter prospective study are available online at www.neuropathyregistry.com.
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Heel pain syndrome of neural origin is an important concept. Historically, heel pain was commonly was attributed to the presence of a medial calcaneal bone spur. This gave rise to medial heel pain’s being related to plantar fasciitis. However, if the traditional treatment for heel pain in the athlete fails to give relief, is it possible that the pain can be of neural origin? And if so, which is the nerve along the anatomic path of which these pain impulses are transmitted? For heel pain symptoms, and especially if they are associated with
Posterior tibial nerve injuries
Combined Great Toe Pulp 100
Left
Combined Heel 100
Right
Right
80 GM/SQ MM
GM/SQ MM
80
Left
60 40 %
%
2 PT Static
40 %
20
20
1 PT
60
1 PT
2 PT Moving
Line indicates 99% Normal Confidence Level (gm/sq mm) 1.6 25.7 1.0 7.8 mm
1 PT
%
2 PT
1 PT
Static 12.8 6.6 mm
2 PT Moving
Line indicates 99% Normal Confidence Level (gm/sq mm) 5.0 50.0 2.8 6.5 mm
11.1 6.2 mm
B *Measurement made at non-normative spacing Figure 9A-16 Physical examination and neurosensory testing related to posterior tibial nerve compression. (A) Clawing, a sign of lateral plantar nerve compression, often is mistaken for hammertoes. In this patient with bilateral severe tarsal tunnel syndrome related to neuropathy, decompression of the four medial ankle tunnels on the right side has permitted reversal of the clawing on one side, while it remains on the other, nonoperated side. (B) Evaluation of the sensory component with the Pressure-Specified Sensory Device results in a computer printout in which the pressure required to discriminate one- from two-point static touch is measured. In this report the left, blue bars are above the 99% confidence limit for pressure for age (the horizontal black bar), indicating abnormal function for the left side, whereas the right side, in red, is below the bar. The asterisk denotes abnormal distance for the measurement, indicating axonal loss. The sensibility is abnormal for both the medial plantar nerve (hallux pulp) and the medial calcaneal nerve (heel, medial surface), indicating that both of these nerves are abnormal and that the location of the compression is in both the medial plantar tunnel and the calcaneal tunnel. The surgical approach is given in Figure 9A-15.
may have been directly injured by repetitive running activities or that a nerve entrapment is due to inflammation or immobilization after an ankle or heel injury. Although x-ray and ultrasound are appropriate for bone and plantar fascia evaluation, traditional electrodiagnostic studies cannot truly measure the small medial calcaneal branches, 219
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poststatic dyskinesia, the treatment modalities must include strapping, stretching, changing shoes, using a heel cup, taking nonsteroidal anti-inflammatory medication, and getting a cortisone injection. The definition of ‘‘recalcitrant heel pain’’ varies, but if heel pain symptoms persist, it is appropriate to consider that a nerve
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Nerve disorders and plantar heel pain
Orgins of the Medial Calcaneal Nerve: One origin
A. 16%
C. 5%
D. 1%
B. 14%
E. 1%
Origins of the Medial Calcaneal Nerve: Three origins
A. 10%
C. 2%
D. 2%
E. 1%
Origins of the Medial Calcaneal Nerve: Two origins
D. 4%
E. 4%
A. 13%
B. 8%
C. 7%
F. 2%
G. 2%
H. 1%
Origins of the Medial Calcaneal Nerve: Four origins
B. 3%
F. 1%
A. 2%
B. 1%
Figure 9A-17 Variations in the innervation of the medial heel. There can be from one to four different nerves innervating the medial heel, with these arising in almost every conceivable variation from the posterior tibial, medial plantar, lateral calcaneal, or any combination of these.55
and techniques that measure the motor or sensory component of the lateral plantar nerve have been used as surrogates.47 The origin of pain from plantar fasciitis presumably is the periosteum, where this fascia originates from the medial calcaneal tubercle. This nerve, as I interpret the concept, is the nerve described first by Rondhuis and Huson in 198648 and subsequently popularized as the source of this heel pain by Baxter’s group.49-51 It was Rondhuis and Huson who first gave this nerve the name ‘‘first branch of the lateral plantar nerve.’’ Ultimately, the nerve has come to be known as ‘‘Baxter’s nerve.’’52 Anatomic studies have defined the saphenous, sural, and tibial contributions to the heel.53,54 Most recently, a detailed analysis of the posterior tibial nerve branches to the heel in 85 patients, performed in a bloodless intraoperative field with 3.5-loupe magnification, has outlined the many variations of the medial calcaneal nerve.55 There are many patients with three or four branches that innervate the medial calcaneal region (Fig. 9A-17). In many patients there is more than one branch from the lateral calcaneal nerve. The first
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branch of the lateral plantar nerve often is clearly not the branch carrying the pain impulses from the periosteum of the medial calcaneal tubercle. Those periosteal nerves always, ultimately, become part of the posterior tibial nerve, and most often are within the lateral plantar nerve. If the site of nerve compression is within the lateral plantar tunnel, then there will be symptoms of numbness or paresthesia present in addition to heel pain, and measurement of the medial calcaneal skin surface will identify an abnormal cutaneous pressure threshold. It is better therefore didactically to say that heel pain can be due to entrapment of a branch of the posterior tibial nerve, which usually is a branch of the lateral plantar nerve, but until the anatomy is defined at surgery, it is not possible to know which branch is the source of the pain. In a recent study,56 approximately 40% of patients presenting with heel pain had abnormal medial calcaneal cutaneous pressure threshold measurements, and another 20% had abnormal medial plantar plus medial calcaneal nerve abnormal cutaneous pressure threshold measurements. The Pressure-Specified
Posterior tibial nerve injuries
Sensory Device was used to make these measurements. Therefore in the patient with heel pain, there may be a neurogenic mechanism, it may be chronic nerve compression, and it can be identified by conducting an evaluation of sensibility. If the surgical approach involves just releasing the nerve to the periosteum, the approach described by Baxter, then the pain either may never be relieved or may take up to 1 year to improve.1,2 Furthermore, Baxter’s approach includes an open medial plantar fasciotomy.1,2,49-52 If an ultrasound examination or MRI is normal for plantar fascial thickness and neurosensory testing is abnormal, then a plantar fascia release theoretically is not necessary. However, if the surgical approach is the same as that described previously for the four medial ankle tunnels, then all the variations of the medial calcaneal nerve can be identified, and each nerve followed and released. In my experience, this is sufficient to treat heel pain of neural origin. A confounding pain problem for heel pain is the patient who has had a medial plantar fasciotomy and who has a painful (DuVries-type) scar.57 This may be called ‘‘failed’’ or ‘‘recurrent’’ fasciitis or heel pain when it actually is a true neuroma of one of these medial calcaneal nerve branches.58 In this situation, the neuroma can be resected, an internal neurolysis of the medial plantar branch from the lateral plantar nerve accomplished, and the proximal end, after neuroma resection, is turned and implanted into the distal flexor hallucis longus muscle (Fig. 9A-18).
Interdigital plantar nerve entrapment is the most appropriate name for the forefoot pain syndrome that athletes experience related to the common plantar nerve, the intermetatarsal ligament, and the metatarsal heads.9 When this pain syndrome occurs to the common plantar digital nerve in the interspace between the third and fourth toe, it traditionally is termed Morton’s neuroma. Repetitive impact on the forefoot in runners, people doing step aerobics or kickboxing, or those wearing athletic shoes that are too pointed are the athletic settings in which this problem may occur. The important distinction to be made is that Morton’s ‘‘neuroma’’ is actually chronic nerve compression and not a true neuroma (Fig. 9A-19). Therefore my approach to this is a neurolysis of the common plantar digital nerve through a dorsal approach.59 The intermetatarsal ligament is completely divided, and fibrous edges to intrinsic muscles are divided. The swelling in the nerve is left alone.
Deep transverse intermetatarsal ligament
Common plantar digital nerve
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Figure 9A-18 Pain in the medial heel in the patient who previously has had a medial plantar fasciotomy may be due to a true neuroma of one of the branches of the medial calcaneal nerve(s). In this intraoperative photo, the previous Devries incision is noted with black marker. The neuroma of the calcaneal nerve is seen. This neuroma will be resected, and the proximal end of the medial calcaneal nerve will be implanted into the flexor hallucis longus muscle proximal to the ankle.58
Figure 9A-19 Interdigital nerve compression. The common plantar nerve must glide beneath the intermetatarsal ligament during the initiation of gait. It can become compressed in this area between the metatarsal heads (left). The swollen nerve may appear to be a neuroma (right), but, in the absence of direct, not repetitive, trauma, it is not a true neuroma. Neurolysis by division of the intermetatarsal ligament instead of nerve resection is recommended (left). Resection creates a true neuroma. It often is stated that this occurs most commonly in the third interspace because the formation of the third interdigital nerve from both the medial and lateral plantar nerves restricts gliding of this common plantar digital nerve; however, there is great variability in the formation of this nerve. (Courtesy www.DellonInstitutes.com Web site, patient-interactive tutorial.)
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Nerve disorders and plantar heel pain
Figure 9A-20 Interdigital plantar nerve compression can occur in adjacent webspaces. This incision permits entry into each webspace, avoiding parallel incisions.59 In this patient, whose foot was crushed, there was an interdigital nerve compression in each interspace. On the left, the incisions are seen at 2 weeks after surgery and on the right 6 months after surgery. Note that the incision is centered over the metatarsal, and the distal end of the incision then goes off into each interspace.
The nerve is left loose to shift its position in the widened space with all phases of gait. There is support for this approach now in several reports, using both an open60,61 and an endoscopic technique.62 In more than 50 patients, I have not had to take a patient back to surgery to resect this nerve (unpublished observations). I have one failure so far in a patient with a painful neuropathy of unknown etiology who remained with forefoot pain after the neurolysis and probably was a poor choice to have only the interdigital neurolysis. This raises the concept of the ‘‘double crush’’ phenomenon,63-65 in which a proximal site of compression renders the distal nerve susceptible for compression, as well. In the posterior tibial nerve region, entrapment of the posterior tibial nerve branches in the medial ankle region will reduce the gliding of the interdigital nerve system, rendering them more susceptible to compression. Each patient with a clinical interdigital nerve compression must be evaluated for a coexisting neuropathy or tarsal tunnel syndrome by measuring the sensibility of the hallux pulp, heel, and dorsal foot surface. It is possible that patients with an interdigital nerve compression in a webspace other than the third have a proximal nerve compression site. For patients with more than one interdigital nerve compression, the adjacent webspaces can be approached through a single incision, as noted by Schon,2 and our preferred incision for this is given in Figure 9A-20.66 Although relief of interdigital nerve
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compression usually can be achieved by inserting a metatarsal bar into the shoe, changing the shoebox to incorporate a wider toe, administering nonsteroidal anti-inflammatory medications and cortisone injections, persistent pain requires surgical treatment. Repetitive cortisone injections may weaken the capsule of the metatarsophalangeal joint or induce tendon or volar plate rupture. The results of resecting the common plantar interdigital nerve can approach 90%,67-69 but failure results in a true neuroma, the correction of which requires a plantar approach and implantation of the resected interdigital nerve into muscle in the arch of the foot.6,8
LESS COMMON LOWER-EXTREMITY PERIPHERAL NERVE PROBLEMS The lateral femoral cutaneous nerve usually is depicted as being below the inguinal ligament and about 2 cm medial to the anterior superior iliac crest. Athletes who fall directly on the anterior iliac crest may have pain related to such a ‘‘hip pointer’’ injury. This may occur in wrestling during a takedown, in football during a tackle, or in rugby. Numbness in the anterior and lateral thigh and anterior hip pain can be the result of acute and then chronic compression of this nerve (Fig. 9A-21).
Less common lower-extremity peripheral nerve problems
Regions of Cutaneous Nerve Distribution:
Nerve Regions Iliohypogastric
Genitofemoral: Genital branch Femoral branch Ilioinguinal Lateral femoral
This problem was known decades ago as meralgia paresthetic or a painful thigh. Because this nerve can extend to the lateral surface of the knee, it can even present as knee pain, which I have seen in a slim, female, longdistance biker. In biking, the repetitive hip flexion/ extension can cause irritation of this nerve, especially when it is located within the inguinal ligament and adjacent to the anterior superior iliac crest. Indeed, this nerve is so commonly found in this location at surgery (Fig. 9A-22), that it prompted a cadaver study, reported in 1995.70 This demonstrated that more than one third of cadavers have this nerve located within the inguinal ligament and adjacent to the bone or the origin of the sartorius muscle. Patients with this nerve compression have discomfort sitting up straight and often will be observed to be sitting in the examining room with the affected leg slightly extended at the hip. Neurosensory testing of the lateral versus the medial thigh skin can document the present of this nerve compression, which is difficult to identify with electrodiagnostic testing.71 In the acute situation, it is important to administer anti-
inflammatory medication and use methods to reduce the swelling while maintaining gliding of the nerve so it does not become scarred. Ultrasound with steroid iontophoresis may be helpful in the subacute phase. If the symptoms have been present for more than 6 months and cannot be relieved by massage or by wearing clothes without a tight belt, then surgical decompression must be considered. The results of neurolysis of lateral femoral cutaneous nerve have been reported showing excellent results in more than 80% of patients.72 Hernia repair in athletes can cause pain in the groin related to either tightening of the inguinal ligament sufficient to cause compression of the lateral femoral cutaneous nerve or iatrogenic injury to the ilioinguinal and iliohypogastric nerves.72 The typical pain pattern (skin innervation territory) for each of these nerves is given in Figure 9A-21. Pain from a neuroma of the ilioinguinal or genitofemoral nerve may be confused with pain from tendinitis of the origin of the gracilis muscle or other adductors from the pubic ramus. The saphenous nerve can be compressed in the midthigh in the adductor canal. This is a rare entrapment.73–75 I have seen it in the setting of cyclists who have fallen and have had bruising in the thigh and in motorcycle riders who have fallen and in whom the bike has compressed the midthigh. This also has been observed in a martial artist as a stretch/traction problem. If this does not resolve, the surgical approach requires a large midthigh incision and division of the fascia between the rectus lateralis and the adductor group of muscles (Figure 9A-23). 223
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Figure 9A-21 Groin pain of neural origin can be evaluated by considering the skin territory innervated by each nerve, shown in different colors, below. The surgical incisions that are responsible for creating neuroma and pain syndrome of these nerves also are shown. The lateral femoral cutaneous nerve has a large territory, and most often this nerve has chronic compression, rather than a true neuroma. Its territory extends to the knee, and compression of this nerve can give rise to knee pain in athletes with repetitive hip flexion, such as cyclists. Pain in the groin after hernia repair is the usual cause of the painful neuromas in the other territories. (Courtesy www. DellonInstitutes.com Web site, patient-interactive tutorial.)
Figure 9A-22 Intraoperative view of neurolysis of the right lateral femoral cutaneous nerve. This nerve is located adjacent to the anterior superior iliac crest. The narrowed area of the nerve is clear after division of the inguinal ligament. The neurolysis must continue proximally dividing the internal oblique fibers until the superficial circumflex iliac vessels is reached.
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Nerve disorders and plantar heel pain
Figure 9A-23 Adductor canal syndrome. This patient had an injury to the left knee and thigh. Previous operations resected the infrapatellar branch of the saphenous nerve, but the patient had persistent pain in the saphenous distribution. With the leg abductor and externally rotated at the hip, a positive Tinel sign was present at the site of the adductor canal, which has been exposed (A). The saphenous nerve is encircled with a vessel loupe (B). For chronic compression, a neurolysis is sufficient. If there is a distal pain syndrome, the saphenous nerve can be resected at this level and implanted into an adductor muscle.
The sural nerve can be entrapped theoretically where it exits the fascia in the distal lateral calf. Its surgical anatomy has been described well, and the variability of the location for the lateral sural joining the medial sural is significant.53 A stretch-traction injury to the sural nerve in this distal location has been described, but it is rare.76 More likely, the athlete will have had a direct injury to this nerve from sports trauma,77 or the nerve will be injured iatrogenically related to a lateral ankle surgery.
REFERENCES 1. Baxter DE: Functional nerve disorders. In Baxter DE, editor: Sports foot and ankle, St Louis, 1994, CV Mosby. 2. Schon LC: Nerve entrapment, neuropathy, and nerve dysfunction in athletes, Orthop Clin North Am 25:47, 1994. 3. Mackinnon SE, Dellon AL: Surgery of the peripheral nerve, New York, 1988, Thieme. 4. Dellon AL, Mackinnon SE, Pestronk A: Implantation of sensory nerve into muscle: preliminary clinical and experimental observations on neuroma formation, Ann Plast Surg 12:30, 1984. 5. Dellon AL, Mackinnon SE: Treatment of the painful neuroma by neuroma resection and muscle implantation, Plast Reconstr Surg 77:427-436, 1986.
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6. Dellon AL: Treatment of recurrent metatarsalgia by neuroma resection and muscle implantation: case report and algorithm for management of Morton’s ‘‘neuroma’’, Microsurgery 10:256, 1989. 7. Dellon AL, Aszmann OC: Treatment of dorsal foot neuromas by translocation of nerves into anterolateral compartment, Foot Ankle 19:300, 1998. 8. Wolfort S, Dellon AL: Treatment of recurrent neuroma of the interdigital nerve by neuroma resection and implantation of proximal nerve into muscle in the arch, J Foot Ankle Surg 40:404, 2001. 9. Larson EE, et al: Accurate nomenclature of forefoot nerve entrapment: a historical perspective, J Am Podiatr Med Assoc 95:298, 2005. 10. Horner G, Dellon AL: Innervation of the human knee joint and implications for surgery, Clin Orthop Rel Res 301:221, 1994. 11. Dellon AL: Clinical grading of peripheral nerve problems, Neurosurg Clin North Am 12:229, 2001. 12. Dellon AL, Mont MA, Hungerford DS: Partial denervation for treatment of persistent neuroma pain after total knee arthroplasty, Clin Orthop Rel Res 316:145, 1995. 13. Dellon AL, et al: Partial denervation for persistent neuroma pain around the knee, Clin Orthop Rel Res 329:216, 1996. 14. Dellon AL, Mont MA, Hungerford DS: Partial denervation for the treatment of painful neuromas complicating total knee arthroplasty. In Insall JN, Scott WN, editors: Surgery of the knee, ed 2. Philadelphia, 2000, WB Saunders. 15. Rab M, Ebmer J, Dellon AL: Innervation of the sinus tarsi: implications for treating anterolateral ankle pain, Ann Plast Surg 47:500, 2001. 16. Dellon AL: Denervation of the sinus tarsi for chronic posttraumatic lateral ankle pain, Orthopedics 25:849, 2002.
References 45. Dellon AL, et al: Cisplatin/Taxol neuropathy: treatment by decompression of peripheral nerve, Plast Reconstr Surg 114:478, 2004. 46. Lee C, Dellon AL: Prognostic ability of Tinel sign in determining outcome for decompression surgery decompression surgery in diabetic and non-diabetic neuropathy, Ann Plast Surg 53:523, 2004. 47. Schon LC, Glennon TP, Baxter DE: Heel pain syndrome: electrodiagnostic support for nerve entrapment, Foot Ankle 14:129, 1993. 48. Rondhuis JJ, Huson A: The first branch of the lateral plantar nerve and heel pain, Acta Morphol Neerl Scand 24:269, 1986. 49. Baxter DE, Thigpen CM: Heel pain: operative results, Foot Ankle 5:16, 1984. 50. Schon LC, Baxter DE: Neuropathies of the foot and ankle in athletes, Clin Sports Med 9:489, 1990. 51. Baxter DE, Pfeffer GB: Treatment of chronic heel pain by surgical release of the first branch of the lateral planar nerve, Clin Orthop 279:229, 1992. 52. Schon LC: Plantar fascia and Baxter’s nerve release. In Myerson M, editor: Current therapy in foot and ankle surgery, St Louis, 1993, Mosby Yearbook. 53. Coert JH, Dellon AL: Clinical implications of the surgical anatomy of the sural nerve, Plast Reconstr Surg 94:850, 1994. 54. Aszmann OC, Ebmer JM, Dellon AL: The cutaneous innervation of the medial ankle: an anatomic study of the saphenous, sural and tibial nerve and their clinical significance, Foot Ankle 19:753, 1998. 55. Dellon AL, Kim J, Spaulding CM: Variations in the origin of the medial calcaneal nerve, J Am Podiatr Med Assoc 92:97, 2002. 56. Rose JD, Malay DS, Sorrento DL: Neurosensory testing of the medial calcaneal and medial plantar nerves in patients with plantar heel pain, J Foot Ankle Surg 42:173, 2002. 57. DuVries, HL: Heel spur (calcaneal spur), AMA Arch Surg 74:536, 1957. 58. Kim J, Dellon AL: Calcaneal neuroma: diagnosis and treatment, Foot Ankle Int 22:890, 2001. 59. Dellon AL: Treatment of Morton’s neuroma as a nerve compression: the role for neurolysis, J Am Podiatr Med Assoc 82:399, 1992. 60. Gauthier G: Thomas Morton’s disease, a nerve entrapment syndrome. A new surgical technique, Clin Orthop 142:90, 1979. 61. Nemoto K, et al: Neurolysis as a surgical procedure for Morton’s neuroma, J Jpn Orthop Assoc 63:470, 1989. 62. Barrett S, Pignetti TT: Endoscopic decompression for intermetatarsal nerve entrapment; the EDIN technique; preliminary study with cadaveric specimens and early clinical results, J Foot Ankle Surg 33:503, 1994. 63. Upton ARM, McComas AJ: The double crush in nerve entrapment syndromes, Lancet 2:35361, 1973. 64. Dellon AL, Mackinnon SE, Seiler WA IV: Susceptibility of the diabetic nerve to chronic compression, Ann Plast Surg 20:117, 1988. 65. Dellon AL, Mackinnon SE: Chronic nerve compression model for the double crush hypothesis, Ann Plast Surg 26:259, 1991. 66. Rosson G, Dellon AL: Surgical approach to multiple interdigital nerve compressions, J Foot Ankle Surg 44:70, 2005. 67. Bradley N, Miller WA, Evans JP: Plantar neuromas, analysis of results following surgical excision in 145 patients, South Med J 69:853, 1976. 68. Mann R, Reynolds JC: Interdigital neuroma: a critical clinical analysis, Foot Ankle 32:38, 1983. 69. Keh RA, et al: Long-term follow-up of Morton’s neuroma, J Foot Surg 31:93, 1992. 70. Aszmann OC, Dellon ES, Dellon AL: The anatomic course of the lateral femoral cutaneous nerve and its susceptibility to compression and injury, Plast Reconstr Surg 100:600, 1997. 71. Coert JH, Connolly J, Dellon AL: Documenting compressive neuropathy of the lateral femoral cutaneous nerve, Ann Plast Surg 50:373, 2003.
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17. Dellon AL, Barrett S: Sinus tarsi denervation: clinical results, J Am Podiatr Med Assoc 95:108, 2005. 18. Mont MA, et al: Operative treatment of peroneal nerve palsy, J Bone Joint Surg 78A:863, 1996. 19. Dellon AL, Ebmer J, Swier P: Anatomic variations related to decompression of the common peroneal nerve at the fibular head, Ann Plast Surg 48:30, 2002. 20. Adkinson DP, et al: Anatomical variations in the course of the superficial peroneal nerve, J Bone Joint Surg 7A:112, 1991. 21. Rosson GD, Dellon AL: Entrapment of the superficial peroneal nerve, Clin Orthop Rel Res 2005. (in press). 22. Styf J, Moberg P: The superficial peroneal tunnel syndrome: Results of treatment by decompression, J Bone Joint Surg 79B:801, 1997. 23. Krause KH, Witt T, Ross A: The anterior tarsal tunnel syndrome, J Neurol 271:67, 1977. 24. Borges LF, et al: The anterior tarsal tunnel syndrome: report of two cases, J Neurosurg 54:89, 1981. 25. Gessini L, Jandolo B, Peitrangel A: The anterior tarsal tunnel syndrome: report of for cases, J Bone Joint Surg 66A:786, 1984. 26. Dellon AL: Deep peroneal nerve release, entrapment on the dorsum of the foot, Foot Ankle 11:73, 1990. 27. Lindenbaum BL: Ski boot compression syndrome, Clin Orthop 140:19, 1979. 28. Francel TJ, Dellon AL: Functional limb salvage combining gastrocnemius neurotization and posterior tibial nerve grafting: a case report, J Reconstr Microsurg 8:209, 1992. 29. Mackinnon SE, Dellon AL: Homologies between the tarsal and carpal tunnels: implications for treatment of the tarsal tunnel syndrome, Contemp Orthop 14:75, 1987. 30. Tassler PL, Dellon AL: Pressure perception in the normal lower extremity and in tarsal tunnel syndrome, Muscle Nerve 19:285, 1996. 31. Dellon AL: Computer-assisted sensibility evaluation and surgical treatment of tarsal tunnel syndrome, Adv Pod 2:17, 1996. 32. Dellon AL: Measuring peripheral nerve function: neurosensory testing versus electrodiagnostic testing. In Slutsky D, editor: Atlas of the hand clinics: nerve repair and reconstruction, Philadelphia, 2005, Elsevier. 33. Naff N, Dellon AL, Mackinnon SE: The anatomic course of the palmar cutaneous branch of the median nerve, including a description of its own unique tunnel, J Hand Surg 18B:316, 1993. 34. Dellon AL: Wound healing in nerve, Clin Plast Surg 17:545, 1990. 35. Dellon AL, et al: Effect of submuscular versus intramuscular placement of ulnar nerve: experimental model in the primate, J Hand Surg 11B:117, 1986. 36. Lau JTC, Daniels TR: Tarsal tunnel syndrome: a review of the literature, Foot Ankle Int 20:201, 1999. 37. Pfeiffer WH, Cracchiolo A: Clinical results after tarsal tunnel decompression, J Bone Joint Surg 76A:1222, 1994. 38. Bailie DS, Kelitian AS: The tarsal tunnel syndrome: surgical technique and functional outcome, Foot Ankle Int 19:65, 1998. 39. Gondring WH, Shields B, Wenger S: An outcomes analysis of surgical treatment of tarsal tunnel syndrome, Foot Ankle Int 24:545, 2003. 40. Mullick T, Dellon AL: Results of decompression of four medial ankle tunnels in the treatment of tarsal tunnel syndrome, J Reconstruct Microsurg, 2007. (in press). 41. Dellon AL: Clinical grading of peripheral nerve problems, Neurosurg Clin North Am 12:229, 2001. 42. Dellon AL: Treatment of symptoms of diabetic neuropathy by peripheral nerve decompression, Plast Reconstr Surg 89:689, 1992. 43. Aszmann OC, Kress K, Dellon AL: Results of decompression of peripheral nerves in diabetics: a prospective, blinded study utilizing computer-assisted sensorimotor testing, Plast Reconstr Surg 106:816, 2000. 44. Aszmann OC, Tassler PL, Dellon AL: Changing the natural history of diabetic neuropathy: incidence of ulcer/amputation in the contralateral limb of patients with a unilateral nerve decompression procedure, Ann Plast Surg 53:517, 2004.
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72. Lee CH, Dellon AL: Surgical management for groin pain of neural origin, J Am Coll Surg 191:137, 2000. 73. Mozes MM, Ouaknine G, Nathan H: Saphenous nervous entrapment simulating a vascular disorder, Surgery 77:299, 1975. 74. Worth RM, et al: Saphenous nerve entrapment, Am J Sports Med 12:80, 1984. 75. Romanoff ME, et al: Saphenous nerve entrapment of the adductor canal, Am J Sports Med 17:478, 1989. 76. Pringle RM, Protheroe K, Mukherjee SK: Entrapment neuropathy of the sural nerve, J Bone Joint Surg 56B:465, 1974.
77. Gould N, Trevino S: Sural nerve entrapment by avulsion fracture at the base of the fifth metatarsal bone, Foot Ankle 2:153, 1981.
FURTHER READING Dellon AL: Deciding when heel pain is of neural origin, J Foot and Ankle Surgery, 40:341-345, 2001.
B. Plantar heel pain Lew C. Schon, Florian Gruber, and Glenn B. Pfeffer
Plantar heel pain is one of the most common foot problems in the athlete/dancer. Running, cutting, pivoting, and jumping, especially on unyielding surfaces, places tremendous, acute, and repetitive stresses on the heel. Often it is difficult to determine the exact etiology of the heel pain because several different underlying problems can occur simultaneously with symptoms. The complex anatomy of the heel challenges the practitioner to distinguish among several potentially pathologic structures that lie within a small area. The difficulty in establishing the specific etiology and subsequently reversing underlying processes correlates with the complexity of achieving a cure. Focal causes of plantar heel pain include the following: 1. Fat pad insufficiency 2. Plantar fascial rupture 3. Insertional plantar fasciosis 4. Midsubstance plantar fasciitis 5. Nerve entrapment: (a) tarsal tunnel syndrome and (b) first branch of the lateral plantar nerve 6. Stress fracture of the calcaneus 7. Tumor. In differentiating these diagnoses, a comprehensive physical examination and medical history are essential. Knowing the onset of the pain (e.g., acute trauma vs. overuse) and the precipitating activity is useful to establish etiology. The exact location, character (i.e., musculoskeletal or neuritic), and duration of pain should be noted. The relationship of pain to a particular action or a specific activity modification is useful for realizing a diagnosis and treatment plan. The history should include an overview of the patient’s general medical and orthopaedic conditions to determine whether there is systemic or more global musculoskeletal disorder contributing to the local problem. Radiculopathy in the L5-S1 distribution should be considered in a patient with back pain, and a
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peripheral neuropathy ruled out when heel pain is diffuse, nonfocal, and bilateral. The seronegative arthropathies should be considered in an athlete with bilateral heel pain.1 Chronic pain at rest is an unusual presentation for plantar heel pain, and if a neurologic cause is not responsible, a tumor of the calcaneus should be considered.
FAT PAD INSUFFICIENCY With each heel strike, the calcaneal fat pad cushions the foot and body from direct and potentially catastrophic impact. A healthy, middle-aged man has a gait velocity of approximately 82 m/minute and a cadence of 116. This rate results in 58 heel strikes per minute with a force of up to 110% of body weight. A sprinter does not place a direct increased stress on the heel, but a middle- or long-distance runner may generate a force of up to 200% of body weight. Considering timing, impact forces, and average heel pain area (23 cm2), the loading pressure of a 70-kg man is approximately 9.3 kg/cm2 when he is running. Anatomic studies of the human heel pad have identified structural specialization capable of withstanding these high loads.2 The anatomy of the heel pad was first described by Tietze in 1921.3 He emphasized the specialized anatomy of the heel pad, with elastic adipose tissue organized as spiral-formed, fibrous tissue septa anchored to one another, the calcaneus, and the skin. Designed to resist and absorb compressive loads, the tissue septa are U-shaped or comma-shaped fat-filled columns with a vertical orientation. The septa are reinforced internally with elastic transverse and diagonal fibers that connect the thicker walls and separate the fat into compartments or cells. The thickness of the heel pad is the most important factor in determining the
Insertional plantar fasciosis
Plantar aponeurosis
Plantar fasciitis
Heel pain syndrome
Fat pad atrophy of shear
Focal causes of plantar heel pain.
stresses seen in the tissues beneath it.4 After age 40, the adipose tissue usually begins to deteriorate gradually, with the insidious loss of collagen, elastic tissue, water, and overall thickness of the heel pad. The result is an inescapable softening, flaccidness, and thinning in the heel pad and a concomitant loss of shock attenuation. Some patients experience these changes earlier because of genetic factors. An athlete with heel pain secondary to fat pad incompetence usually complains of diffuse plantar heel discomfort aggravated by sports on harder surfaces, such as a basketball court, concrete floors, or cinder track. By clinical examination the patient has a soft, flattened heel pad that allows easy palpation of the calcaneal tubercles. Sometimes the pad has a particularly small surface area or thickness. Compression of this area by the examiner duplicates the symptoms, with pain maximal over the central weight-bearing portion of the heel pad overlying the bone. Initially there is no radiation of the pain, and the plantar fascia is not tender. The area of maximal tenderness is proximal and central on the heel (Fig. 9B-1). With prolonged duration of the condition, patients may develop calcaneal stress fractures, fasciitis/fasciosis, or local neuralgia. The only intervention for this condition is avoidance of high-impact activity, especially on unyielding hard surfaces, using a cushioned heel cup and/or shock-
absorbent footgear. A plastic or silicone heel cup that elevates the heel may be helpful both by protecting the painful area and by shifting some of the weight bearing more anteriorly. Cross training with swimming or biking is useful in maintaining physical condition while avoiding the offending activity. Avoidance of cortisone injections for this condition limits further atrophy. There is no surgical treatment for this condition.
INSERTIONAL PLANTAR FASCIOSIS The most common site for plantar heel pain is where the plantar fascia and intrinsic muscles arise from the medial calcaneal tuberosity on the anteromedial aspect of the heel (Fig. 9B-1). During sports activities, particularly long-distance running, the plantar fascia is placed under repetitive traction, which contributes to high stresses at the bone-fascia junction. The plantar fascia arises predominantly from the medial calcaneal tuberosity and inserts distally through several slips into the plantar plates of the metatarsophalangeal joints, the flexor tendon sheaths, and the base of the proximal phalanges of the digits.5,6 When the metatarsophalangeal joints are dorsiflexed with running or jumping, the inelastic plantar fascial fibers place traction on the calcaneus.5 227
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Figure 9B-1
Compression of the first branch of the lateral plantar nerve
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Typically with recurrent stresses the junction of two structures with different biomechanical properties will be the site of stress concentration. This is particularly true in the heel, where the plantar fascia, which is strong under traction or tension stresses, meets the calcaneus, which is strongest in compression load. Over time, microtears can occur in the plantar fascia near the medial calcaneal tuberosity. A reparative response develops, along with continued traumatic fatigue in the fascia. Surgical biopsy specimens of the origin of the plantar fascia in athletes with chronic heel pain reveal collagen necrosis, angiofibroblastic hyperplasia, chondroid metaplasia, and matrix calcification. Thus it is appropriate to use the term ‘‘fasciosis’’ to reflect a degenerative process, rather than ‘‘fasciitis,’’ an inflammatory process. Periostitis of the medial calcaneal tuberosity often occurs in conjunction with degenerative changes in the plantar fascia, causing a positive delayed technetium-99 bone scan in the majority of painful heels.7 Because of the close proximity of the medial calcaneal tuberosity and the origin of the plantar fascia, it is not possible to differentiate clinically a fascial or bony source of an athlete’s pain. Both structures usually are involved, much like other insertional tendon and fascial conditions.8 Patients may have local, soft-tissue swelling and focal tenderness over the medial calcaneal tuberosity directly and the plantar fascia distally for several millimeters. The examiner often must apply a considerable amount of pressure to localize the painful area. Interestingly, patients almost never have increased pain or duplication of symptoms with passive dorsiflexion of the toes, which causes traction on the plantar fascia by the Windlass mechanism (Fig. 9B-2). Associated tightness of the Achilles tendon is commonly seen with this condition, because limited ankle dorsiflexion places increased stress on the plantar fascia. Insertional plantar fasciosis is insidious in onset and is seen most often as an overuse condition of long-distance runners.8 In athletes with an acute onset of symptoms, rupture of the plantar fascia should be considered9 (Fig. 9B-3). Rupture is much less common than chronic insertional plantar fasciosis and easily can be differentiated on the basis of physical examination and history. A palpable defect in the plantar fascia is present when a rupture occurs, and often there is ecchymosis. The fascia will be less taut with a rupture than with fasciosis. An old partial rupture of the plantar fascia can present with a palpable nodularity in the fascia near the medial calcaneal tuberosity and a lower arch. Athletes with insertional plantar fasciosis usually experience symptoms during the first minutes of walking, especially in the morning when first out of bed. The pain gradually decreases. Discomfort is intensified by athletic activity, especially jumping or running. Some athletes have symptoms only during periods of
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Figure 9B-2
Windlass mechanism.
Figure 9B-3
Rupture of plantar fascia.
prolonged running. It is not unusual for athletes to complain of heel pain that occurs only during the first few miles of a workout. No clear correlation between insertional plantar fasciosis and pes planus or pes cavus has been established. A positive correlation with obesity exists, although most athletic patients do not have this concern. A lateral x-ray of the heel will exclude a stress fracture or tumor of the calcaneus. Even among highperformance athletes, a stress fracture is extremely rare.
Insertional plantar fasciosis
cast for 2 to 6 weeks followed by a custom-made orthosis may help break a painful cycle. An off the shelf boot brace typically is not helpful in this condition because the orthosis tends to concentrate the stresses on the heel. In athletes with refractory symptoms, a steroid injection often is beneficial. Care should be taken to inject the steroid deep to the plantar fascia so as not to cause atrophy of the fat pad. A medial approach of the injection is best used so that the steroid can be spread along the broad origin of the plantar fascia. A 25-gauge needle is walked across the anterior border of the calcaneus just deep to the plantar fascia, thereby avoiding the plantar nerves (Fig. 9B-4). Two to three milliliters of an equal mixture of lidocaine, bupivacaine, and long-acting steroid should be administered. Multiple steroid injections may predispose the athletic patient to plantar fascia rupture and should be avoided.14 A majority of patients respond to these conservative measures. A patient may have some persistent symptoms for up to 6 months, but usually only 4 to 6 weeks will be lost from training or competitive athletics if treatment is started early. Extracorporeal shock wave therapy (EWST) has been introduced for the treatment of chronic plantar fasciosis. Alvarez15 reported on the use of high-energy shock wave before surgical management is considered. The safety and early preliminary efficacy of the high-energy
Figure 9B-4 A steroid injection from the medial side of the heel. To avoid steroid-induced atrophy of the fat pad, the solution is injected deep into the plantar fascia. The heel spur arises within the origin of the flexor digitorum brevis muscle.
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Leg lengths always should be examined when evaluating athletes with chronic heel pain. If one leg is longer than the other, often there is a history of repeated injury to the shorter leg. Heel pain is seen more often in the shorter leg and may be treated effectively with an appropriate lift. A functional short-leg syndrome can result from running on the same tilt of road or in the same direction on the track. In both instances, after many miles of training, one heel will be more stressed than the other. By using both sides of the road or intermittently changing directions on a training track, stress between both heels can be equalized. The cornerstone of conservative treatment in athletes is modification in training. Mileage reduction, alternating activities, work reduction, and shortened workouts should be considered.10 Low-resistance cycling and swimming pool running are effective cardiovascular activities that usually are not stressful to the heel. Oral anti-inflammatory agents, contrast baths, ice massage, and soft-soled shoes or sneakers also are used. Plantar fascia stretching exercises should be instituted. If the athlete has Achilles tightness, this should be stretched as well. A study of 101 patients (complete data for 66 patients) with symptoms longer than 10 months compared a specific plantar fascia stretching program (group A) with an Achilles stretching program (group B) for 8 weeks.11,12 Patients in both groups used full-length, prefabricated orthoses. Patients in group A were instructed to perform a stretch by placing the affected foot on the thigh of the contralateral leg. While hyperextending the toes with the ipsilateral hand until a stretch in the arch is felt, the contralateral hand palpates the degree of tension of the plantar fascia. This position was held for 10 seconds and repeated 10 times. The plantar–ascia-stretching group was advised to perform the stretching before any weight bearing. All patients in the other group were instructed to stretch three times a day. After this treatment period, the Achilles tendon group was given the plantar fascia-specific stretching protocol. The results were evaluated after 8 weeks and 2 years. At 8 weeks the plantar–fascia-stretching group had significantly fewer complaints of pain at its worst and pain at the first steps in the morning. At the 2-year follow-up, there was no statistically significant difference between the groups. After 2 years, 94% reported less or no pain and 58% reported no pain. The majority of patients (62%) achieved the best results within the first 6 months. Low dye taping and a one-eighth-inch medial heel wedge may be added in an attempt to reduce the stress on the plantar fascia. A night splint ankle-foot orthosis with the ankle fixed in 5 degrees of dorsiflexion also may be indicated. Using this technique, Wapner et al.13 had a 79% success rate after an average of 4 months of splint use. In refractory cases, a short-leg
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shock wave using the OssaTron was evaluated. Twenty heels of 20 patients were treated with 1000 extracorporeal shock waves from the OssaTron to the affected heel after administration of a heel block. Each patient underwent an extensive evaluation, including x-ray, KinCom, physical examination, and a 10-cm visual analog scale. Of the 20 patients treated, 17 were improved or pain free. There were no complications or adverse effects attributed to the procedure. Zingas and colleagues16 also studied the safety and efficacy of musculoskeletal shock wave therapy in 29 patients with chronic plantar fasciitis. In this study the patients were enrolled in a randomized, 1:1 allocated, placebo-controlled, prospective, double-blind clinical study with two groups: one receiving ESWT with the Dornier Epos Ultra and the other receiving sham treatment. The authors concluded that shock wave therapy is useful in the treatment of chronic plantar fasciitis that has failed conventional conservative methods. The Food and Drug Administration now has approved this treatment for chronic plantar fasciitis, but only some insurance plans cover the treatment. The decision whether to use high-energy or lowerenergy shock wave also has been debated. To date there is no consensus on how to define the terms high-dose and low-dose shock wave. An advantage of the lower energy machine is that the patient does not need general anesthesia or an invasive nerve block to tolerate the procedure. An advantage of the high-energy machines is that typically only one treatment is required, as opposed to three for the lower-energy machines. Different therapy-regimens seem to result in different efficacy of treatment. In 2003, Speed et al.17 found no significant difference between the treatment and placebo group. In their study the authors applied shock waves (0.12 mJ/mm2) monthly for 3 months. The authors concluded that efficacy may be highly dependent on machine types and treatment protocols. Porter et al.18 concluded that ESWT was less effective than a single corticosteroid injection in patients who underwent a standardized Achilles tendon and plantar fascia stretching program. Kudo et al.19 found significantly better outcome of an ESWT group in comparison with a placebo group 3 months after treatment. Treatment consisted of approximately 3800 total shock waves (10) reaching an approximated total energy delivery of 1300 mJ/mm2 (EDþ) in a single session versus placebo treatment. Several studies focusing on the durability of pain relief show good results for EWST for chronic plantar fasciitis for follow-up times from 2 to 6 years.20,21 Further research is needed to develop evidence-based recommendations for using ESWT for treatment of this condition. A recent therapeutic approach for plantar fasciitis is local injection of botulinum toxin A. Placzek et al.22 performed a pilot study with 25 patients using a single
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subfascial injection of 100 units of botulinum toxin A in the first 6 patients to determine the optimal treatment dose and with 200 units in the other 19 patients. The group that received 200 units reported a substantial reduction of maximal and continuous pain 2 and 14 weeks after the injection and no signs of muscular weakness in a clinical exam. Babcock et al.23 presented a randomized placebo-controlled, double-blind study of 27 patients (43 feet). They applied 40 units at the tender area at the medial tuberosity of the calcaneus and 30 units between an inch distal of the heel and the middle of the foot. The placebo group received injections with the same volume of saline. Main outcome measures included the pain visual analog scale, Maryland foot score, pain relief visual analog scale, and pressure algometry response. Patients were assessed before injection, at 3 weeks, and at 8 weeks. The botulinum group improved significantly in all measures and showed no adverse side effects. Another possible treatment option for enthesopathies that has been used for patients with elbow tendinosis involves injection of platelet-rich plasma (PRP). Mishra and Pavelko24 studied 20 patients with persistent pain for a mean of 15 months despite conservative therapy. The pain level measured with a visual analog scale from 0 to 100 was 82 on average (60-100). Fifteen patients received a single percutaneous injection of PRP. The control group (n ¼ 5) got an injection with bupivacaine. Eight weeks after treatment, the patients in the PRP group had a 60% improvement in visual analog scores and the control group showed only 16% improvement (p ¼ .001). Only the platelet-injection group could be observed in further follow-up. At 6 months and at final follow-up after a mean 25.6 months (range, 12-38 months), 81% and 93% of these patients noted improvement in their pain visual analog score. The authors concluded that PRP injection reduces pain significantly in their patient group. Research is needed to determine whether this result is applicable to treatment of plantar fasciitis. In those few patients who fail prolonged, conservative treatment, surgical release of the plantar fascia should be considered. However, every attempt should be made to avoid this procedure in competitive athletes. Release of the plantar fascia may have a detrimental effect on function. Daly et al.25 demonstrated in their study a change in both arch height and the ratio of arch height to arch length following a plantar fascia release. A less energetic pattern of walking following a plantar fascia release also was seen. Further, if the plantar fascia is divided surgically, increased compressive forces are transmitted to the dorsal aspect of the midfoot, with decreased flexion forces on the metatarsophalangeal joint complex.6 These changes can lead to dorsal midfoot pain and metatarsalgia postoperatively (Fig. 9B-5).
Insertional plantar fasciosis
Figure 9B-5 If the plantar fascia is divided surgically, there are increased compressive forces transmitted to the dorsal aspect of the midfoot and decreased flexion forces on the metatarsophalangeal joint complex.
Surgical technique Plantar fascia release may be performed using a regional anesthetic with intravenous sedation and a standby general anesthetic. An ankle block is highly useful, using a 1:1 solution of 0.25% bupivacaine hydrochloride (Marcaine) and 1% lidocaine, both without epinephrine. An oblique incision is begun along the inferomedial aspect of the heel, just anterior to the calcaneus where the inferior abductor fascia joins the medial plantar fascia (Fig. 9B-6). This 2.5- to 4-cm incision is planned anterior to the medial calcaneal branch of the posterior tibial nerve, avoiding inadvertent division of the nerve and the formation of a painful postoperative neuroma. Care should be taken to search for this nerve branch during the operative approach because its course can be more anterior than expected. Using blunt dissection, the medial edge of the plantar fascia origin is visualized easily. Isolate the fascia from the adipose tissue, which lies inferiorly, and the fascia of the abductor hallucis muscle, which lies superiorly. If necessary, the incision can be extended a few centimeters transversely across the nonweight-bearing aspect of the sole.29 A Freer elevator is used to isolate the plantar fascia along its origin on the calcaneus. The plantar fascia often will be thickened in this area from chronic changes. A scalpel then is used to divide the plantar fascia as it arises from the calcaneus. Any degenerated portions of the plantar fascia should be excised. Typically a piece of fascia is removed measuring 3 to 4 mm wide and a thickness of 2 to 4 mm. The depth of the release should be 4 to 5 mm. 231
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If surgery is performed, it is necessary to discuss the role of the spur with the patient. In general, resection of the heel spur is not performed because it does not contribute to the pathophysiology. In addition, resection of the spur can lead to a slightly more aggressive release of the fascia to gain exposure and may lead to some more bleeding because of the presence of raw bone. On the other hand, at times the spur is quite large and the patient is fixated on its presence. It can be easier to remove the spur than to explain at each visit that the pain that remains while he or she is healing is common and will resolve. It is useful to advise the patient that the heel spur arises deep to the plantar fascia in the nonweight-bearing substance of the flexor brevis muscle and therefore is probably not involved in producing the pain. Most patients are informed that the calcaneal spur was of great importance in the treatment of heel pain historically. They also are told that many patients without heel pain have spurs and that many patients without spurs have pain. Tanz26 demonstrated that only 50% of patients with plantar heel pain had a heel spur and that 16% of nonpainful heels also had a heel spur. Rubin and Whitton27 determined that only 10% of patients with heel spurs were symptomatic. Finally they are told that the spur can be left alone, but that they still can have successful conservative or surgical treatment for the plantar fasciitis. Lapidus and Guidotti28 showed that the successful treatment of heel pain was not contingent on the surgical removal of a heel spur and concluded that plantar calcaneal spurs do not cause the painful heel, as they have been postulated to do. We leave the decision about spur resection to the surgeon’s discretion.
CHAPTER 9
Nerve disorders and plantar heel pain
Figure 9B-6 Incision used to release the plantar fascia. The incision may be extended along the nonweightbearing aspect of the foot.
If a heel spur is present in the origin of the flexor brevis muscle, it easily can be removed using a small osteotome and rongeur. Care should be taken not to remove cortical bone of the calcaneus and thereby create a stress riser. A reciprocating rasp works well for both gross reduction and final smoothing of the calcaneal surface. One should protect the first branch of the lateral plantar nerve (nerve to the abductor digiti quinti), which runs across the heel just deep to the heel spur and the flexor brevis muscle. If a tourniquet is used, it should be deflated and hemostasis obtained. A bulky compression dressing is used, and the patient is instructed not to bear weight for 3 to 4 days to allow for wound healing. After the fourth day, weight bearing can progress as tolerated using crutches. Minimal incision surgery is not recommended for release of the plantar fascia. Direct visualization of the plantar fascia is required to gain an adequate release, and inadvertent division of the medial calcaneal sensory nerve easily can occur when an incision of 1 cm or less is used. Benton-Weil reported on percutaneous plantar fascia release in a retrospective study with 35 patients using a questionnaire and the visual analog score at an average follow-up time of 34 months. He described improvement of the visual analog score from 8.2 to 2.1. In 83% the results of the procedure met or exceeded the patient’s expectations. An interesting technique that has been used for plantar fasciosis involves drilling the calcaneus. Some authorities add this to their surgical protocol when there is any suspected calcaneal stress fracture, determined on the basis of a hot bone scan or tenderness along the wall of the calcaneus. Schon uses this method as an adjuvant for these cases but at times has drilled only the
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calcaneus and had good results. Hassab and El-Sherif 30 drilled the os calcis to obtain relief of recalcitrant heel pain. They performed 68 operations in 60 patients and reported excellent results in 62, good in 2, and poor in 4. Santini et al.31 presented a retrospective study of 25 feet in 21 patients treated with drilling of the calcaneus. The indication was chronic heel pain in combination with increased uptake in the delayed bone scans. Under local anesthesia, three holes were drilled in the medial cortex of the calcaneus. After an average follow-up time of 21 months, the authors noted a decrease in pain from 8.8 (4-10) preoperatively and 2.4 (0-10) using the visual analog score. Six of seven patients who had another bone scan postoperatively showed resolution of the increased uptake. The outcome was worse in patients with rheumatoid and other systemic diseases and Haglund deformity. Santini states that his results of calcaneal drilling are comparable to other surgical options for treatment of chronic heel pain. Endoscopic plantar fascia release is another method for treating this condition. The technique was first popularized by Barrett and Day,32 who proposed this technique as causing less tissue damage than open treatment. In a follow-up, multicenter study of 652 procedures, they reported 62 complications in 53 patients but felt that it afforded satisfactory results. O’Malley and associates33 reviewed the surgical results following endoscopic plantar fasciotomy in 16 patients (20 feet) with an average preoperative duration of symptoms of 4 years. Nine had complete relief of pain, and another 9 feet were improved. One patient with bilateral symptoms had no relief in either foot. The average American Orthopaedic Foot and Ankle Society hindfoot score
Entrapment of the first branch of the lateral plantar nerve
improved from 62 to 80, a statistically significant difference. Patients with unilateral symptoms did better than those with bilateral symptoms. There were no iatrogenic nerve injuries. Other authors have reported various complications from endoscopic plantar fascial release, including stress fractures,34 pseudoaneurysm formation,35 and recurrence of pain.36 A prospective study by Saxena37 compared uniportal endoscopic release of the medial 50% of the plantar fascia in athletes versus nonathletes. All patients had undergone at least 8 months of conservative treatment. Good and excellent results were reported in all 16 athletically active patients using the Modified Plantar Fascia Score (MPFS) and an average return-to-activity time of 2.6 months. Of the 10 patients in the control group (at time of surgery 12 years older than athletic patients), 5 had poor outcome. All of the control patients had a body mass index (BMI) higher than 27. Most authors believe that only the medial one half or medial two thirds of the plantar fascia be released because of the high incidence of lateral foot pain following more aggressive release.
ENTRAPMENT OF THE FIRST BRANCH OF THE LATERAL PLANTAR NERVE One of the most commonly overlooked causes of chronic plantar heel pain in the athlete is entrapment of the first branch of the lateral plantar nerve38-40
(Fig. 9B-7). The first branch innervates the periosteum of the medial calcaneal tuberosity, the long plantar ligament, and the abductor digiti quinti and flexor brevis muscles.41 Entrapment of the nerve accounts for approximately 20% of chronic heel pain. Entrapment occurs as the nerve changes from a vertical to a horizontal direction around the medial plantar aspect of the heel (Fig. 9B-8). The exact site of compression is between the heavy, deep fascia of the abductor hallucis muscles and the medial caudal margin of the medial head of the quadratus plantae muscle (see Fig. 9B-9). Athletes who spend a significant amount of time on their toes, such as sprinters, ballet dancers, and figure skaters are prone to entrapment of the first branch of the lateral plantar nerve by the well-developed abductor hallucis. The medial calcaneal nerve branches that innervate the plantar medial aspect of the heel pass superficial to the abductor hallucis muscle and are not involved with entrapment of the first branch. Another potential site of entrapment of the first branch is the point at which the nerve passes just distal to the medial calcaneal tuberosity.40 Inflammation and spur formation in the origin of the flexor brevis muscle can produce sufficient swelling to cause compression of the nerve against the long plantar ligament (Fig. 9B-10). The inflammatory changes of heel pain syndrome (HPS) therefore can predispose to chronic entrapment of the nerve. The diagnosis of entrapment of the first branch of the lateral plantar nerve is made on the basis of clinical grounds. It therefore is incumbent on the examiner to differentiate first-branch entrapment from other, more
First branch of lateral plantar nerve
Medial plantar nerve
Nerve tomedial calcaneal tuberosity
First branch of the lateral plantar nerve.
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Figure 9B-7
Lateral plantar nerve
CHAPTER 9
Nerve disorders and plantar heel pain
Calcaneal nerve
Quadratus plantae
First branch of the lateral plantar nerve
Lateral plantar nerve
Medial plantar nerve
Figure 9B-8 Entrapment of the first branch of lateral plantar nerve occurs as the nerve changes direction from vertical to horizontal around the medial plantar aspect of the heel. Medial plantar nerve Lateral plantar nerve Quadratus plantar (medial and lateral heads)
Abductor digiti quinti Pronation Flexor brevis
Abductor hallucis
Plantar fascia Site of nerve compression Heel spur (if present)
Figure 9B-9
Site of compression of the first branch of the lateral plantar nerve.
common causes of heel pain (Fig. 9B-11). Early-morning pain is not as prominent with nerve entrapment, which tends to cause pain more at the end of the day or after prolonged activity. The pathognomonic sign of entrapment of the first branch of the lateral plantar nerve is maximal tenderness where the nerve is compressed between the taut deep fascia of the abductor hallucis muscle and the medial caudal margin of the quadratus plantae muscle. Chronic inflammation of the plantar fascia may predispose to entrapment of the first branch
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of the lateral plantar nerve. The patient therefore may have some tenderness over the proximal plantar fascia and medial calcaneal tuberosity. Without maximal tenderness over the course of the nerve on the plantar medial aspect of the foot, however, the diagnosis of entrapment should not be made (see Fig. 9B-1). Some patients may have paresthesias elicited with pressure over the nerve at the entrapment site, although this does not occur commonly. Entrapment of the isolated medial plantar nerve, ‘‘jogger’s foot,’’ occurs more distally at
Entrapment of the first branch of the lateral plantar nerve
Entrapment of nerve to the abductor digiti quinti m. between deep fascia of the abductor hallucis m. and the medial caudal margin of the quadratus plantae m.
Figure 9B-11 Entrapment of nerve to the abductor digiti quinti.
the level of the navicular tuberosity and should not be confused with entrapment of the first branch of the lateral plantar nerve more proximally. Motor weakness in the abductor digiti quinti muscle may on occasion be detected, although no cutaneous sensory deficit occurs. Electromyography and nerve conduction studies are not yet consistent in diagnosing
Surgical Technique The surgical approach to release the first branch of the lateral plantar nerve should be from the medial side of the heel. The patient is supine on the operating table. No tourniquet is required, although an ankle tourniquet can be used. A 4-cm oblique incision is made on the medial heel over the proximal abductor hallucis muscle. The incision is centered over the course of the first branch of the lateral plantar nerve. The medial calcaneal sensory nerve branches are not encountered as they course posterior to the incision. Care is taken, however, to preserve any aberrant branches. 235
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Figure 9B-10 The plantar fascia is retracted. The first branch of lateral plantar nerve is exposed (arrow). A large heel spur is marked (S). (From Kenzora JE: The painful heel syndrome: an entrapment neuropathy, Bull Hosp Joint Dis 47:178, 1987.)
entrapment of the first branch of the lateral plantar nerve.42 Measurement of nerve conduction slowing across the site of entrapment is technically demanding, and denervation potentials in the intrinsic foot muscles may occur only rarely because of the possible dynamic nature of this particular compression neuropathy. A comparison may be drawn to the diagnosis of a posterior interosseous nerve entrapment in the upper extremity. Treatment for athletes with entrapment of the first branch of the lateral plantar nerve is similar to that of HPS, with rest, nonsteroidal anti-inflammatory agents, contrast baths, ice massage, physical therapy, and steroid injection serving as the foundation for conservative care. A shock-absorbent viscoelastic heel insert also will help to decrease inflammation in the area. In athletic patients with excessive pronation, especially long-distance runners, a nonrigid, mediolongitudinal arch support can decrease compression of the nerve. In 1984, Baxter and Thigpen39 presented the first large clinical series of patients treated operatively for entrapment of the first branch of the lateral plantar nerve. Twenty-six patients with 34 involved heels underwent operative decompression; 82% of the patients experienced complete relief of their symptoms. In 1992, Baxter and Pfeffer38 published a series of 69 heels in 53 patients with chronic heel pain who had surgical release of the first branch of the lateral plantar nerve. The average duration of heel pain symptoms was 23 months. No patient had fewer than 6 months of conservative treatment before surgery. The average duration of preoperative conservative treatment was 14 months. Postoperatively 61 heels (89%) had excellent or good results. The average follow-up was 49 months. Approximately half the patients in Baxter’s second study developed heel pain as a result of a sports activity, usually long-distance running. Other activities included aerobics, basketball, volleyball, and tennis. Eighty-five percent of this group had good or excellent results from surgery. The mean recovery time of the athletic subgroup to resumption of sports activities was 3 months. This amount of time was not considered excessive, given the mean of 23 months of preoperative symptoms.
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Nerve disorders and plantar heel pain
The superficial fascia of the abductor hallucis is divided with a no. 15 blade, and the muscle is retracted superiorly using a Ragnell retractor. A section of deep fascia of the inferior abductor hallucis is removed directly over the area where the nerve is compressed between this taut fascia and the medial border of the quadratus plantae muscle. A small portion of the medial plantar fascia may be removed to facilitate exposure and clearly define the plane between the deep abductor fascia and the plantar fascia. The deep fascia of the abductor hallucis then is divided from inferior to superior to sufficiently free the nerve from entrapment. If present, a heel spur is removed, using a Freer elevator to protect the nerve that runs superiorly. The abductor hallucis muscle belly and its superficial fascia are left intact. A plantar fascia release is not performed unless the patient has been symptomatic over the plantar aspect of the medial calcaneal tuberosity and direct visualization provides evidence of pathology in the proximal portion of the plantar fascia. At the end of each case, a small hemostat is used to palpate along the course of the nerve to make sure it is free from any adhesions proximally or distally. The wound is closed with interrupted horizontal mattress nylon sutures. No subcutaneous sutures are used. A bulky dressing is placed. Patients are allowed to bear weight in a postoperative shoe as tolerated and to gradually return to sports activities after 3 to 4 weeks. A plantar heel spur forms in the insertion of the flexor brevis muscle on the calcaneus. The first branch of the lateral plantar nerve courses from medial to lateral directly above this muscle. Although it is unlikely that a heel spur is a direct mechanical cause of plantar heel pain, inflammation in the area of the spur is a theoretical source of compression of the first branch of the lateral plantar nerve as it passes above the spur. A heel spur, if present, therefore should be excised. Care should be taken when excising the spur to protect the first branch of the lateral plantar nerve. The plantar fascia should not be divided to preserve its biomechanical advantage during sports activities.
TARSAL TUNNEL SYNDROME Another nerve entrapment capable of producing chronic heel pain is tarsal tunnel syndrome. Posttraumatic adhesions, bony spurs, chronic inflammation, benign tumors, and varicosities all can all cause compression of the posterior tibial nerve within the tarsal tunnel. Excessive pronation in a long-distance runner may predispose to tarsal tunnel syndrome by placing repeated stress on the structures on the medial side of the heel. Hindfoot varus, in association with excessive pronation, also may be associated with tarsal tunnel syndrome.
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The salient clinical feature of tarsal tunnel syndrome is direct focal tenderness over the nerve as it passes beneath the flexor retinaculum. Percussion of the nerve in this area will reproduce the patient’s symptoms, which can include pain, burning, or tingling on the plantar aspect of the foot. Subjective numbness of the toes may occur, although objective decreased sensibility is rarely demonstrated. Some patients may complain of proximal radiation of their symptoms. Electromyography and nerve conduction studies can be helpful in making a diagnosis. A normal study, however, does not exclude the diagnosis of tarsal tunnel syndrome. In general, the plantar heel pain produced by tarsal tunnel syndrome is more diffuse and less focal than that of either HPS or entrapment of the first branch of the lateral plantar nerve. A careful clinical examination should easily distinguish among these three entities. A medial heel wedge will decrease tension on the nerve. Steroid injection into the tarsal tunnel also may be beneficial but usually produces only transient relief of symptoms. Surgical release of the flexor retinaculum and exploration of the tarsal tunnel can be expected to provide relief of symptoms in 90% of athletic patients. Decompression of both the medial and lateral plantar nerves into the midfoot should be performed in any patient with preoperative tenderness along the course of these nerves (Fig. 9B-12). Internal neurolysis of the nerve is rarely indicated.
MIDSUBSTANCE PLANTAR FASCIITIS Tenderness over the plantar fascia in the midfoot is aptly called midsubstance plantar fasciitis. This condition presents with tenderness over the midportion of the plantar fascia. As opposed to insertional plantar fasciosis, dorsiflexion of the toes almost always exacerbates the patient’s symptoms by the Windlass mechanism stretching the midfascial fibers (Fig. 9B-13). There is usually is only minimal tenderness over the most proximal fascial fibers, which are painful in insertional plantar fasciosis. Plantar fasciitis is seen more often in sprinters and middle-distance runners, who spend more time on their toes during athletic activity. Tendinitis of the flexor hallucis longus tendon can present with pain in the plantar medial midfoot. This condition can be distinguished easily from plantar fasciitis. Passive dorsiflexion of the great toe aggravates both plantar fasciitis and flexor hallucis longus tendinitis, but resisted flexion of the toe is painful only with involvement of the tendon. Careful palpation with motion of the tendon usually is sufficient to confirm the diagnosis. A painful plantar fibromatosis involving the midplantar fascia also can be detected by careful examination.
Summary
Tibialis posterior
Flexor digitorum longus
Posterior tibial artery and nerve
Flexor retinaculum
Abductor hallucis
Figure 9B-12 Decompression of medial and lateral plantar nerves into the midfoot should be performed in any patient with preoperative tenderness along the course of the nerves.
eighth-inch medial heel wedge may take tension off the plantar fascia. If these modalities fail, the cornerstone of treatment is the University of California Biomechanics Laboratory (UCBL) orthosis.43 The theory of the UCBL orthosis is to hold the foot in a position that relieves tension on the plantar fascia. The orthosis accomplishes this reduction in tension by holding the heel in inversion and applying forces against the navicular and lateral aspect of the forefoot, without direct pressure on the soft tissue underneath the longitudinal arch. The UCBL insert usually is not helpful in patients with insertional plantar fasciosis because the rigid material used in constructing the insert often aggravates the inflamed heel. It is extremely unusual to operate on a patient for true midfoot plantar fasciitis. If prolonged, conservative treatment of more than 6 months fails, however, a similar operative approach to that used for insertional plantar fasciosis is indicated.
SUMMARY
A mediolongitudinal arch support often is not tolerated in a patient with plantar fasciitis because it pushes up on the plantar fascia and increases tension on its fibers. Circumferential taping of the foot with 1-inch adhesive tape applied over a nonadhesive elastic wrap usually is beneficial. Rest, alteration of training, nonsteroidal anti-inflammatory agents, ice massage, contrast baths, and physical therapy, including ultrasound and plantar fascial stretching, also are indicated. A one-
Ninety-eight percent of patients with heel pain can be treated successfully with conservative treatment. If treatment is begun soon after the onset of symptoms, most athletes can minimize their downtime to 6 weeks or less. Understandably many athletic patients are reluctant to give up or significantly modify their sports activities. They continue to train through the pain and thereby establish a chronic and refractory condition. In those few patients who require surgery, an excellent result can be obtained if the correct diagnosis is made and the surgeon addresses the specific cause of the athlete’s plantar heel pain. 237
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Figure 9B-13 Dorsiflexion of the toes causing tension on the plantar fascia. The symptoms of true plantar fasciitis are reproduced with this maneuver.
CHAPTER 9
Nerve disorders and plantar heel pain
C A S E S T U D Y 1
C A S E S T U D Y 4
A 23-year-old, nationally ranked middle-distance runner had chronic heel pain. She failed all conservative treatment, including prolonged physical therapy, heel cups, an orthotic device, and shoe modification. She did not want to use a cast. She had maximal tenderness over the medial plantar hindfoot consistent with the diagnosis of entrapment of the first branch of the lateral plantar nerve. Her symptoms had been present for 1 year. Under regional anesthesia she had a surgical release of the deep abductor fascia, freeing up the nerve. Her plantar fascia was left intact. Six weeks later she resumed training with complete relief of pain.
A 24-year-old, female, long-distance runner had a plantar fascia release. Postoperatively she developed metatarsalgia and dorsolateral midfoot pain. She was seen in consultation after repeated attempts at conservative treatment failed to relieve her midfoot pain. Her plantar heel pain had resolved after surgery. She required 8 weeks of casting to alleviate the midfoot symptoms.
C A S E S T U D Y 5
C A S E S T U D Y 2
A 44-year-old, competitive long-distance runner had 2 years of heel pain consistent with insertional plantar fasciosis. His mileage had decreased from 80 miles per week to 0. Under regional anesthesia through an oblique medial incision his plantar fascia was released. No heel spur was present. His plantar heel pain gradually resolved over 4 months. He returned to 40þ miles per week.
An aerobics instructor was seen for chronic hindfoot pain following a plantar fascia release. A longitudinal incision had been used. A small portion of the medial heel was numb. A neuroma in the superficial medial calcaneal nerve was identified. Symptoms persisted despite two steroid injections into the neuroma. The nerve was resected surgically to its origin within the tarsal tunnel. The patient experienced continued tenderness at the nerve ending. Another patient with a similar problem developed a reflex sympathetic dystrophy that remained refractory to conservative treatment.
REFERENCES
C A S E S T U D Y 3
A 23-year-old, male volleyball player was seen for a second opinion regarding chronic heel pain. Surgery had been recommended. The diagnosis was midfoot plantar fasciitis. He wore a rigid, plastic orthotic device, which did not help. The orthotic device was discarded and circumferential taping of the midfoot over a nonadherent wrap was begun. He began a program of physical therapy three times a week to stretch the Achilles tendon and plantar fascia and decrease inflammation. A nonsteroidal anti-inflammatory agent, ice massage, and contrast baths also were used. His symptoms sufficiently improved so that surgery was not required.
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1. Gerster JC: Plantar fasciitis and Achilles tendinitis among 150 cases of seronegative spondarthritis, Rheumatol Rehabil 19:218, 1980. 2. Jahss MH, et al: Investigations into the fat pads of the sole of the foot: anatomy and histology, Foot Ankle 13:233, 1992. 3. Tietze A: Ueber den Architektonischen Aurbau des Bindegenebes in der Neuschilchen Fuss-sohle, Beitr Z Klin Chir 123:493, 1921. 4. Jahss MH, Kummer F, Michelson JD: Investigations into the fat pads of the sole of the foot: heel pressure studies, Foot Ankle 13:227, 1992. 5. Hicks JH: The plantar aponeurosis and the arch, J Anat 88:25, 1954. 6. Sarrafian FK: Functional characteristics of the foot and plantar aponeurosis under tibiotalar loading, Foot Ankle 8:4, 1987. 7. Williams PL, et al: Imaging studies of the painful heel syndrome, Foot Ankle 7:345, 1987. 8. Snider MJ, Clancy WG, McBeath AA: Plantar fascia release for chronic plantar fascitis in runners, Am J Sports Med 11:215, 1983. 9. Leach R, Jones R, Silva T: Rupture of the plantar fascia in athletes, J Bone Joint Surg 60A:537, 1978.
References 25. Daly PJ, Kitaoka HB, Chao EYS: Plantar fasciotomy for intractable plantar fasciitis: clinical results and biomechanical evaluation, Foot Ankle 13:188, 1992. 26. Tanz SS: Heel pain, Clin Orthop 28:168, 1963. 27. Rubin G, Witton M: Plantar calcaneal spurs, Am J Orthop 5:38, 1963. 28. Lapidus PW, Guidotti FP: Painful heel: report of three hundred twenty-three patients with three hundred sixty-four painful heels, Clin Orthop 39:178, 1965. 29. Ward WG, Clippinger RW: Proximal medial longitudinal arch incision for plantar fascia release, Foot Ankle 8:152, 1987. 30. Hassab HK, El-Sherif AS: Drilling of the os calcis for painful heel with calcanean spur, Acta Orthop Scand 45:152, 1974. 31. Santini S, et al: Percutaneous drilling for chronic heel pain, J Foot Ankle Surg 42:296, 2003. 32. Barrett SL, Day SV: Endoscopic plantar fasciotomy for chronic plantar fasciitis/heel spur syndrome: surgical technique-early clinical results, J Foot Surg 30:568, 1991. 33. O’Malley MJ, Page A, Cook R: Endoscopic plantar fasciotomy for chronic heel pain, Foot Ankle Int 21:505, 2000. 34. Sammarco GJ, Idusuyi OB: Stress fracture of the base of the third metatarsal after an endoscopic plantar fasciotomy: a case report, Foot Ankle Int 19:157, 1998. 35. Gentile AT, et al: Traumatic pseudoaneurysm of the lateral plantar artery after endoscopic plantar fasciotomy, Foot Ankle Int 18:821, 1997. 36. Jerosch J: Endoscopic release of plantar fasciitis—a benign procedure? Foot Ankle Int 21:511, 2000. 37. Saxena A: Uniportal endoscopic plantar fasciotomy: a prospective study on athletic patients, Foot Ankle Int 25:882, 2004. 38. Baxter DE, Pfeffer GB: Treatment of chronic heel pain by surgical release of the first branch of the lateral plantar nerve, Clin Orthop 279:229, 1992. 39. Baxter DE, Thigpen CM: Heel pain—operative results, Foot Ankle 5:16, 1984. 40. Kenzora JE: The painful heel syndrome: an entrapment neuropathy, Bull Hosp Joint Dis 47:178, 1987. 41. Rondhuis JJ, Huson A: The first branch of the lateral plantar nerve and heel pain, Acta Morphol Neerl Scand 24:269, 1986. 42. Schon LC, Glennon TP, Baxter DE: Heel pain syndrome: electrodiagnostic support for nerve entrapment, Foot Ankle 14:129, 1993. 43. Campbell JW, Inman VT: Treatment of plantar fasciitis and calcaneal spurs with the UC-BL shoe insert, Clin Orthop 103:57, 1974.
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10. Leach RE, Seavey NS, Salter DK: Results of surgery in athletes with plantar fasciitis, Foot Ankle 7:155, 1986. 11. Digiovanni BF, et al: Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up, J Bone Joint Surg Am 88:1775, 2006. 12. DiGiovanni BF, et al: Tissue-specific plantar fascia-stretching exercise enhances outcomes in patients with chronic heel pain. A prospective, randomized study, J Bone Joint Surg Am 85:1270, 2003. 13. Wapner KL: The use of night splints for treatment of recalcitrant plantar fasciitis, Foot Ankle 12:135, 1991. 14. Sellman JR: Plantar fascia rupture associated with corticosteroid injection, Presented at the AOFAS, Banff, Canada, 1990. 15. Alvarez RG: Preliminary results on the safety and efficacy of the OssaTron for treatment of plantar fasciitis, Presented at the Summer Meeting, American Orthopaedic Foot and Ankle Society, Boston, July 1998. 16. Zingas CN, Collon D, Anderson K: Shock wave therapy for plantar fasciitis, presented at the Summer Meeting, American Orthopaedic Foot and Ankle Society, Vail Colorado, 2000. 17. Speed CA, et al: Extracorporeal shock wave therapy for plantar fasciitis. A double blind randomised controlled trial, J Orthop Res 21:937, 2003. 18. Porter MD, et al: Intralesional corticosteroid injection versus extracorporeal shock wave therapy for plantar fasciopathy, Clin J Sport Med 15:119, 2005. 19. Kudo P, et al: Randomized, placebo-controlled, double-blind clinical trial evaluating the treatment of plantar fasciitis with an extracorporeal shockwave therapy (ESWT) device: a North American confirmatory study, J Orthop Res 24:115, 2006. 20. Hammer DS, et al: Extracorporeal shock wave therapy (ESWT) in patients with chronic proximal plantar fasciitis: a 2-year follow-up, Foot Ankle Int 24:823, 2003. 21. Wang CJ, et al: Long-term results of extracorporeal shockwave treatment for plantar fasciitis, Am J Sports Med 34:592, 2006. 22. Placzek R, et al: Treatment of chronic plantar fasciitis with botulinum toxin A—an open pilot study on 25 patients with a 14-week follow-up, Z Orthop Ihre Grenzgeb 144:405, 2006. 23. Babcock MS, et al: Treatment of pain attributed to plantar fasciitis with botulinum toxin A: a short-term, randomized, placebocontrolled, double-blind study, Am J Phys Med Rehab 84:649, 2005. 24. Mishra A, Pavelko T: Treatment of chronic elbow tendonsis with buffered platelet-rich plasma, Am J Sports Med 34:1774, 2006.
.........................................C H A P T E R 1 0 Arthritic, metabolic, and vascular disorders Gregory Rowdon and David Taylor CHAPTER CONTENTS ...................... Introduction
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Metabolic disease
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Inflammatory/rheumatologic
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Vascular/lymphatic disorders
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Other
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INTRODUCTION Foot and ankle problems are common complaints to the physician who cares for athletes. Most of these complaints can be attributed directly to the athlete’s training and competition with their sport. However, athletes are not immune from disease. Most of these athletes will present to the sports medicine physician assuming their complaints are related to their participation, and many will try to explain their complaints as being secondary to some aspect of their training. Although the vast number of complaints evaluated by the sports medicine physician is directly attributable to a primary musculoskeletal source, the physician must maintain an appropriate differential diagnosis to include those disease states that also can affect the musculoskeletal system. The foot and ankle are common sites for these disease states to present as they mimic sports injuries. Many of the individuals who present to a sports medicine clinic are not ‘‘highly competitive’’ athletes but are athletes nonetheless. These individuals are commonly referred to as ‘‘recreational athletes’’ and generally are older. They strive to maximize their abilities in their own chosen activity while attempting to reap the myriad of benefits of a healthy lifestyle. This group of athletes may have concurrent disease states that must be taken into account as they attempt to maintain their healthy, active lifestyle. Diseases such as diabetes, gout, thyroid conditions, osteoporosis, and so forth can present with musculoskeletal complaints. The purpose of this chapter is to review those disease states, which may mimic a primary musculoskeletal problem in both the competitive and recreational athlete. Knowledge of these conditions is essential to the physician caring for athletes.
INFLAMMATORY/RHEUMATOLOGIC Still’s disease (adult onset) Still’s disease is a seronegative polyarthritis that usually affects young adults. It is characterized in its initial manifestation as a spiking fever and a red/salmon colored rash, usually over the trunk and extremities. The rash is transient and appears at the time of the fever spikes. The inflammatory arthritis is a polyarthritis or oligoarthritis. It commonly affects the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints, as well as the wrists, knees, hips, and shoulders. Occasionally, the cervical spine, intertarsal joints, temporomandibular joints (TMJ), and the distal interphalangeal (DIP) joints are affected. It may lead to fusion of the carpal-metacarpal and the intercarpal joints. Laboratory evaluation commonly shows an elevated white blood cell count as well as an elevated erythrocyte sedimentation rate (ESR). Anemia of chronic disease is commonly present. Secondary nonmusculoskeletal findings include lymphadenopathy, hepatosplenomegaly, pericarditis, and carditis. The disease is treated with either high-dose aspirin or other nonsteroidal anti-inflammatory medicines. Often, oral steroids are required to control the disease. Overall, Still’s disease has a good prognosis. Ankylosing spondylitis Ankylosing spondylitis is an insidious onset seronegative inflammatory condition affecting young individuals, that is, generally younger than 40 years old. It has a uniform sex distribution, but the disease seems to be milder in females. Also, females have more peripheral involvement, rather than spine involvement. Ankylosing
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spondylitis affects the sacroiliac (SI) joints, followed by the spine and peripheral joints, respectively. There usually is symmetric loss of spine movement. The peripheral joint involvement occurs in 20% to 30% of ankylosing spondylitis patients and has a predilection for the lower extremities. Achilles’ tendinitis, plantar fascitis, and costochondritis also are associated with the disease process. It is common to have fatigue, weight loss, low-grade fever, and in more severe cases, uveitis, pulmonary fibrosis, and cardiac abnormalities. Laboratory findings include an elevated ESR. The natural history of ankylosing spondylitis is poorly defined, with some patients experiencing minimal disease and some patients experiencing severe disease. Treatment usually involves physical therapy and anti-inflammatories.
Reiter’s syndrome Reiter’s syndrome involves the triad of arthritis, uveitis, and conjunctivitis. It commonly occurs following an episode of either genitourinary or gastrointestinal infection. It has associated features of inflammatory eye lesions, balanitis, oral ulcers, and keratodermatitis. Reiter’s syndrome has a male to female occurrence of 5:1. The arthritis experienced in Reiter’s syndrome is a reactive arthritis rather than an infectious arthritis. It usually occurs 2 to 6 weeks following the onset of an infectious episode. It is asymmetric and mainly affects knees and ankles. It is usually of acute onset. There may be diffuse swelling of fingers and toes, that is, sausage digits. There is commonly inflammatory change at both the Achilles’ tendon insertion and the plantar fascial origin. There also may be associated low-back pain with involvement of the SI joints, making it difficult to distinguish it at times from ankylosing spondylitis. The conjunctivitis in Reiter’s syndrome is either unilateral or bilateral. It usually is mild and transient and is a noninfectious source like the arthritis. Common skin lesions in Reiter’s syndrome are small, shallow, painless, penile ulcers called balanitis circinata. Another associated skin lesion is keratoderma blenorrhagica, which represents hyperkeratotic skin lesions mainly involving the soles of the feet, but they also can be found on the palms and the scrotum. Radiographic findings may demonstrate erosions or periosteal changes, particularly at the Achilles’ tendon insertion or plantar fascial origin. Also, an asymmetric sacroiliitis may be present that is in contrast to the symmetric involvement of ankylosing spondylitis. Reiter’s syndrome also is seronegative but usually demonstrates an elevated ESR and elevated white blood count. Treatment for Reiter’s syndrome involves anti-inflammatory medications and intra-articular steroid injections as well as physical therapy. Systemic oral steroids have been shown to be of minimal benefit. Topical steroids are used for the skin lesions and for the conjunctivitis. The prognosis for Reiter’s syndrome usually
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falls into one of three courses; the majority of athletes experience recurrent attacks of arthritis, whereas others experience a single, self-limited episode or a continuous, unremitting course.
Psoriatic arthritis Psoriatic arthritis is the combination of psoriasis and inflammatory arthritis. To make a definitive diagnosis of psoriatic arthritis, skin or nail changes of psoriasis must be present at some point in the course of the disease. The arthritic changes can be present before skin changes develop. The joint pattern in psoriatic arthritis is variable but commonly includes a pauciarticular asymmetric arthritis involving the peripheral joints. It is common to have the spine involved in combination with peripheral joints as well as inflammation of tendon and insertion points of tendons, that is, enthesitis. Digits may become sausage like. There often are associated eye changes, including conjunctivitis, iritis, and episcleritis. Psoriatic arthritis has an equal sex distribution and usually has onset in the 30to 40-year-old age group. Laboratory results are often normal, but some athletes will present with an elevated ESR and/or a normocytic normochromic anemia. Synovial fluid evaluation typically reveals a mild inflammatory process. Radiographs often reveal DIP erosive disease, sacroiliitis, and enthesopathy and/or periostitis. Treatment of psoriatic arthritis involves the use of anti-inflammatory medications, physical therapy, and intra-articular corticosteroids to treat the inflammatory arthritis. The focus of treatment, however, involves treating the athlete’s skin lesions. Oral methotrexate is a common therapeutic choice because it treats both the skin lesions and the arthritis. Overall, psoriatic arthritis has a good prognosis. Enteropathic arthritis Enteropathic arthritis is arthritis associated with inflammatory gastrointestinal (GI) conditions including ulcerative colitis and Crohn’s disease, and infectious GI conditions, including Shigella, Salmonella, Campylobacter, Yersinia, and Whipple’s disease. The arthritis, when associated with ulcerative colitis or Crohn’s disease, usually is one of a peripheral arthritis with associated sacroiliitis and less often enthesopathies. It often is a transient, oligoarticular, migratory, nondestructive arthritis associated with the bowel disease activity. The knees and ankles are most often involved. Synovial fluid from the affected joints contains mild to severe inflammation. There are a variety of associated cutaneous lesions with the disease, and mucosal, serosal, and ocular lesions may occur. The arthritis with ulcerative colitis and Crohn’s disease often resolves with medical or surgical treatment of the intestinal disease. The arthritis associated with enteropathic infection often comes on a few weeks following the bowel symptoms. The arthritis, in this case, is a reactive arthritis
Inflammatory/rheumatologic
Rheumatoid arthritis Rheumatoid arthritis is a chronic, systemic inflammatory disease characterized by significant joint involvement. It affects multiple systems extensively, and thus a full detailed description of the disease is beyond the scope of this chapter. It involves symmetric upper extremity, knee, and foot destructive changes, sparing the DIP joints of the hands and feet. It results in progressive joint destruction and deformity. Again, there are multiple extra-articular features, including rheumatoid nodules, arteritis, neuropathies, scleritis, and pericarditis. Lymphadenopathy and splenomegaly are common. The incidence in females is two to three times greater than in males. It may occur at any age and increases in frequency with increasing age. Hand, wrist, knee, and foot are most commonly involved, but any diarthrodial joint can be affected. The elbows, shoulders, sternoclavicular (SC) joints, hips, ankles, and temporomandibular joints (TMJ) are less commonly involved. Spine involvement is limited to the upper cervical spine. Feet and ankle changes are similar to those seen in the hands. Cocking up of the toes may occur secondary to subluxation of the metatarsal heads. This gives the digits a claw-like appearance. Fibular deviation of the first through fourth toes may occur. Bursal inflammation about the foot/ankle also occurs with the retrocalcaneal bursa being most common. Laboratory evaluation usually shows a normocytic, normochromic or hyperchromic anemia. There often is an elevated ESR and positive rheumatoid factor. Joint fluid evaluation reveals mild inflammation. Treatment involves anti-inflammatory medications, as well as physical therapy. Intra-articular corticosteroid injections are used for symptomatic joints not responsive to initial treatment. Second-line therapy involves disease-modifying antirheumatic drugs (DMARDs) with the trend toward more aggressive/earlier use of these drugs. Systemic lupus erythematosus (SLE) SLE is a chronic, multisystem inflammatory disease affecting bone, joints, tendons, skin, kidney, heart, lungs, GI tract, and central nervous system (CNS). Again, a full and detailed description of the disease process is beyond the scope of this text. SLE has a 9:1
female to male ratio. The arthralgias and arthritis are a common presenting complaint. The arthralgia/ arthritis often is symmetric. Joint capsule, ligamentous, and tendon involvement can be prominent in the disease, and hand or foot deformities may develop. There often are marked laboratory abnormalities, including a normocytic, normochromic anemia, leukopenia, thrombocytopenia, elevated ESR, and positive antinuclear antibody (ANA) and double-stranded DNA. Treatment is with anti-inflammatories, topical/oral steroids, antimalarials, and immunosuppressive agents.
Gout The pathogenesis of gouty arthropathy involves tissue deposition of uric acid crystals from a supersaturated extracellular fluid. Gout involves recurrent attacks of severe articular or periarticular inflammation. Late involvement of the disease involves crystal deposition of uric acid within articular, osseous, soft tissue, and cartilaginous structures. These tophi occur late (>10 years) in the disease. There may be renal impairment with or without uric acid urinary calculi. Hyperuricemia may be demonstrated in individuals without gout and uric acid levels may be within the normal range in individuals showing clinical gouty arthropathy. Gout is a disease of middle-aged men and postmenopausal women. It increases in frequency with age. An acute, gouty, arthritic flare most commonly involves the great toe metatarsophalangeal (MTP) joint but also commonly involves the ankle. It usually involves a single joint with an acute onset, often during the evening hours. The joint often appears warm, red, and swollen and usually is exquisitely tender. The flare may subside spontaneously 3 to 10 days following onset without treatment. Individuals often are symptom free following an acute attack, but over time, if untreated, the attacks may increase in frequency, increase in the number of joints affected, and increase in duration of symptoms when flared. The flares may be triggered by trauma, alcohol, drugs, stress, or medical illness. Tophi when present occur most commonly in the synovial tissue, subchondral bone, olecranon bursa, patellar and Achilles’ tendons, subcutaneous tissue on the extensor surface of the forearms, and overlying joints. Radiographic findings in gout usually are negative. Often they are obtained to rule out other joint processes, such as a septic joint, or to evaluate for the presence of chondrocalcinosis. More chronic cases can show periarticular erosions and frank degenerative changes, especially in the great toe MTP joint. The gold standard for diagnosis is monosodium uric crystals demonstrated in joint fluid. The white blood cell count from a symptomatic joint usually reveals moderate inflammation. Treatment in the acute setting may involve colchicine, antiinflammatory medications, steroids, or intramuscular adrenocorticotrophic hormone (ACTH). Treatment in
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and, again, affects mainly knees and ankles. There also may be axial joint involvement. Enthesopathies, although not common in association with ulcerative colitis and Crohn’s disease, are common in association with infectious GI conditions and typically involve the plantar fascia and Achilles’ tendon insertions. The arthritis is usually self-limited, resolving weeks to months after the bowel infection. Treatment is symptomatic involving the use of anti-inflammatory medications, physical therapy, and intra-articular corticosteroid injections.
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the chronic setting may also involve the use of colchicine as well as allopurinol or probenecid.
Pseudogout Pseudogout involves acute, gout-like, inflammatory attacks that occur secondary to calcium pyrophosphate dihydrate crystal deposition within joints. The incidence of clinically symptomatic pseudogout is one half that of true gout. Calcium pyrophosphate dihydrate crystal deposition may occur as an incidental finding in a symptom-free joint with radiographic evaluation. The term ‘‘chondrocalcinosis’’ is used to describe this x-ray appearance. The male to female ratio of pseudogout is 1.4:1 and is in marked contrast to the distribution in gout. The pseudogout flare usually involves one or more joints lasting for several days. It usually is abrupt in onset but self-limited. Findings may be as severe as in true gout, but typically the attacks of pseudogout are less painful. The knee is the most commonly affected joint, but all joints are susceptible, including the first MTP joint. The flare may be triggered by trauma, surgery, stress, or medical illness. Individuals usually are symptom free between flares. Treatment is with anti-inflammatory medications and intra-articular steroid injections.
4 PEARL Suspect inflammatory disease in a joint that has no history of trauma and that is swollen and warmer than expected for the history.
4 PEARL Suspect inflammatory disease if there is a history of multiple joint involvement or other systemic complaints that is, skin, GI, constitutional, and so forth.
C A S E S T U D Y 1 : G O U T
A 46-year-old, male runner awakens with a swollen, warm, red right ankle, which is exquisitely painful. He denies injury but did go for his usual 3-mile run 1 day ago. The rest of his history is noncontributory. On physical examination he demonstrates an effusion to the ankle
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with the joint erythemic and warm. The ankle is diffusely and significantly tender. The rest of the examination is noncontributory. X-rays are normal. Laboratory studies show a normal complete blood count (CBC), ESR, renal function, and uric acid. Joint aspiration demonstrates a mild to moderate inflammatory response and is positive for monosodium urate crystals. The patient was treated with indomethacin and demonstrated a complete response over the next few days.
C A S E S T U D Y S Y N D R O M E
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R E I T E R ’ S
A 24-year-old, professional basketball player presents with a left ankle that is painful, swollen, red, and warm. He also notes several toes that are swollen and right heel pain. His past medical history and family history are noncontributory, except that he was treated for a Chlamydia infection 1 month ago. He is on no medications except for Visine for ‘‘irritated’’ eyes. Physical examination demonstrates an erythemic, warm left ankle with mild effusion. Several sausage digits are noted. The right plantar fascia origin is tender. Both conjunctiva are injected. The rest of the examination is noncontributory. X-rays are normal. Laboratory studies are negative, including an inflammatory workup, except that the ESR is elevated and the WBC is at the upper limits of normal. The athlete was treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy. The athlete returned to baseline and there were no recurrences.
OTHER Lyme disease Lyme disease is a multisystem illness caused by the tickborne spirochete Borrelia burgdorferi. The disease is characterized by a rash at the bite site (erythema chronicum migrans), constitutional symptoms, neurologic abnormalities, cardiac involvement, musculoskeletal complaints, and a reactive arthritis. Early in the disease course, there often is migratory pain without specific inflammation to the joints. Tendon, bursal, and muscular inflammation is common. The reactive arthritis usually occurs in intermittent attacks. It can be monoarticular to oligoarticular and has a preference for large joints, especially the knees. It can last for months, with
Metabolic disease
Sarcoidosis Sarcoidosis is a multisystem illness characterized by noncaseating epithelioid granulomas in affected tissues. It has a tendency to affect young adults of either sex. It most often begins as bilateral hilar lymphadenopathy, pulmonary infiltrates, and skin and eye lesions. However, there may be bone lesions, localized muscular granulomas, and acute inflammatory arthritis. The arthritis is the most common rheumatologic manifestation and can be the initial complaint. The arthritis most commonly affects the ankles and knees. The most severe attacks usually occur during active disease. These flares usually last for 2 to 3 weeks. Chronic arthritic changes are much less common. The prognosis in sarcoidosis is favorable. Treatment usually is anti-inflammatory medication or a short course of oral corticosteroids.
METABOLIC DISEASE Metabolic diseases are an uncommon cause of concern in the athletic foot and ankle. The most common metabolic disease that may present with foot and ankle issues is diabetes mellitus. The neuropathy and microvasculopathy in the extremities, especially the foot and ankle, can result in a wide range of sequelae. Metabolic bone disease is another common metabolic disease that uncommonly affects an athlete’s foot and ankle. In cases of recurrent stress fractures, metabolic bone disease such as osteoporosis may be the underlying cause. Medications and/or supplements can cause metabolic bone disease or can cause other conditions that are risk factors for metabolic bone disease. Examples include steroid use (or abuse), which causes drug-induced osteopenia, or vitamin B12 deficiency, which can cause a neuropathy that may present with diabetes-like complications.
Diabetes mellitus Diabetes mellitus is a common disorder. Younger athletes are more likely to be type I, but many type II diabetics are involved with athletics, especially on a recreational or fitness level. The most important factor is achieving optimal control of the athlete’s diabetes. Tighter control usually equates with fewer complications. In the setting of the foot and ankle, the most important complication is peripheral neuropathy, which usually occurs in a long standing diabetic. Peripheral neuropathy leads to the possibility of skin breakdown and subsequent ulceration and infection. In an athlete’s
foot and ankle, skin integrity can be a concern, regardless of diabetes. Callus formation, blisters, abrasion, and fungal infections are very common in athletes. In the setting of diabetes, these conditions can lead to ulceration and bacterial infection and potentially may develop a serious complication faster than in a nondiabetic athlete. Skin ulceration is a significant concern for all diabetic athletes. Cellulitis can develop quickly. Even worse is the possibility of osteomyelitis. Left untreated, these complications could be career altering or even career ending. Most plantar wounds or ulcers in a diabetic are polymicrobial. Superficial skin infections on the dorsum of the foot or around the ankle may be less likely to be polymicrobial, but if empiric treatment is warranted, standard regimens to cover typical pathogens for diabetic ulcerations should be used. Proper wound care is essential, and weight-bearing activities may have to be restricted temporarily. One special note is that deep foot ulcers with signs of cellulitis may be infected with Pseudomonas because athletic shoes may harbor these bacteria. Lastly, deep ulcers need debridement and/or other investigation to search for osteomyelitis, although this would be unusual in the athlete. Diagnosis and testing of diabetes is beyond the scope of this chapter, but it is important to note that monofilament tactile and vascular examinations are essential for the evaluation and monitoring of diabetic neuropathy. Routine diabetic care is essential for tight control of glucose levels and prevention of complications. It also is important to note that sports participation should be encouraged in the diabetic population because physical activity can have beneficial effects on the disease as a whole. Simply keep in mind that more attention must be paid to lower-extremity skin care in the athlete. In individuals with foot alignment prone to callus formation, such as a cavus foot, professional callus shaving may be warranted. Orthotics may be useful in spreading out load-bearing surface of the foot and may help to alleviate pressure spots before they can ulcerate. Diabetics have other complications that can affect the athlete’s performance and general health, but one that can have specific foot and ankle relevance is the fact that diabetics have a higher incidence of osteoporosis and may have an increased rate of stress fractures. The key is focusing on the foot and ankle but remembering to see the athlete as a whole person.
Metabolic bone disease Metabolic bone disease encompasses any disorder that changes the mineralization of the normal skeleton. Osteoporosis is the most common metabolic bone disease that could affect the foot or ankle. This is a concern primarily in the mature or elderly athlete. Osteoporosis and osteopenia are common disorders, especially in postmenopausal women. However, they 245
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chronic flares over several years. The treatment for Lyme disease early in its course is tetracycline, penicillin, or erythromycin. Late in the course of the disease, intravenous penicillin usually is the treatment of choice.
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do not usually affect the foot and ankle. The most common sites of fracture in osteoporosis are the spine, wrist, ribs, pelvis, hip, and humerus. Osteoporosis is a concern in mature or elderly athletes because weaker bones may lead to an increased fracture rate or recurrent fractures. Osteoporosis and osteopenia are abnormalities of the bony matrix, where bone is less dense but of normal architecture. Other metabolic bone diseases may not have normal bony architecture, such as osteomalacia. Bone densitometry (dual energy x-ray absorptiometry [DEXA] scan) is the test of choice for diagnosis of osteoporosis. Standard radiographs are unreliable. DEXA scanning will differentiate osteoporosis from osteopenia. A DEXA score of 2.5 standard deviations below the mean is diagnostic of osteoporosis. Scores of 1.0 to 2.5 are diagnostic of osteopenia. Treatment of osteoporosis is beyond the scope of this chapter, but a brief summary follows. The best treatment is prevention. Calcium intake should be at least 1000 mg/day in an adult, and vitamin D is needed to aid in the absorption of the calcium. Weight-bearing resistance exercise also is important in building and maintaining strong bones. Once osteoporosis has been diagnosed, several treatment options exist. Calcium and vitamin D need to be taken, but they will not adequately increase bone density. At this time bisphosphonates (e.g., alendronate and risedronate) are a first-line treatment for increasing bone density. Estrogen increases bone density in postmenopausal osteoporosis but has other significant tissue effects that need to be taken into account before use. Selective estrogen-receptor modulators (raloxifene and tamoxifen) can prevent bone density loss and decrease fractures. Calcitonin can directly inhibit osteoclasts and prevent further bone loss. Parathyroid hormone actually can stimulate osteoblastic activity if the concentration is not too high. Follow-up DEXA scanning is important to monitor therapy. Most cases of osteoporosis are idiopathic, age-related, or postmenopausal. There are many secondary causes that are not as common but need to be kept in mind. Please see Table 10-1 for a list of these secondary causes. The majority of patients with osteoporosis will be older recreational athletes, but bone loss can occur in a younger athlete. The classic scenario in a younger patient would be a college-age, female runner with recurrent stress fractures and an eating disorder and who is anovulatory. This is the classic female athletic triad (see Chapter 24). The results of the female athletic triad syndrome include metabolic bone disease and can lead to an increased rate of stress fractures. Any patient with recurrent stress fractures or problems healing existing fractures must be evaluated for possible metabolic bone disease. Clinical judgment is needed to determine when to test an athlete for metabolic bone disease in the setting of recurrent stress fractures. There are no
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Table 10-1 Secondary causes of osteoporosis Nutritional Inadequate calcium intake Malabsorption Bulimia or anorexia nervosa Exogenous Substances Glucocorticoids Some chemotherapeutic agents Excessive alcohol Some anticonvulsants Cyclosporine Tacrolimus Thyroxine Bone Marrow Disease Leukemia Lymphoma Myeloma Metastatic carcinoma Bone cysts Rheumatologic/Connective Tissue Disease Rheumatoid arthritis Marfan’s syndrome Ehlers-Danlos syndrome Osteogenesis imperfecta Endocrine Disease Diabetes mellitus Hyperparathyroidism Hyperthyroidism Cushing’s syndrome Vitamin D deficiency (rickets/osteomalacia)
Vascular/lymphatic disorders
Table 10-1
Secondary causes of osteoporosis (cont’d)
Hypogonadism Growth hormone deficiency Functional
In addition, medications, supplements, or deficiency states can lead to other conditions that can affect the foot and ankle. Vitamin B12 or folate deficiency can lead to a peripheral neuropathy, which in turn could lead to some of the same concerns that a diabetic athlete may have. The bottom line is to search for clues to the underlying cause and, if possible, correct the disorder, discontinue the medicine or replete the deficiency.
Prolonged immobilization or disuse Miscellaneous Postsurgical
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F E M A L E
Subtotal gastrectomy
Renal Renal tubular acidosis Hypercalciuria
established guidelines for the number or frequency of fractures that necessitate further investigation. In our opinion there is no specific number of fractures needed to prompt workup for metabolic bone disease, but if there is enough clinical evidence to suggest metabolic bone disease, a work-up is warranted (i.e., two to three stress fractures within a 2-year period). Workup for metabolic bone disease is directed toward the suspected cause. For example, in a mature fitness athlete with recurrent stress fractures the cause is most likely to be a result of idiopathic or primary osteoporosis, and initial workup would start with a DEXA scan. A significantly different approach would be the case for a teenage girl with recurrent stress fractures and would include a more detailed dietary and menstrual history, as well as laboratory workup.
Medications/supplements/deficiency states Several medications, supplements, or deficiencies can result in disease-like states that can result in foot and ankle issues in an athlete. Most cases concern medications or supplements that result in metabolic bone disease. Table 10-1 has several examples of medications that can cause osteoporosis. Also, deficiencies can result in metabolic bone disease. The obvious is calcium deficiency, but other states can lead to osteoporosis as well. Examples include growth hormone deficiency, thyroid hormone deficiency, and hypogonadism. Please see Table 10-1 for more examples. In some cases, excess states can lead to metabolic bone disease. Hyperparathyroidism and Cushing’s disease would be examples.
A 19-year-old, female, college freshman, cross country/ track athlete presents with a 2-week history of gradually worsening left foot pain. The pain initially was present at the start of her runs and became worse as she tried to run through the pain. Now the pain is present with activities of daily living (ADLs). Over the last 24 hours, her pain has worsened significantly. She has noted some mild swelling in the area of her dorsal midfoot/forefoot. About 1 month ago she added some runs outside of her usual training runs/practices. She has concern for a possible stress fracture as she has a history of prior stress fractures (three fractures during her senior and junior years of high school). The rest of her history of present illness is noncontributory. She is on no medications but admits to the use of over-the-counter (OTC) diet pills. She has a history of ‘‘spotty’’ periods and has not had a period since she was a sophomore in high school. The rest of her past medical history is noncontributory. Physical examination demonstrates a height of 5 feet 6 inches and a weight of 105 lb (BMI ¼ 17), minimal erosions of the enamel of the teeth and fine hair on the arms but is otherwise noncontributory. X-rays show a completed fourth metatarsal stress fracture. Laboratory studies including CBC, electrolytes, thyroid, and hormonal status tests are noncontributory. DEXA testing shows bone mineral density 2.5 standard deviations below the mean of young adults. A multiteam approach was used to treat the athlete and involved the team internist, a dietician, and a sports psychologist. Treatment included a walking boot for the stress fracture with activity modification, increased caloric intake and calcium supplementation to 1500 mg per day, hormonal supplementation, counseling, and involvement of the athlete’s family for emotional support.
VASCULAR/LYMPHATIC DISORDERS Arterial disease Arterial disease represents decreased blood flow to the lower extremity. The most common cause is occlusive 247
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disease secondary to atherosclerosis and associated embolic phenomenon. It is uncommon in young healthy athletes unless there is a genetic predisposition or severe risk factors. It is most common in middle-aged to olderaged recreational athletes, especially those who have concurrent disease, that is, diabetes or elevated triglycerides or cholesterol. It presents as claudication of the lower extremities, which is defined as exercise-related pain. Evaluation at rest, unless late in the disease, may be entirely normal, although decreased lower-extremity pulses may be present. The disease usually is progressive, causing increased pain at lesser workloads. Evaluation may include arteriography, and definitive treatment may require vascular surgery. Claudication in a young athlete may be caused by popliteal artery entrapment (see Chapter 20). Its cause is either an entrapment of the popliteal artery in the popliteal fossa secondary to an anatomic variation of the popliteal artery and surrounding myofascial structures or a functional entrapment compressing the artery by the exercising muscles and surrounding bone. It has an 85% male preponderance and usually occurs in the second or third decade. It is bilateral in 25% of cases. The athlete usually complains of cramping to the calf and foot with associated numbness or paresthesias. In 10% of patients, there are acute or chronic ischemic changes of the lower extremity, including skin and temperature changes as well as rest pain and possible tissue necrosis. Physical examination usually is normal, but the diagnosis may be suspected if pulses diminish in the affected extremity with maximal ankle dorsiflexion or with active plantarflexion with the knee fully extended. However, these examination findings also are found in normal individuals who have no lowerextremity complaints. Evaluation usually includes noninvasive vascular studies, including lower-extremity Doppler, preexercise and postexercise ankle/brachial blood pressure indices, continuous wave Doppler ultrasound with provocative maneuvers, mentioned previously, and a duplex ultrasound that combines anatomic evaluation with quantitative and qualitative analysis of arterial blood flow. The gold standard for evaluation, however, is arteriography. Treatment involves surgical release of the entrapped artery. Although few long-term studies exist regarding the prognosis of popliteal artery entrapment syndrome, studies suggest that the prognosis is most favorable if no arterial damage has occurred at the time of diagnosis and treatment. Raynaud’s phenomenon is manifested by pallor and cyanosis of the digits in response to some type of stressor, usually exposure to the cold but also possibly secondary to an emotional distress. It can present at any age but is most common in women between the ages of 20 and 40 years. It has an unknown etiology. Patients usually have no findings at the time of physical
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examination. Occasionally, some bluish discoloration of the tips of the digits may be present between attacks. A typical attack causes the digits to become pale and cyanotic with a sharp demarcation of these findings with the skin more proximally. Raynaud’s may be associated with other diseases such as scleroderma, and when this occurs it is referred to as Raynaud’s phenomenon. When just the Raynaud’s findings are present without concurrent other disease, then it is called Raynaud’s disease. The prognosis for Raynaud’s patients generally is good. For athletes who are exposed to cold weather conditions, protective clothing is usually sufficient. More severe cases may require a pharmacologic treatment, which may include calcium channel blockers, alpha-adrenergic blockers, or vasodilators. Another condition that may affect the foot during cold weather outdoor activities is chilblain or pernio. Chilblain is an inflammatory disorder of the skin induced by cold temperature. It often affects women in the second or third decade of life. The etiology of chilblain is unknown. It presents as bluish red edematous areas of the skin overlying the lower extremities. Patients may complain of itching/burning to the areas of skin change. Repeated exposure may cause the lesions to become chronic and ulcerative. The lesions generally resolve with avoidance of the cold. Often, however, there will be a permanent area of hyperpigmentation at the prior site of the lesions.
Venous disease Thrombophlebitis is uncommon in a young, healthy athlete. It may occur from direct trauma from a contact sport, especially in association with postgame travel in an away team returning to the home location or following limited activity after a significant injury or elective surgery. A previous history of thrombophlebitis may predispose an individual to a second episode. Three factors as part of Virchow’s triad may lead to the formation of a thrombosis, and these include venous stasis, injury to the venous wall, and a hypercoagulable state. Any unexplained swelling associated with lower-extremity erythema and increased temperature should raise the suspicion of a venous thrombus. The main concern in detecting a venous thrombus is to determine whether the lesion occurs within the superficial venous system or the deep venous system. Superficial lesions are treated symptomatically and may present as tender, erythemic, palpable cords within the subcutaneous tissue. However, because of the potential serious complications of a deep venous thrombus, definitive study should be obtained to rule out any deep system involvement if there is any question regarding the presentation. Testing involves noninvasive, lower-extremity Doppler examination that provides an approximate 90% accuracy. If deep venous thrombosis
Vascular/lymphatic disorders
Lymphatic disease Other sources of edema of the lower extremities, but usually not associated with pain, are abnormalities of the lymphatic system. Lymph vessels serve to transport lymph fluid back to the venous system through the thoracic duct at the left jugular vein. At lymph node junctions along the lymph system, immunologic and filtering is done to the lymph fluid. Lymphatic channels, which normally follow the venous tree, are susceptible
to many of the same forces that affect the venous system and include trauma, mechanical obstruction, and surgical removal of lymph nodes as well as venous hypertension. Primary lymph edema is a disease of the lymph systems with an unknown cause. It is most common in females and often is unilateral. It usually has onset before the age of 40. The diagnosis may be confirmed with either lymphogram or contrast lymphangiography. Treatment is symptomatic and aimed at reducing the lower-extremity edema with elevation, support stockings and, occasionally, diuretics. Chronic lymphedema may cause recurrent skin infections, which in turn lead to an overload of the lymph system, causing further edema. Rarely, surgical intervention may be necessary.
C A S E S T U D Y 4 : P O P L I T E A L A R T E R Y E N T R A P M E N T
A 17-year-old, high school senior CC runner presents with a several-month history of exercise-related left calf and foot pain. The pain is described as cramp-like in quality and has become progressively worse with time. The pain has become more intense and has onset earlier in his runs. There are no associated paresthesias, increased tension to the calf musculature, or loss of foot or ankle control during the runs. The pain will resolve after several minutes of rest but with return to running after resolution the pain will return almost immediately. There are no symptoms noted on the right or symptoms outside of activity. Past medical history and family history are noncontributory. Physical examination is noncontributory except that with the knee in full extension and forced dorsiflexion or active plantarflexion the dorsalis pedis and posterior tibialis pulses diminish. X-rays are negative. Superficial and deep posterior chronic exertional compartment testing is negative. Arteriography demonstrates entrapment of the artery at the knee. The athlete is treated surgically with release of the artery and makes a gradual return to running.
In summary, inflammatory metabolic, vascular diseases are common in the general population but uncommon causes of foot and ankle concerns in athletes. However, being attuned to the possibility of these disease processes complicating an athlete’s ability to perform his or her chosen sport can allow the physician to address these issues and enhance the athlete’s performance or enjoyment of sport.
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is discovered, treatment involves rest and initiation of anticoagulation therapy. Anticoagulation therapy usually is instituted for 3 to 6 months for the first episode and may require chronic anticoagulation therapy for repeated episodes. Anticoagulation reduces the likelihood of further formation of the thrombus and lessens the potential complications of embolic phenomenon. Measures aimed at correcting any underlying risk factors such as minimizing immobilization and treating any cause for the hypercoagulable state, also are recommended. Varicose veins are prominent, abnormally distended, tortuous, superficial veins of the lower extremities that occur in approximately 20% of adults. The cause is usually one of defective valves within the veins or congenitally absent valves. They are more common in females and often are associated with a family history of varicosities. Any condition that decreases venous outflow from the lower extremities, that is, pregnancy, also may cause varicosities. Normal venous return from the lower extremities usually is accomplished by contraction of the lowerextremity musculature to pump the blood back up the venous gradient. Intact/competent venous valves prevent back flow. When the valves are incompetent or absent, pooling blood distends the veins, leading to further obstruction that causes worsened flow from the lower extremities. An exercising athlete with varicose veins further worsens this condition because of increased arterial flow into the exercising lower extremities. Usually this worsening of the venous return during exercise has little effect on exercise tolerance. Some athletes, however, may complain of a nonspecific heavy sensation to the extremities with exercise. This vague, exerciserelated discomfort is known as ‘‘venous claudication.’’ If venous congestion of the superficial system progresses it may lead to involvement of the deep venous return. This may then result in chronic edema, venous dermatitis, and/or stasis ulcers. Treatment is initially symptomatic using elevation and support stockings. Surgical vein stripping also may be an option for persistent problems, which do not respond to a more conservative approach. Proper skin care to treat the chronic dermatitis and any ulcers that may develop also is necessary.
.........................................C H A P T E R 1 1 Dermatologic, infectious, and nail disorders Kevin Gebke CHAPTER CONTENTS ...................... Introduction
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Infectious disorders
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Dermatologic disorders: environmental/anatomic
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Nail disorders
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Dermatologic disorders: traumatic
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References
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INTRODUCTION Athletes present with a wide range of dermatologic afflictions, including traumatic conditions, anatomic abnormalities, and various infections. Identifying patterns of wear and anatomic variation may give key insight into the cause of the presenting complaint. The purpose of this chapter is to discuss the more common disorders seen in sports medicine and to give insight into the treatment options. The ultimate goal is to assist in early recognition of common problems and to prevent performance impairment in our athletic patients. Initial examination of the foot and ankle always should include a thorough inspection of the skin and nails.
DERMATOLOGIC DISORDERS: ENVIRONMENTAL/ANATOMIC Contact dermatitis Contact dermatitis (Fig. 11-1) is fairly common in an athletic population. Athletes encounter multiple exposures, including adhesive tape, compound of benzoin, topical medications (antibiotics, antifungals, and antiseptics), and rubber-containing sports equipment. Some athletes even have reactions to the leather products of which most sports shoes are composed. Contact dermatitis presents as an inflammatory response of the skin to an offending irritant. The main pathologic feature of contact dermatitis is intracellular edema of the epidermis, resulting in intraepidermal vesicle and bullae
formation in acute cases. In chronic cases, a presentation with papules, scarring, and lichenification can be seen.1 Allergic contact dermatitis will be seen in individuals who previously have been sensitized to the allergen. A delayed hypersensitivity reaction will be seen over the course of several hours. In athletes, contact dermatitis is seen most commonly on the dorsum of the foot and toes. Fisher2 stressed that the moist environment within the athletic shoe is a major component in the development of contact dermatitis. It was stated that feet that were kept dry would not develop this form of dermatitis. The initial approach to treatment of contact dermatitis is to remove exposure to the offending agent. A wet compress with an astringent such as aluminum acetate is effective in soothing the affected areas. Topical and systemic steroids are used for their anti-inflammatory and mineralocorticoid effects. Antihistamines are used when significant pruritus is associated with the dermatitis. As the dermatitis starts to resolve, it is advocated to apply emollients to moisturize the healing skin.
4 PEARL Clinical pearls in treatment and prevention of contact dermatitis include regular changing of damp footwear, avoidance of potentially irritating or allergenic substances applied to the foot and ankle, and early identification of signs and symptoms of dermatitis. It is recommended to maintain a high index of suspicion for secondary bacterial infections and to treat with systemic antibiotics as needed.
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Figure 11-1 Contact dermatitis. (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 92, Figure 4-16.)
Frostbite Injury induced by cold exposure has been recognized for thousands of years.3 Frostbite involves the skin and potentially the soft tissues of the foot and ankle in athletes that are exposed to prolonged cold environments. Injury can occur, however, even with brief exposure of an unprotected foot to a cold, conductive surface (metal, concrete). Several terms are used to describe this phenomenon, including frostnip, chilblains, and frostbite. Frostnip is described as nonfreezing injury to the skin tissues that can commonly be seen in the toes. Associated symptoms include numbness and tingling. Cellular injury is absent in frostnip. Chilblains is associated with a more significant nonfreezing cold injury seen at temperatures below 59 F in which mild tissue damage is seen in the form of minor vascular injury and tissue swelling. Frostbite is the destruction of body tissues because of freezing (below 32 F) and ice crystal formation in the tissues, which causes cell lysis and tissue destruction. The tissue damage seen in association with frostbite is caused by two distinct mechanisms. First, ice crystal formation in the intracellular space leads to cellular dehydration and destruction. Second, damage to the vascular endothelium leads to inefficient delivery of blood to the injured tissues, further complicated by edema and swelling. Ultimately, further cell deterioration is seen secondary to hypoxia.4 Several classification schemes have been used to categorize frostbite injury. Historically, frostbite has been categorized into four degrees of injury, with first degree being described as a numb central white plaque with surrounding erythema. Second-degree injury is described as blister formation of clear or milky fluid with surrounding erythema and edema, all seen within the first 24 hours. Third-degree injury is characterized by blisters filled with a dark fluid, possibly appearing
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hemorrhagic, that eventually results in a black eschar within a couple of weeks. Fourth-degree injury generally refers to complete tissue necrosis. Considering that it is nearly impossible to classify frostbite into one of these categories on initial presentation, many clinicians simply describe frostbite as either superficial or deep. Superficial frostbite includes the first- and second-degree types described and deep describes the third- and fourthdegree categories. Physical examination findings on initial presentation can allow the clinician to arrive at a general prognosis. Findings such as sensation to pinprick, normal skin color, and enlarged blisters with clear fluid are favorable indicators that predict more of a superficial injury. On the other hand, if dark fluidfilled blisters; hard, nondeforming skin; and nonblanching cyanosis are seen, this is more diagnostic of a deeper injury. Patients with frostbite of the foot are likely to have involvement of the toes. They typically will complain of symptoms of numbness and tingling with possible associated electric–shock-type sensations. Symptoms of cold sensitivity, sensory loss, and hyperhidrosis may be described for months to years following the injury. The diagnosis of frostbite is made on the basis of history and physical examination. It is difficult to predict the degree of tissue injury for weeks following the exposure. With severe injury, it may take months before a clear delineation of viable versus nonviable tissue can be made. There is no current radiologic technique that can reliably distinguish the line of demarcation of injured tissues in the immediate postinjury period. Continued research using technetium scintigraphy and magnetic resonance techniques is needed to identify whether any available radiographic procedure may allow for early distinction of viable tissues.4 The treatment of frostbite injuries can be divided into three phases, including initial evaluation, acute care, and long-term follow-up. McCauley et al.5 described a treatment protocol for frostbite. This protocol can be applied to active individuals who suffer injuries to the lower extremity. Initially, the athlete should be admitted for rapid rewarming of the affected area in warm water (104 to 108 F for 15 to 30 minutes or until thawing has completed). After the completion of rewarming, the affected parts should be treated as follows: white blisters should be debrided and topical treatment with aloe vera should be applied every 6 hours. Hemorrhagic blisters should be left intact, with topical aloe vera administration every 6 hours. The patient’s lower extremities should be elevated and splinted as needed. The athlete should be given antitetanus prophylaxis. Regular administration of anti-inflammatory medications is recommended. Analgesia should be accomplished using narcotic medications. Antibiotic coverage should be started and continued for the first 2 to 3 days or until signs of superinfection have cleared. Daily hydrotherapy
Dermatologic disorders: environmental/anatomic
4 PEARL Clinical pearls in the treatment and prevention of frostbite include many commonsense principles. First of all, athletes should be educated on the use of appropriate clothing not only to protect the lower extremities but also to help maintain core body temperature. As the core body temperature begins to decrease, blood is shunted away from the lower extremity, further predisposing to frostbite injury. Adequate hydration should be stressed. Regular changing of damp socks and footwear should be recommended. Lastly, during times of anticipated cold exposure, it should be recommended that the athlete wear two pairs of socks, with the inner layer made of synthetic fiber such as polypropylene to wick away water from the skin and an outer layer made of wool or cotton for increased insulation.
Hyperhidrosis Hyperhidrosis is defined as excessive sweating outside the range required for normal thermal regulation. It typically presents in early childhood or adolescence and can affect the soles of the feet. The condition can be idiopathic or secondary to systemic disease, metabolic disorder, febrile illness, or medication use. Three forms of hyperhidrosis are described, including emotionally induced, localized, and generalized. The sole of the foot can be affected by the emotionally induced and localized types. It occurs equally in both sexes and there seems to be a predisposition in those of Japanese descent. Athletes will seek medical attention most commonly after they have suffered secondary effects from the plantar hyperhidrosis. They will describe excessive sweating in this area and a history of recurrent skin maceration, blistering, dermatitis, and/or infections. Depending on the pattern of hyperhidrosis described, a workup for an underlying systemic disorder may be justified. People
who develop hyperhidrosis later in life warrant a workup for systemic disease on presentation. The treatment for hyperhidrosis can be challenging. Topical agents such as glutaraldehyde solution can be administered in an attempt to reduce perspiration through the denaturation of keratin with resultant occlusion of the pores of the sweat glands. Aluminum compounds such as aluminum chloride function as antiperspirants and can be used topically, as well. Darrigrand et al.6 studied the application of antiperspirants to the feet of cadets in an attempt to decrease foot sweat accumulation and injuries. They demonstrated a 50% decrease in foot sweat accumulation and a reduced occurrence of trench foot and friction blisters. There was, however, an increased incidence of contact dermatitis. Oral administration of anticholinergic agents such as propantheline, glycopyrrolate, benztropine, and oxybutynin also has been advocated. In addition, neuromuscular blocking agents such as botulinum toxin can be used to inhibit transmission of nerve impulses at the neuromuscular junction of skeletal muscle and/or the autonomic ganglia. It is recommended to perform a nerve block of the posterior tibial nerve and the sural nerve before to botulinum toxin treatment for plantar hyperhidrosis.7
4 PEARL Clinical pearls in the treatment of hyperhidrosis include early multimodality intervention in an attempt to control sweating. It is important to remember that hyperhidrosis is not associated with mortality, but multiple morbidities can be seen that will impair athletic participation and performance. Many times, a dermatologist will need to be consulted, especially if botulinum toxin therapy is considered.
Hyperkeratosis Hyperkeratosis (Fig. 11-2) in the form of corns and calluses is a standard feature for many athletes. These lesions are produced as pressure and friction are applied repeatedly to the skin overlying the osseous structures. In an attempt to protect from skin breakdown, the body produces these regions of hyperkeratotic tissue. Many athletes who have symptoms related to their hyperkeratosis complain of localized pain and discomfort. Interestingly, the hyperkeratotic tissue itself is not what causes the pain, but rather underlying bursitis and nerve irritation. The most common types of hyperkeratosis include helomas, tylomas, and intractable plantar keratoma. Helomas are synonymous with corns and usually are found on the toes. Tylomas also are known as calluses and they usually are found over bony prominences, 253
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should be implemented for 30 to 45 minutes at a temperature of 104 F. Lastly, the patient should avoid smoking during this time to prevent peripheral vasoconstriction. When evaluating and treating patients with frostbite, the clinician should avoid rubbing the involved region because this can cause additional damage to the injured tissue. It also is important to ensure that there is not a possibility of refreezing after the rewarming process has taken place. If the potential for refreezing exists, rewarming should be delayed until further cold injury can be avoided. If refreezing does occur, significantly more tissue injury can manifest. Most athletes with frostbite injuries of the foot and ankle will present with findings consistent with a superficial injury. After rewarming, the athlete can be treated in an outpatient setting using appropriate topical formulations and analgesics. Close follow-up is necessary.
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Figure 11-2 Hyperkeratosis (corn). (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 928, Figure 27-5.)
especially in the region of the metatarsal heads. Intractable plantar keratoma is defined as a cone-shaped keratotic plug within a tyloma. Corns usually are broken down into two types. Hard corns are located over the lateral aspect of the proximal interphalangeal (PIP) joint of the fifth toe or over the proximal or distal interphalangeal joints of the second, third, and fourth toes dorsally. Athletes with hammertoe deformities and mallet-toe deformities are particularly predisposed to developing hard corns. Soft corns appear between the toes and can be attributed to the moist environment and high pressure seen with improper footwear. Large, hyperkeratotic, boggy masses can appear over time and develop central ulceration. The most common location is the interdigital space of the third, fourth, and fifth toes. Treatment of hard corns can be achieved using scalpel debridement techniques and/or regular buffing with a pumice stone. The athlete should be educated on proper footwear, with close attention to an appropriate size toe box to ensure adequate toe spacing and decreased potential for rubbing. Soft corns can be treated with debridement of the loose skin and adjustments in footwear. The athlete should be encouraged to attempt to keep the feet as dry as possible and can be instructed
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on the placement of padding between the toes. Surgical treatment usually is aimed toward correction of an underlying bony deformity but is rarely necessary. Calluses are seen almost universally on the feet of athletes. As described earlier, this is the body’s response to wear and tear. Many times, athletes are protected from skin breakdown and potential infection by this hyperkeratotic process. Callus formation becomes problematic when there is an overproliferation of the keratin tissue leading to underlying bursitis, neuroma, or neuritis.8 Intractable plantar keratoma is a highly painful lesion in the region of the plantar aspect of the metatarsal heads. Intractable plantar keratoma can be extensive and symptomatic enough to affect an athlete’s performance.9 Deformities of the metatarsophalangeal joint that produce increased plantarflexion in this area lead to the development of intractable plantar keratoma in the metatarsal head regions receiving the most plantar pressure. Calluses should be treated systematically. Early scalpel debridement and intervention by means of footwear changes are essential. Daily work on these lesions with a pumice stone or callus file should be advocated. Metatarsal pad fabrication and placement of custom foot orthotics will aid in prevention of recurrence.
Dermatologic disorders: traumatic
Clinical pearls for treatment of hyperkeratotic conditions primarily focus on prevention. Try to personalize footwear for your athletes through identification of predisposing factors such as bony deformities, lesions currently present, and history of previous complications. Also, avoid aggressive treatment to prevent exacerbation of symptoms and always assess for other potential causes (viral warts).
Xerosis Xerosis simply is severely dried skin. Skin drying is more pronounced in cold environments and especially during the winter months in temperate regions. Low humidity in the air leads to increased drying of the skin that manifests as roughening and fine scaling. In more severe forms of xerosis, the scaling becomes coarser and fissures may occur. Athletes that are exposed to chemicals (swimmers) and adhesives are particularly at risk. For the most part, xerosis is a benign condition and athletes will complain of pruritus in the lower leg and dorsal foot. This drying can predispose to fissure formation, allowing fungal or bacterial organisms to colonize the area. The treatment of xerosis should include regular emollient therapy. More severe cases respond well to 12% lactate lotion. Temporary relief of pruritus symptoms can be achieved using antihistamines such as diphenhydramine and cetirizine.
4 PEARL Clinical pearls for the treatment and prevention of xerosis include decreasing shower frequency and duration, minimizing hot water use, using regular emollient therapy, and protecting from epidermal excoriation.
Sunburn Sun exposure for prolonged periods of time in barefoot sports such as sand volleyball, swimming, and surfing lead to light-induced skin changes manifest as either suntan or sunburn. A suntan is the body’s protection mechanism from photoinjury after exposure to ultraviolet light. Suntan occurs in two stages; the first stage involves a photochemical change of existing melanin to produce a darkening of the skin color, whereas the second stage involves the synthesis of new melanin in the dermal layer that typically becomes visible within 72 hours.10 Sunburn occurs as a response to excess ultraviolet exposure with the degree of damage being dependent on duration of exposure and sensitivity of the skin. Individuals with a light
complexion are much more predisposed to this type of injury. The dorsum of the foot is a region that is not often sun exposed and is prone to severe burn. Sunburn reaction occurs in several stages, including immediate erythema, delayed erythema, vascular permeability with the development of edema and blisters, and finally desquamation. Immediate erythema is seen within a few minutes before fading. This gives way to a delayed erythema after a period of time. With more severe injury, vascular permeability with intradermal edema and epidermal blister formation will be seen within the span of a few hours. The desquamation process takes place within a week, giving way to new skin, albeit sun-damaged skin. Sun damage has an additive effect. Long-term changes increase the risk of skin cancers such as melanoma, squamous cell carcinoma, and basal cell carcinoma. Treatment after sun exposure depends on the degree of injury. Less severe burns can be treated with cool, wet compresses, emollient therapy, and protection from further exposure. Severe burns may need to be treated with a 4- to 6-day course of oral steroids in an attempt to prevent intense immune reaction. Again, it should also be stressed that these injuries should be protected from further ultraviolet exposure.
4 PEARL The key clinical pearl for sunburn treatment and prevention is preparation. Any anticipated sun exposure should be preceded by application of a sunscreen compound. Sun protection factor (SPF) is an indicator of sunscreen efficacy, with a higher SPF being more protective. When treating sunburn acutely, topical anesthetic preparations containing benzocaine should be avoided secondary to a photosensitization effect.
DERMATOLOGIC DISORDERS: TRAUMATIC Black heel (calcaneal petechiae, talon noir) Darkening of the posterior and posterolateral aspect of the heel was first described by Crissey and Peachey11 in basketball players. This discoloration is caused by repeated lateral shearing force of the epidermis sliding over the rete pegs of the papillary dermis, resulting in intraepidermal hemorrhage.12 The dark appearance gave rise to the terms black heel and calcaneal petechiae. In addition to basketball players, black heel (Fig. 11-3) has been described in other sports that require frequent starting and stopping such as lacrosse and football. The pathophysiologic changes previously described are caused by heel trauma from rubbing against the back 255
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Figure 11-3 Black heel. (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 375, Figures 12-18a and b.)
of the shoe. It is seen most commonly in adolescents and young adults and usually is asymptomatic. Sports activities should not be limited by this condition. The diagnosis of black heel usually will be readily apparent by history and physical examination. The lesions usually appear as multiple petechiae with central aggregation and scattered satellite patches. Often the dyschromia is horizontally arranged across the posterior and lateral aspect of the heel but can be seen in circular and oval patches, as well. If the diagnosis is in doubt, other diagnoses such as viral warts and malignant melanoma must be considered. Rarely, skin biopsy with histochemical staining is required to confirm the diagnosis of black heel and to rule out malignant melanoma.13 The treatment of black heel is quite simple. The clinician should educate and reassure the athlete that this condition is benign and will resolve with cessation of the causal mechanism.
4 PEARL The most important clinical pearl in black heel evaluation is distinguishing this lesion from malignant melanoma. If there is any doubt, an excisional biopsy should be performed with dermatopathology evaluation. Black heel can be prevented by placing a felt pad in the heel of the shoe. If a cosmetic effect is desired, the lesion can be pared down with a scalpel with nearly complete clearance of the dyschromia.
Piezogenic pedal papules The term piezogenic refers to ‘‘pressure giving rise to.’’ Piezogenic papules occurring in the heel are more common than previously thought. Zaidi et al.14 described 80 subjects out of a random sample of 100 people to
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have these pedal papules. They arise from herniation of the subcutaneous fat into the dermis. Their presence is identified easily while pressure is being applied, but they usually disappear with the removal of that force. The distribution of piezogenic papules in an athletic population is primarily along the medial and lateral plantar heel pad. The potential exists for these lesions to become painful, especially in long-distance runners, who place a great deal of repetitive stress on their feet. When painful, piezogenic papules can be detrimental to athletic performance. It is thought that the pain associated with the papular lesions is secondary to inflammatory changes in the deep dermal layers.15 Treatment options for piezogenic papules are limited. Some degree of symptomatic relief may be achieved with heel cups or shoe orthotics. There are no medical or surgical therapies described for this malady.
4 PEARL Regarding treatment pearls, with piezogenic pedal papules it is more of a case of what not to do than what to do. Corticosteroid injections into painful lesions are contraindicated. If steroid injections are administered, the athlete will be predisposed to fat atrophy and weakening of the supportive collagen matrix in this region that can be complicated by an even more painful heel.
Friction blisters Repetitive rubbing of the skin has been shown to produce blisters in multiple controlled trials. These frictional forces cause a mechanical separation of the epidermal cells at the level of the stratum spinosum. With continued mechanical trauma and separation of the epidermal cells, midepidermal necrosis will occur and a clear transudate
Infectious disorders
4 PEARL Clinical pearls for the treatment and prevention of friction blisters focus primarily on decreasing the amount of frictional force across a given dermatologic region. Some studies including Knapik et al.19 have shown foot antiperspirants to be efficacious in the reduction of foot blisters during recreational sports activities. It should be noted, however, that the use of antiperspirants on the feet as a prevention for friction blisters is controversial. Also, the use of antiperspirant agents is confounded by a high incidence of irritant contact dermatitis, which can be more debilitating than the original friction blisters. Knapik et al.20 identified a reduction in frictional blister formation with the use of polyester-lined socks. With this information, now it is recommended that endurance athletes use acrylic-based socks or thin polyester socks combined with a thick polypropylene sock. Neoprene insoles combined with appropriately fitted shoes are a great starting point for those initiating training activities. Early exposure to low-intensity frictional coefficients allows for cellular adaptation and epidermal thickening which may reduce the likelihood of blisters, as well.17
INFECTIOUS DISORDERS Viral warts It is estimated that approximately 10% of the adolescent population in the United States is affected by plantar warts (Fig. 11-4). With this in mind, it becomes evident that many athletes will fall into this category. Human papillomavirus (HPV) types 1, 2, and 4 are responsible for this form of hyperkeratotic lesion. After exposure to the virus, HPV attacks the epidermal layers of damaged, cracked skin. Unlike viral wart lesions elsewhere on the body, plantar warts grow deep into the tissue secondary to the constant pressure application to the sole of the foot. Plantar warts seem to thrive in the warm, moist environment of the shoe. The virus typically is encountered by direct contact of the bare foot to a surface harboring the virus. Johnson21 identified that the use of public locker rooms increased the risk of contracting plantar warts, especially when the subjects used communal showers. The diagnosis of plantar warts can be challenging because these lesions sometimes are difficult to distinguish from callus formation. Athletes will present with symptoms of pain in the region corresponding to the lesion. Direct observation may identify centralized cratering of a warty lesion. If the diagnosis remains in doubt, the hyperkeratotic tissue should be pared away using a no. 15 blade scalpel until the hypertrophic epithelium gives way to a dermal layer revealing multiple ‘‘seeds.’’ These seeds represent the thrombosed vessels that supply the warty lesion.22 Localized spread along the plantar surface results in a cluster of warty lesions that may resemble a mosaic. Plantar warts can be seen anywhere along the plantar surface but tend to spare the region corresponding to the metatarsal heads. Plantar warts are benign, and most will resolve spontaneously. Many forms of therapy have been described to eradicate plantar warts. Close attention should be paid to the potential adverse reactions associated with a given therapy. If lesions are causing symptoms of pain or impairment in function, a noninvasive therapeutic approach should be considered. Paring of the hyperkeratotic superficial layer should be followed by regular application of keratolytic agents such as salicylic acid (15% to 60%), cantharidin, or dichloroacetic acid. Daily application of these topical therapies with regular use of a pumice stone will aid in the gradual resolution of plantar warty lesions without significant impairment in function. Multiple other therapeutic modalities are described, including cryotherapy, injection therapy, immunotherapy, electrical therapy, chemical destruction, and surgical therapy.23 More aggressive/invasive treatments 257
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will accumulate in this space.16 These blisters are more likely to occur in skin areas that have a thick, horny layer held tightly to underlying structures, such as the soles of the feet.17 Moisture of the foot can either exacerbate or relieve the degree of frictional force present. A damp skin surface will see an increase in the frictional force, whereas very moist/wet feet actually will benefit from a lubrication effect. Friction blisters can be seen in many parts of the body in many types of athletes but are most common on the feet of distance runners. In addition to a damp environment, friction blisters also can be caused by poorly fitted shoes, bulky socks that bunch up and cause an area of increased pressure, and training on hard surfaces such as concrete or pavement. The diagnosis of friction blisters usually can be made by history alone. A physical examination will identify a bullous-appearing lesion corresponding to the region of discomfort. Friction blisters tend to be tender to palpation and are fluctuant when pressure is applied. The clinician should examine the region surrounding a friction blister carefully to evaluate for the possibility of a superficial infection (cellulitis). The consensus is that blisters should be drained, multiple times if needed, within the first 24 hours. Cortese et al.18 described a shorter healing time with this early intervention. They also stressed that the blister region healed more rapidly if the overlying roof was kept intact. Again, close attention should be paid for signs of infection, with appropriate use of systemic antibiotics to treat early cellulitis or impetigo. Placement of padding (moleskin) over the blister region is advocated until healing has occurred.
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Figure 11-4 Plantar warts. (From DeLee J, Drez D, Miller, M: DeLee and Drez’s orthopedic sports medicine, ed 2, Philadelphia, 2002, Elsevier, Figure 30-J-73.)
should be reserved for recalcitrant cases of plantar warts that have not responded to conservative management.
4 PEARL The first clinical pearl to remember is that plantar warts cause localized pain symptoms but can be overlooked on physical examination. Many athletes present with painful plantar lesions that are mistaken as overuse injuries such as metatarsal stress fractures because a plantar dermatologic examination was not performed. Encouraging the use of shower thongs or sandals in communal showers can reduce the risk of HPV exposure. Surgical treatment should be strongly discouraged because the resultant scar tissue can lead to symptoms of continued pain.
Tinea pedis The term athlete’s foot refers to the most common infection in sports participants. Fungal infection of the feet usually affects the interdigital spaces, especially between the fourth and fifth toes. The warm, moist environment within an athletic shoe provides an ideal environment for fungus to prosper. The dermatophyte linked to tinea pedis (Fig. 11-5) in most cases is Trichophyton rubrum. Less commonly, Trichophyton mentagrophytes and Epidermophyton floccosum are isolated. Men are affected more commonly than women or children. A 70% rate of lifetime incidence is estimated.24 Much like the viruses associated with plantar warts, dermatophytes can survive on the warm, moist floors of locker rooms and communal showers.
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Figure 11-5 Tinea pedis. (From Rakel: Textbook of family practice, ed 6, Philadelphia, 2002, WB Saunders, Figure 41-28.)
The interdigital spaces are most commonly affected in tinea pedis; however, a moccasin distribution also can be identified on physical examination. The ‘‘moccasin’’ distribution refers to scaling along the medial and lateral sides of the foot and potentially also the plantar surface. Physical examination findings will vary depending on
Nail disorders
the stage of infection. Early infection presents as fine scaling with associated pruritus. As the infection progresses, maceration of the superficial skin occurs, with gradual epidermal breakdown. At this point, superinfection by resident bacteria progresses skin breakdown and increases symptomatology. Leyden and Kligman25 demonstrated progressively decreased rates of fungal recovery as the severity of symptoms worsened. Conversely, more severe symptomatology correlated with increasing numbers of resident aerobic bacteria, especially large colony diphtheroids. In rare cases, highly inflamed sterile vesicles and pustules can be seen distant from the tinea infection. This is referred to as a ‘‘dermatophytid’’ or ‘‘id’’ reaction, representing an immunologic response to the fungus.26 Dermatophyte infections of the interdigital space usually respond well to topical therapy with antifungal agents of the imidazole and allylamine groups. Examples from these groups include clotrimazole 1% and terbinafine, respectively. Other potential choices include econazole, ketoconazole, miconazole, oxiconazole, ciclopirox, naftifine, and butenafine. Topical therapy must be continued for 4 weeks with clotrimazole and 1 to 4 weeks with terbinafine. Patients with moccasin-type tinea pedis can be difficult to treat and occasionally will require oral antifungal therapy. Oral antifungals include itraconazole, terbinafine, fluconazole, ketoconazole, and griseofulvin. Fluconazole should be administered 150 mg daily for a total of 2 to 4 weeks for recalcitrant cases. If the diagnosis of tinea pedis is in doubt after several weeks of topical and/or oral therapy, a potassium hydroxide preparation with microscopic examination for hyphae should be performed to confirm the diagnosis. Oral antibiotic therapy should be prescribed for severe cases with associated cellulitis. Immunocompromised individuals are especially prone to this complication. Coverage for typical skin flora including Staphylococcus and Streptococcus is appropriate. First-line therapy is dicloxacillin 500 mg every 6 hours for 7 days (Gilbert et al.27). Erythromycin can be substituted if penicillin is contraindicated. Other interventions in treating tinea pedis include the use of drying agents such as aluminum acetate solution and keratolytic agents such as ammonium lactate lotion. The prevention of tinea pedis is challenging.
NAIL DISORDERS Subungual hematoma Many sports predispose participants to direct foot trauma, especially to the toes. This trauma may be in the form of repetitive pounding against the anterior shoebox or it may be suffered as a result of another player’s stepping on the foot. Subungual hematoma (Fig. 11-6) formation can occur as a result of this trauma. Blood collects in the space between the nail bed and the toenail, with pain generated from increasing pressure within this space. Symptoms range from mild discomfort to extreme pain. Acute traumatic injuries tend to be more painful. Associated injuries include phalanx fractures and soft-tissue contusion. The evaluation process for a subungual hematoma should include a thorough history, including the timing of the injury and musculoskeletal, neurologic, and vascular assessment. With repetitive pounding injuries as seen in runners and tennis players, the physical examination may reveal early subungual discoloration, but this may be delayed. Acute traumatic injuries usually will have a more obvious subungual bloody accumulation that is identified easily on examination.
4 PEARL Figure 11-6 Subungual hematoma. (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 882, Figure 25-36.)
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Clinical pearls include education of athletes to avoid direct contact of the feet with flooring in showers and locker rooms. Also, maintaining a dry environment for the feet can limit the potential for fungal growth. Lastly, sharing footwear and towels should be discouraged.
CHAPTER 11
Dermatologic, infectious, and nail disorders
The treatment for subungual hematoma depends on symptomatology and the degree of involvement. Athletes presenting with extreme pain, especially with a brief period of symptoms, will benefit from a decompression procedure. Decompression can be achieved in one of three ways: a battery-operated cautery device can be used to burn a small hole through the nail, a largediameter needle can be used to bore into the nail to create a hole, or a paper clip tip can be heated to burn through the nail plate as well. All of these interventions will allow the blood to drain, effectively relieving the pressure and pain. On occasion, a nail bed laceration will be identified. This requires nail removal and laceration repair.28 Early intervention will allow for prevention of nail dystrophy and further impairment.
4 PEARL Clinical pearls for the prevention of subungual hematoma include working with athletes to choose appropriate footwear. Excessive forefoot anterior motion and tight dorsal toe boxes can exacerbate this problem. During the recovery phase from subungual hematoma, it is beneficial to provide pressure relief over the involved toes by cutting the leather overlying the involved digits.29
Onychocryptosis Ingrown toenails can lead to severe functional impairment, especially in those who depend on their feet in competition. Onychocryptosis (Fig. 11-7) is the most common of all toenail problems in athletes, and the lateral margins of the great toe are most often affected. The condition also can be complicated by paronychia formation, which can lead to osteomyelitis or sepsis. Ingrown toenails can be seen secondary to abnormal nail plate anatomy or secondary to external factors. Abnormal nail plate anatomy can be hereditary or secondary to previous trauma. When there is an improper fit of the nail plate in the nail groove, sharp spicules of the lateral nail margin are driven gradually into the dermis of that region. A foreign body reaction is seen, leading to localized erythema, edema, purulence, and granulation tissue. Compromise of the tegument can lead to the introduction of typical skin flora into the break in the skin. Typically, ingrown toenails are divided into three stages: the first stage involves erythema, edema, and focal tenderness. The second stage is marked by crusting and expressible purulence at the nail fold and nail plate junction. The third stage shows signs of chronic infection, with protuberant granulation tissue extending over and under the nail plate. The prevalence of ingrown toenails is 3:1, male to female.30 The factors that put athletes at risk for onychocryptosis include
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Figure 11-7 Onychocryptosis (ingrown toenail). (From Habif, Clinical dermatology, St Louis, 2004, Mosby: p. 881, Figure 25-35.)
improper nail care (aggressive nail trimming), excessive foot moisture, and repetitive trauma. Initial evaluation for onychocryptosis should involve a thorough history and focused physical examination. Symptoms described will vary from minimal discomfort to incapacitating pain. A family history of ingrown nails or a previous history of similar problems may aid in determining the underlying cause. Physical examination of type 1 lesions will reveal erythema, edema, and tenderness to palpation in the involved nail border. The nail can be lifted easily to identify an intact layer of skin within the nail groove. Type 2 lesions will be characterized by crusting at the nail fold and nail plate junction, with or without an expressible purulence. Lifting the lateral nail border will reveal early dermal breakdown. Stage 3 lesions appear very uncomfortable and have signs of chronic infection and extensive granulation tissue (proud flesh). Evaluation of nail morphology may point toward a specific causal factor (incurvated nail plate, subungual exostosis, or nail dystrophy). Treatment approach to ingrown nails varies depending on the stage of involvement. Ilfeld31 described a successful therapy for onychocryptosis with stage 1 findings. The treatment consisted of placement of a collodion-coated cotton wisp between the edge of the ingrown nail and the adjacent soft tissue. This waterproof barrier allows for immediate pain relief and provides a firm runway for further growth of the nail. This procedure may need to be repeated after 3 to 6 weeks
Nail disorders
4 PEARL Clinical pearls for the treatment of this malady include early intervention in an attempt to avoid advanced-stage lesions. Treatment interventions can lead to symptom exacerbation and further loss of performance capacity. There is not absolute contraindication to participation after nail resection unless the athlete has signs/symptoms of systemic infection. Participation should be based on pain tolerance. Nail resection should be reserved for those athletes who are unable to perform or whose schedule allows for a period of recovery. Lastly, complete nail extraction should be avoided if possible because this can predispose to further nail dystrophies.
Onychomycosis (tinea unguium) Onychomycosis (Fig. 11-8) is the most common cause of toenail thickening. Up to 20% of the population in various age groups is afflicted with this problem.10 The most common pathogens include the dermatophytes Trichophyton rubrum and Trichophyton mentagrophytes.
Figure 11-8 Onychomycosis. (From Rakel: Textbook of family practice, ed 6, Philadelphia, 2002, WB Saunders, Figure 41-30.)
Less commonly, Candida albicans and nonpathogenic fungi are implicated. The most common distribution is the distal subungual region. Other patterns include white superficial onychomycosis, proximal subungual onychomycosis, and Candida onychomycosis. In distal subungual onychomycosis, the dermatophytes invade the distal area of the nail bed leading to the development of an accumulation of hyperkeratotic debris. This subsequent nail thickening causes separation from the underlying nail bed and allows the fungus to grow further into the substance of the plate. With time, this invasion slowly moves more proximally with the potential to involve the entire nail. Proximal subungual onychomycosis is caused by the same organisms, but is more associated with immunosuppressed states. Psoriasis should be kept high on the differential diagnosis because this disorder can cause similar nail features. Factors that predispose individuals to the development of onychomycosis are humidity, heat, trauma, diabetes mellitus, and underlying tinea pedis.32 Historically, affected individuals will present with a chronic history of gradual nail thickening and discoloration. Runners seem to be predisposed to this condition secondary to repetitive trauma to the nail from contact with the toe box, whereas basketball players are more predisposed secondary to the direct trauma of having their toes stepped on by other competitors. Physical examination will reveal hyperkeratosis of the nail bed, with a yellowish to brown discoloration and onycholysis. The diagnosis should be confirmed with both a potassium hydroxide (KOH) examination and a fungal culture. On confirmation of a fungal offending agent, therapeutic modalities can be discussed. Within recent years, effective systemic antifungal therapy has become available for the treatment of onychomycosis. Included in the treatment options are fluconazole, itraconazole, and terbinafine. These drugs have replaced griseofulvin as the systemic treatment options. Terbinafine should be administered at a dosing schedule of 250 mg/day 261
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or sooner if displacement occurs. A similar intervention can be applied initially for stage 2 involvement. The collodion-coated cotton wisp can be inserted between the lateral nail edge and the soft tissues if there is not significant spicule formation. If there is a component of the nail that has broken through the dermal layer that prevents placement in a reasonable fashion, the lateral nail border should be removed. This therapeutic approach is contiguous with that recommended for stage 3 onychocryptosis. Wedge-shaped nail resection is recommended on the involved side in the following manner: first, a digital block should be performed using 1% or 2% lidocaine injection at the base of the digit. Next, a tourniquet should be placed proximal to the toenail. After thorough cleansing with Betadine solution, a nail splitting scissors should be inserted under the ingrown nail plate parallel to the lateral nail fold. On meeting resistance proximally in the region of the matrix, the wedge should be cut and removed. Any granulation tissue present should be treated with silver nitrate application or removed via curettage. Wound care following this procedure entails regular application of wet compresses until inflammation has subsided. Gentle cleansing is recommended but should be delayed for the first 24 to 48 hours. For cases of recurrent ingrown nails, athletes may require the use of liquid phenol for permanent destruction of the lateral nail matrix. This should be applied immediately after wedge resection, with care taken to avoid the soft tissues other than the nail matrix. Ingrown toenails will be encountered on a fairly regular basis.
CHAPTER 11
Dermatologic, infectious, and nail disorders
for a total of 12 weeks. Itraconazole can be administered at 200 mg/day for a total of 12 weeks or through pulse dosing at 400 mg/day for the first week of 4 consecutive months. Lastly, fluconazole is an option at 150 mg once weekly for a total of 6 to 12 months (Gilbert et al.27). Extreme care should be taken to avoid the use of these medications in individuals with hepatic insufficiency. A review of potential drug interactions also is advocated. Onychomycosis is a fairly benign entity but can be complicated by symptoms of localized pain or secondary bacterial infection. Many athletes will opt to defer systemic treatment, but those who wish to proceed with therapy should be monitored closely for adverse reactions or drug interactions. Educating the individual that it may take 6 to 12 months for the nail to grow out will minimize the number of callbacks within the first few months.
REFERENCES 1. Michael JA: Dermatitis, contact, www.eMedicine.com 2. Fisher AA: Contact dermatitis, Philadelphia, 1986, Lea & Febiger. 3. Post PW, Donner DD: Frostbite in a pre-Columbian mummy, Am J Phys Anthropol 37:187, 1972. 4. Murphy JV, et al: Frostbite: pathogenesis and treatment, J Trauma 48:171, 2000. 5. McCauley R, et al: Frostbite injuries: a rational approach based on the pathophysiology, J Trauma 23:143, 1983. 6. Darrigrand A, et al: Efficacy of antiperspirants on feet, Mil Med 157:256, 1992. 7. Fujita M, et al: Surgical pearl: use of nerve blocks for botulinum toxin treatment of palmar-plantar hyperhidrosis, J Am Acad Dermatol 45:587, 2001. 8. Robbins JM: Recognizing, treating, and preventing common foot problems, Cleve Clin J Med 67:45, 2000. 9. Mann R, Duvries H: Intractable plantar keratosis, Orthop Clin North Am 4:67, 1973. 10. Habif TP: Clinical dermatology a color guide to diagnosis and therapy, ed 3, St Louis, 1996, Mosby.
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11. Crissey J, Peachey J: Calcaneal petechiae, Arch Derm 83:501, 1961. 12. Levine N, Baron J: Black heel (calcaneal petechiae), www. emedicine.com/derm/topic53.htm (Last updated Oct. 2, 2006). 13. Hafner J, et al: Benzidine stain for the histochemical detection of hemoglobin in splinter hemorrhage (subungual hematoma) and black heel, Am J Dermatopathol 17:362, 1995. 14. Zaidi Z, et al: Piezogenic papules—a study of 100 cases, J Pak Med Assoc 45(4):93, 1995. 15. Schlappner L, et al: Painful and nonpainful piezogenic pedal papules, Arch Dermatol 106:729, 1972. 16. Chima K, Lambert WC, Schwartz RA: Friction blisters, www.eMedicine.com. 17. Knapik JJ, et al: Friction blisters. Pathophysiology, prevention and treatment, Sports Med 20:136, 1995. 18. Cortese T Jr, et al: Treatment of friction blisters, Arch Dermatol 97:717, 1968. 19. Knapik JJ, Reynolds K, Barson J: Influence of an antiperspirant on foot blister incidence during cross-country hiking, J Am Acad Dermatol 41:655, 1998. 20. Knapik JJ, et al: Influence of boot-sock systems on frequency and severity of foot blisters, Mil Med 161:594, 1996. 21. Johnson LW: Communal showers and the risk of plantar warts, J Fam Pract 40:136, 1995. 22. Esterowitz D, et al: Plantar warts in the athlete, Am J Emerg Med 13:441, 1995. 23. Landsman MJ, Mancuso JE, Abramow SB: Diagnosis, pathophysiology, and treatment of plantar verruca, Clin Podiatr Med Surg 13:55, 1996. 24. Martin ES, Elewski BE: Tinea pedis, www.eMedicine.com 25. Leyden JJ, Kligman AM: Interdigital athlete’s foot. The interaction of dermatophytes and resident bacteria, Arch Dermatol 114:1466, 1978. 26. Noble SL, Forbes RC, Stamm PL: Diagnosis and management of common tinea infections, Am Fam Physician 58:163, 1998. 27. Gilbert DN, Moellering RC, et al: The Sanford guide to antimicrobial therapy, Hyde Park, UT, 2004, Sanford. 28. Kukula CL, Fell SD: Subungual hematoma, www.eMedicine.com. 29. Levine N: Dermatologic aspects of sports medicine, J Am Acad Dermatol 3:415, 1980. 30. Craig T, Egland AG: Ingrown nails, www.eMedicine.com. 31. Ilfeld FW: Ingrown toenail treated with cotton collodion insert, Foot Ankle 11:312, 1991. 32. Rich P: Nail disorders. Diagnosis and treatment of infectious, inflammatory, and neoplastic nail conditions, Med Clin North Am 82:1171, 1998.
.........................................C H A P T E R 1 2 Nonsurgical treatment of acute and chronic ankle instability Jon Karlsson and Mikael Sansone CHAPTER CONTENTS ...................... Introduction
265
Prevention
268
Acute ligament injuries
265
Conclusion
270
Chronic ankle joint instability
267
References
270
INTRODUCTION Ligament injuries to the lateral ankle ligaments are the most common sports-related injuries. It is estimated that these injuries account for approximately 25% of all sportsrelated injuries, and the incidence has been shown to be approximately 5600 injuries daily in the United Kingdom and 23,000 in the United States. There are three different strategies in terms of treatment alternatives, that is, cast immobilization, surgical treatment, and functional treatment. Despite the extremely high number of injuries, there are only a few well-conducted studies, and even though many or even most authors advocate early mobilization, there is little scientific evidence to support it. The best studies are summarized in three Cochrane reviews. All three reviews concluded that more highquality studies are needed.
ACUTE LIGAMENT INJURIES It has been shown in several studies that early diagnosis, functional treatment, and rehabilitation are the keys to prevention of chronic lateral ligament instability of the ankle.1-3 The on-field treatment of fresh ruptures is well known, for example, the rest, ice, compression, and elevation (RICE) principle. The most vulnerable of the lateral ligaments is the anterior talofibular ligament (ATFL; Fig. 12-1, A), followed by a combined rupture of this ligament and the calcaneofibular ligament (CFL; Fig. 12-1, B). Other injuries, such as injuries to the medial deltoid ligament are much less frequent and occur with a
frequency of less than 10% of all injuries.2,3 The mechanism of injury to the lateral ligaments is most commonly a plantarflexion inversion injury from landing (Fig. 12-2). Prevention of ligament injuries has gained much attention recently, because it has been shown that approximately 75% of all injuries are recurrences and may thus potentially be prevented, provided a sound protocol is used.4-6 Prevention by either coordination training using balance boards or by external support can significantly reduce the number of ligament injuries. Ankle tape and/or functional splinting, proficiently completed by the use of a stirrup splint (Fig. 12-3) is preferred by many athletes. It also has been shown that there is hardly any place for surgical repair after acute ligament ruptures.7,8 After the recommended treatment using a rehabilitation program with functional treatment, active range of motion exercises, coordination training, peroneal strengthening, and early weight bearing, the functional results are reported as excellent or good in approximately 80% to 90%, whereas 10% to 20% of patients develop secondary symptoms of chronic instability and/or pain.9,10 Despite this, the treatment of acute lateral ankle ligament injuries is still controversial; some authors have recommended that these injuries be treated with early mobilization, whereas others recommend cast or brace immobilization for 3 to 6 weeks or even early surgical repair. However, even though there is substantial evidence to suggest that early mobilization with active rehabilitation probably is the treatment of choice, there are only a few randomized, controlled studies comparing different treatment modalities.11 In a recent meta-analysis it was shown that no treatment of lateral ankle ligament ruptures led to an increased number of residual
CHAPTER 12
Nonsurgical treatment of acute and chronic ankle instability
Figure 12-1 Anterior talofibular ligament (ATFL) (A) and calcaneofibular ligament (CFL) (B). Note ATFL (A) over probe and peroneal tendons running posterior to fibula. Note CFL under probe with peroneal tendons removed.
Figure 12-3 Ankle stirrup brace used in rehabilitation after acute and chronic lateral ankle instability.
Figure 12-2 Mechanism of injury for lateral ankle ligament sprain. Position at time of landing is plantarflexion and inversion.
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symptoms.12 Surgical treatment produced better results than functional treatment; however, functional treatment was found to be superior to cast immobilization for 6 weeks. The authors pointed out that surgical treatment was associated with higher costs, as well as increased risk
Chronic ankle joint instability
of complications, such as disturbance of wound healing, nerve damage, and possibly infections. In one Cochrane review, it has been shown that functional treatment appears to be the favorable strategy for treating acute ankle ligament injuries when compared with immobilization.13 Concerning surgical versus nonsurgical treatment for acute injuries of the ligament complex, there is insufficient scientific evidence from randomized, controlled studies to determine the relative effectiveness of surgical and conservative treatment of these injuries, as concluded in a second Cochrane review.14 This might imply that surgical treatment is not necessarily superior. It also is obvious that in case of failed conservative treatment, late reconstructive procedures can be performed with satisfactory results, even several years after the initial injury. The extent of injury, that is, being grade I, II, or III, might play a role. Two prospective, randomized studies have evaluated the effect of early range of motion training, full early weight bearing, combined with either an ankle stirrup brace or specially designed compression pads. Both studies showed that early functional treatment resulted in significantly shorter sick leave and facilitated earlier return to sports, without the risk of inferior functional results in the long term. One Cochrane review compared different functional treatment strategies for the treatment of acute ankle ligament injuries.15 It was shown that the use of elastic bandage was correlated with fewer complications than tape but was associated with slower return to work and sport. Semirigid ankle braces produced less ankle laxity than elastic bandages. Lace-up ankle support was more effective in reducing swelling in the short term compared with semirigid braces, elastic bandage, and tape. Thus either semirigid brace or lace-up support probably is preferred. It appears that early weight training, combined with range of motion training, is beneficial. The long-term prognosis likely is unaffected by early functional training.16,17 Studies have shown that the best external support is strong evertor muscles. Therefore a combination of isokinetic strength training with proprioception training is most favorable; this combination can shorten rehabilitation and serve as secondary prophylaxis.
participate in sports with high demands of stable ankle joints, such as soccer, volleyball, basketball, and all sports involving jumping, sidestepping, turning, and twisting. In the literature, more than 50 different surgical methods have been described to correct chronic ankle joint instability.4,6,9,10,19 The clinical diagnosis initially is based on a thorough clinical assessment, for instance, testing the anterior drawer sign (Fig. 12-4) and the inversion (supination) test (Fig. 12-5). Comparison always must be made with the contralateral ankle. It must be remembered, however, that functional instability is a complex syndrome, and there are several factors at play, such as increased laxity, proprioceptive deficit, and peroneal muscle weakness, either alone or most often in combination. Excessive laxity must be corrected with some kind of surgical procedure, but proprioceptive deficit and muscular weakness can and should be treated by rehabilitation.20 In the acute phase the main objective is for pain relief, but soon after injury the treatment is aimed at restoring range of motion, and this should be done without any loss of proprioception. The general principle is that early rehabilitation is the main goal. Immobilization probably should never be used, not even in case of grade III injury. There are several studies in the literature comparing immobilization and early mobilization, and none favor immobilization. In fact, immobilization may result in joint stiffness, muscle atrophy, and loss of proprioception. Some clinicians do use intermittent immobilization for the acute phase of recovery, allowing early mobilization also, but there is no literature documenting this approach. Rehabilitation can be divided into four phases, that is, the initial phase, early rehabilitation, late rehabilitation, and functional phase. The length of each phase depends much on the individual process of healing. The initial
L
CHRONIC ANKLE JOINT INSTABILITY
Figure 12-4 Radiograph of ankle demonstrating the subluxation that occurs with an anterior drawer test for lateral ankle instability with anterior talofibular ligament (ATFL) ligamentous laxity.
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It has been shown in several studies that chronic lateral ankle joint instability may develop in approximately 10% to 30% of all patients who sustain an acute injury of the ligaments.18-20 The functional instability, irrespective of the mechanical laxity (indeed, there is no constant correlation between the functional instability and the laxity of the joint), does not always produce disability of such grade that surgical reconstruction is needed. Surgical reconstructions have been well described during the last 3 decades and are needed most often in athletes who
CHAPTER 12
Nonsurgical treatment of acute and chronic ankle instability
Figure 12-6 Balance board used in rehabilitation after acute and chronic lateral ankle instability.
Figure 12-5 Radiograph of ankle demonstrating the subluxation that occurs with a talar tilt test for lateral ankle instability with calcaneofibular ligament (CFL) ligamentous laxity.
phase is directed at reduction of swelling, most often with compression bandage but also with anti-inflammatory medication, short rest (maximum of 1 to 2 days), ice and elevation, that is, the RICE principle. Sometimes ultrasound and electrotherapy are added, but their effect has not been shown with any convincing evidence. In order not to lose neuromuscular coordination, gait training including early weight bearing and balance board training, is started as early as possible. The initial phase is for the most part the first week after injury. The second phase, that is, weeks 2 to 4, the early rehabilitation phase is aimed at restoring normal range of motion of the ankle with active exercises, and sometimes manual treatment and kinetotherapy are added. Sometimes, gentle passive movement of the ankle joint can be used to increase the range of motion in the sagittal plane. Stretching of the calf muscles also is important during this phase, especially to increase dorsiflexion. The tilt or balance board exercises (Fig. 12-6) are used progressively during this phase, both in terms of time and intensity. The training is aimed first at balance on both legs, and thereafter on one leg (the injured one). Cryotherapy may be continued during this phase, as well as anti-inflammatory medication. During this phase, the athlete is allowed to return to sports activities, provided an external support is used, such as ankle tape or functional bracing.16 The late rehabilitation phase usually is reached around week 5, and the weight-bearing exercises are
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increased. The main goal of this phase is training of muscular strength, endurance, and neuromuscular function. The final functional phase starts around week 9 and is aimed at return to full sports activity, including jumping, turning, and twisting. External support should be worn during the entire functional phase, and one of the main aims is to reduce the risk of recurrence of the ankle sprain. Supervised programs such as the one described and detailed in Table 12-1, can be used both after first-time injury and in the case of chronic or recurrent ankle insufficiency. Before any decision is made on surgical treatment in the case of the chronically unstable ankle, a well-planned rehabilitation protocol (such as the one shown in the Table 12-1) should be carried out. This protocol is based on isokinetic strength training of the peroneal muscles and proprioceptive training. One study has shown that approximately 50% of patients with chronic ligament insufficiency will regain satisfactory functional stability after a 12-week program.16 The obvious goal of the rehabilitation program is to decrease the muscle weakness, regain normal or near-normal proprioceptive function, and reestablish the protective reflexes. The last few weeks of the rehabilitation program should concentrate on sports activity. Patients with the highest grade of ligament laxity are those least likely to benefit from this protocol. The program is described in detail in Table 12-1.
PREVENTION The best way to treat ligament injuries obviously would be to prevent them, and even though this is practically impossible, it is true that prevention can play a significant role. The two main methods that have been proven
Prevention
Table 12-1 Rehabilitation program for patients who have chronic instability of the ankle
Weeks 5-8 Increased strength training:
Week 1
2 20 repetitions
Range of motion exercises (flexion-extension), for increased blood circulation
Toe raises in one leg
3 20 repetitions; 3 times/day
Step-ups using two boxes, 1 m apart
Cycling
Jog up and down with different steps in between the boxes
Weeks 2-4
Step-ups on a box back and forth and from side to side
Isometric contractions in flexion, extension, and pronation
Use a weight shoe for heavy weight training of flexion, extension, and pronation
3 10 sec; relax for 2-6 sec between each contraction
Week 9
Foot exercises 3 minutes, 2 times/day Roll a small ball under the foot back and forth and side to side
Increased coordination training: Walk on uneven surfaces Use different kinds of jumps
Wrinkle a towel
Jog in intervals
Pick up marbles and/or small rocks
Train with a ball
Closed chain (weight bearing)
Weeks 10-12
Balance and coordination training Bilateral toe raises Walk on tiptoe Jog in place and jog on a soft mattress Walk along zigzag lines, back and forth, and side to side The training should be increased from week to week by increasing the tempo and by turning 90/180 degrees Walk with a surgical tube around the ankle, back and forth, and side to side Stand on one leg (hold the balance), and when this is easily accomplished, then stand on one leg and flex and extend the knee Hold for 10-30 sec Stand on one leg, with the eyes closed for 40 sec Increase the balance training by standing on a balance board, first on both feet and thereafter on one foot while flexing and extending the knee simultaneously. The knee should be kept over the ankle as much as possible Stand on the balance board on one foot; roll a ball around the balance board with the other foot Use 2-3 balance boards and try to walk from one to another, and keep the balance at the same time Endurance and strength training Training with a surgical tube—flexion, extension, and pronation; 3 20 repetitions Increase the training after a while by shortening the surgical tube Stretch the gastrocnemius and soleus muscles with straight and flexed knee 2 15-20 sec
Add to the program: Turnings while jogging Starts, stops, and rushes Cone training Slope training Sports activity, individual and team training A modified program also can be successfully used after acute ligament injuries. (Modified from Karlsson et al., 1991.)
successful in clinical practice are proprioceptive training and external ankle support. There is, however, little scientific evidence to support the preventive effect of ankle taping. A few studies have shown that balance board training can reduce the risk of ankle ligament injuries, especially in those with previous injuries.21-23 However, the effect is either less pronounced or unknown in athletes with previously uninjured ligaments.18,24 This means that the question whether the first-time ligament injury can be prevented using proprioceptive training is still unanswered. The second measure is external ankle support, either ankle tape or brace.25-27 There is little evidence for the use of ankle tape, and the mechanism behind the function of ankle tape is not fully understood. It has been suggested that tape may reduce ankle laxity, limit the extremes of ankle motion, and/or shorten the reaction time of the peroneal muscles, thereby affecting the proprioceptive function of the ligaments and joint capsule around the ankle joint.28 However, as the tape becomes loose after 15 to 30 minutes of use, it never has been proven how it really works.29,30 Despite this, ankle tape is extremely common and has 269
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3 20 repetitions
CHAPTER 12
Nonsurgical treatment of acute and chronic ankle instability
been found empirically to be useful. There is more evidence for the use of ankle braces, especially the semirigid Air-stirrup brace.31-37 Taken together, treating deficits of the proprioceptive system probably is the most important aspect of ankle rehabilitation after lateral sprains. Consideration of improvements in proprioception should be the most important when deciding on a rehabilitation protocol. Moreover, a combination of different exercises and modalities should always be a part of a thorough rehabilitation program. Ankle disk training and/or semirigid ankle brace appear to the effective cornerstones of treatment and prevention.38-41
CONCLUSION Ankle ligament injuries are common, time consuming, and expensive. Most of the injuries are to the lateral ligament complex, and the outcome may be satisfactory, even without treatment. However, nonsurgical treatment of acute ligament injuries may lead to shorter sick leave and faster return to sports activities without risking the functional outcome in the short term and medium term. Well-planned rehabilitation protocol has been shown repeatedly to produce satisfactory outcome in terms of functional stability and return to sports. Despite this, approximately 10% to 30% of all patients will suffer from sequels in the short term and medium term. The symptoms usually are pain and/or functional instability. Studies have shown that approximately 50% of all patients who have chronic ligament insufficiency will recover after having undergone a 12-week rehabilitation program based on strength and proprioceptive training. However, it should be borne in mind that even though rehabilitation programs may work well, prevention is the most important nonsurgical treatment.
REFERENCES 1. Balduini FC, et al: Management and rehabilitation of ligamentous injuries of the ankle, Sports Med 4:364, 1987. 2. Brostro¨m L: Sprained ankles: A pathologic, arthrographic, and clinical study, dissertation, Karolinska Institute, Stockholm, 1966. 3. Karlsson J: Chronic lateral instability of the ankle joint. A clinical radiological and experimental study, Dissertation, Go¨teborg University, Sweden, 1989. 4. Freeman MAR, Dean MRE, Hanham IWF: The etiology and prevention of functional instability of the foot, J Bone Joint Surg 47B:678, 1965. 5. Karlsson J, Andre´asson GO: The effect of external ankle support in chronic lateral ankle joint instability. An electromyographic study, Am J Sports Med 20:257, 1992. 6. Karlsson J, Lansinger O: Lateral instability of the ankle joint, Clin Orthop Rel Res 276:253, 1992.
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7. Glick JM, Gordon RB, Nishimoto D: The prevention and treatment of ankle injuries, Am J Sports Med 4:136, 1976. 8. Hertel J, Denegar CR, Buckely WE: Effect of rear foot orthotics on postural sway after lateral ankle sprain, Arch Phys Med Rehabil 82:1000, 2001. 9. Karlsson J, et al: Lateral instability of the ankle treated by the Evans procedure. A long-term clinical and radiological follow-up, J Bone Joint Surg 70B:476, 1988. 10. Karlsson J, et al: Reconstruction of the lateral ligaments of the ankle for chronic lateral instability, J Bone Joint Surg 70A:581, 1988. 11. Karlsson J, Eriksson BI, Swa¨rd L: Early functional treatment for acute ligament injuries of the ankle joint, Scand J Med Sci Sports 6:341, 1996. 12. Pijenburg ACM, et al: Treatment of ruptures of the lateral ankle ligaments: a meta-analysis, J Bone Joint Surg 82A:761, 2000. 13. Kerkoffset GM, Struijs PA, et al: Different functional treatment strategies for acute lateral ankle ligament injuries in adults, Cochrane Database Syst Rev 3:CD002938. DOI: 10.1002/ 14651858:CD002938, 2002. 14. Kerkoffset GM, Handholl HH, et al: Surgical versus conservative treatment for acute injuries of the lateral ligament complex of the ankle in adults, Cochrane Database Syst Rev 3:CD000380. DOI: 10.1002/14651858:CD000380, 2002. 15. Kerkoffs GM, Rowe BH, et al: Immobilisation and functional treatment for acute lateral ankle ligament injuries in adults, Cochrane Database Syst Rev 3:CD003762. DOI: 10.1002/ 14651858. CD003762, 2002. 16. Karlsson J, Lansinger O, Faxe´n E: Conservative treatment of chronic lateral instability of the ankle, Swedish Med J 88:1404, 1991. 17. Karlsson J, Faxe´n E, Eriksson BI: Ankle joint ligament injuries: prevention, evaluation and treatment, Crit Rev Phys Rehab Med 8:183, 1996. 18. Konradsen L, Ravn JB: Ankle instability caused by prolonged reaction time, Acta Orthop Scand 61:388, 1990. 19. Krips R, et al: Long-term outcome of anatomical reconstruction versus tenodesis for the treatment of chronic antero-lateral instability of the ankle joint: a multicenter study, Foot Ankle Int 22:415, 2001. 20. Komi PV, Viitasalo JT, Rauramaa R: Effect of isometric strength training on mechanical, electrical and metabolic aspects of muscle function, Eur J Appl Physiol 40:45, 1978. 21. Osborne MD, Chou LS, Laskowski ER: The effect of ankle disk training on muscle reaction time in subjects with a history of ankle sprain, Am J Sports Med 29:627, 2001. 22. Sheth P, Yu B, Laskowski ER: Ankle disk training influences reaction time of selected muscles in a simulated ankle sprain, Am J Sports Med 25:538, 1997. 23. Uh BS, Beynnon BD, Helie BV: The benefit of a single-leg strength training program for the muscles around the untrained ankle, Am J Sports Med 28:568, 2000. 24. Lephart SM, Pincivero DM, Giraldo JL: The role of proprioception in the management and rehabilitation of athletic injuries, Am J Sports Med 25:130, 1997. 25. Asthon-Miller JA, Ottaviani RA, Hutchinson C: What best protects the inverted weight-bearing ankle against further inversion, Am J Sports Med 24:800, 1996. 26. Eils E, Rosenbaum D: A multi-station proprioceptive exercise program in patients with ankle instability, Med Sci Sports Exerc 33:1991, 2001. 27. Lynch SA, Renstro¨m PA: Treatment of acute lateral ankle ligament rupture in the athlete: conservative versus surgical treatment, Sports Med 27:61, 1999. 28. Simpson KJ, Cravens S, Higbie E: A comparison of the Sport Stirrup, Malleoloc, and Swede-O ankle orthoses for the foot ankle
References
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32.
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35. Stacoff A, Reinschmidt C, Nigg BM: Effects of foot orthoses on skeletal motion during running, Clin Biomech 15:54, 2000. 36. Stover CN: Air-Stirrup management of ankle injuries in the athlete, Am J Sports Med 8:360, 1980. 37. Thonnard JL, Bragard D, Willems PA: Stability of the braced ankle, a biomechanical investigation, Am J Sports Med 24:356, 1996. 38. Makuloluwe RTB, Mouxas GL: Ultrasound in the treatment of sprained ankles, Practioner 218:586, 1977. 39. Mascaro TB, Swanson LE: Rehabilitation of the foot and ankle, Orthop Clin North Am 25:147, 1994. 40. Evans DL: Recurrent instability of the ankle. A method of surgical treatment, Proc R Soc Med 46:343, 1953. 41. Zo¨ch C, Fialka-Moser V, Quitton M: Rehabilitation of ligamentous ankle injuries: a review of recent studies, Br J Sports Med 37:291, 2003.
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kinematics of a rapid lateral movement, Int J Sports Med 20:396, 1999. Vaes P, et al: Comparative radiologic study of the influence of ankle bandages on ankle stability, Am J Sports Med 13:46, 1985. Vaes PH, Duquet W, Castelyn PP: Static and dynamic roentgenographic analysis of ankle stability in braced and nonbraced stable and functionally unstable ankles, Am J Sports Med 26:692, 1998. Lo¨fvenberg R, Ka¨rrholm J: The influence of an ankle orthosis on the talar and calcaneal motions in chronic lateral instability of the ankle, Am J Sports Med 21:224, 1993. Matsuaka N, Yokoyama S, Tsurusaki T: Effect of ankle disk training combined with tactile stimulation to the leg and foot on functional instability of the ankle, Am J Sports Med 29:25, 2001. Nester CJ, Hutchins S, Bowker P: Effect of foot orthoses on rear foot complex cinematics during walking gait, Foot Ankle Int 22:133, 2001. Raikin SM, Parks BG, Noll KH: Biomechanical evaluation of the ability of casts and brace to immobilize the ankle and hindfoot, Foot Ankle Int 22:214, 2001.
.........................................C H A P T E R 1 3 Ankle sprains, ankle instability, and syndesmosis injuries Thomas O. Clanton CHAPTER CONTENTS ...................... Introduction
273
Failed lateral ankle ligament reconstruction
278
Surgical treatment
273
Medial ankle sprains
280
Results
275
Chronic medial ankle instability
284
Complications
275
Syndesmosis injury
286
Direct ligament repair (modified Brostrom procedure)
275
References
290
INTRODUCTION Because it generally is agreed that most acute lateral ankle sprains can be treated nonoperatively while acknowledging an incidence of late problems in 10% to 20% it is no surprise that lateral ankle ligament reconstruction is commonplace.1 This approach to the treatment of lateral ankle sprains is reasonable only if reconstructive procedures for the lateral ankle ligaments can be as successful as primary repair. Recent consensus of orthopaedic opinion supports this viewpoint. However, there is still controversy that persists regarding the best method of treatment of acute lateral ankle sprains because of the paucity of scientific studies in this field that meet the requirements for proof of method in outcomes-based research.2 Most patients with chronic lateral ankle sprains and instability present with either recurrent ankle sprains after an initial acute sprain or with the feeling of looseness in the ankle and the sensation of ‘‘giving way.’’ These patients may complain of ankle pain, but it is not a prerequisite feature of this problem, although the examination confirms the presence of a positive anterior drawer test and/or a positive inversion stress test. Tenderness may be present, but often is more indicative of associated pathology, as noted later. The examiner must be thorough enough to rule out other sources of symptoms (Table 13-1) because the clinical
diagnosis of chronic lateral ankle instability has been associated with the intraoperative findings of peroneal tendon pathology (tenosynovitis, tears, dislocation), anterolateral impingement lesions, ankle synovitis, intraarticular loose bodies, talar osteochondral lesions, and medial ankle tenosynovitis.3 A comprehensive physical therapy program should be initiated first. Symptoms often will resolve with correction of the deficits in proprioception, strength, and flexibility. Regardless, therapy can improve the results in patients who ultimately require surgery. The nonoperative treatment also includes activity and/or shoe modification (e.g., lateral heel wedge), an ankle-foot orthosis, and/or orthotic devices incorporating a lateral heel wedge. Brostrom4 found that symptoms of instability remained in 20% of his patients who were treated in a conservative fashion. Athletes may use a nonoperative approach to get through a season but rarely consider this an acceptable long-term solution unless their symptoms are minimal.
SURGICAL TREATMENT Indications for surgical treatment include young to middle-aged, active individuals who have failed a welldesigned, nonoperative treatment program. I use the radiographic criteria of an anterior drawer greater than 1 cm (or a side-to-side difference of >3 mm), and a
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
Table 13-1
Sources of chronic pain or instability after ankle sprain
Articular injury
Impingement
Chondral fractures
Anterior tibial osteophyte
Osteochondral fractures
Anterior inferior tibiofibular ligament
Nerve injury
Miscellaneous conditions
Superficial peroneal
Failure to regain normal motion (tight Achilles)
Posterior tibial
Proprioceptive deficits
Sural
Tarsal coalition
Tendon injury Peroneal tendon (tear or dislocation) Posterior tibial tendon Other ligamentous injury
Meniscoid lesions Accessory soleus muscle
Unrelated ongoing pathology masked by routine sprain Unsuspected rheumatologic condition
Syndesmosis
Occult tumor
Subtalar
Chronic ligamentous laxity (collagen disease)
Bifurcate
Neuromuscular disease (Charcot-Marie-Tooth disease)
Calcaneocuboid
Neurologic disorders (L5 radiculopathy, poststroke )
talar tilt greater than 15 degrees (or a side-to-side difference of >10 degrees) as guidelines but have found that the symptoms and signs are most critical. An in-office mini C-arm is a convenient tool to confirm the radiographic instability. Contraindications to surgery include other causes of instability (collagen diseases, tarsal coalitions, neuromuscular diseases, neurologic disorders, or functional instability), older patients with sedentary lifestyles, patients with serious medical conditions that would preclude anesthesia and major surgery, circulatory impairment, presence of ongoing infection, lateral ankle pain without documented lateral instability, history of complex regional pain syndrome, or degenerative arthritis. A relative contraindication is failure of the patient to participate in a preoperative rehabilitation program. The goals of a reconstruction or repair procedure are correction of instability, elimination of pain, and avoidance of surgical morbidity. Anatomic repair or reconstruction is preferable in restoring normal joint kinematics. If there is associated pathology present, it must be recognized and treated simultaneously. Inadequate local tissue to stabilize the ankle may dictate the use of a tendon transfer or tendon graft. Such occasions
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might include patients with known collagen disease, unusually large individuals (e.g., patients larger than 250 lb), or patients with a failure of a prior anatomic repair. Avoidance of nerve injury and preservation of ankle and subtalar joint motion are major factors in preventing morbidity when performing lateral ankle stabilization. Diagnostic and surgical arthroscopy is warranted before ankle stabilization. Chondral injury is the most common problem discovered at arthroscopy, with almost 30% of acute ankle injuries and 95% of chronic ankles having this lesion in one study of an athletic population.5 A more recent study by Komenda and Ferkel6 found only a 25% incidence of chondral injury in their chronic ankle instability series. Regardless, the value of ankle arthroscopy, particularly in cases of chondral fracture, loose bodies, and soft-tissue impingement has been confirmed in several studies.6-9 Hintermann and co-workers9 concluded that essential information was obtained by performing ankle arthroscopy at the time of surgery for ankle instability. Operations for stabilization of the lateral ankle in cases of chronic instability are numerous. When instability persists despite conservative treatment, the surgeon
Direct ligament repair (modified Brostrom procedure)
can choose from more than 50 methods of reconstructing the lateral ankle ligaments. Fortunately, the reported short-term success rate is greater than 80% for all these procedures, according to the literature.10 The primary difference in the various procedures is whether or not they are designed to anatomically reconstruct the ligaments. In a manner reminiscent of the surgical history of shoulder and knee instability, more anatomic reconstructions are gaining popularity for ankle instability. This began with the introduction of the secondary repair of the previously injured ligaments by Lennart Brostrom in 1966.11 It has taken almost four decades for the accumulation of scientific evidence to cast doubt on the tenodesis procedures described by Evans, Watson-Jones, Larsen, and Chrisman and Snook.12-16 The following discussion focuses on the anatomic procedures, whether by direct repair in the tradition of Brostrom or by the use of tissue transfer or tissue grafts done through anatomically placed bone tunnels. Brostrom described his anatomic repair as a delayed procedure for chronic lateral ankle instability. The procedure is a straightforward division and imbrication of the anterior talofibular ligament. The calcaneofibular ligament is not addressed. Various modifications have been described, the most popular being a reinsertion into a bony trough,17 imbrication of the calcaneofibular ligament,18 and reinforcement with the inferior extensor retinaculum.19 Other authors have described the use of different graft sources to rebuild the lateral ankle ligaments while emphasizing the anatomic placement of bone tunnels. Graft sources for this include the plantaris tendon,20-22 the split peroneus brevis tendon,23,24 hamstring tendons,25-27 and allograft tendons.28,29
well as having the greatest mechanical strength.38 Another study, a prospective, randomized comparison of Chrisman-Snook and modified Brostrom, found that both procedures had greater than 80% good or excellent results, but there were more complications in the Chrisman-Snook group (five with wound problems, eight with sural nerve injury, and six with the feeling that the ankle was ‘‘too tight’’). Brostrom complications were almost nonexistent and included no wound problems, no nerve injury, and only two with a feeling that the ankle was ‘‘too tight.’’13 In a long-term, multicenter outcome study of anatomic reconstruction versus tenodesis, Krips and associates39 found that more patients with tenodesis procedures had positive anterior drawer signs, medial ankle degenerative changes, higher mean talar tilt, and anterior talar translation. In addition, significantly fewer patients in the tenodesis group had excellent results, and more patients had a fair or poor result. In a follow-up study, patients who underwent tenodesis procedures underwent more revision procedures, demonstrated more osteoarthritis, more instability, tenderness, chronic pain, and limited dorsiflexion. Good to excellent results were found in 80% of patients at 30-year follow-up after anatomic reconstruction, versus only 33% after Evans tenodesis.40 Overall, it appears that tenodesis procedures fail to restore the normal anatomy, resulting in lessened mechanical stability and a decrease in patient satisfaction. Because of these well-documented inherent problems of nonanatomic tenodesis procedures, anatomic ligamentous reconstruction is the preferable treatment approach in almost all circumstances.
COMPLICATIONS
Results of the Brostrom anatomic reconstruction are excellent. In Brostrom’s original study, 51 of 60 patients demonstrated minimal or no instability at follow-up.11 Other reported results from the Brostrom procedure or a modification thereof include large and small series of patients from around the world, with more than 500 cases reported and results ranging from 85% to 100% successful.13,30-37 Lesser results are associated with heel varus, inadequate rehabilitation, nerve injury, preexisting arthritis, and significant repeat sprains. Objective results of comparison studies that include anatomic procedures such as the Brostrom versus tenodesis procedures all favor the former procedure. In a cadaveric study comparing the Chrisman-Snook, Watson-Jones, and modified Brostrom procedures, the modified Brostrom procedure produced the least amount of talar tilt and anterior drawer translation, as
Neurologic damage and wound complications are not infrequent. Injury to the superficial nerves is the most common complication following operative repair of the lateral ankle ligaments. Depending on the report and the type of surgical approach used, the incidence ranges from 7% to 19%.41 The sural nerve is at greater risk with tenodesis procedures.42 Wound dehiscence, superficial and deep infection, loss of ankle and/or subtalar motion, and deep venous thrombosis are less-often reported complications. Wise patient selection and good surgical technique are paramount in keeping these complications to a minimum.
DIRECT LIGAMENT REPAIR (MODIFIED BROSTROM PROCEDURE) For most cases of chronic lateral ankle instability in the athletic population, a modified Brostrom technique is 275
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Ankle sprains, ankle instability, and syndesmosis injuries
applicable. Its advantage is that it is an anatomic repair, with no tenodesis effect and no major change in the ankle and subtalar joint biomechanics. A second advantage is that it does not sacrifice adjacent healthy tissue. Indications include those patients with chronic lateral ankle ligament instability who are unresponsive to physical therapy. Contraindications include patients with structural varus deformities, previously failed lateral ligament reconstructions, genetic collagen disorders (Marfan’s and Ehlers-Danlos syndromes), or posttraumatic conditions with soft-tissue loss. Relative contraindications are obese patients (more than 250 lb) or patients whose instability exceeds 10 years duration with history of multiple severe sprains.17 For these patients, consideration is given to use a free tendon graft (allograft or autograft) for augmentation. My operative technique includes planned day surgery or a 23-hour hospital stay. General, spinal, or regional anesthesia may be used. The patient is positioned supine with a bolster under the ipsilateral hip. A thigh tourniquet is placed. The procedure is performed through an anterior lateral incision paralleling the border of the fibula unless a more extensile longitudinal incision is necessary to address additional pathology.
Technique 1. The incision begins at the level of the plafond and extends distally to the level of the peroneal tendons (Fig. 13-1). The lateral branch of the superficial peroneal nerve and the sural nerve are protected. 2. Dissection is carried down to the capsule. To isolate the remaining portion of the anterior talofibular ligament (ATFL), it is helpful to enter the anterolateral capsule at the plafond level and carefully dissect distally to expose the ATFL fibers. If the ligaments appear stretched (Fig. 13-2) and there is no obvious rupture, the capsule and ligament are divided a few millimeters from their fibular origin and imbricated. 3. To locate the calcaneofibular ligament (CFL), the peroneal sheath is opened and the peroneal tendons are first checked for a tear. Then the tendons are retracted exposing the CFL, and the quality of the CFL is determined. A ligament that is simply stretched can be divided and imbricated (Fig. 13-3). The previously ruptured ATFL or CFL often is scarred down to capsule and tendon sheath and requires dissection to disclose their location and character. For the CFL, it is necessary to determine whether the remaining tissue can be used in the secondary repair. A distal avulsion from the calcaneus can be reattached with suture anchors. I prefer to use a bioabsorbable anchor to avoid problems from retained
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276
Figure 13-1 Anterior lateral incision paralleling the border of the fibula used for anatomic repairs and reconstructions. (Courtesy Matthew Morrey, MD.)
Figure 13-2 Stretched anterior lateral ligaments found in typical chronic ankle sprains. (Courtesy Matthew Morrey, MD.)
hardware in the event of future ankle problems that might call for a drill hole in this location. A proximal avulsion can be reattached with sutures through drill holes in the fibula (being careful to consider the anterior talofibular reconstruction) or with a suture anchor. The greatest
Direct ligament repair (modified Brostrom procedure)
in neutral dorsiflexion and slight eversion (Fig. 13-5). The surgeon must be careful to ensure that there is no anterior displacement force on the ankle while the sutures are being tied. To prevent this, a bump is placed under
Figure 13-3 Imbrication of stretched ligaments in anatomical reconstructive procedure. (Courtesy Matthew Morrey, MD.)
Figure 13-4 Bony trough used for attachment of anterior talofibular and calcaneofibular ligaments to bone. (Courtesy Matthew Morrey, MD.)
Figure 13-5 Sutures tied over bony bridge on anterior lateral fibula. (Courtesy Matthew Morrey, MD.)
277
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difficulty arises with a midsubstance tear that has extensively scarred to the surrounding tissue. Careful dissection usually will define a ligamentous remnant that can be imbricated. 4. In the case of an ATFL avulsed from the fibula, and to be certain of sufficient tissue for the ATFL reconstruction, a periosteal flap that is continuous with the capsule and the anterior talofibular scar can be created. 5. Nonabsorbable or slowly absorbable sutures are placed in the ligament. A small bony trough is created above the anterior and inferior border of the distal end of the fibula, and several drill holes are made with a small drill bit or Kirschner wire (Fig. 13-4). This permits imbrication of the ends of the cut ligament and capsule, as well as the anchoring of the ligament into bone. In the few cases in which the ATFL has avulsed from the fibula, it also is feasible to reattach the ATFL with suture anchors. As mentioned under number 3 previously, it is preferable to use bioabsorbable anchors here to avoid the potential problem of extricating a metal anchor that is situated in the exact location where a bone tunnel must be placed for a tendon graft reconstruction should the anatomic reconstruction fail or be disrupted in a future injury. 6. The sutures are tied over a bony bridge on the lateral aspect of the fibula, with the ankle held
CHAPTER 13
7.
8. 9.
10. 11.
Ankle sprains, ankle instability, and syndesmosis injuries
the distal leg to relieve any anterior directed force on the heel. Sutures are placed in the CFL first, followed by the ATFL, and then the lateral capsule. The sutures are tagged or grouped to be tied only after all sutures are in place. Sutures are tied beginning with the CFL, then the ATFL, and concluding with the anterior capsule. The ankle is positioned in relaxed plantarflexion when the sutures in the CFL are secured and in slight dorsiflexion and eversion for tying the sutures in the ATFL. After securing the repair, the stability is checked and further imbrication performed as needed. Before closure, attention is directed to the inferior extensor retinaculum, which is imbricated or sutured to the periosteum over the fibula (Fig. 13-6). This provides additional stability to the subtalar area and protection to the ATFL and may add some proprioceptive feedback. I believe that it is an important addition to the Brostrom technique, as noted by Gould and others.35,43-45 The subcutaneous tissues are reapproximated with absorbable sutures, and the skin is closed with a subcuticular technique. A U-shaped splint and a posterior splint or a walking boot is applied.
Postoperative care For athletes, the patient is placed in a short-leg splint with the foot in neutral dorsiflexion and slight eversion. The splint remains in place until the first postoperative visit, which usually occurs between 6 and 10 days from the day of surgery. The patient is on crutches— nonweight bearing until this visit. At the first postoperative visit, the patient is placed in a walking boot or cast and begins weight bearing as tolerated. This is continued for 3 to 4 weeks until the next office visit. During this second phase, the patient may start dorsiflexion and eversion movement if in a boot, and at 4 weeks, the patient is placed in an ankle stirrup brace. Gentle active inversion is begun at 4 weeks in association with Achilles stretching. At the same time, proprioceptive training and resistive exercises with rubber tubing are begun. The patient is allowed to progress from stationary biking to pool running to outdoor walking and straight-line running. As long as the patient shows no pain or undue swelling, rehabilitation continues as tolerated with figure-eight running in progressively smaller loops, and ultimately, cutting drills are instituted. The athlete then is allowed to resume activities specific to his or her sport, with return to competition once each task of the sport can be accomplished. For 6 months following the repair, the patient is instructed to use a protective ankle brace and/or taping to protect the repair. The typical return to competitive sport participation is 12 weeks (range 10 to 16 weeks), although it may take closer to 6 months for swelling and discomfort to resolve fully. For nonathletes, a 10- to 12-week period of protection is warranted, the first 4 to 6 weeks with the patient being in a cast or walking boot with limited exercise and the second 6 weeks with the patient being in a removable brace or walking boot when a more aggressive rehabilitation program is begun. Resumption of vigorous exercise or recreational sports generally takes longer in this population. Although I believe in individualizing the rehabilitation program to the patient and the pathology, a table is provided as a general guideline (Table 13-2).
FAILED LATERAL ANKLE LIGAMENT RECONSTRUCTION
Figure 13-6 Imbrication of inferior extensor retinaculum to periosteum of distal fibula. (Courtesy Matthew Morrey, MD.)
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278
Of patients who undergo a lateral ankle reconstruction, 5% to 15% may proceed to failure, requiring further intervention. Perhaps the most common cause for failure is recurrent instability. The primary surgical procedure may have been inadequate, the patient may have reinjured the ankle, or there may have been inherent factors that predisposed a patient to failure (benign joint
Failed lateral ankle ligament reconstruction
Rehabilitation program for surgically reconstructed lateral ankle ligaments
Doctor visits
Days (weeks)
Immobilization
Weight bearing
Rehabilitation
Surgery to first postoperative visit
0-7 (1)
Immobilized in splint or walking boot
Crutches nonweight bearing
No exercises with ankle but general conditioning as tolerated
First visit to second visit
8-28 (2-4)
Walking boot with dorsiflexion and eversion allowed
Crutches with weight bearing as tolerated, progressing to full weight and no crutches
General conditioning, stationary bike starting with stirrup brace and weight on heel, pool walking and running, light balance work
Second visit to third visit
29-42 (5-6) 43-56 (7-8)
Stirrup brace at all times except sleep Stirrup brace for exercise
Full weight
Biking with increased resistance, outdoor walking and straight line running, aggressive proprioceptive education Start figure-8 running, cutting, sports-specific drills
Third visit to return to play
57-70 up to 84 (9-12)
Brace or tape for practice
hypermobility syndrome, Marfan’s syndrome, or EhlersDanlos syndrome).42 The patient often describes a loose feeling in the ankle or the sensation of ‘‘giving way’’ or ‘‘turning easily.’’ Another cause of failure in lateral ankle reconstruction is chronic pain, constant or only during activity, resulting from intra-articular pathology or postoperative stiffness. In addition to a thorough history, it is important to obtain a record of the primary procedure, if possible. Stress tests of the lateral ligaments should demonstrate laxity. Limited range of motion of the ankle and subtalar joints can be observed in patients who were overtightened at their original reconstructive procedure. The alignment of the hindfoot should be evaluated. Varus alignment of the heel will predispose a patient to failure of a lateral ligament reconstruction. Radiographs of the foot and ankle should be obtained to evaluate the presence of bony pathology. Stress radiographs or fluoroscopy can aid in the diagnosis of recurrent instability or an excessively tight reconstruction. Intra-articular pathology, such as osteochondral lesions, can be diagnosed with magnetic resonance imaging (MRI). Computed tomography (CT) scans are helpful in defining previous bone tunnels. Nonoperative measures may be effective in the
Progress drills, speed and endurance
management of recurrent instability; however, these patients typically require a second attempt at surgical stabilization.
Treatment Reconstructing the lateral ligament with a free tendon transfer using the semitendinosus or the gracilis tendon is recommended, performed in a manner similar to the method used when harvesting for an anterior cruciate ligament autologous graft. After the graft has been harvested, it is prepared by sizing it for diameter and length. Generally, the doubled semitendinosus is 9 to 11 cm in length and approximately 5 to 6 mm in diameter, whereas the gracilis is somewhat smaller. It also is possible to use an allograft tendon, and a larger tendon such as the anterior tibial tendon can be cut to the appropriate diameter for drill holes. The lateral ankle is exposed through one of two incisions chosen on the basis of the underlying pathology. When the pathology is limited to the previously reconstructed lateral ligamentous complex, a small, curvilinear incision paralleling the anterior and distal border of the fibula is used, similar to the incision for the previously described Brostrom procedure (see Fig. 13-1). For cases with more extensive pathology (peroneal tendon tears 279
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Table 13-2
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
or anterior osteophytes), a longitudinal incision is made over the posterior border of the fibula, curving distally to the sinus tarsi and the anterior process of the calcaneus. With both approaches, the ankle joint is exposed and the anterolateral capsule is divided, preserving as much potentially useful tissue as possible. For proper graft placement, the insertion sites of the ATFL (talus and distal fibula) and CFL (distal fibula and calcaneus) are exposed. The surgeon then drills a 4.5- to 6.0-mm tunnel in the talus, depending on the size of the graft and the size of the interference fit screw being used. Bioabsorbable screws currently vary in size from 4 to 11 mm. I have found that the 5- to 5.5-mm screw works best in the ankle. The tendon graft is captured with a suture loop using the Arthrex Biotenodesis System and inserted into the bone tunnel to a depth of approximately 20 mm before the bioabsorbable screw is tightened against the tendon within the bone tunnel. Another option is to drill a tunnel in the talus to a depth of 25 to 30 mm and use a Beath pin to pass the sutures from the end of the tendon graft through the tunnel in the talus and out the medial side of the foot. With tension applied to the tendon through the sutures, an interference screw can be placed next to the tendon to secure the graft in the talus. Once the graft is secure in the talus, a tunnel is drilled from the anterior distal fibula at the origin of the ATFL through the distal fibula and into the area of the proximal peroneal groove. When the procedure is performed through a Brostrom-type incision, a separate 2-cm incision is made for insertion of a retractor to protect the peroneal tendons. A second fibular bone tunnel is drilled at the origin of the CFL and passed posterior to exit at the posterior fibula at the same exit site as the previously drilled fibular tunnel. Now a V-shaped channel in the distal fibula exists. A suture passer is placed through the posterior fibular tunnel, exiting anterior, and the sutures in the tendon graft are passed into the fibula, creating an ATFL graft. The suture passer next is passed posterior through the distal fibular tunnel, and the sutures in the tendon graft are passed out the distal fibula to create a CFL graft. It is important to keep a clamp around the graft at the posterior fibula to allow tensioning of the separate limbs of the graft. A tunnel is drilled in the lateral calcaneus at the site of insertion of the CFL for the tendon graft, with the depth of the tunnel being sufficient enough to pull the entire tendon graft length into the bone tunnel. A Beath pin or Keith needle then is used to pass the tendon graft sutures through the plantar medial heel. While holding the ankle in neutral dorsiflexion and neutral inversion/eversion, the surgeon applies tension to the graft. A bioabsorbable screw is placed with an interference fit in the calcaneal bone tunnel to secure the graft (Fig. 13-7). Alternatively, the Arthrex
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280
Figure 13-7 Bioabsorbable screws placed with an interference fit in the talar and calcaneal bone tunnels to secure the tendon graft.
Biotenodesis System can be used to insert the tendon in the bone tunnel and fixate the graft with the bioabsorbable screw. Once the graft is secured and the tension is judged to be adequate, the ankle is tested for stability and range of motion, and stress radiographs are performed under fluoroscopy. If the ankle is still unstable, the screw in the calcaneus is removed, the graft further tensioned, and the screw replaced with the heel in slight eversion. The graft is secured to the periosteum of the fibula at the entrance and exit holes with absorbable suture. The inferior extensor retinaculum or other local tissue can be used for augmentation if further stability is required. Postoperatively, the ankle is protected in a splint or boot, nonweight bearing for 1 to 2 weeks. After this time period, progressive weight bearing is allowed over 2 to 3 weeks, with discontinuation of crutches by 4 weeks postoperatively. Compliant patients, under supervision, can be managed in a removable walking boot and started on active range of motion immediately. The typical ankle rehabilitation program for range of motion, strength, Achilles stretching, and proprioceptive reeducation begins at about 3 to 4 weeks and progresses as tolerated. Other pathology often dictates any alterations that must be made to this general protocol.
MEDIAL ANKLE SPRAINS The medial ankle ligamentous complex is composed solely of the deltoid ligament. The overwhelming majority of deltoid ligament injuries occur in association with
Medial ankle sprains
Anatomy and biomechanics The deltoid ligament is a broad, fan-shaped complex of ligaments that together serve as the medial collateral ligament of the ankle. The deltoid ligament consists of both a superficial layer and a deep layer and has enough anatomical variation that there has been some confusion in the nomenclature.51-54 Milner and Soames’51 detailed anatomic study found six different bands, with three being consistently present (two superficial and one deep), and three bands were not found in all specimens. The constant superficial bands originate from the anterior colliculus of the medial malleolus and are divided into the tibiospring ligament (TSL) and tibionavicular ligament (TNL). The less constant portions of the superficial deltoid are the tibiocalcaneal ligament (TCL) and superficial posterior tibiotalar ligament (STTL) (Fig. 13-8). By their nature, the medial ligaments blend together, forming an indistinct origin from the medial malleolus, and are characterized primarily by their distal attachment. The constant band of deep deltoid ligament is the deep posterior tibiotalar ligament (PTTL). The deep anterior tibiotalar ligament (ATTL) was found in only 10% of specimens51 (Fig. 13-9). The deep bands cross only the single joint of the ankle, whereas the superficial
Deltoid ligament Posterior tibitalar Tibiocalcaneal Tibionavicular Anterior tibiotalar
Figure 13-8 Superficial deltoid ligaments. (A) Tibial spring ligament. (B) Tibionavicular ligament. (C) Tibiocalcaneal ligament.
Tibionavicular/ Tibiospring (reflected)
Deep anterior tibiotalar
Deep posterior tibiotalar
Figure 13-9 Deep deltoid ligaments. (A) Deep posterior tibiotalar ligament. (B) Deep anterior tibiotalar ligament.
ligaments cross two joints (ankle and either talocalcaneal or talonavicular). The deep layer of the deltoid originates from the intercollicular groove and posterior colliculus of the medial malleolus. The deltoid ligament is the primary restraint to valgus tilting of the talus within the ankle mortise.55 Both the superficial deltoid and the deep deltoid individually resist eversion of the hindfoot. Valgus tilting of the talus does not occur if only the superficial or the deep portion of the deltoid is divided.55,56 Complete rupture of the entire deltoid complex is required to produce valgus tilting of the talus in otherwise intact ankles.55 The deep deltoid ligament is also a secondary restraint against both lateral talar shift and anterior talar excursion, with the fibula and lateral ankle ligaments being the primary restraint.55 Multiple anatomic studies have shown that, with an intact deltoid, up to 3 mm of lateral talar shift is possible if the lateral malleolus has been resected.55,57,58 Conversely, no increase in lateral shift or anterior excursion of the talus occurs when the entire deltoid is sectioned if the lateral malleolus and ligaments are intact.57 However, sectioning of the entire deltoid, or just the tibiospring (or tibiocalcaneal) portion of the superficial deltoid, has been shown to dramatically decrease tibiotalar contact area and increase peak ankle joint pressures up to 30%. These significant changes in contact area and peak pressures occur before radiographic evidence of medial talar tilt is present.59,60 The deltoid ligament clearly is involved in rotary stability of the talus within the mortise, but its exact function in this regard is the subject of some debate.56,61,62 281
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lateral malleolus fractures, syndesmotic disruptions, or injuries to the lateral ankle ligaments. Isolated deltoid ligament sprains account for only 2% to 3% of all ankle sprains.46-48 Chronic medial ankle instability is rarely a clinical problem, but its prevalence probably is underestimated.49,50
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
Mechanisms of injury Although the deltoid ligament may be injured in conjunction with the lateral ligamentous structures by a variety of mechanisms, the classic mechanism of injury for an isolated deltoid rupture is forced abduction or eversion.63 In these forced abduction injuries, the superficial deltoid ligament ruptures first, followed by the deep deltoid.64 The deep deltoid has a significantly higher load to failure than the lateral collateral ankle ligaments, with its dominant mode of failure being an intrasubstance rupture near its talar insertion.65,66 Consequently, a deltoid injury requires considerably more force than the average lateral ankle sprain. Athletic injuries to the deltoid typically involve jumping sports or contact sports such as football or wrestling. A basketball player might sustain an eversion injury by landing on another player’s foot after coming down from a jump, whereas a football player might sustain a forced abduction injury when an opponent falls on or steps on his lateral ankle with the foot in a pronated position. Garrick67 noted an inordinately high frequency of ankle sprains in wrestlers, presumably resulting from their wide stance and having their feet everted to gain traction on the mat. Diagnosis As stated previously, the majority of deltoid injuries occur in conjunction with lateral ankle sprains, syndesmosis injuries, or fibula fractures. Obtaining an accurate description of the patient’s mechanism of injury may provide important clues to the presence of these associated injuries. Patients with acute deltoid ligament ruptures usually recall the specific injury and often feel or hear a pop on the medial side of their ankle. A history of immediate pain and swelling over the deltoid ligament is typical, along with a variable degree of difficulty with ambulation and a feeling of medial instability. Because of the high prevalence of associated injuries, examination of an athlete with a suspected deltoid ligament injury should include evaluation of the entire lower leg. Careful palpation of the entire length of the fibula should be performed to assess for a high fibula fracture that might be seen with a Maisonneuve-type injury. An injury to the ankle syndesmosis must be ruled out by squeeze test (Fig. 13-10) or external rotation test (Fig. 13-11) or, if still in question, by MRI. A thorough assessment of each of the lateral ankle ligaments also must be performed. When examining the medial ankle structures, it is important to keep in mind the intimate spatial relationships of the deltoid ligament to the contents of the tarsal tunnel. Careful localization of the point of maximal tenderness and evaluation of tendon function can help to distinguish between deltoid ligament ruptures and injuries of the posterior tibial, flexor digitorum longus (FDL), or flexor hallucis longus
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Site of pain localization
Figure 13-10 Squeeze test for syndesmosis injury.
(FHL) tendons or to the spring ligament. The patient with a deltoid injury may develop an increasingly flat foot or pronated foot deformity with weight bearing after the injury that is actively correctable with contraction of the posterior tibial muscle.50 Finally, a brief sensory examination of the foot and ankle, including attempts to elicit a Tinel’s sign, can help to identify acute traction injuries of the tibial or saphenous nerves. Radiologic evaluation should begin with standard views of the ankle to detect associated ankle fractures or frank diastasis of the syndesmosis. Supplemental anterior-posterior (AP) and lateral views of the leg should be obtained if the physical examination is suggestive of a high fibula fracture or proximal tibiofibular pathology. Weight-bearing AP ankle radiographs may show valgus tilt in a complete deltoid rupture. If an isolated deltoid ligament rupture is clinically suspected, manual valgus stress radiographs should be obtained. Greater than 5 degrees of valgus talar tilt with valgus stress in neutral ankle flexion, or a side-to-side difference of greater than 2 degrees, is indicative of an isolated complete deltoid injury.68 It should be noted that plain radiographs typically are normal in patients with ruptures of only the superficial portion of the deltoid ligament.
Medial ankle sprains
External rotation test for syndesmosis injury.
Although MRI is considered the gold standard for visualizing the deltoid ligament, it has been used rarely in clinical practice except in professional athletes. As with lateral ligament injuries, MRI can be helpful in the evaluation of associated ankle pathology in a patient who fails conservative management. MRI also is useful in special cases in which the diagnosis of an acute deltoid rupture must be objectively confirmed. Clinical correlation between MRI and physical examination findings is critical because MRI is highly sensitive and may demonstrate clinically insignificant changes in the deltoid ligament.69 Schneck et al.70 have emphasized the importance of separate dorsiflexion and plantarflexion imaging sequences to optimally visualize the individual components of the deltoid ligament. With newer high field strength magnets, updated three-dimensional imaging software, and the use of a dedicated ankle coil, foot position may be less important.71 When ordering an MRI to evaluate the deltoid, direct consultation with the radiologist before the study helps to determine the appropriate imaging protocol for their specific equipment. Another alternative for diagnosis when nonoperative treatment fails is arthroscopy of the ankle and direct assessment of the ligamentous integrity, as described
by Hintermann et al.50 He suggests using the criteria described in Table 13-3 for grading the degree of instability by arthroscopy.
Treatment In general, the treatment of acute deltoid ligament ruptures is nonoperative. However, the presence of an associated fibular fracture or syndesmotic injury most often will require operative treatment for these entities. Although it is the subject of historical controversy, most recent studies have concluded that the deltoid does not need to be surgically repaired once the lateral malleolus and/or syndesmosis have been anatomically reduced and stabilized.72-77 The anatomy of the deltoid ligament allows for maintained apposition of its torn ends if the talus is appropriately stabilized within the mortise.20,78,79 The main indication for deltoid ligament surgery is the infrequent case in which the deltoid or posterior tibial tendon becomes entrapped between the talus and the medial malleolus, preventing anatomic reduction of the talus within the mortise. In these cases, medial ankle arthrotomy with exploration of the posterior tibial tendon and repair of the deltoid is recommended. There are other situations that occasionally 283
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Figure 13-11
CHAPTER 13
Table 13-3
Ankle sprains, ankle instability, and syndesmosis injuries
Arthroscopic grading and findings in medial ankle instability
Grade of instability
Opening medially (mm)
Stable
Device used
Finding
Up to 3
2-mm hook probe/2.7-mm scope
Minimal translation of talus
1
3-4
2-mm hook probe/2.7-mm scope
Translation discernible with probe, scarring seen in superficial deltoid
2
4-5
5-mm scope/ 4.5-mm shaver
Obvious translation with easy movement of large joint scope into medial tibiotalar space, scarring of medial ligaments or disruption both deep and superficial
3
More than 5
5-mm scope/ 4.5-mm shaver
Obvious translation with easy movement of large joint scope into medial tibiotalar space with free visualization to the posterior aspect of the ankle joint even without valgus stress applied
Modified from Hintermann B, et al: Medial ankle instability—a missed diagnosis, Presented at AAOS Annual Meeting, AOFAS Specialty Day, March 13, 2004.
warrant repair of the deltoid in association with syndesmosis disruption, and the best determinant that I have found is stress evaluation intraoperatively following the lateral side repair. Treatment of athletes with low-grade, isolated, deltoid ligament sprains is similar to the nonoperative treatment of acute lateral ankle sprains, but return to sports generally is more prolonged. Immediate cold therapy, antiedema measures, and the use of a functional stirruptype brace or walking boot are begun as quickly as possible, with return to sports in 3 to 6 weeks. For high-grade sprains or complete ruptures of the deltoid, anatomic reduction must be confirmed before treatment, with 6 to 8 weeks of immobilization in a walking cast or walking boot to prevent external rotation of the talus as the deltoid heals. Although I do not routinely perform surgery on athletes with complete deltoid ligament ruptures (even in conjunction with fibular fracture or syndesmosis injury), I consider failure to achieve anatomic alignment of the medial clear space an indication for surgical repair.80 Determining this may require examination under anesthesia and arthroscopy. There is very little in the scientific literature regarding the acute repair of deltoid ligament injuries. Jackson et al.81 have described the surgical repair of an isolated, complete rupture of the anterior portion of the deltoid in a high-performance football player. Jackson used a Kessler-type suture tied over drill holes in the medial malleolus and has described his post-operative protocol in detail. At 6 weeks, the patient began weight bearing
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in a hinged ankle brace; at 9 weeks, he was running with his ankle taped; and at 12 weeks, he was running patterns without pain or instability. One of Brostrom’s4 early reports of a series of ankle sprains included eight isolated deltoid ruptures. All patients underwent arthrography to confirm the diagnosis; three were treated operatively, one was casted, and four were treated with ankle strapping. At a mean follow-up of 3.8 years, he reported no residual symptoms in any of the deltoid ligament treatment groups. It is unclear whether surgical repair of complete deltoid ruptures offers any advantage in terms of quicker return to sports or improved outcome when compared with conservative treatment. Nevertheless, extrapolating from the findings of Hintermann et al.50 related to chronic medial instability, examination under anesthesia, arthroscopy, and acute repair with sutures or suture anchor can be justified in the athlete with an acute injury who is suspected to have instability. Until further scientific work elucidates a clear difference between the results of operative and nonoperative repair, controversy will persist in determining the best approach to the acute, severe medial ankle sprain.
CHRONIC MEDIAL ANKLE INSTABILITY Chronic medial ankle instability is an uncommon but severely disabling problem.20,49,82 When chronic deltoid
Chronic medial ankle instability
insufficiency does occur, it usually can be related to lateral ankle pathology. Deformity of the lateral malleolus from fibular fracture malunion or distal physeal arrest, as well as chronic syndesmotic diastasis, can all be contributing factors.15,82,83 In these cases, the lateral malleolus fails to appropriately buttress the talus within the mortise, causing the deltoid to heal in a lengthened position or to gradually attenuate. Additionally, arthroscopic findings in patients with chronic ankle instability indicate that combined medial and lateral ankle instability is more than twice as common as medial ankle instability alone.49 Patients with chronic medial ankle instability usually complain of recurrent episodes of giving way along with medial ankle pain. Physical examination may reveal mild pes planovalgus, tenderness over the deltoid ligament and anteromedial joint line, and a variable degree of instability to valgus stress. The ability of the patient to correct the planovalgus or pronation deformity actively while weight bearing by contracting the tibialis posterior muscle is confirmatory.50 Manual valgus stress radiographs in neutral ankle flexion should be obtained to document the degree of valgus talar tilt. Although fibular length can be adequately evaluated by plain radiographs, a rotational malunion of the fibula or a subtle syndesmosis deformity is assessed more easily with axial CT imaging. MRI also is reasonable in these cases, because Hintermann et al.49 have reported a high association of talar articular cartilage lesions with complete ruptures of the deltoid ligament. Treatment of chronic medial ankle instability depends on the associated pathology. In patients with fibular malunion, derotational and/or lengthening fibular osteotomy should be performed before addressing the deltoid ligament. Similarly, chronic syndesmosis injuries first require stabilization or reconstruction of the syndesmosis. In cases of chronic medial ankle instability without associated lateral ankle pathology, patients may benefit from a period of conservative treatment. This
Split posterior tibial tendon graft for deltoid ligament reconstruction.
285
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Figure 13-12
may include any combination of supportive taping, bracing (e.g., short articulated ankle foot orthosis [AFO]), casting, functional rehabilitation, and orthoses (e.g., medial heel wedge and first metatarsal lift). If the athlete’s symptoms are not reduced to a tolerable level with conservative measures, surgical reconstruction of the deltoid ligament is warranted. Several different methods of deltoid ligament reconstruction have been described in detail. If the remaining ligamentous tissue is of adequate quality, simple imbrication using a method analogous to the lateral Brostrom procedure may be performed.82 When possible, it seems advantageous to advance the ligament to bone using suture anchors in the talus and naviculum to accomplish this goal.84 Alternatively, when the remaining deltoid is of poor quality, ligamentous reconstruction with a tendon graft is recommended. Wiltberger and Mallory85 have described a method for deltoid reconstruction using the anterior half of the posterior tibialis tendon. The split tendon graft is left attached at its insertion and the free end is passed through a bone tunnel in the medial malleolus before being tied back on itself (Fig. 13-12). In view of the serious potential problems created by posterior tibial tendon pathology, it seems less than ideal to take a portion of the posterior tibial tendon for use as a graft to reconstruct the deltoid ligament. More complex reconstruction of the deltoid in a patient with traumatic loss of the medial malleolus using a free tendon graft also has been described.86 Allograft tendon or autologous hamstring tendon grafts can be used with bioabsorbable interference fit screw fixation into bone tunnels. The postoperative protocol recommended by Jackson includes 2 weeks of nonweightbearing immobilization in a short-leg cast. This is followed by 4 weeks of weight bearing as tolerated in a walking boot, while active range-of-motion exercises are initiated. Strengthening exercises are started at 6 weeks, and the patient may begin weight bearing in a hinged ankle brace. At 9 weeks, light running is
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
Posterior
Anterior
Insertion site of interosseous ligament
Attachment of interosseous membrane
inferior tibiofibular ligament (PITFL), and (3) the interosseous ligament. The AITFL runs obliquely at approximately a 45-degree angle from the anterolateral tubercle of the tibia to the anterodistal fibula (Fig. 13-14). It is the most often-injured ligament in syndesmosis sprains and in frank diastasis.64 The PITFL has two components (Fig. 13-15). The superficial component runs from the posterolateral tubercle on the
Fibular notch AITF origin
Figure 13-13
Anatomy of the fibular notch. Anterior tibiofibular ligament
allowed, and by 12 weeks, a gradual return to the athlete’s specific sport begins. Return to competition is expected at 4 to 6 months.81
Anterior talofibular ligament
SYNDESMOSIS INJURY Syndesmosis injury, or the high ankle sprain, has become the injury de rigueur in the sports medicine world related to the foot and ankle. No National Football League injury report is complete, it seems, without there being some athlete who is out of action because of this entity. Although the injury clearly has been around since antiquity, it does seem to be diagnosed presently with more frequency. This probably is due not only to the larger, faster, and stronger athletes playing on surfaces with more torsional friction but also to improved diagnostic tools and physician awareness.
Anatomy and biomechanics The stability of the distal tibiofibular complex is dependent on bony and ligamentous anatomy, and the distal tibia and fibula comprise the bony anatomy of the syndesmosis. The fibular notch (Fig. 13-13), or incisura fibulare, is a vertically oriented triangular groove in the lateral tibia with which the fibula articulates. As the fibula rests in this notch, it is supported anteriorly and posteriorly by the distal tibial tubercles. The size of these tubercles correlates with the depth of the notch. Radiographically, the notch appears concave only 75% of the time, and in 16% of patients it takes on a convex appearance.87 There are three main ligaments that add stability to the distal tibiofibular syndesmosis: (1) the anterior inferior tibiofibular ligament (AITFL), (2) the posterior
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Figure 13-14
Anatomy of the anterior syndesmosis.
Posterior tibiofibular ligament Posterior talofibular ligament Deltoid ligament Calcaneofibular ligament
Figure 13-15
Anatomy of the posterior syndesmosis.
Syndesmosis injury
suspected to have an abduction component, a rupture of the deltoid ligament or a fracture of the medial malleolus will produce tenderness at the medial ankle. The examiner also must ensure that the fibula is palpated from distal to proximal, including the proximal tibiofibular joint, to rule out the possibility of a Maissoneuve’s fracture or a proximal tibiofibular joint disruption. Delayed swelling and ecchymosis are frequent findings.
Mechanism of injury Most clinicians agree that external rotation is the most significant force in a syndesmosis injury.20,64,92,93 The AITFL is the first to fail with an external rotation force, followed by the interosseous ligament and membrane. The PITFL usually is preserved. A syndesmosis sprain may also occur with an abduction force, requiring rupture of the deltoid ligament or fracture of the medial malleolus.
Special clinical tests The ‘‘squeeze test,’’ described in 1990 by Hopkinson et al.,93 is a method of detecting ‘‘stable’’ syndesmosis injuries (see Fig. 13-10). A recent biomechanical study confirmed separation at the origin and insertion sites of the AITFL caused by compression of the fibula and tibia proximal to the midpoint of the calf.95 The authors further reported that the distance of separation increased as the syndesmotic ligaments were sectioned sequentially. The pain elicited during this maneuver could be caused by tension in the remaining fibers of the distal tibiofibular complex. I have not found the squeeze test to be a reliable indicator of syndesmosis injury. When the injury is isolated to the syndesmosis, one expects the anterior drawer and talar tilt test to be negative. These tests should be performed routinely. The external rotation test is the most reliable test for syndesmosis injury, with a high interrater correlation (Fig. 13-11).96 The test is performed by stabilizing the leg with the knee flexed at 90 degrees while externally rotating the foot. Pain is produced at the syndesmosis when it is injured. The tibiofibular shuck test or Cotton test is another adjunctive test to detect instability in the distal tibiofibular articulation.97-99 The distal leg is steadied with one hand while the plantar heel is grasped with the opposite hand and the heel is moved side to side. Excessive movement when compared with the opposite ankle suggests an unstable mortise. A medial or lateral malleolus fracture should be ruled out before performing this test.
Clinical diagnosis Patients with acute syndesmosis injuries generally have anterolateral ankle pain directly over the anterior syndesmosis. The pain and swelling may be more precisely localized than in patients with the traditional lateral ankle sprain, but this is not always the case, particularly after the first 24 hours. Uys and Rijke94 studied the clinical association between acute lateral ankle sprain and syndesmotic ligament involvement and found that severe syndesmosis injuries were not associated with tears of the lateral ankle ligaments. Although one would expect minimal tenderness over the ATFL or CFL in syndesmosis injuries, this often is not the case, and the physical examination is notoriously unreliable in ankle sprain injuries. When the mechanism of injury is
Radiographic diagnosis Routine radiography is the next step in the evaluation of a patient with a suspected syndesmosis sprain. Careful evaluation of the distal tibiofibular relationship with regard to the medial clear space, the tibiofibular clear space, and the tibiofibular overlap is crucial (Fig. 13-16). An increase in the medial clear space is defined as a widening in the space between the medial malleolus and the medial border of the talus, normally no more than 2 to 4 mm.100 The tibiofibular clear space at the incisura fibularis tibiae and the absolute amount and percentage of overlap of the tibia and fibula at the incisura are other radiographic landmarks. A radiograph of the uninjured ankle can be used to clarify the relationship between the uninjured distal tibia and fibula. Criteria for the diagnosis 287
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posterior surface of the tibia to the posterior aspect of the distal part of the fibula. It covers the back of the tibiotalar joint. The deep portion of the PITFL is called the transverse tibiofibular ligament. It lies anterior to the superficial component of the PITFL and forms the most distal aspect of the tibiotalar articulation. It functions as a virtual labrum and deepens the tibiotalar articulation. The combination of strength and elasticity makes the PITFL the last syndesmotic structure to tear.20 The interosseous ligament interconnects the tibia and fibula from 0.5 to 2 cm above the plafond. It surrounds the synovial recess that extends up approximately 1 cm from the tibiotalar joint. Although it is the shortest structure interconnecting the distal tibia and fibula, it is considered the primary bond between these two bones at the ankle.58,88,89 At the superior margin, the interosseous ligament blends with the interosseous membrane. The membrane itself adds very little additional strength to the stabilizing effect of the syndesmotic ligaments. In the normal relationship between the tibia and fibula, there is motion in the frontal, transverse, and sagittal planes.90 An increase in the intramalleolar distance of about 1.5 mm takes place from full plantarflexion to full dorsiflexion. Rotation of the ankle also is possible through the syndesmosis. A rotation of the tibia on the talus of 5 to 6 degrees occurs during dorsiflexion and normal walking.58 In addition, the fibula migrates distally an average of 2.4 mm during the stance phase of gait.91
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
A B C D 1 cm 1 cm E F
A. B. C. D. E. F. CD. BC. EF.
Lateral border of fibula Lateral border of anterior tibial prominence Medial border of fibula Lateral border of posterior tibial malleolus Medial border of talus Lateral border of medial malleolus Tibiofibular clear space Tibiofibular overlap Medial clear space
Figure 13-16 Landmarks for radiologic diagnosis of syndesmosis injury.
of diastasis are (1) medial clear space widening, (2) increased tibiofibular clear space, and (3) less tibiofibular overlap. However, the absence of radiographic findings does not completely rule out the possibility of a significant sprain. Stress radiographs with application of an external rotation and abduction force can expose an occult diastasis (Fig. 13-17). Some clinicians advocate the use of stress radiography as standard practice in the diagnosis of syndesmosis injury.101 Other clinicians question its role.102,103 Bone scan, CT, and MRI are other radiographic modalities used in the diagnosis of syndesmosis injury. Bone scan can be a particularly useful diagnostic tool in evaluating a patient with chronic pain after a lateral ankle sprain.90 CT is excellent for showing bony detail of the tibiofibular syndesmosis and can be more precise in evaluating the presence of a diastasis. In one study, CT was able to detect 2- and 3-mm diastases that were not otherwise apparent on routine radiographs.104 MRI allows an accurate picture of ligamentous anatomy and the distal tibiofibular joint. MRI has become the preferred diagnostic study when syndesmosis injury is suspected in professional and collegiate athletes in the United States. The criteria for making an MRI diagnosis of a syndesmosis injury are (1) ligament
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288
Figure 13-17 External rotation and abduction stress x-ray to expose a latent diastasis.
discontinuity, (2) wavy or curved ligament contour, and (3) nonvisualization of the ligament (Fig. 13-18, A and B). Using these criteria, Oae et al.105 found a sensitivity of 100%, a specificity of 93%, and an accuracy of 97% in diagnosing a syndesmosis injury.
Treatment The treatment of syndesmosis injuries discussed here will focus on those cases in which etiology is traumatic. In the acute injury, initial management includes rest, ice, compression, and elevation (RICE). The affected extremity should be immobilized, the patient should remain nonweight bearing, and the appropriate diagnostic tests ordered. Sprains without diastasis can be treated nonsurgically. Patients may bear weight as tolerated in a walking boot or brace. Crutches are used if pain prevents weight bearing. Physical therapy can start when pain subsides and weight bearing becomes easier. These injuries take longer than most sprains to return to normal activity. One study showed that although 86% of patients reported good to excellent ankle function, stiffness and activity-related pain were persistent.106 Patients with latent diastasis can be treated conservatively once a congruent distal tibiofibular joint is confirmed after reduction. After confirmation of the anatomical reduction by CT or MRI, the patient is immobilized in a non-weight-bearing cast or cast boot. Weight-bearing radiographs should be done at 2 to 3 weeks postinjury to confirm anatomic reduction. Gradual weight bearing can be allowed at 4 weeks, with full weight bearing by
Syndesmosis injury
Figure 13-18 Magnetic resonance image of syndesmosis injury with tear of anterior inferior tibiofibular ligament, interosseous ligament, and avulsion of posterior inferior tibiofibular ligament. (A) Axial section. (B) Coronal section.
through small percutaneous incisions to reduce the diastasis. Be certain to correct the malrotation during the reduction (usually by internal rotation pressure). 6. If this reduction is confirmed to be anatomic by fluoroscopic imaging, then the AITFL is repaired. 7. If reduction is difficult or impossible, a medial incision is made to confirm that there is no debris or infolded ligament blocking the reduction. The deltoid ligament is repaired with sutures or by using a suture anchor. The anatomic reduction is confirmed before continuing with the syndesmosis repair. 8. Fix the anatomically reduced fibula with a transsyndesmotic screw. a. Direct the drill slightly anterior, starting at the posterolateral fibula, 2 to 3 cm above the plafond. b. Four cortices are penetrated, and two 4.5-mm, fully threaded cortical screws are placed. Placing the screws across a four-hole plate provides some additional stability and protection to the 289
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8 weeks postinjury. In some situations, such as the elite athlete, latent diastases may do better with surgical treatment. On the other hand, frank diastasis always requires surgical management, unless there are overriding medical contraindications. Any lateral displacement of the mortise and fibula requires internal fixation. My preferred technique for acute syndesmosis injuries with diastasis and without fracture is as follows:90 1. Make a 4- to 6-cm anterolateral incision centered over the ankle joint. 2. Curve the incision slightly posterior at its distal arm, beginning at the level of the plafond, to expose the AITFL insertion on the fibula. 3. Expose and avoid the superficial peroneal nerve by using blunt dissection through the subcutaneous layers. Be certain to warn the patient preoperatively about the probability of at least temporary numbness on the dorsal foot following the operation. 4. Identify the remnant of the AITFL. 5. A large bone-reduction forceps clamped to the medial malleolus and the fibula can be used
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Ankle sprains, ankle instability, and syndesmosis injuries
fibula when the syndesmosis screws are removed. A screw across four cortices allows better purchase and provides a portion to retrieve if the screw breaks. Although this is my preference, there is no current scientific evidence to suggest that the use of one or two syndesmosis screws, the use of a plate, or the penetration of three or four cortices results in any difference in outcome. 9. Suture the subcutaneous tissues and skin and place in well-padded posterior and U-shaped splint or a walking boot. At the conclusion of the procedure, the tibiofibular joint should be anatomically reduced and rigidly fixed, and the medial clear space should be reestablished to the normal range. The surgeon must pay attention to correcting rotational deformity and use anatomic landmarks, fluoroscopy, and/or routine and comparison radiographs for intraoperative confirmation of the reduction. Postoperatively, the patient should remain nonweight bearing for 6 weeks. At the end of 6 weeks, partial weight bearing is started and progressed to full weight bearing in a cast boot by 12 weeks. At 12 weeks, the transsyndesmotic screw can be removed percutaneously in the operating room. If the patient weighs more than 220 lb, the screw may be left in longer, at the surgeon’s discretion. Full activity should be reached by 6 to 8 months. Subacute and chronic syndesmosis injuries require meticulous attention. A subacute injury (3 weeks to 3 months) usually is the result of a missed injury and is not as uncommon as it would seem, because the most difficult part of the treatment is actually making the diagnosis. Treatment is the same for this as it is for acute injuries. Autologous or allogeneic tissue may be needed to substitute for an inadequate AITFL remnant. If this fails, an iatrogenic synostosis can be created for stability. Chronic syndesmosis injuries (>3 months) are treated with the same treatment goals in mind as those for acute and subacute injuries. The difference is the presence or absence of degenerative changes in the tibiotalar joint. With degenerative changes, the outcome already may be determined, and the reliability of reconstruction is decreased. With no articular changes, syndesmosis reconstruction can proceed. A synostosis may occur with reconstruction of chronic injuries and should not be considered a poor outcome. Patients often can return to a high level of athletic performance even with a synostosis.7
REFERENCES 1. Kannus P, Renstrom P: Current concepts review: treatment for acute tears of the lateral ligaments of the ankle—operation, cast, or early controlled mobilization, J Bone Joint Surg 73A:305, 1991.
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2. Kerkhoffs GM, et al: Surgical versus conservative treatment for acute injuries of the lateral ligament complex of the ankle in adults, Cochrane Database Syst 3:CD000380, Rev 2002. 3. DiGiovanni BF, et al: Associated injuries found in chronic lateral ankle instability, Foot Ankle Int 21:809, 2000. 4. Brostrom L: Sprained ankles. V. Treatment and prognosis in recent ligament ruptures, Acta Chir Scand 132:537, 1966. 5. Taga I, et al: Articular cartilage lesions in ankles with lateral ligament injury. An arthroscopic study, Am J Sports Med 21:120, 1993. 6. Komenda GA, Ferkel RD: Arthroscopic findings associated with the unstable ankle, Foot Ankle Int 20:708, 1999. 7. Ogilvie-Harris DJ, Gilbart MK, Chorney K: Chronic pain following ankle sprains in athletes: the role of arthroscopic surgery, Arthroscopy 13:564, 1997. 8. Kibler WB: Arthroscopic findings in ankle ligament reconstruction, Clin Sports Med 15:799, 1996. 9. Hintermann B, Boss A, Schafer D: Arthroscopic findings in patients with chronic ankle instability, Am J Sports Med 30:402, 2002. 10. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby. 11. Brostrom L: Sprained ankles. V. Surgical treatment of ‘‘chronic’’ ligament ruptures, Acta Chir Scand 132:551, 1966. 12. Bahr R, et al: Biomechanics of ankle ligament reconstruction. An in vitro comparison of the Brostrom repair, Watson-Jones reconstruction, and a new anatomic reconstruction technique, Am J Sports Med 25:424, 1997. 13. Hennrikus WL, et al: Outcomes of the Chrisman-Snook and the modified Brostrom procedures for chronic lateral ankle instability. A prospective, randomized comparison, Am J Sports Med 400, 1996. 14. Rosenbaum D, et al: Functional evaluation of the 10-year outcome after modified Evans repair for chronic ankle instability, Foot Ankle Int 18:765, 1997. 15. Rosenbaum D, et al: Tenodeses destroy the kinematic coupling of the ankle joint complex. A three-dimensional in vitro analysis of joint movement, J Bone Joint Surg 80B:162, 1998. 16. Schmidt R, et al: Reconstruction of the lateral ligaments: do the anatomical procedures restore physiologic ankle kinematics? Foot Ankle Int 25:31, 2004. 17. Karlsson J, et al: Surgical treatment of chronic lateral instability of the ankle joint. A new procedure, Am J Sports Med 17:268, 1989. 18. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby. 19. Gould N, Seligson D, Gassman J: Early and late repair of lateral ligament of the ankle, Foot Ankle Int 1:84, 1980. 20. Kelikian H, Kelikian A: Disorders of the ankle, Philadelphia, 1985, WB Saunders. 21. Brunner R, Gaechter A: Repair of fibular ligaments. Comparison of reconstructive techniques using plantaris and peroneal tendons, Foot Ankle Int 11:359, 1991. 22. Schon LC, Hansen ST Jr: Anatomic reconstruction of the lateral ligaments of the ankle using the plantaris tendon: the modified Kelikian procedure. American Academy of Orthopaedic Surgeons Comprehensive Foot and Ankle Course, Chicago, November, 1998. 23. Colville MR, Grondel RJ: Anatomic reconstruction of the lateral ankle ligaments using a split peroneus brevis tendon graft, Am J Sports Med 23:210, 1995. 24. Clanton TO, Schon LC: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 6, St Louis, 1993, Mosby. 25. Coughlin MJ, Matt V, Schenck RC Jr: Augmented lateral ankle reconstruction using a free gracilis graft, Orthopaedics 25:31, 2002.
References 50. Hintermann B, et al: Medial ankle instability: an exploratory, prospective study of fifty-two cases, Am J Sports Med 32:183, 2004. 51. Milner CE, Soames RW: The medial collateral ligaments of the human ankle joint: anatomical variations, Foot Ankle Int 19:289, 1998. 52. Sarafian SK: Anatomy of the foot and ankle, ed 2, Philadelphia, 1993, Lippincott. 53. Siegler S, Block J, Schneck CD: The mechanical characteristics of the collateral ligaments of the human ankle joint, Foot Ankle Int 8:234, 1988. 54. Pankovich AM, Shivaram MS: Anatomic basis of variability in injuries of the medial malleolus and the deltoid ligament. I. Anatomical studies, Acta Orthop Scand 50:217, 1979. 55. Harper MC: Deltoid ligament: an anatomical evaluation of function, Foot Ankle Int 8:19, 1987. 56. Rasmussen O, Kromann-Anderson C, Boe S: Deltoid ligament. Functional analysis of the medial collateral ligamentous apparatus of the ankle joint, Acta Orthop Scand 54:36, 1983. 57. Harper MC: An anatomic study of the short oblique fracture of the distal fibula and ankle stability, Foot Ankle Int 4:23, 1983. 58. Close JR: Some applications of the functional anatomy of the ankle joint, J Bone Joint Surg 38A:761, 1956. 59. Clarke HJ, et al: Tibio-talar stability in bimalleolar ankle fractures: a dynamic in vitro contact area study, Foot Ankle Int 11:222, 1991. 60. Earll M, et al: Contribution of the deltoid ligament to ankle joint contact characteristics: a cadaver study, Foot Ankle Int 17:317, 1996. 61. Michelson JD, et al: Kinematic behavior of the ankle following malleolar fracture repair in a high-fidelity cadaver model, J Bone Joint Surg 84A:2029, 2002. 62. Sasse M, Nigg BM, Stefanyshyn DJ: Tibiotalar motion—effect of fibular displacement and deltoid ligament transection: in vitro study, Foot Ankle Int 20:733, 1999. 63. Lauge-Hansen N: ‘‘Ligamentous’’ ankle fractures: diagnosis and treatment, Acta Chir Scand 97:544, 1949. 64. Rasmussen O: Stability of the ankle joint: analysis of the function and the traumatology of the ankle ligaments, Acta Orthop Scand Suppl 211:1, 1985. 65. Attarian DE, et al: Biomechanical characteristics of human ankle ligaments, Foot Ankle Int 6:54, 1985. 66. Beumer A, et al: A biomechanical evaluation of the tibiofibular and tibiotalar ligaments of the ankle, Foot Ankle Int 24:426, 2003. 67. Garrick JM: The frequency of injury, mechanism of injury, and epidemiology of ankle sprains, Am J Sports Med 5:241, 1977. 68. Leith JM, et al: Valgus stress radiography in normal ankles, Foot Ankle Int 18:654, 1997. 69. Schneck CD, et al: MR imaging of the most commonly injured ankle ligament. Part II. Ligament injuries, Radiology 184:507, 1992. 70. Schneck CD, et al: MR imaging of the most commonly injured ankle ligament. Part I. Normal anatomy, Radiology 184:499, 1992. 71. Klein MA: MR imaging of the ankle: normal and abnormal findings in the medial collateral ligament, Am J Roentgenol 162:377, 1994. 72. Baird RA, Jackson ST: Fractures of the distal part of the fibula with associated disruption of the deltoid ligament. Treatment without repair of the deltoid ligament, J Bone Joint Surg 69A:1346, 1987. 73. Geissler W, Tsao A, Hughes J: Fractures and injuries of the ankle. In Fractures in adults, Philadelphia, 1996, Lippincott-Raven. 74. Hahn D, Colton C: Malleolar fractures. In AO principles of fracture management, Stuttgart, 2000, AO Publishing.
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26. Jeys LM, Harris NJ: Ankle stabilization with hamstring autograft: a new technique using interference screws, Foot Ankle Int 24:677, 2003. 27. Coughlin MJ, et al: Comprehensive reconstruction of the lateral ankle for chronic instability using a free gracilis graft, Foot Ankle Int 25:231, 2004. 28. Horibe S, et al: Reconstruction of lateral ligaments of the ankle with allogeneic tendon grafts, J Bone Joint Surg 73A:802, 1991. 29. Sugimoto K, et al: Reconstruction of the lateral ankle ligaments with bone-patellar tendon graft in patients with chronic ankle instability: a preliminary report, Am J Sports Med 30:340, 2002. 30. Karlsson J, et al: Reconstruction of the lateral ligaments of the ankle for chronic lateral instability, J Bone Joint Surg 70A:581, 1988. 31. Javors JR, Violet JT: Correction of chronic lateral ligament instability of the ankle by use of the Brostrom procedure. A report of 15 cases, Clin Orthop 198:201, 1985. 32. Ahlgren O, Larsson S: Reconstruction for lateral ligament injuries of the ankle, J Bone Joint Surg 71B:300, 1989. 33. Liu SH, Jacobson KE: A new operation for chronic lateral ankle instability, J Bone Joint Surg 77B:55, 1995. 34. Golz RJ, et al: Reconstruction of the lateral ankle ligaments for chronic instability, Orthop Trans 16:341, 1992. 35. Gould N, Seligson D, Gassman J: Early and late repair of lateral ligament of the ankle, Foot Ankle Int 1:84, 1980. 36. Sjolin SU, Dons-Jensen H, Simonsen O: Reinforced anatomical reconstruction of the anterior talofibular ligament in chronic anterolateral instability using a periosteal flap, Foot Ankle Int 12:15, 1991. 37. Hamilton WG, Thompson FM, Snow SW: The modified Brostrom procedure for lateral ankle instability, Foot Ankle Int 14:1, 1993. 38. Liu SH, Baker CL: Comparison of lateral ankle ligamentous reconstruction procedures, Am J Sports Med 22:313, 1994. 39. Krips R, et al: Long-term outcome of anatomical reconstruction versus tenodesis for the treatment of chronic anterolateral instability of the ankle joint: a multicenter study, Foot Ankle Int 22:415, 2001. 40. Krips R, et al: Anatomical reconstruction and Evans tenodesis of the lateral ligaments of the ankle: clinical and radiological findings after follow-up for 15 to 30 years, J Bone Joint Surg 84B:232, 2002. 41. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby. 42. Sammarco VJ: Complications of lateral ankle ligament reconstruction, Clin Orthop 391:123, 2001. 43. Leach RE, et al: Secondary reconstruction of the lateral ligaments of the ankle, Clin Orthop 160:201, 1981. 44. Moller-Larsen F, et al: Comparison of three different treatments for ruptured lateral ankle ligaments, Acta Orthop Scand 59:564, 1988. 45. Aydogan U, Glisson RR, Nunley JA II: Biomechanical comparison of the Brostrom and the Gould modified Brostrom repair utilizing inferior extensor retinaculum. Presented at AAOS Annual Meeting, AOFAS Specialty Day, March 13, 2004. 46. Brostrom L: Sprained ankles. I. Anatomic lesions in recent sprains, Acta Chir Scand 128:483, 1964. 47. Brostrom L: Sprained ankles: III-Clinical observations in recent ligament ruptures, Acta Chir Scand 130:560, 1965. 48. Brostro¨m L: Sprained ankles: V-Treatment and prognosis in recent ligament ruptures, Acta Chir Scand 132:537, 1966. 49. Hintermann B, Boss A, Schafer D: Arthroscopic findings in patients with chronic ankle instability, Am J Sports Med 30:402, 2002.
CHAPTER 13
Ankle sprains, ankle instability, and syndesmosis injuries
75. Harper MC: The deltoid ligament: an evaluation of need for surgical repair, Clin Orthop 226:156, 1988. 76. Stromsoe K, et al: The repair of a ruptured deltoid ligament is not necessary in ankle fractures, J Bone Joint Surg 77B:920, 1995. 77. Zeegers AV, van der Werken C: Rupture of the deltoid ligament in ankle fractures: should it be repaired? Injury 20:39, 1989. 78. Bonnin JG: Injury to the ligaments of the ankle, J Bone Joint Surg 47A:609, 1965. 79. Glick JM: Traumatic injuries to the soft tissues of the foot and ankle. In Du Vries’ surgery of the foot, St Louis, 1978, Mosby. 80. Clanton TO, Porter DA: Primary care of foot and ankle injuries in the athlete, Clin Sports Med 16:435, 1997. 81. Jackson R, Wills RE, Jackson R: Rupture of the deltoid ligament without involvement of the lateral ligament, Am J Sports Med 16:541, 1988. 82. Leach RE, Schepsis AA: Acute injuries to ligaments of the ankle. In Surgery of the musculoskeletal system, New York, 1990, Churchill Livingstone. 83. Berg EE: Recurrent medial ankle instability: the result of distal fibular growth arrest, Foot Ankle Int 15:218, 1994. 84. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby. 85. Wiltberger BR, Mallory TM: A new method for the reconstruction of the deltoid ligament of the ankle, Orthop Rev 1:37, 1972. 86. Boyer MI, Bowen V, Weiler P: Reconstruction of a severe grinding injury to the medial malleolus and the deltoid ligament of the ankle using a free plantaris tendon graft and vascularized gracilis free muscle transfer: case report, J Trauma 36:454, 1994. 87. Hocker K, Pachucki A: The fibular incisure of the tibia: the cross-sectional position of the fibula in the distal syndesmosis, Unfallchirurg 92:401, 1989. 88. McCullough CJ, Burge PD: Rotatory stability of the loadbearing ankle: an experimental study, J Bone Joint Surg 62A:460, 1980. 89. Outland T: Sprains and separations of the inferior tibiofibular joint without important fracture, Am J Surg 59:320, 1943. 90. Clanton TO, Paul P: Syndesmosis injuries in athletes, Foot Ankle Clin North Am 7:529, 2002.
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91. Scranton PE, McMaster JH, Kelly E: Dynamic fibular function, Clin Orthop 118:76, 1976. 92. Fritschy D: An unusual ankle injury in top skiers, Am J Sports Med 17:282, 1989. 93. Hopkinson WJ, et al: Syndesmosis sprains of the ankle, Foot Ankle Int 10:325, 1990. 94. Uys HD, Rijke AM: Clinical association of acute lateral ankle sprain with syndesmotic involvement. A stress radiography and magnetic resonance imaging study, Am J Sports Med 30:816, 2002. 95. Teitz CC, Harrington RM: A biomechanical analysis of the squeeze test for sprains of the syndesmotic ligaments of the ankle, Foot Ankle Int 19:489, 1998. 96. Alonso A, Khoury L, Adams R: Clinical tests for ankle syndesmosis injury: reliability and prediction of return to function, J Orthop Sports Phys Ther 27:276, 1998. 97. Bassewitz HL, Shapiro MS: Persistent pain after ankle sprain: targeting the causes, Physician Sportsmed 25:58, 1997. 98. Cotton FJ: Fractures and joint dislocations, Philadelphia, 1910, Saunders. 99. Takao M, et al: Arthroscopic diagnosis of tibiofibular syndesmosis disruption, Arthroscopy 17:836, 2001. 100. Shereff MJ: Radiographic analysis of the foot and ankle. In Disorders of the foot and ankle, Philadelphia, 1991, Saunders. 101. Boytim MJ, Fischer DA, Neumann L: Syndesmotic ankle sprains, Am J Sports Med 19:294, 1991. 102. Xenos JS, et al: The tibiofibular syndesmosis: evaluation of the ligamentous structures, methods of fixation, and radiographic assessment, J Bone Joint Surg 77A:847, 1995. 103. Ogilvie-Harris DJ, Reed SC: Disruption of the ankle syndesmosis: diagnosis and treatment by arthroscopic surgery, Arthroscopy 10:561, 1994. 104. Ebraheim NA, et al: Radiographic and CT analysis of the tibiofibular diastasis: a cadaver study, Foot Ankle Int 18:693, 1997. 105. Oae K, et al: Injury of the tibiofibular syndesmosis: value of MR imaging for diagnosis, Radiology 227:155, 2003. 106. Taylor DC, Englehardt DL, Bassett FH: Syndesmosis sprains of the ankle and the influence of heterotopic ossification, Am J Sports Med 20:146, 1992.
.........................................C H A P T E R 1 4 Osteochondral lesions of the talus and occult fractures of the foot and ankle Michael Bowman CHAPTER CONTENTS ...................... Occult fractures of the hindfoot
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Occult fractures of the talus
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Talonavicular avulsion injuries
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Osteochondral lesions of the talus
317
Cuboid fractures
303
References
336
Fractures of the anterolateral process of the calcaneus
305
OCCULT FRACTURES OF THE HINDFOOT Occult fractures of the hindfoot represent a common source of prolonged pain and disability after athletic injuries. Increased knowledge about the existence and mechanisms of such injuries and a healthy suspicion about ‘‘soft-tissue injuries’’ that do not get better allow the health care provider to make a prompt diagnosis of occult foot and ankle fractures. Through history, physical examination, and proper use of diagnostic tests one can confirm the diagnosis and select the proper treatment.
Pertinent anatomy With 28 bones, multiple joints, and connecting ligaments, the foot and ankle are vulnerable to compression and avulsion injuries with many complex movements during competitive sports. The bones comprising the hindfoot are the tibia, fibula, talus, calcaneus, navicular, and cuboid. The talus is especially prone to injury because it is involved in both dorsiflexion/plantarflexion and inversion/eversion motions. The talus is connected at the ankle joint to the tibia medially through the deltoid ligament (Fig. 14-1, A) and to the fibula laterally through the anterior talofibular ligament and posterior talofibular ligament (Fig. 14-1, B). The talus is connected to the calcaneus by the talocalcaneal interosseous ligament and the cervical ligament (Fig. 14-2, A). Thedorsal (see Fig. 14-2, A) and plantar (Fig. 14-2, B) talonavicular ligaments connect the talus and navicular. The talus is unique in that it has no direct muscular attachments. Approximately 60% to 70% of the talar
surface is articular1,2 with the ankle joint superiorly, the talonavicular joint anteriorly, and the subtalar joint inferiorly. Blood supply to the talus therefore is limited,1,3 coming from its ligamentous attachments and a leash of vessels surrounding the talar neck that receive contributions from the artery to the tarsal canal medially, the dorsalis pedis artery anteriorly, and the artery to the sinus tarsi laterally (Fig. 14-3, A through C). The internal vasculature of the talus varies considerably4 (Fig. 14-4). External athletic injuries to the talus that involve disruption of the vascular leash or the ligamentous attachments often produce vascular insult to the talar body or talar neck and may produce talar fractures or compression injuries that heal slowly or do not heal. The lateral process of the talus is a wide, triangularshaped process that slopes down to meet the lateral calcaneus (see Fig. 14-5, A). On the lateral view it is wedge-shaped and articulates superiorly with the fibular surface and inferiorly with the calcaneus (see Fig. 14-5, A). The lateral talocalcaneal ligament attaches to the lateral process (Fig. 14-5, B). The posterior process of the talus originates from the convex-curved posterior half of the talar dome and slopes down and back to form the posterior talar ‘‘beak.’’ Inferiorly, it is concave and articulates with the posterior subtalar facet of the calcaneus. The posterior process has both a posteromedial tubercle and posterolateral tubercle. In between lies the flexor hallucis longus, which is commonly involved in posterior talar injuries (Fig. 14-6). This posterior process is widely variable in shape, from a short, rounded end to a long ‘‘beak’’ that is prone to injury.
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Fibula
Deltoid ligament
Ant. talofibular ligament
Post. talofibular ligament
Talus
Calcaneus Calcaneofibular ligament
B
A
Figure 14-1 Hindfoot anatomy of the ankle. Note the (A) medial attachment of the talus the tibia with the deltoid and (B) laterally to the fibula with the anterior and posterior talofibular ligaments.
Cuboid Navicular
Dorsal talonavicular ligament Interosseous talocalcaneal ligament
Plantar calcaneonavicular “spring” ligament
Talus
Plantar talonavicular ligament
Calcaneus
Calcaneus
Cervical ligament
A
B
Figure 14-2 Hindfoot anatomy of the subtalar joint. Note the attachment of the talus to the calcaneus via the (A) talocalcaneal and cervical ligaments and the talus to the navicular via the (A) dorsal and (B) plantar talonavicular ligaments.
The posterolateral tubercle (Stieda’s process) is larger than the posteromedial tubercle. In approximately 7% to 10% of humans a separate os trigonum may exist— connected to the posterolateral tubercle by a fibrous cartilaginous synchondrosis (Fig. 14-7, A and B). The
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posterior talofibular ligament attaches the fibula to the posterolateral tubercle or the os trigonum (see Fig. 14-7, B). The posterior deltoid or posterior talotibial ligament attaches the posterior tibia to the posteromedial tubercle of the talus. The Y-shaped transverse or bifurcate ligament
Occult fractures of the hindfoot
Dorsalis pedis artery branches
Artery to the sinus tarsi Dorsalis pedis artery Peroneal artery
Artery to the tarsal canal
Artery to the sinus tarsi branches
A
Post. tibial artery
Figure 14-4
Artery to the tarsal canal
Internal vasculature anatomy of the talus.
Dorsalis pedis artery
Artery to the sinus tarsi
Lateral talar process
Peroneal artery
A B Ant. talofibular ligament
Dorsalis pedis artery Post. tibial artery
Calcaneofibular ligment Peroneal artery
Talocalcaneal ligament Artery to the sinus tarsi
Figure 14-3 Vasculature supply anatomy for the talus. Note contributions from the (A-C) dorsal pedis artery, (A-C) peroneal (artery to the sinus tarsi), (A) artery to the tarsal canal, and (A and C) posterior tibial artery.
B Figure 14-5 Anatomy of the talus. Note the (A) predominance of articular surface and (B) laterally the attachment of the talocalcaneal ligament to the lateral process.
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C
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
FHL Post. inferior tibiofibular ligament
Transverse ligament
Posterolateral tubercle
Posteromedial tubercle
Post. deltoid ligament Post. talofibular ligament
Posteromedial tubercle
Posterolateral tubercle FHL
Figure 14-6 Posterior anatomy of the talus. Note the (A) posterior process of the talus, the (B) flexor hallucis longus between the two tubercles of the posterior talus, and (C) the posterior ligamentous anatomy.
Synchondrosis
Flexor hallucis longus Os trigonum
A
B
Os trigonum
Figure 14-7 (A) Lateral view. Anatomy of the os trigonum. Note that the os trigonum is the posterior process that is attached to the talus via a synchondrosis and (B) is attached to the posterior talofibular ligament (axial view).
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Occult fractures of the hindfoot
Fibula Talus
Calcaneofibular ligament
Calcaneus
is a thickening in the posterior ankle capsule that holds the two tubercles together and restrains the flexor hallucis longus. A meniscus-like ‘‘marsupial meniscus’’ also often exists in the posterior ankle superior to the posterior process of the talus (Fig. 14-8). The calcaneus is a complex, bony structure providing attachment for the Achilles posteriorly and the plantar fascia and plantar intrinsic muscles of the foot inferiorly. It articulates with the talus superiorly, as well as with the cuboid and navicular anteriorly. The anterolateral process of the calcaneus extends forward to form the calcaneocuboid joint. The saddle-shaped anterior surface articulates with the cuboid anteriorly, and the superior tip articulates to a varying degree with the lateral navicular. The extensor digitorum brevis also originates from this calcaneal process. The blood supply to the calcaneus is quite robust, and fractures of the calcaneus tend to heal more easily. The ligamentous attachments at the calcaneus are the talocalcaneal interosseous ligament, lateral talocalcaneal ligament and cervical ligament to the talus and the calcaneofibular ligament laterally (Fig. 14-9). The posterior, lateral, and anterior calcaneocuboid ligaments and the plantar calcaneonavicular (spring ligament) and lateral calcaneonavicular ligaments connect the calcaneus anteriorly to the cuboid and navicular, respectively. The strong plantar calcaneonavicular or ‘‘spring’’ ligaments acts as a ‘‘sling’’ to hold the talar head in place. The bifurcate ligament (Y-ligament) is composed of the anterior and lateral calcaneocuboid ligament (Fig. 14-10, A and B) and is commonly injured during ‘‘sprain-type’’ inversion injuries, producing an avulsion fracture at the anterolateral process of the calcaneus. Inversion/adduction injuries of the midfoot also may produce avulsion fractures at the base of the cuboid.
Cervical ligament
Figure 14-9 Calcaneal ligaments. Note laterally the calcaneofibular, cervical, and lateral talocalcaneal ligaments.
The saddle-shaped cuboid articulates with the anterior process of the calcaneus and may be involved in either compression or avulsion tension-type injuries. The tarsal navicular is a ‘‘C’’ or saucer-shaped bone articulating with the talus posteriorly and the cuboid laterally. The dorsal talonavicular ligament and capsule may produce avulsion injuries of the navicular from plantarflexion-type injuries. Compression-type injuries also may be produced by the impact of the talar head on the navicular. The blood supply to the midportion of the navicular is poor (Fig. 14-11) and may contribute to delayed healing or nonunion of such fractures. The articulation between the cuboid and the navicular varies from a true articulating joint to a fibrous connection to a bony bridge (tarsal coalition). Various important and powerful tendons attach to the hindfoot; these produce considerable forces during athletic activities and can create injuries. The posterior tibial tendon attaches to the navicular (Fig. 14-12, A and B), producing inversion/supination and adduction while elevating the arch. It fires twice during each gait cycle or step—both eccentrically as a shock absorber and concentrically during push-off. The anterior tibial tendon, with attachments to the cuneiform and first metatarsal, is the primary dorsiflexor for the ankle and also inverts the foot. It also fires eccentrically during heel strike to decelerate and cushion the landing foot. The peroneus brevis and longus tendons (Fig. 14-13) both evert the foot and ankle and resist inversion injuries. The peroneus brevis attaches to the base of the fifth metatarsal. The peroneus longus wraps around the cuboid at the trochlea to insert broadly underneath the foot near the base of the first metatarsal, which allows the longus also to help plantarflex and stabilize the medial foot. 297
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Figure 14-8 A meniscus-like ‘‘marsupial meniscus’’ often noted in the posterior ankle superior to the posterior process of the talus.
Interosseous talocalcaneal ligament
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Anterior Fibula Talus
Lateral calcaneonavicular ligament
Navicular
Calcaneus
Medial
Lateral
Anterior calcaneocuboid ligament
Bifurcate ligament
Posterior Cuboid Long calcaneocuboid lig.
A
Lateral calcaneocuboid Deep calcaneocuboid ligament ligament
Calcaneus
Talus Long CC ligament Deep CC ligament
Lateral CC ligament
Spring ligament
Navicular Cuboid
B Figure 14-10 Lateral plantar transverse tarsal ligaments.
TALONAVICULAR AVULSION INJURIES Incidence and mechanism Avulsion fractures involving the tarsal navicular or talar head are not unusual after a plantarflexion injury of the ankle (Fig. 14-14). The dorsal talonavicular capsule or ligament pulls off a small fragment with this injury (see Fig. 14-14). This injury is more
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298
Figure 14-11 Vasculature anatomy of the tarsal navicular. Note the central area of decreased blood supply corresponding to areas of navicular stress fractures.
common than thought, because many occur and are not treated immediately. They are seen in practices such as mine years later, asymptomatic with x-ray findings on films taken for an unrelated injury. Many of these minor fractures heal untreated by either painless bony or fibrous nonunion. However, a painful nonunion also may occur. Bony union of the fracture can result in the athlete’s having pain from a bony prominence over the joint (Fig. 14-15) or painful arthritis of the talonavicular joint. An avulsion fracture from the medial or proximal end of the tarsal navicular at the distal insertion of the posterior tibial tendon is less common in athletics. This injury occurs in running sports in which a sudden change of direction is common. The athlete plants the foot, decelerates, and twists a plantarflexed foot to reaccelerate and push off. The force of the posterior tibial tendon on the navicular may produce an avulsion at its insertion. In cases in which the athlete has a congenital accessory navicular, the injury may occur through the cartilaginous synchondrosis between the main and ‘‘extra’’ (or accessory) bone (Fig. 14-16).
Diagnosis With dorsal navicular avulsion fractures, the athlete complains of anterior ‘‘ankle’’ pain after a sprain-type injury. In acute cases, ecchymosis may exist over the anterior ankle. Point tenderness will be noted over the dorsum of the navicular (Fig. 14-17) or the talar head. Inversion or eversion may produce pain and plantarflexion of the foot. In chronic cases, a firm, bony ‘‘lump’’ (tender or nontender) will be noted over the dorsal navicular or talar head. In medial navicular avulsion injuries, the athlete will have ecchymosis, swelling, and tenderness over the
Talonavicular avulsion injuries
Tibia
Posterior tibial tendon Fibula
Talus
Talus
Navicular
Peroneus brevis tendon
Navicular Calcaneus Cuboid
Calcaneus
5th met.
A
Peroneus longus tendon
Figure 14-13 Anatomy lateral ankle depicting peroneus longus and brevis tendons.
Long plantar ligament
Peroneus longus tendon
Peroneus brevis tendon
B Figure 14-12 Posterior tibial tendon anatomy. Note the attachment to the medial navicular, medial cuneiform, and lateral cuneiform that produces inversion, supination, and adduction.
medial and plantar navicular. Posterior tibial tendon function usually is still intact but may be painful against resistance to plantarflexion and inversion.
Treatment For acute, minimally displaced (less than 1 mm) fractures, boot immobilization for 6 to 8 weeks usually will result in healing, either a bony union or a painless, fibrous nonunion. The unusual large fragment (greater than 5 mm) fracture may require internal fixation if displaced. The athlete is protected in a boot postoperatively, and nonweight bearing for approximately 6 weeks until the fracture is healed. When a painful nonunion develops, an injection of corticosteroid sometimes will relieve the symptoms. 299
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Post. tibial tendon
Imaging X-rays usually will show a wafer-like avulsion fracture on the dorsum of the navicular or talar head (Fig. 14-18). In chronic cases, x-ray may show a rounded-off nonunion of the fragment or a healed, bony, beak-like projection, often with some arthritic changes in the dorsal talonavicular joint (Fig. 14-19). More involved navicular body fractures also occur in the athlete but are not common. These larger body fractures require a computed tomography (CT) scan with axial and lateral views (Figs. 14-20 and 14-21) to assess joint alignment and fracture orientation for surgical decision making. A CT scan also is helpful in chronic cases for assessment of joint irregularities and arthritis and to rule out a navicular stress fracture. In medial navicular avulsion fractures, x-rays will show calcified flecks or fragments on the medial navicular (Fig. 14-22). Additional supination oblique views (Fig. 14-23) sometimes are helpful, especially when an accessory navicular is present. Widening of the synchondrosis may or may not be seen.
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-16 Anterior-posterior radiograph of athlete’s foot depicting painful medial accessory navicular attached by synchondrosis.
Figure 14-14 Fracture of navicular caused by plantarflexion of foot and ankle with avulsion of dorsal fragment.
Figure 14-15 Nonunion of dorsal navicular avulsion fracture. This can cause a dorsal prominence and pain in the athlete.
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Figure 14-17 Clinical examination of athlete’s foot depicting area of pain noted on foot with dorsal avulsion fracture of navicular.
Talonavicular avulsion injuries
Figure 14-20 Computed tomography (coronal view) demonstrating more involved navicular body fracture with comminution.
Figure 14-19 Radiographic findings of chronic, dorsal, navicular nonunion. Note rounded edges and smooth contour in distinction from acute fracture in Fig 14-18.
Figure 14-21 Computed tomography (axial view) demonstrating navicular body fracture with displacement.
Alternative shoe lacing (Fig. 14-24), or a donut-type pad may reduce pressure in the area. If conservative treatment fails, the usual surgical treatment is excision of the fragment through a small dorsal longitudinal incision. Postoperatively the patient is nonweight bearing in a boot for approximately 2 weeks, followed by progressive weight bearing and active range of motion (AROM). In chronic cases in which a bony union has resulted in a painful bony prominence or dorsal talonavicular joint arthritis, conservative treatment is nonsteroidal anti-inflammatory drugs (NSAIDs), alternative shoe lacing or a donut-type pad dorsally, and molded foot orthoses with good arch support. A cortisone injection
also may be helpful. If nonsurgical care is unsuccessful, the prominent and arthritic portion of the talus or navicular may be resected in a V-shaped fashion (Fig. 14-25), leaving healthy joint behind. In severe cases of posttraumatic talonavicular arthritis, fusion may be needed. Treatment of acute medial navicular fractures usually is conservative. Protection in a nonweight-bearing boot for 6 weeks until nontender followed by appropriate therapy for the posterior tibial tendon, usually will produce good results. The avulsion fragments may or may not demonstrate bony union on follow-up x-rays in successful cases. The rare large displaced fragment may require open reduction internal fixation (ORIF) (Fig. 14-26, A and B). The conservative treatment may be tried for nondisplaced 301
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Figure 14-18 Radiographic findings of dorsal, wafer-like fracture with acute injury.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Painful area
Figure 14-22 Anterior-posterior radiograph of foot demonstrating comminute medial navicular avulsion fracture.
Figure 14-24 Lacing pattern on athlete’s shoe to decrease pressure on a painful dorsal prominence of the foot such as a dorsal navicular avulsion nonunion.
Figure 14-25 V-shaped excision of dorsal prominence and portion of joint that has become arthritic.
by protection in a nonweight-bearing boot for 6 weeks, may be needed.
Figure 14-23 Supination oblique (10 to 15 degrees of supination) demonstrating clear view of accessory navicular. This view also can give a clearer view of a navicular stress fracture.
accessory navicular injuries but in my experience is less successful. Excision of the accessory navicular and repair of the posterior tibial tendon to the navicular with bony anchors (Fig. 14-27, A through G, followed
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Rehabilitation and return to sports Postoperative care of the previously described injuries involve nonweight-bearing protection in a boot until the fracture and associated ligament/tendon injury are healed (usually 6 weeks), followed by an ankle rehabilitation program working on edema control, range of motion (ROM), proprioception, and progressive resisted exercises (PREs) (especially the posterior tibial tendon). Running is added first and jumping activities are added next, followed by sports-specific exercises. The athlete may return to practice/play on successful completion of the program (6 to 10 weeks postinjury).
Cuboid fractures
Figure 14-26 Fixation of large accessory navicular with two screws. (A) Anterior-posterior and (B) lateral radiographs depicting placement of screws.
Incidence and mechanism Cuboid fractures are much more rare in an athletic foot and ankle practice but tend to be overlooked and dismissed as a foot sprain. Two basic types are seen as athletic injuries: (1) an avulsion injury, caused by an inversion/adduction injury while landing (basketball, volleyball, and so forth) or rapid direction change (soccer, rugby, football) and (2) a compression injury, caused by forced eversion while plantarflexed or dorsiflexed in a pileup (e.g., football, rugby). In the avulsion cuboid injury, the calcaneocuboid capsule and plantar C-C ligament are torn, producing a usually small avulsion fragment off the plantar posterior cuboid. In the compression injury, the cuboid is crushed between the calcaneus and fifth metatarsal. Diagnosis The athlete will complain of lateral foot pain, swelling, and difficulty walking, especially during push-off. Examination
will show swelling and possible ecchymosis of the lateral foot, just proximal to the insertion of the peroneus brevis. There will be tenderness to palpation over the cuboid and possible pain with manipulation of the calcaneocuboid joint.
Imaging The small avulsion fractures may be seen with careful inspection of lateral or oblique x-rays (Fig. 14-28). Compression injuries of the cuboid often do not show on standard x-rays. Posthealing x-rays may show increased radiodensity (Fig. 14-29). A magnetic resonance imaging (MRI) (Fig. 14-30, A and B) or bone scan (Fig. 14-31) can be used to confirm the fracture. Healing then must be followed by either routine radiographs or CT. Treatment Usually conservative treatment is used to successfully treat both types of cuboid injuries. Avulsion-type cuboid fractures are treated with a protective boot and allowed weight bearing as tolerated (WBAT). Ice and edema control are started immediately. Running and return to sports exercises are initiated 303
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CUBOID FRACTURES
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-27 Radiographs (A and B) of displaced accessory navicular requiring (C-F) excision of fragment, repair of posterior tibial tendon to medial navicular, and (continued on page 305)
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Fractures of the anterolateral process of the calcaneus
Figure 14-27 cont’d. (G) postoperative anterior-posterior radiograph noting excision of accessory bone.
Figure 14-28 Oblique radiograph of foot demonstrating small fracture of cuboid.
when weight bearing is comfortable in a shoe. Usually a painless, fibrous nonunion of the fragment will result. In the rare case of a painful fragment, excision is performed. Compression cuboid injuries also are treated with edema control and WBAT in the boot. When the athlete is pain free, walking in the boot, and nontender to palpation, weight bearing in the shoe and progressive activities are allowed.
FRACTURES OF THE ANTEROLATERAL PROCESS OF THE CALCANEUS
Figure 14-29 Lateral radiograph of foot depicting increased density of cuboid indicating healing of prior occult cuboid fracture.
The second mechanism of injury to the anterolateral process is an eversion abduction injury (Fig. 14-33) that produces a compression-type horizontal fracture through 305
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Incidence and mechanism The anterolateral process fracture represents up to 23% of all calcaneus fractures.5 Two mechanisms of injury to the anterolateral process of the calcaneus have been noted.6,7 An inversion injury to a plantarflexed foot (much like the mechanism for a common ankle sprain) will produce an avulsion fracture of the tip of the anterolateral process through tension on the bifurcate ligament (Fig. 14-32).
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-31 Bone scan of athlete with occult cuboid fracture. Note increased signal center over area of cuboid.
Figure 14-30 (A) Sagittal and (B) axial magnetic resonance imaging (MRI) demonstrating increased bone edema with occult compression fracture of cuboid.
the calcaneus.5,7 Degan et al.7 proposed the following classification for fractures of the anterior lateral process of the calcaneus: type I—nondisplaced tip avulsion, type 2—displaced avulsion fracture not involving the calcaneocuboid joint, and type 3—displaced larger fragments involving the calcaneocuboid joint.
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Figure 14-32 Diagram of right foot demonstrating supination and inversion of hindfoot causing avulsion of anterior process of calcaneus with tension on bifurcate ligament.
Diagnosis Athletes with a fracture of the anterolateral process will complain of lateral ankle and foot pain, increased by weight-bearing activity, push-off, or a change in direction. A history of an ‘‘inversion sprain’’ may be
Fractures of the anterolateral process of the calcaneus
Figure 14-33 Diagram of right foot demonstrating dorsiflexion and compression of calcaneocuboid joint with fracture of anterior process of calcaneus.
Figure 14-35 Clinical photograph of right foot demonstrating assessment of transverse tarsal instability by stressing the hindfoot in (A) supination and (B) pronation.
obtained. Often the diagnosis is delayed, and the athlete will give a history of an ankle sprain treated by the normal rest, ice, compression, and elevation (RICE) mechanism and physical therapy regimen that do not lead to improvement. Initial x-rays may have been taken and interpreted as negative. Examination will show point tenderness over the bifurcate ligament and the anterolateral process of the calcaneus (Fig. 14-34). Lateral ankle instability tests (drawer test, talar tilt test, and flexion rotation drawer test) often are negative. Often pain may be produced
Imaging As stated previously, initial x-rays may be interpreted as negative if the fracture is nondisplaced. However, review of the old x-rays or new anterior-posterior (AP), lateral, and oblique x-rays of the foot may show a displaced fracture through the tip of the anterolateral process of the calcaneus (Fig. 14-36). Alternatively, a large, blunted, irregular and indistinct process may be visualized (Fig. 14-37). In cases in which point tenderness exists over the anterolateral process but x-rays are not conclusive, a CT scan (Fig. 14-38, A through C) often will show the 307
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Figure 14-34 Clinical photograph of right foot demonstrating area of hindfoot that is tender with underlying anterior process fracture of calcaneus.
by inversion stress through the subtalar joint (distracting the fragment). There may be instability of the transverse tarsal joint, which is tested by holding the heel stable with one hand and pronating and supinating the midfoot with the other hand (Fig. 14-35, A and B).
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-36 Lateral radiograph of hindfoot demonstrating small anterior process fracture (arrows) of calcaneus.
Figure 14-37 Lateral radiograph of hindfoot demonstrating healed fracture of anterior lateral process (ALP) of calcaneus.
fracture and help in assessing the amount of healing. The CT also is helpful in surgical planning (ORIF vs. excision). A bone scan is used as a screening tool to distinguish this injury from other soft-tissue types of lateral ankle injuries.
Treatment For acute, nondisplaced fractures (less than 8 weeks) and small fractures less than 2 mm, cast or boot immobilization and nonweight bearing for approximately 6 weeks is used until the fracture is healed. For acute or semiacute fractures that are displaced (more than 5 mm in diameter), either excision or open reduction internal fixation is suggested. If any instability of the transverse tarsal joint exists on testing, the bifurcate ligament may be repaired back to the remaining process of the calcaneus with a suture anchor or with internal fixation of the fragment.
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In cases of chronic nonunion of the anterolateral process of the calcaneus, asymptomatic athletes are treated with observation only. For large fragments greater than 1 cm or involving a significant portion of the articular surface, the fracture site is debrided and internal fixation is applied. For smaller fragments, the fragment is excised. The calcaneocuboid joint is inspected and debrided if necessary. The bifurcate ligament may be repaired back to the calcaneal process if any instability of the transverse tarsal joint exists. For cases of malunited fractures of the anterolateral process of the calcaneus, arthritic changes in the superior portion of the calcaneocuboid joint and/or the junction between the process of the calcaneus and navicular may exist. In these cases, a trial injection of cortisone in the calcaneocuboid joint and calcaneonavicular space may provide relief or help to establish the diagnosis of arthritic changes. A CT scan or MRI with magnified views will help to provide information about the joints. Surgical treatment involves open resection of a portion of the anterolateral process of the calcaneus, trimming it back to a point at which a healthy calcaneocuboid joint is present. Recently, arthroscopic resection through a subtalar approach has been described.8
Rehabilitation and return to sports In cases in which excision is required, boot immobilization and nonweight bearing are used for 2 weeks, followed by gentle AROM of the foot and protected weight bearing in the boot for an additional 4 weeks. General ankle rehabilitation then is begun, followed by sports-specific exercises. Athletes with anterolateral process fractures treated by ORIF or excision and ligament repair are placed in a non-weight-bearing boot for 6 weeks until healed. General ankle rehabilitation followed by sports-specific exercises then is started. Return to sports usually is within 8 to 12 weeks.
OCCULT FRACTURES OF THE TALUS Occult fractures of the talus fall into several categories: posterior process fractures, lateral process fractures, global compression injuries of the talus (GCTs), and osteochondral lesions of the talus (OLTs).
Posterior talus fractures/posterior impingement syndrome (see also Chapter 2)
............................................................. Incidence and mechanism As noted previously, athletes with a long, slender, posterior talar ‘‘beak’’ may be more prone to posterior talar injuries.
Occult fractures of the talus
Figure 14-38 (A) Sagittal reconstruction, (B) coronal, and (C) axial computed tomography view of occult anterior process fracture (arrows) of calcaneus. Plain radiographs did not reveal fracture but athlete had tenderness over anterior process.
applied to the back of a dorsiflexed ankle at the bottom of a scrum or pileup (Fig. 14-40) may produce an avulsion fracture of the posteromedial tubercle by traction on the posterior deltoid ligament (see Fig. 14-39, B).6,11-13 A similar 309
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Two major athletic mechanisms exist that produce posterior process fractures.6,9,10 A forced ankle dorsiflexion and pronation injury such as forced planting of the foot backward with force applied (Fig. 14-39, A) or weight
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Post. deltoid ligament
Posteromedial tubercle of the talus
B Figure 14-39 (A) Lateral view of posterior talus process fracture caused by forced dorsiflexion of the ankle against a planted foot. (B) Posterior view, showing avulsion forces produced by the posterior deltoid ligament on the posterior medial tubercle of the talus.
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Occult fractures of the talus
Tibia
Talus
Figure 14-40 Posterior talus process fracture caused by force on the back of the ankle, causing avulsion of the posterior talar process through tension on the posterior deltoid ligament.
Figure 14-41 Common mechanism for posterior process fracture with compression of posterior process between calcaneus and posterior tibia in severe plantarflexion of ankle.
posterior ankle pain, or pain with push-off, jumping, and landing.
Diagnosis The diagnosis of posterior process fracture often is delayed. In one study, five to eight physician visits were necessary until the diagnosis was made.18 The posterior ‘‘ankle sprain’’ that does not get better should alert the physician to the possible presence of this fracture. The athlete often will give a history of posterior ankle pain worse with planting the foot back (tennis, football, racquetball), jumping and landing (basketball, volleyball), kicking (swimming), or tiptoe position (ballet). They may give a history of an ankle sprain or ‘‘Achilles pain.’’ 311
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forced dorsiflexion/inversion injury also may produce injury to the posterolateral tubercle or os trigonum by traction on the posterior talofibular ligament.2,9,13 Another and more common mechanism for producing posterior talar process fractures/os trigonum injuries is forceful plantarflexion.13-15 Repetitive plantarflexion and push-off activities (ballet, running, soccer), jumping and landing activities (gymnastics, basketball, volleyball, football), or twisting the ankle in a plantarflexion/inversion ‘‘sprain’’ position16,17 force the long talar beak/os trigonum against the posterior tibia and produce a fracture (Fig. 14-41). Injuries to the posterior talus may result in chronic posterior impingement syndrome,6,9 in which athletes complain of
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Examination Ankle ROM may be normal or painful posteriorly with limits at both dorsiflexion (traction) and plantar fraction (compression). Passive subtalar joint motion, producing inversion and eversion with the ankle slightly plantarflexed, also may produce posterior ankle pain because the subtalar joint also may be affected. The ‘‘pinch test’’ posteromedially or posterolaterally just posterior to the ankle (Fig. 14-42) will produce pain. The posterior impingement test (Fig. 14-43, A and B) will produce pain and possibly clicking. Manipulation of the great
Figure 14-42 Clinical demonstration of ‘‘pinch test.’’ Compression of posterior process fracture of talus (os trigonum) in athlete just behind ankle from medial and lateral sides cause pain.
toe, producing stretch on the flexor hallucis longus, also may produce posterior ankle pain. Acutely, there also may be ecchymosis in the posterolateral or posteromedial ankle region.
Imaging AP, lateral, and oblique x-rays may be negative if the fracture is nondisplaced or at a slight angle (Fig. 14-44, A). An os trigonum may appear normal. Repeat x-rays (especially lateral views) later may show the fracture (Fig. 14-44, B). A CT scan or MRI (Fig. 14-44, C) can be the standard for establishing the diagnosis, showing presence of the fracture, location, and size.19 An MRI also will show compression injuries of the posterior talus (Fig. 14-45) that did not exhibit a discreet fracture line, as well as surrounding edema. A bone scan (Fig. 14-46) is useful to confirm a symptomatic os trigonum injury.19-21 An injection of cortisone into the os trigonum synchondrosis may provide temporary relief and help with the diagnosis. Treatment For acute nondisplaced fractures/os trigonum injury, immobilization in a boot/cast and limited weight bearing may lead to healing in 4 to 6 weeks. A repeat CT scan may be needed in subtle fractures to demonstrate healing. For large displaced fractures (especially ones that extend into the weight-bearing talar body region), internal fixation through a posterolateral or posteromedial approach with cannulated 4.5 screws or headless screws is indicated.22-25 The flexor hallucis longus and medial
Figure 14-43 Clinical demonstration of ‘‘posterior compression test.’’ Forced maximal plantarflexion (A and B) of ankle produces pain in athlete with posterior process fracture (os trigonum).
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Occult fractures of the talus
Figure 14-44 Lateral radiograph and magnetic resonance imaging (MRI) ankle demonstrating os trigonum. Lateral x-ray shows (A) intact posterior process but repeat lateral radiograph demonstrated os trigonum with mild displacement. MRI clearly demonstrates the os trigonum as a separate fragment and area of chronic fracture.
Figure 14-46 Lateral bone scan image of ankle demonstrating increased uptake in posterior ankle consistent with posterior ankle impingement and painful os trigonum.
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Figure 14-45 Sagittal magnetic resonance imaging of talus demonstrating occult fracture of posterior facet, which causes posterior ankle pain in athlete and can be similar in presentation to posterior ankle impingement. Note edema in posterior talus and fluid posterior ankle.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
neurovascular bundle must be protected with this approach. The head of the screws should be countersunk. For smaller fractures/symptomatic os trigonum that do not heal or chronic fracture cases, excision of the posterior tubercle (Fig. 14-47, A through D) and debridement of the adjacent ankle and subtalar joint is the method of treatment.16,17 Although Marumoto and Ferkel26 and others5,27 have advocated arthroscopic resection of the os trigonum, most surgeons still prefer resection through a small posteromedial9,28 or posterolateral16 approach for medial process/lateral process fractures, respectively.
Rehabilitation and return to sports Postoperatively, in cases in which internal fixation is required, the athlete is placed in a protective boot,
nonweight bearing for 6 weeks with early AROM out of the boot to prevent stiffness. When the fracture is healed, progressive weight bearing and ankle rehabilitation is begun, followed by sports-specific exercises. ROM and strengthening of the flexor hallucis longus (FHL) is emphasized. After excision of the fracture fragment or os trigonum, the athlete is protected nonweight bearing in a boot for 2 weeks with gentle AROM of the ankle and subtalar joint allowed out of the boot. At 2 weeks, progressive WBAT in the boot is allowed, and the athlete is weaned back into a shoe as tolerated. At 4 to 6 weeks postoperatively (depending on comfort), general ankle rehabilitation is permitted, followed by sports-specific exercises. Athletes may return to sports on successful rehab completion, ranging from 4 to 8 weeks postinjury.
Figure 14-47 Symptomatic os trigonum. (A) Lateral radiograph and (B) sagittal magnetic resonance imaging confirm os trigonum. (C) Clinical appearance of os trigonum removed through lateral incision and (D) lateral radiograph demonstrating excision.
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Occult fractures of the talus
Lateral process fractures of the talus ............................................................. Incidence and mechanism Lateral process fractures of the talus are another commonly missed hindfoot injury in athletes. They represent the second-most common talar body fracture (almost 25%).2,13 It is estimated that they are present in 0.86% of all lateral ankle sprains.28 Although more commonly seen in motor vehicle accidents and high-energy traumatic injuries to the ankle, athletically produced lateral process fractures of the talus have increased to an estimated 2000 per year in the U.S.29 because of the recent popularity of snowboarding. They account for 2.5% of all snowboarding injuries.30 In ‘‘snow boarder’s ankle,’’ dorsiflexion and inversion applied to the ankle and talus are the most accepted mechanism for production of athletic lateral process fractures of the talus.13,28,29,31,32 However, experimental studies suggest that external rotation applied to a dorsiflexed inverted foot (Fig. 14-48) may produce a force to the lateral process and result in a fracture.6,32 Both the body and the snowboard act as a lever arm on the ankle and talus. The leading leg is injured twice as often.29,30 Diagnosis The athlete may give a history of a twisting injury to the ankle and complain of lateral ankle pain increased with weight bearing. Examination Athletes may exhibit ecchymosis on the lateral ankle. Tenderness is present inferior to the lateral malleolus,
and pain may be produced with dorsiflexion and plantarflexion and/or inversion.
X-rays An AP, lateral, and oblique ankle x-rays may show an avulsion-type fragment laterally (Fig. 14-49, A) or be negative if the fracture is nondisplaced (Fig. 14-49, B and C). The mortise view is felt to be best to visualize these fractures.32 A CT scan is the gold standard for identification of lateral talar process fractures, aiding in sizing and surgical planning (Fig. 14-50). MRIs also may show associated talar cartilage and/or bony injuries.33 A bone scan may be useful as a screening tool in cases of chronic lateral pain in which the fracture was undetected. Classification Two commonly used classifications for lateral talus process fracture exist: the Hawkins classification13: type1— simple two-part fracture, type 2—comminuted fracture, and type 3—avulsion fracture of the anterior inferior process and the Funk classification29 (Fig. 14-51): type A—small, minimally displaced, extra-articular avulsion fracture, type B—a medium-sized fracture involving only the talocalcaneal joint surface, and type C—a larger fracture involving both the talocalcaneal and talofibular joint articulations. Treatment For acute, nondisplaced lateral process fractures, immobilization in a boot and nonweight bearing for 4 to 6 weeks is indicated. Repeat CT scan may be necessary
Lateral talar process
Figure 14-48 Diagram noting mechanism for lateral process fractures of talus. Forced external rotation with the ankle in dorsiflexion and inversion results in a lateral process fracture.
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Figure 14-49 (A) Anterior-posterior (AP) radiograph of ankle demonstrating lateral process fracture of talus (arrows) noted just inferior to the tip of fibula. (B) Lateral and AP radiographs of athlete with lateral process fracture not able to be visualized on x-rays.
to document healing. For small, displaced fractures (less than 5 mm) conservative treatment with boot or cast immobilization and nonweight bearing also is indicated. Early excision of displaced small fragments and progressive weight bearing also has been proposed.30 For larger displaced fractures (>1 cm) and/or with joint surface irregularity greater than 2 mm, open reduction internal fixation5,6,13,19,28,30 with headless or countersunk screws through a subfibular approach with sectioning
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of the calcaneofibular ligament for exposure is indicated. Postoperative, nonweight-bearing boot immobilization is used, with immediate, gentle AROM until healing is accomplished. For chronic cases (previously undetected) or cases of nonunion after immobilization, treatment of large fragments (greater than 1 cm) or fragments involving the articular surfaces require debridement and/or internal fixation. Small fragments (less than 1 cm) may be excised.13
Osteochondral lesions of the talus
Figure 14-50 Axial computed tomography scan of talus demonstrating lateral process fracture that was not identified on ankle radiographs in athlete.
Dorsal
Posterior
Type A
Type B
Type C
Figure 14-51 Funk classification for lateral process fracture talus. Type A involves only a small avulsion fragment, type B involves only the talocalcaneal joint, and type C involves both the talocalcaneal and talofibular articulations.
OSTEOCHONDRAL LESIONS OF THE TALUS Intra-articular ankle injuries to the talar body are a common source of athletic disability. Cartilage injuries to the 317
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Posterior
Rehabilitation and return to sports Postinjury, athletes are treated in a nonweight-bearing boot until the fracture is healed. In most cases a repeat CT scan is needed to assess healing. Athletes with intraarticular lateral talus fractures requiring internal fixation are allowed to start gentle AROM exercises of the ankle and subtalar joints during this healing and nonweightbearing phase to maintain joint mobility. When all fractures are healed, progressive weight bearing and ankle rehabilitation are begun, followed by sports-specific exercises and return to sports. In cases involving the subtalar joint, this may be up to 3 months.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
talus may be partial thickness or full thickness, or may involve bone (OLTs).
Mechanism Historically, various origins for OLT have been presented. Ko¨nig34 coined the term ‘‘osteochondritis desiccans’’ to describe loose osteochondral fragments in the knee, and the theory of spontaneous necrosis for these lesions in the knee and ankle was postulated. Various theories concerning vascular insult to the talus have been described.2,27,34-36 The body of the talus has a generally poor blood supply because of its large articular surface, as noted earlier. There also is considerable variation in the intra-articular blood supply of the talar body. Embolic phenomena, sickle cell anemia, and corticosteroid use have been noted as causes for bony infarcts in the talar body.1,36 Inflammatory conditions such as rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, and ankylosing spondylitis, as well as genetic predisposition, parathyroid disease, and osteoarthritis have been associated with OLTs.1,36 However, these cases of nontraumatic talar body osteochondral lesions generally are more diffusely involved than the discrete OLT seen with sports injuries that we will discuss in this chapter. The more well-defined and distinct OLTs seen in the athletic population usually result from an acute traumatic injury or chronic lateral ligament instability of the ankle. Most OLTs are located in the anterolateral (Fig. 14-52, C and D) or posteromedial corner (see Fig. 14-52, C and D). Bruns and Behrens37 postulated that an inversion injury to a plantarflexed foot (Fig. 14-52, A and B), similar to a common ankle sprain, would produce shear forces on the lateral talus and compression forces in the medial talus.13 The posteromedial lesions likely occur with more concomitant ankle plantarflexion, and anterolateral lesions occur with more ankle dorsiflexion with inversion. Such forces could produce a compressive injury to the subchondral bone posteromedially and lead to shear forces with avulsion on the lateral talus. Berndt and Harty35 experimentally produced lateral OLTs with application of inversion to a dorsiflexed foot while the tibia is internally rotated. Medial OLTs were produced by applying inversion force to a plantarflexed foot with tibial external rotation. Yao and Weiss38 postulated that eversion of dorsiflexed ankles with the tibia internally rotated produces lateral OLTs. The overlying articular cartilage coverage still may be intact or partially intact while producing an injury to the underlying bone. The subchondral fracture fragment has no direct blood supply. Left unrecognized, with continued weight bearing, the bony defect may not heal, leading to a fibrous nonunion or collapse, and result in a cartilage defect, loose osteochondral fragment, and cystic changes. Scranton and McDermott39 and Ferkel40 have postulated that an articular cartilage defect produced
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by such an injury may lead to cystic changes in the subchondral bone when joint fluid is forced repetitively into the defect under pressure. Chronic lateral ankle instability after an ankle sprain also may produce repetitive forces on the talus resulting in an OLT.1,16 GCTs represent a small minority of athletic injury to the talus. Usually the results of massive trauma, they can cause significant ankle pain and synovitis and inability to bear weight, and their diagnosis may be delayed because of lack of initial findings on routine radiographs (Fig. 14-53, A and B). An MRI best defines the lesion, with significant signal changes indicating edema and bony injury in the talar neck and/or body (Fig. 14-53, C and D). Because of the poor blood supply of the of the talar body, these lesions are slow to heal, if they heal at all. Literature reports of the natural history and my anecdotal experience show that talar collapse, chondrolysis, and gross ankle arthritis may be the result of such injuries.
Incidence Ankle sprains occur at the rate of approximately 27,000,000 per year. OLTs have been estimated to occur in approximately 6.5% of these injuries.16,41-43 Thirty-eight percent of supination and external rotation-4 type ankle injures are felt to produce an OLT.16 Sixteen percent to 23% of cases treated surgically for chronic instability of the ankle are found to have an OLT.13,16 Posteromedial lesions are more common than anterolateral and tend to be deeper in thickness. The average patient is 25 to 35 years of age, male (70%),13,16 with 10% to 25% incidence of bilaterality.16 OLT is most commonly seen in sports in which running, jumping, or change of direction are common, all factors that typically lead to the production of ankle sprain injuries.
Diagnosis and evaluation ............................................................. Diagnosis The diagnosis of OLT often is delayed. In several studies and in my own practice, there often are 5 to 9 months between the initial injury and the definitive diagnosis.37,44,45 The diagnostic tools have improved, but a high index of suspicion on the part of the surgeon for ‘‘ankle sprains that do not get better’’ is essential. The history of an ‘‘ankle sprain’’ is common. The athlete may give a history of continued anterior ankle pain and swelling despite initial radiographs that were read as negative and appropriate conservative treatment for an ankle sprain. A history of ‘‘catching’’ or ‘‘locking’’ may suggest a loose osteochondral fragment. Another common scenario is that of an ‘‘old ankle sprain’’ months or years before presentation in which the initial symptoms seemed to improve and then recur without addition injury. These cases most likely
Osteochondral lesions of the talus
Medial compression Lateral shear
B Anterior
Lateral
Medial
C
Medial
Posterior
Lateral
D
Figure 14-52 Osteochondral lesions of the talus. Mechanism is (A) inversion of the ankle causing a (B) shear force on the lateral dome and compression force on medial talus. (C and D) Location of resultant lesions are anterolateral and posteromedial in the talus.
Examination Physical examination in acute OLT cases may closely resemble that of an acute ankle sprain with ecchymosis
and tenderness in the anterior ankle or posteromedial ankle. There also may be swelling or an ankle effusion and synovitis. A drawer or talar tilt test (see Chapters 12 and 13) may be positive. There may be crepitus or ‘‘catching’’ with ankle ROM when a displaced OLT exists. In cases associated with chronic ankle instability, the anterior drawer test, talar tilt test, and/or flexion/rotation 319
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represent progression of the disease process. A third presentation is one in which an initial ankle sprain results in chronic lateral ankle instability, producing painful ‘‘giving way’’ episodes and further talar injury.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-53 Global talar compression injury. Routine radiographs (A and B) fail to demonstrate talus injury. Magnetic resonance imaging notes edema and ‘‘fracture’’ line (arrows) on (C) coronal and (D) sagittal images.
drawer test will be positive. In chronic cases, only swelling and joint tenderness may be present.
Imaging Initial radiographs often are negative unless the fracture is displaced.46 Serial or subsequent x-rays may show a
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subchondral fracture line, displacement of a fragment, or an area of radiolucency on the anterolateral or posteromedial talus (Fig. 14-54, A). A mortise view taken with a 4-cm heel rise may increase detection with conventional radiographs (Fig. 14-54, B). A bone scan, CT scan, or MRI may be used as a screening tool for chronic
Osteochondral lesions of the talus
Figure 14-54 Anterior-posterior radiograph of ankle (A) demonstrating radiolucency in talus (arrows) suggesting medial dome osteochondral lesion of talus. Oblique radiograph of ankle (B) showing clear evidence of large medial dome cyst and osteochondral lesion of talus.
Finally, intra-articular ankle injection with Xylocaine and Marcaine is helpful in cases in which there is doubt about whether the osteochondral lesion is producing the patient’s symptoms. I use MRI as a screening tool to detect OLTs when routine radiographs are negative, to localize and size osteochondral lesions preoperatively, and to assess and confirm healing of osteochondral lesions. However, as discussed later, actual treatment often depends on arthroscopic evaluation and determination of the intactness and viability of the cartilage.
Classification Several classification and staging systems for OLTs have been devised as diagnostic capabilities have developed. The Berndt and Harty35 radiograph-based classification introduced in 1959 is still the most widely used classification (Fig. 14-56). Stage I represents an area of osteochondral compression. Stage II is a partially loose fragment. Stage III is a completely detached fragment without displacement. Stage IV represents a completely detached and displaced fragment. This has been appended to include Stage 0, which is an x-raynegative but MRI-positive lesion. Scranton and others have added stage V39,50 to describe lesions with deep cystic changes (Fig. 14-57). Ferkel51 advanced a classification system based on CT in 1996 (Fig. 14-58). Hepple et al.43 presented an MRI-based classification system in 1999. Pritsch et al.,52 Ferkel,40 Mintz et al.,47 and Taranow et al.53 have all noted that arthroscopic evaluation of these lesions is essential to assess the overlying cartilage. An arthroscopic classification system was proposed by Ferkel.51 321
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ankle pain. A CT scan with 1-mm overlapping cuts, axial, coronal, and sagittal views is the gold standard for lesion location, sizing, and surgical planning.16 Similar views on MRI are helpful in evaluating early or compression injuries, demonstrating the amount of edema associated with the injury and assessing cartilage injuries. Arthroscopic evaluation47,48 has been proven to be essential for demonstrating the viability and stability of the overlying cartilage and whether the cartilage surface is still intact. At arthroscopic evaluation, the underlying subchondral bone can also be probed to determine its structural integrity. CT and MRI, however, have been shown to allow better assessment of the size of the OLT.49 Although Verhagen et al.46 found that CT and MRI evaluation were equally valuable in assessing OLTs, my experience has shown that MRI tends to show a much larger lesion because of the bony edema surrounding the fracture (Fig. 14-55, A through E). An MRI usually is much better in assessing early-stage lesions and as a screening tool. When an OLT is present with a more global compression injury, CT scan is helpful to accurately localize the specific osteochondral fracture. The history, physical examination, and these diagnostic tests all are helpful together to detect an OLT, to determine its size and location and to help with staging. However, the surgeon should be cautioned to determine that the presence of an osteochondral lesion is in fact the lesion producing the athlete’s symptoms. I personally have seen several cases in which a chronic asymptomatic OLT was detected on evaluation or was sent to me on discovery, and, in fact, another condition was causing the patient’s symptoms. We discuss treatment of asymptomatic OLTs later. However, the lesson here is to treat the patient not the imaging study.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-55 Osteochondral lesion of lateral dome of talus. (A) Anterior-posterior radiograph of ankle demonstrating lateral dome of talus osteochondral lesion. Coronal and sagittal (B and C) computed tomography images and (D and E) magnetic resonance imaging delineates more clearly chronic and cystic nature of lesion.
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Osteochondral lesions of the talus
Stage II
Stage III
Stage IIIA
Stage IV
Figure 14-56 Berndt and Hardy classification for osteochondral lesions of talus. Stage I represents an area of osteochondral compression. Stage II is a partially loose fragment. Stage III is a completely detached fragment without displacement. Stage IV represents a completely detached and displaced fragment.
Treatment of acute injuries Nonoperative treatment commonly is used for acute OLTs.3,13,35,40,41,54 Immobilization, nonweight bearing and crutches are used until healing is complete. Followup routine x-rays, CT scan, or MRI may be used to fully evaluate healing. Cases that are not healed may be treated as chronic cases. There is some controversy whether immobilization and/or nonweight bearing are critical to the success rate of nonoperative treatment.1,40 Acute OLTs that are displaced have been treated most commonly by arthroscopy and excision (if less than 1 cm) or by arthroscopy/arthrotomy and ORIF.40 Bioabsorbable pins or headless screws also may be used. For posterior medial lesions, transmalleolar pinning through a drill hole (Fig. 14-59) or a medial malleolar osteotomy have been used. Anterolateral lesions often can be approached through an arthroscopic approach or by a small arthrotomy and/or excision of a small anterolateral edge of the distal tibia.50,55 In the case of a nonunion, the patient is then treated as a chronic case. Treatment of chronic injuries Nonoperative treatment with or without immobilization has been shown to produce only approximately 50% good to excellent results1,3,38,42 and less than 33% good to excellent results in younger patients. Arthroscopic evaluation is essential in selecting the proper operative treatment of symptomatic patients with OLTs. A
combination of x-ray, CT scan, and/or MRI evaluation along with arthroscopic assessment of the cartilage surface allows accurate staging. Most cases of chronic OLT involve partially or totally displaced cartilage and bony fragments. Excision of the OLT alone yields approximately 38% good to excellent results.3 Excision and curettage (Fig. 14-60, A through C) yields 78% good to excellent results, whereas excision, curettage and drilling, or microfracture (Fig. 14-61, A and B) have produced 86% good to excellent results.1,18,56 For deep cystic lesions (stage V), excision, curettage, and bone grafting have yielded reasonable results.6 ‘‘Second look’’ procedures have shown the fibrocartilage tissue39 that forms in the lesions treated by excision and drilling or when microfracture is present (Fig. 14-61, C). The thickness and biomechanics of this fibrocartilaginous tissue is not identical to normal articular cartilage11 but often can produce a good functional result. For OLTs in which the articular cartilage is found to be intact on arthroscopy, retrograde drilling of the talus and bone grafting has been suggested (Fig. 14-62, A through I).53,57 Under simultaneous arthroscopic and fluoroscopic control, a Micro Vector drill guide is used to place a guidepin from a lateral incision across the talus to just underneath the posteromedial lesion (Fig. 14-62, F and G). A cannulated drill bit then is used to drill a 4.5-mm ‘‘tunnel’’ just up to the lesion. Any necrotic bone in the lesion is removed with small ring curette (Fig. 14-62, F and G). Four-millimeter bone plugs are taken from the lateral calcaneus (Fig. 14-62, H) and tamped into place until the articular cartilage surface 323
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OLT Treatment .............................................................
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Stage I
Stage II
Stage III
Stage IV
Stage V 39,50
Figure 14-57 Classification of osteochondral lesions with addition of stage V cystic changes.
‘‘tents up’’ a millimeter while visualized through the arthroscope (Fig. 14-62, I). When excision, curettage and drilling, or microfracture do not produce a satisfactory result in treating an OLT (Fig. 14-63, A), osteochondral transfer or osteochondral autograft transfer system (OATS) procedures have proven useful (Fig. 14-63, B through F). Introduced by Hangody in 199758 and supported by several other studies,59-63 cartilage and bone ‘‘plugs’’ are harvested from nonweight-bearing portions of the femoral condyle arthroscopically (Fig. 14-63, C and D) or through a knee arthrotomy. Various-size plugs then are implanted into a similarly sized hole drilled into the OLT (Fig. 14-63, E). The plugs may be single or
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to describe lesions with deep
‘‘nested’’ for larger lesions. For osteochondral lesions on the flatter part of the talus, the intercondylar notch of the knee is preferable as a donor site, where the lateral femoral ridge is used for OLTs located in the ‘‘corner’’ region of the talus.64,65 Despite the thicker articular cartilage of the knee as compared with the talus, good results have been achieved. Sammarco and Makwana66 described using the nonweight-bearing articular surface of the talus as an ipsilateral donor site. Most cartilage/bone plugs used in OATS procedures are approximately 1 cm in depth. Deeper plugs have been used for treating cystic, type-V lesions.39 All of the previously mentioned procedures have been used to treat focal, reasonably well-circumscribed lesions
Osteochondral lesions of the talus
Stage I
Stage IIA
Stage III
Stage IV
Classification of osteochondral lesions as described by Ferkel51 based on computerized
Figure 14-59 Diagram demonstrating transmalleolar pinning of medial dome osteochondral lesion through drill hole in medial malleolus.
of the talus. Their success rates fall when matched against more diffuse areas of articular cartilage damage. Autologous chondrocyte implantation (ACI) has been one of the newer methods to help treat larger (>1.5 cm) talar chondral lesions. Brittberg et al.67 described treatment for articular lesions of the knee in 1994, using cultured chondrocytes implanted under a periosteal blanket. The OLT is debrided back to stable cartilage borders and down to subchondral bone. Chondrocytes obtained from an initial cartilage biopsy are cultured and grown for later implantation. Fibrin ‘‘glue is used to secure and seal the periosteal cover. Giannini in 200168 reported use of this technique for resurfacing talar lesions. OLTs up to 3.3 cm were treated with improvement to an American Orthopaedic Foot and Ankle Society (AOFAS) ankle score of 91. Patients were begun on continuous passive ROM and kept nonweight bearing for 12 weeks. Kouvalis et al.69 described a series of patients treated with ACI that had failed previous surgery. Good results were achieved with ACI and weight bearing after 6 to 7 weeks. Schafer1 and Ferkel70 suggested that this method could be used to treat patients up to 55 years of age with unipolar lesions that were constrained and with a history of previous failed 325
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Figure 14-58 tomography.
Stage IIB
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-60 Arthroscopic views of (A) osteochondral lesion (OCL), (B) curettage, and (C) postexcision and curettage. Note bloody base and stable rim (arrows) at donor site for OCL.
surgery. Results treating ‘‘shoulder’’ lesions have not been as good.70 ‘‘Sandwich’’ procedures with cultured chondrocytes between two periosteal layers have been used to cover deeper, cystic, type-V lesions filled with cancellous bone graft. Recently, various commercially prepared collagenbased ‘‘scaffolds’’ or matrices that can be impregnated with cultured chondrocytes have been introduced to replace periosteum as the ‘‘blanket’’ holding the chondrocytes. This Matrix-induced Autologous Chondrocyte Implantation (MACI) offers to eliminate harvesting of periosteum. These methods are an exciting new opportunity to treat larger OLTs that previously had been left untreated or treated with fusion or total ankle replacement. The technique is expensive, demanding, and often considered ‘‘experimental’’ by many health insurers but likely will be more widely available in the future as more good long-term results are reported. Recently, Bently et al.65 reported 89% good results with
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ACI in the knee versus 69% using mosaicplasty, although other studies show equivalent results.71 Talar body partial or total allografts recently have been reported for use in the treatment of more global talar cartilage damage. In 2001, Gross et al.72 noted using matched allograft talar replacements (Fig. 14-64). Meehan et al.73 have presented initial good results with this technique. However, long-term follow-up has shown complications of resorption, graft fracture, and failure. Tissue matching is not required for this procedure. Access to a large tissue bank where size-matched allograft can be obtained is essential for this new procedure, thereby limiting availability. The technical and immunologic complexity of this technique must be weighed against the alternatives of ankle fusion or replacement. Review of the literature shows very little detailed, evidence-based information about the role of weight bearing or nonweight bearing in the treatment of these lesions. The literature also is scarce on surgical treatment options
Osteochondral lesions of the talus
Figure 14-61 Osteochondral lesion treated with (A) K-wire drilling or (B) microfracture results in (C) replacement with fibrocartilage noted at second-look arthroscopy.
My suggested treatment ............................................................. Acute injuries (less than 4 to 6 weeks) For acute lesions I prefer to use the Berndt and Harty classification but I often obtain a CT scan to further evaluate the size and position of the lesion. For stage
0 and 1 lesions, the athlete is treated nonweight bearing with active ankle ROM. Salter76 reported that ROM is helpful in cartilage nutrition and healing. When swelling is down and tenderness of the talus to palpation is gone, a progressive weight-bearing program is begun, followed by general ankle rehabilitation focusing on edema control, ROM, PREs (especially the posterior tibial tendon and peroneal tendons), and proprioception. If the talus remains painful to palpation, a repeat CT scan may be performed to evaluate healing. After successfully completing sports-specific exercises, the athlete may return to sports. Stage 2 lesions with a fracture line present are treated by nonweight bearing in a boot without AROM until radiographic evidence of healing. A CT scan may be needed to document healing. Return to sports comes after successful completion of ankle rehabilitation and 327
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on GCTs other than to recognize that they exist and that fusion or total ankle replacement is difficult when such a lesion is present. Mont74 has written about drilling these talar lesions if conservative measures fail. Methyl methacrylate or talar body prosthetic replacements75 have been proposed in isolated cases. A talar body allograft may be used.72,73 Tibiocalcaneal fusion or ankle replacement also have been described as treatment.
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-62 Medial dome osteochondral lesion (OCL) treated with retrograde drilling and bone graft. (A and B) Anterior-posterior and lateral radiographs noting only mild medial dome radiolucency, whereas (C and D) coronal and sagittal magnetic resonance imaging clearly demonstrate medial lesion.
sports-specific exercises. In some cases involving professional players and large fragments, arthroscopy and pinning with bioabsorbable pins or headless screws may allow earlier ROM, healing, and return to sports.
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Stage 3 and stage 4 lesions are treated with excision and either drilling or microfracture if less than 1 cm. ORIF is performed, either arthroscopically or through a malleolar osteotomy, if the OLT is more than 1 cm.
Osteochondral lesions of the talus
Figure 14-62 cont’d. (E-G) Micro Vector drill guide is used to place a guidepin from a lateral incision across the talus to just underneath the posteromedial lesion. (H) Bone graft taken from calcaneus is (I) tamped into area curetted out under OCL causing mild tenting up of cartilage surface.
in a boot with gentle AROM until routine radiographs or a repeat CT scan reveal healing, General ankle rehabilitation is then initiated, followed by sports-specific exercises. 329
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Choice of fixation is either bioabsorbable pins or headless screws, depending on the size of the fragment. Any fibrous tissue under the fragment is curetted. These patients are treated postoperatively nonweight bearing
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Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-63 (A) Osteochondral lesion (OCL) treated with microfracture with continued pain and poor cartilage production. This lesion required (B-F) osteochondral grafting by taking (C and D) 10-mm autograft plug from medial femoral condyle of knee and (continued on page 331)
Chronic OLT lesions (more than 6 weeks old or failed previous treatment) It is important to assess the patient’s symptoms and the imaging study when caring for these athletes. As noted previously, the presence of an OLT on x-ray, CT scan, or MRI does not make it the source of the patient’s current symptoms. It is critical to properly assess the athlete and his or her complaints to make sure the symptoms or disability are indeed from the OLT. This evaluation is sometimes difficult.
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Treatment of asymptomatic OLTs visualized on incidental radiographs, CT scan, or MRI presents a treatment and ethical dilemma for the sports physician. Several of my colleagues and I have been consulted when an athlete has a totally asymptomatic OLT found on imaging studies of the ankle obtained for unrelated problems. In such situations, the OLT is almost always chronic. In these situations the best option is complete education of the patient. I explain to the athlete that the lesion may become partially or totally loose and
Osteochondral lesions of the talus
Figure 14-63 cont’d. (E) placement into the OCL site of talus via a (F) medial malleolar osteotomy fixed with two cannulated screws.
If the articular cartilage surface of the talus is intact with either a stage 1 or stage 5 lesion, the preferred treatment is retrograde drilling of the talus, with bone grafting for stage 5 lesions. Postoperatively, athletes begin early AROM and are in a boot nonweight bearing until an x-ray or CT scan demonstrates bone healing. General ankle rehabilitation followed by sports-specific exercises then is started. For lesions at stage 2, 3, or 4 that are shallow (less than 2 mm deep) and less than 1 cm in diameter, excision of the lesion and drilling or microfracture (depending on the location of the lesion) are performed. Athletes are nonweight bearing with AROM, as described previously, for 6 to 8 weeks until swelling and tenderness are gone. Rehabilitation and weight bearing then are started as discussed previously. When treating stage 2, 3, and 4 OLT lesions in which the surface area is more than 1 cm I prefer osteochondral transfer from the knee (OATS procedure). As long as the lesion appears to be located on the edge or medial or lateral surface of the talus and can be reached by a malleolar osteotomy or arthroscopy, single or nested matched osteochondral plugs provide very good results. Careful orientation of the drill holes perpendicular to the articular surface is critical. Proper matching of the plug contour to the natural contour of the talus also is important. As other authors have described,64 the plug or plugs are left very slightly ‘‘proud’’ at the time of surgery. The postoperative regimen is the same as described previously. For cystic lesions at stage 2, 3, or 5 (in which the cartilage surface is disrupted) less than 1 cm, excision, curettage, and placement of cancellous bone graft as suggested by Lanny Johnson have proven successful. The same nonweight bearing and early AROM 331
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symptomatic in the future, with the possibility of ankle arthritis. The nature of surgical treatment with accompanied risks, such as becoming symptomatic, is also discussed. The patient is presented with two general options: first is serial evaluation at yearly intervals with a repeat x-ray and/or MRI. The patient is told to call or report immediately if he or she has any ankle discomfort or swelling. I have followed several patients with large OLTs for several years that are completely asymptomatic and continue to run and engage in recreational athletics without pain or discomfort. Patients with asymptomatic stage 1 lesions are encouraged to take this option. The other option is prophylactic surgical treatment, often at the end of the current athletic season. In the case of cystic lesions without an overlying osteochondral fragment, it is not unreasonable to offer the athlete retrograde drilling and bone grafting during the off season. Patients are nonweight bearing with AROM for approximately 6 weeks until healing is confirmed by repeat radiographs or CT scan. Rehabilitation then is begun. For asymptomatic stage 2 or 3 lesions, arthroscopy, excision, curettage and drilling with microfracture, or osteochondral transfer is selected. Athletes must understand that this treatment may result in increased symptoms and therefore must be approached with caution. In treating symptomatic chronic OLTs, ankle radiographs are obtained for baseline evaluation and to help with serial examinations. MRI is used as a screening tool and to evaluate the extent of bony edema. Often a CT scan may be used to clearly define the location and size of the OLT before surgery. Patients are advised that the exact treatment depends on the findings noted at the time of arthroscopy.
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-64 Anterior-posterior radiograph after allograft total ankle. Note two screws in tibia to hold graft in place and increased density of allograft in tibia and talus.
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Osteochondral lesions of the talus
333
cont’d. (continued)
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Figure 14-64
CHAPTER 14
Osteochondral lesions of the talus and occult fractures of the foot and ankle
Figure 14-64 cont’d.
postoperative protocol is prescribed. On occasions in which I have had the opportunity to do a ‘‘second look’’ procedure on these patients, the fibrocartilage healing is similar to those with more shallow lesions treated by excision and drilling/microfracture. For larger cystic lesions at stage 2, 3, or 4, an osteochondral transfer with a deeper plug may be used, or cancellous bone graft may be inserted39 before placing the plug. In cases in which initial surgical treatment for OLT has failed, medial malleolar osteotomy and the OATS procedure seem to be the procedure of choice for lesions
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less than 3 cm. Larger lesions (>1.5 cm diameter) may be treated with ACI or MACI. I do not have any experience with this technique, although increasingly reports seem to indicate this is the procedure of choice for these large lesions. Expense and insurance approval are major hurdles to its use. Larger lesions or bipolar lesions involving both talar and tibial surfaces lend to treatment with talar allografts.16 Immunologic difficulties, limited access to a large, talar bone bank, and lack of long-term experience have limited the use of this salvage procedure.
Osteochondral lesions of the talus
Treatment of GCTs As noted previously, these injuries are commonly missed, both in the acute or chronic setting after a significant compression and/or twisting injury to the
ankle. The initial radiographs usually are negative and the diagnosis rests with initial suspicion, talar tenderness on palpation, and MRI confirmation. Acute or chronic GCT is treated with protection in a boot, nonweight
Figure 14-65 Global compression injury of talus treated with drilling as preferred by me. (A) Sagittal magnetic resonance imaging denoting global talar edema, with (B) normal cartilage noted on arthroscopy. (C-F) Fluoroscopically guided drilling of talus with multiple passes to improve blood supply and encourage healing.
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Figure 14-65
Osteochondral lesions of the talus and occult fractures of the foot and ankle
cont’d.
bearing with early AROM. I place the patients on calcium and vitamin D supplementation and use a bone stimulator. Weight bearing is permitted when the talus is nontender to palpation and swelling is diminished. Healing often is prolonged because of the poor blood supply of the talus and may take several months. If healing of the fracture or progress is in doubt, a repeat MRI is obtained at 3-month intervals. Usually I allow weight bearing in the boot first, followed by weight bearing in shoes. Appropriate therapy then is started followed by sports-specific exercises. For GCT lesions in which the talus remains painful and healing is delayed (>6 months of treatment), I prefer arthroscopic and fluoroscopic-directed drilling of the talus in a retrograde fashion (see Fig. 14-65, A through F). Multiple passes are made with a 2-mm drill bit into the area indicated on the recent MRI. When the talus is nontender and/or the MRI shows resolution, weight bearing and therapy are initiated. I have obtained roughly 50% good results with this approach. Failure of CGT treatment may lead to progressive ankle arthritis or talar avascular necrosis and collapse. Both ankle fusion and arthroplasty are difficult salvage procedures because of poor bone quality and obviously preclude competitive sports participation.
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20. Johnson RP, Collier BD, Carrera GF: The os trigonum syndrome: use of bone scan in the diagnosis, J Trauma 24:761, 1984. 21. Sopov J, Liberson A, Grosher D: Bone scintigraphic findings of os trigonum: a prospective study of 100 soldiers on active duty, Foot Ankle Int 21:822, 2000. 22. Ebraheim NA, Padanilam TG, Wong FY: Posterior process fractures of the talus, Foot Ankle Int 16:734, 1995. 23. Nadim Y, Tosic A, Ebraheim N: Open reduction and internal fixation of fracture of the posterior process of the talus: a case report and review of the literature, Foot Ankle Int 20:50, 1999. 24. Kanbe K, et al: Fracture of the posterior medial tubercle of the talus treated by internal fixation; a report of two cases, Foot Ankle Int 16:164, 1995. 25. Giuffrida AY, et al: Pseudo os trigonum sign: missed posteromedial talar facet fracture, Foot Ankle Int 24:642, 2003. 26. Marumoto JM, Ferkel RD: Arthroscopic excision of the os trigonum: a new technique with preliminary clinical results, Foot Ankle Int 18:777, 1997. 27. Lombardi CM, Silhanek AD, Connolly FG: Modified arthroscopic excision of the flexor hallucis longus tendon: operative techniques and case study, J Foot Ankle Surg 38:347, 1999. 28. Tucker DJ, Feder JM, Boylan JP: Fractures of the lateral process of the talus: two case reports and a comprehensive literature review, Foot Ankle Int 19:641, 1998. 29. Funk JR, Srinivasan SCM, Crandall JR: Snowboarder’s talus fractures experimentally produced by eversion and dorsiflexion, Am J Sport Med 31:921, 2003. 30. Kirkpatrick DP, et al: The snowboarder’s foot and ankle, Am J Sport Med 26:271, 1998. 31. Heckman JD, McLean MR: Fractures of the lateral process of the talus, Clin Orthop 199:108, 1985. 32. Valderrabano V, et al: Snowboarder’s talus fracture: treatment outcome of 20 cases after 2.5 years, Am J Sport Med 33:871, 2005. 33. Sanders TG, Ptaszek AJ, Morrison WB: Fracture of the lateral process of the talus: appearance at MR imaging and clinical significance, Skeletal Radiol 28:236, 1999. 34. Ko¨nig F: Ueber freie korper in den celeken, Deutsch Z Chir 27:90, 1888. 35. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus, J Bone Joint Surg Am 41A:988, 1959. 36. Nunley J: Allograft placement for osteochondral lesions of the talus. In Easley ME, et al, editors: Osteochrondral lesions of the talus: current therapeutic dilemmas, American Academy of Orthopaedic Surgeons 72nd annual meeting ICL# 306, Rosemont, IL, 2005. 37. Brunes J, Behrens P: Etiological and pathophysiologic aspects of osteochondrosis dissecans, Arthroskopie 11:166, 1998. 38. Yao J, Weiss E Jr: Osteochondritis dissecans, Orthop Rev 14:190, 1985. 39. Scranton PE, McDermott JE: Treatment of type V osteochondral lesion of the talus with ipsilateral knee osteochondral autografts, Foot Ankle Int 22:380, 2001. 40. Ferkel RD: Arthroscopic treatment of osteochondral lesions, soft-tissue impingement and loose bodies, In Pfefer G, editor: Arthroscopic treatment of osteochondral lesions, soft-tissue impingement and loose bodies, American Academy or Orthopedic Surgeons (AAOS) monograph series, Rosemont, IL, 2000. 41. Giannini S, Vannini F: Operative treatment of osteochondral lesions of the talar dome: current concepts review, Foot Ankle Int 25:168, 2004. 42. Schachter AK, et al: Osteochondral lesions of the talus, J Am Acad Orthop Surg 13:152, 2005. 43. Hepple S, Winson IG, Glew D: Osteochondral lesions of the talus: a revised classification, Foot Ankle Int 20:789, 1999.
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67. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation, N Engl J Med 331:889, 1994. 68. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint, Foot Ankle Int 22:513, 2001. 69. Kouvalis D, Shultz W, Heyden M: Autologous chondrocyte transplantation for osteochondritis dissecans of the talus, Clin Orthop 395:186, 2002. 70. Ferkel RD: Autologous chondrocyte implantation. In Easley ME, et al., editors: Osteochrondral lesions of the talus: current therapeutic dilemmas, American Academy of Orthopaedic Surgeons 72nd annual meeting ICL# 306, Rosemont, IL, 2005.
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71. Smith GD, Knutsen G, Richardson JB: A clinical review of cartilage repair techniques, J Bone Joint Surg 87B:445, 2005. 72. Gross AE, Zgnidis Z, Hutchinson CR: Osteochondral defects of the talus treated with fresh osteochondral allograft transplant, Foot Ankle Int 22:385, 2001. 73. Meehan R, et al: Fresh ankle osteochondral allograft transplant for tibiotalar joint arthritis, Foot Ankle Int 26:793, 2005. 74. Mont MA, et al: Avascular necrosis of the talus treated by core decompression, J Bone Joint Surg 78B:827, 1996. 75. Harnroongroj T, Vanadurongwan V: The talar body prosthesis, J Bone Joint Surg 79A:1313, 1997. 76. Salter RB: The biologic concept of continuous passive motion of synovial joints the first 18 years of basic research and its clinical application, Clin Orthop 242:12, 1989.
.........................................C H A P T E R 1 5 Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions Scott T. Sauer, Travis W. Hanson, and John V. Marymont CHAPTER CONTENTS ...................... Introduction
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Tarsal coalition
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Anatomy
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Calcaneonavicular coalitions
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Subtalar instability
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Talocalcaneal coalitions
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Sinus tarsi syndrome
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Acknowledgment
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Subtalar dislocation
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References
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INTRODUCTION Pathology in the subtalar joint can be debilitating, difficult to diagnose, and can lead to significant loss of time for the athlete. Subtalar instability is becoming more recognized in association with lateral ankle instability and also as an isolated source of ‘‘giving way’’ in the athlete. We try to elucidate some recent advancements in this sometimes-confusing area. Sinus tarsi syndrome has been a common complaint in the past and we try to update our readers regarding how to diagnose this syndrome and how to differentiate it from other forms of subtalar pathology. Tarsal coalitions often are symptomatic in the athlete. Although the coalition is found in approximately 2% of the population, the athlete often becomes symptomatic with its presence.
of the intermediate root of the inferior extensor retinaculum and the cervical ligament. The deep layer consists of the medial root of the inferior extensor retinaculum and the interosseous talocalcaneal ligament (Fig. 15-1). The joints move in a triaxial plane, which allows for the motions of flexion/extension, inversion/eversion, and adduction/abduction. The sinus tarsi is a space on the lateral aspect of the foot that lies anterior to the posterior facet between the talus and the calcaneus. It is in continuity with the tarsal canal. The tarsal canal is a cone-shaped opening within the subtalar joint and is situated in a posteromedial-to-anterolateral direction. Soft tissues within the sinus tarsi include the artery of the tarsal canal, bursae, nerve endings, and multiple ligaments.
SUBTALAR INSTABILITY ANATOMY The subtalar joint is comprised of three articulating surfaces, referred to as the posterior facet, the middle facet, and the anterior facet. The bony articulations provide inherent stability and soft tissues provide additional stabilization. The lateral soft-tissue stabilizers have been classified into three separate layers.1 The superficial layer is composed of the lateral root of the inferior extensor retinaculum, the lateral talocalcaneal ligament, and the calcaneofibular ligament. The intermediate layer consists
The role that instability of the subtalar joint plays in the patient with lateral ankle instability has been elucidated only recently. It has been estimated that 10% to 30% of patients with functional ankle instability, that is, patients that have pain, swelling, or a sense of ‘‘giving way’’ of the ankle, have evidence of instability of the subtalar joint.2,3 Some have suggested that consideration should be given to the concept of global hindfoot instability rather than simply functional instability about the ankle joint.4
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Figure 15-1 The anatomy of the subtalar joint. (From Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, CV Mosby, p 1147, Figure 26-57.)
Instability of the subtalar joint was first described in 1962 by Rubin and Whitten.5 They proposed a series of stress radiographs to further evaluate this disorder. Brantigan et al.6 were the first to detect radiographic evidence of subtalar instability in their series of three patients. Chrisman and Snook7 in 1969 were able to document clinical subtalar instability in three of seven patients who were undergoing their tendon transfer procedure for lateral instability. Clanton and Berson8 described subtalar injuries as a continuum of other injuries in athletes, particularly sprains of the lateral ankle ligaments.
Clinical presentation The typical injury that leads to instability of the subtalar joint is a severe supination or supination-inversion force applied to the hindfoot. This results in a progressive injury to the talonavicular ligament and talonavicular capsule, followed by injury to the calcaneofibular and lateral talocalcaneal ligaments.8 The presenting complaint often is a sensation of giving way of the ankle. The patient may report pain localized to the region of the sinus tarsi. Athletic activities can exacerbate the symptoms, resulting in a dependence on bracing or taping. Uneven surfaces may cause pain and a feeling of instability. It is difficult to differentiate lateral ankle instability from subtalar instability on the basis of patient history. A thorough clinical and radiographic workup can help define the source of the athlete’s complaints, but the differentiation still can be elusive.
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Physical examination The most notable finding on physical examination is increased inversion of the subtalar joint. This should be compared with the presumably uninjured opposite limb. The increased inversion can result from subtalar instability or a combination of subtalar and ankle instability.4,8 It is extremely difficult to detect the location of increased inversion by examination. In addition to increased inversion of the hindfoot, an increased translation of the calcaneus in the medial direction has been noted by Thermann et al.9 In their study, a valgus stress was applied to the calcaneus, followed by an abrupt internal rotation stress. Results showed a medial shift of the calcaneus in relation to the talus or an opening of the talocalcaneal angle in patients with subtalar instability. Following an acute injury, there may be swelling, bruising, and tenderness laterally. In the more chronic setting, increased inversion and lateral tenderness are more likely. It is easier to detect instability in the chronic setting because the athlete will be less apt to guard because of pain. Radiographic evaluation The initial radiographic workup of the patient with subtalar instability involves a weight-bearing anteriorposterior, lateral, and mortise view of the affected ankle, as well as weight-bearing anterior-posterior, lateral, and oblique radiographs of the affected foot to rule out evidence of bony pathology.
Subtalar instability
4 PEARL When possible, obtain weight-bearing radiographs to assess the bony articulations under physiologic stress. Plain radiographs often are negative, and further investigation must be carried out to arrive at the diagnosis. There have been multiple investigations into the use of stress radiographs in the workup of subtalar instability
(Fig. 15-2).6,10-12 In a series of three patients, Brantigan et al.6 were able to radiographically demonstrate subtalar instability. They attributed the instability to an injured calcaneofibular ligament. Heilman et al.12 sequentially sectioned ligaments in cadaver limbs and then obtained lateral and Broden’s radiographs. They found that sectioning of the calcaneofibular joint caused a 5-mm opening of the subtalar joint. With subsequent sectioning of the interosseous ligament, the joint opened up to 7 mm. The usefulness of stress radiographs has come into question by multiple authors.13-15 Harper13 reported a wide range of subtalar tilt with stress radiographs in his group of asymptomatic patients. Louwerens et al.14 examined 33 patients with chronic ankle instability and 10 control patients who were asymptomatic. Broden’s views were checked under fluoroscopy and they detected no difference between symptomatic and asymptomatic feet with regard to subtalar tilt or medial shift. Van Hellemondt et al.15 examined both stress radiographs and stress computed tomography (CT) scans in 15 patients with unilateral chronic ankle instability with suspected subtalar instability. Although three of the symptomatic feet and one of the asymptomatic feet had increased subtalar tilt on plain films, there was no significant difference between the symptomatic and asymptomatic sides. None of the patients had increased subtalar tilt on the stress CT scans. The authors therefore doubted that a Broden’s stress examination reveals the true amount of subtalar tilt.
Nonoperative treatment In an acute injury, the usual treatment regimen for lateral ankle sprains will suffice for subtalar ligamentous injuries, as well. Rest, ice, compression, and elevation (RICE) are part of a good protocol, as well as immobilization and physical therapy, when needed. The same can be said for management of chronic subtalar instability. The routine nonoperative regimen used for chronic lateral ankle instability is initiated. This may include proprioceptive training, peroneal strengthening, and bracing or strapping.8,16 With bracing, it is important to understand the delicate balance in providing an athlete with enough support without impeding his or her performance. Taping by an athletic trainer before participation can be effective. Wilkerson17 examined a modification of the standard method of ankle taping with the incorporation of a ‘‘subtalar sling.’’ He found that addition of the sling enhances the protective function of taping but cautioned that it may impede performance of certain activities.
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Figure 15-2 Stress radiographs. (A) Stress anteriorposterior (AP) radiograph with subtalar tilt. (B) Stress Broden view showing subtalar instability.
Surgical treatment Patients with residual symptomatic instability despite an adequate program of nonoperative management will require a surgical stabilization of their subtalar joint. If both ankle and subtalar instability exist and require surgery, both problems should be corrected at the time of surgery.4 Surgical stabilization involves direct ligament repair or tendon transfers to substitute for the irreparable ligaments.
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Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions
Lateral malleolus
Lateral malleolus
Anterior talofibular ligament
Extensor retinaculum
Extensor retinaculum
Peroneal tendons
Calcaneofibular ligament
D
Calcaneofibular ligament
E
Peroneal tendons
Figure 15-3 (A) Chrisman-Snook modification of Elmslie procedure. (B) Triligamentous reconstruction. (C) Larsen procedure. (D) Lateral ankle ligament reconstruction. (E) Reinforcing repair with inferior extensor retinaculum. (A-E from Mann RA, Coughlin M.J., editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, CV Mosby; A from p 1128, Figure 26-35; B from p 1153, Figure 26-64; C from p 1127, Figure 26-34; D and E from p 1128, Figure 26-36.)
Surgical techniques resulting in ankle and subtalar stability concurrently are numerous (Fig. 15-3, A through C).2,7,9,18-26 Most techniques require some form of extraarticular tendon transfer to provide stability. Kato25 and Pisani26 described techniques involving intraarticular ligament reconstruction of the interosseus ligament between the calcaneus and talus. A less invasive technique that, according to Clanton and Berson8 and Gould et al.,22 provides a good treatment for subtalar instability is the Brostrom-Gould reconstruction technique for lateral ankle instability (Fig. 15-3, D and E). With the reconstruction of the
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calcaneofibular ligament (CFL) and anterior talofibular ligament (ATFL) buttressed by the inferior extensor retinaculum, subtalar stability is effectively restored.8,22
SINUS TARSI SYNDROME Symptoms of sinus tarsi syndrome may overlap with those associated with subtalar instability. Some authors consider this syndrome simply a variant of subtalar instability.27 Sinus tarsi syndrome describes pain localized
Sinus tarsi syndrome
to the region of the sinus tarsi. Characteristic findings on clinical and radiographic examination have not been well defined. Likewise, the pathologic changes found at the time of surgery are unclear. The most widely reported description of the pathologic anatomy associated with this condition is degenerative changes to the soft tissues of the sinus tarsi.28,29 The majority of cases are posttraumatic in nature but also may be related to inflammatory arthropathies, gout, ganglion cysts, and structural foot abnormalities.30,31
Clinical presentation The typical complaint is pain over the lateral and anterolateral ankle and hindfoot centered in the region of the sinus tarsi. The patient may report a sensation of mild hindfoot instability. It has been estimated that as many as 70% of patients with sinus tarsi syndrome have had a previous inversion injury to the hindfoot.32 Physical examination Tenderness over the lateral ankle and hindfoot overlying the sinus tarsi is the most common finding on clinical examination. Patients may have findings of mild subtalar instability; however, this is difficult to elicit and often absent. Swelling overlying the sinus tarsi is variably present. Radiographic evaluation Plain films often are negative in this condition. Stress views may reveal mild subtalar instability, but, as stated in the previous section, these are of uncertain value. Subtalar arthrograms have been used in the workup of this condition. The normal subtalar joint will accept 3 ml of contrast dye and will demonstrate multiple recesses and interdigitations within the joint capsule.18
Under normal circumstances there is a small recess that projects anteriorly from the subtalar joint. The absence of this synovial recess has been associated with sinus tarsi syndrome.30,32 The use of magnetic resonance imaging (MRI) in the evaluation of sinus tarsi syndrome has been investigated. The key MRI features have been reported as replacement of the normal fat signal intensity in the sinus tarsi with fluid, inflammatory tissues, or fibrosis.31,32 The inflammatory changes often will obscure the ligaments that normally are visualized in the sinus tarsi. Additional findings may include ligament injury, ganglion cysts, and degenerative joint disease.33
Nonoperative treatment Injections of local anesthetic and steroid into the sinus tarsi may be both diagnostic and therapeutic. If the patient does not report even temporary relief following injection, then skepticism must be directed at a diagnosis of sinus tarsi syndrome. Some patients may report permanent resolution of their symptoms after a series of injections.18 Surgery is indicated if pain recurs after a series of one to three injections. Surgical treatment Open and arthroscopic techniques are available. Open excision of the tissue filling the sinus tarsi has been reported to have good results.18,29,30 Typically a lateral oblique incision is made over the region of the sinus tarsi. The lateral branch of the superficial peroneal nerve is avoided. The inferior extensor retinaculum and the origin of the extensor digitorum brevis are reflected distally. The sinus tarsi is entered, and debridement is performed. Arthroscopic exploration (Fig. 15-4) of the sinus tarsi for diagnosis and treatment has been
Figure 15-4 (A) Arthroscopic examination of the subtalar joint with anterior working portal. (B) Posterior working portal.
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Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions
described with good results, but often the postoperative diagnosis is changed from sinus tarsi syndrome to another more anatomic pathology, following direct visualization of the sinus tarsi area and the subtalar joint.27
SUBTALAR DISLOCATION A subtalar dislocation involves the dislocation of the talocalcaneal and talonavicular joints. With this injury there is no associated dislocation of the calcaneocuboid or tibiotalar joints. It was first described separately by DuFaurest34 and Judcy35 in 1811. Broca36 later classified these injuries as medial, lateral, and posterior. In 1856, Malgaigne37 revised this classification and added anterior subtalar dislocations as a specific entity. Frequency of the different subtypes of subtalar dislocations has been reported as 80% medial, 17% lateral, 2% posterior, and 1% anterior.38
Clinical presentation These injuries typically are the result of high-energy mechanisms such as motor vehicle accidents or falls from a height. They also can result from a twisting athletic injury. In 1964, Grantham39 used the term ‘‘basketball foot’’ to describe medial dislocations because four of the five patients in his series injured their foot playing basketball. Low- and high-energy mechanisms create two subtypes of subtalar dislocations. High-energy injuries are more likely to be open, more likely to be lateral, have a higher incidence of associated fracture, and have a worse long-term prognosis.40 Forced inversion of the foot results in a medial subtalar dislocation, whereas eversion causes a lateral dislocation. During medial dislocations, the sustentaculum tali serves as the fulcrum around which the foot rotates. With lateral dislocations, the foot rotates around the anterior process of the calcaneus. Significant foot deformity is found in all patients with subtalar dislocation, although this may be somewhat obscured by swelling. Approximately 20% to 40% of subtalar dislocations are open.41-43 However, open injuries are unusual in the athlete. Physical examination The deformity is usually clinically obvious. With medial dislocations, the skin is tented over the lateral malleolus and the dorsolateral talar head. With lateral dislocations, the skin is tented over the prominent medial talar head and the medial malleolus. A thorough neurovascular examination should be performed, although ischemia of the foot is uncommon with these injuries, especially in the athlete. There is a risk of local ischemia to the
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soft tissues in the region of the tented skin if reduction is not prompt.
Radiographic evaluation A standard three-view series of the foot and/or ankle (anterior/posterior, lateral, oblique) is obtained but can be suboptimal, given the distortion of normal anatomic relationships in the midfoot. The most helpful radiograph is the anterior-posterior view of the foot. The relationship between the talar head and navicular can best be evaluated. The relationship of the talar head to the concave proximal side of the navicular on this view normally is congruent on all views of the foot. On the lateral radiograph, the talar head lies superior to the navicular with medial subtalar dislocations. With lateral subtalar dislocations the opposite is true, and the talar head appears inferiorly displaced. Associated fractures about the foot and ankle are common. These are better identified on postreduction radiographs. DeLee and Curtis44 reported a 47% incidence of associated osteochondral fractures of the talonavicular or talocalcaneal joints in their series of 17 patients. Osteochondral fractures were more common with lateral subtalar dislocations in this series. Other series have reported an incidence of associated foot and ankle injuries of 64% to 88%.42,43 Because of the difficulty in identifying associated fractures on plain radiographs, postreduction CT scans have been recommended as a means of identifying associated injuries.44 Bohay and Manoli45 reported four cases of patients who had normal films following reduction of subtalar dislocations. CT scans revealed intra-articular fractures in all four cases. The authors recommended CT scanning in all patients with normal radiographs following reduction of subtalar dislocations. Diagnosis is important because associated intraarticular fractures have been associated with a poor prognosis.43,44,46 Nonoperative treatment The majority of subtalar dislocations can be reduced using closed methods. Depending on the time from injury, reduction can be achieved with minimal sedation. Injuries left unreduced more than a few hours may require heavier sedation in the emergency department or operating room. The reduction process involves bending the knee to relax the gastrocnemius. Traction is applied to the heel and countertraction is applied to the thigh. As traction is being applied, the deformity is accentuated by inverting the foot for medial dislocations and everting it for lateral dislocations. The deformity then is reversed as direct pressure is placed over the prominent talar head to aid in reduction.
Tarsal coalition
Surgical treatment The indications for operative intervention are open injuries and inability to achieve a congruent reduction using closed methods. Lateral dislocations are more likely to require open reduction than medial dislocations.43,47 In their series of 25 patients, Bibbo et al.43 reported that closed reduction was unsuccessful in 8 patients (32%). Four of these cases had identifiable soft-tissue interposition that blocked reduction. None of the patients with a low-energy mechanism of injury required an open reduction. Blocks to reduction with medial dislocations may include buttonholing of the talar head through the extensor retinaculum or capsule of the talonavicular joint.48,49 There have been reports of the deep peroneal nerve interposition blocking reduction, as well.48 Finally, the lateral navicular bone may impact into the medial talar head and thereby block reduction.49 With lateral dislocations, impingement of the posterior tibial or flexor digitorum longus tendons, as well as impaction of the medial navicular bone onto the lateral talar head, may block reduction.49-51 For open reduction of medial dislocations, a longitudinal anteromedial incision is made along the talar neck extending to the talar head. This allows access to the structures that have entangled the talar head. At the same time, inspection of impaction fractures of the articular surfaces can be carried out. For lateral dislocations, a more medial longitudinal incision is made over the prominent talar head. Interposed tendons are released and joint surfaces are inspected. Any tears found in the tendons should be repaired.
TARSAL COALITION Tarsal coalition involves a congenital union between two or more tarsal bones. This union may be bony, cartilaginous, or fibrous in nature. The two most common locations for coalition are at the talocalcaneal and
calcaneonavicular joints. These locations account for approximately 90% of all coalitions.52 Less commonly, coalitions have been described at the talonavicular, calcaneocuboid, navicular cuneiform, and cuboid navicular joints. Previously it had been suggested that the etiology of tarsal coalition involved the incorporation of accessory ossicles into adjacent tarsal bones.53 In 1955, Harris54 performed microscopic dissection of fetal hindfeet and demonstrated a failure of mesenchymal separation. This failure of segmentation has become the most widely accepted theory regarding the etiology of this disorder. It generally is described as an autosomally dominant disorder with incomplete penetrance.55,56 The incidence of tarsal coalition has been estimated to be less than 1%.57 The incidence probably was underestimated before the use of CT scans. Further confounding the incidence is the asymptomatic nature of a large percentage of coalitions. In 1974, Leonard58 studied the first-degree relatives of 31 patients with tarsal coalition. He found that 39% of the first-degree relatives had coalitions on radiographs, but all were asymptomatic. Approximately 50% of coalitions are bilateral, with calcaneonavicular coalitions more likely to occur bilaterally.57,59
Clinical presentation Patients with this condition often are asymptomatic until ossification of the fibrous or cartilaginous coalition occurs. Before this time, some degree of motion is preserved at the affected joint. Once the coalition ossifies, the motion at the affected joint is lost and symptoms may arise. The timing of this ossification may vary, depending on the location of the coalition. Patients with calcaneonavicular coalitions may become symptomatic earlier (age 8-12 years) than patients with talocalcaneal coalitions (age 12-16 years).60 Patients with tarsal coalition can present with pain, stiffness, and/or a deterioration of athletic performance. Increased stresses are placed on surrounding structures as motion in the hindfoot is restricted, and this may lead to pain. Although a planovalgus position of the foot has been classically described, feet with normal arches or even a cavovarus deformity may contain a coalition.61 The symptoms are often low grade and not severe enough to prompt a visit to the doctor until a traumatic event causes a flare-up of pain. Recurrent ankle sprains often are described in athletes with tarsal coalitions.62 Forced motion beyond that which can be accommodated by the abnormal joints may lead to partial or complete ligamentous injuries. The abnormal joints are unable to dissipate the forces generated by athletic activities, and therefore the 345
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Following reduction, the foot is placed into a bulky splint. Slight eversion of the hindfoot in the splint will help to stabilize medial dislocations, and inversion will hold lateral dislocations. Plain radiographs then are obtained to verify reduction. A CT scan is recommended to rule out associated fractures. Dislocations without fractures are immobilized for 4 weeks to allow soft-tissue healing. Injuries with associated fractures will require a longer period of immobilization, typically in the range of 6 to 8 weeks. Following casting, a program of strengthening and range of motion exercises is initiated.
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Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions
increased stresses are transferred to the ligamentous structures.
Physical examination Patients tend to have a rigid flatfoot involving heel valgus, loss of the midfoot arch, and abduction of the forefoot.
4 PEARL This should be differentiated from an asymptomatic flexible flatfoot, in which heel varus and medial arch is restored with single-foot and double-foot heel rise. The degree of the deformity can be quite variable. Talocalcaneal coalitions are associated with a more severe hindfoot valgus deformity than coalitions at other sites.63 Talocalcaneal coalitions typically eliminate motion of the subtalar joint.
4 PEARL Calcaneonavicular coalitions may cause only a partial reduction of subtalar motion, with more restriction of Chopart’s motion. The patient may be tender about the hindfoot/midfoot, depending on the location of the coalition. Calcaneonavicular coalitions often cause anterolateral tenderness directly over the joint. Talocalcaneal coalitions may cause lateral tenderness over the sinus tarsi and peroneal tendons, as well as medially just anterior to the medial malleolus. A bony eminence from talocalcaneal coalitions has been described as a cause of tarsal tunnel symptoms. In one series, 30% of patients with tarsal tunnel syndrome were found to have an eminence from a talocalcaneal coalitions as a source of the symptoms.64 Peroneal spasm may or may not be present. This finding has been suggested as part of the classic presentation of this disorder; however, it is found only in the minority of cases.57,65
Radiographic evaluation Initial evaluation of the patient should include weightbearing anterior-posterior, lateral, and oblique radiographs of the affected foot. An axial heel view should be added to these three views of the foot so that the talocalcaneal joint can be inspected. These may identify the presence of a coalition and degenerative changes in the surrounding joints. A calcaneonavicular bar is best seen on the 45-degree medial oblique view. A lateral x-ray may show the ‘‘anteater nose,’’ a projection from the anterior process of the calcaneus to the navicular
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(Fig. 15-5, A) that is a sign of the calcaneonavicular coalition, as described by Oestreich et al.66 The axial heel view is the best plain radiograph for diagnosing coalitions of the middle facet of the subtalar joint. Secondary signs of a talocalcaneal coalition also may be detected on the lateral view. These include narrowing of the posterior facet of the subtalar joint, blurriness of the middle facet of the subtalar joint, beaking of the dorsal head of the talus, and rounding of the lateral process of the talus.67 CT has been established as the gold standard study for the identification of talocalcaneal coalitions.68,69 A CT scan (Fig. 15-5, B) allows one to identify the coalition, determine the extent of joint involvement, and assess any areas of surrounding degenerative changes. It can be particularly useful for preoperative planning and determining whether a coalition is resectable. It also may be used postoperatively to assess the completeness of resection, progressive degenerative changes, and recurrence of the coalition. Less commonly, MRI has been used in the workup of tarsal coalitions (Fig. 15-5, C). It may better identify nonosseous coalitions.70 The surrounding joints and soft tissues can be evaluated, as well. A radionuclide bone scan also may be useful in the diagnosis of the symptomatic patient with suspected tarsal coalition, particularly as a screening procedure.71 This test can be positive when the patient is symptomatic. Accumulation of the radionuclide most likely is the result of increased stresses at the surrounding joints or within the coalition itself.
Nonoperative treatment Typically a trial of nonoperative management is indicated in the treatment of tarsal coalitions. A study by Jayakumar and Cowell72 in 1977 found that one third of their patients responded favorably to conservative treatment. When the diagnosis is made in the adolescent who is a competitive athlete, then definitive treatment on a more expedient basis may be appropriate. In this manner, the time off from competition may be reduced. Morgan and Crawford73 looked at 12 adolescent athletes with coalitions (8 calcaneonavicular and 4 talocalcaneal). Nonoperative treatment was successful in none of the patients, and 8 of the 12 elected to undergo surgery. The usual regimen of nonoperative management for patients with mild symptoms includes anti-inflammatory medications and orthotics. For more severe symptoms, patients may undergo a trial of a short-leg walking cast for a period of 6 weeks. If the patient responds favorably to immobilization, then orthoses are used. The patient is considered to have failed nonoperative treatment if pain persists after two cast applications.
Tarsal coalition
Figure 15-5 (A) Radiograph of calcaneonavicular coalition, with ‘‘anteater nose’’ projection from anterior process of calcaneus to navicular. (B) Computed tomography scan. (C) Magnetic resonance imaging of middle facet coalition.
adolescent athletes, they reported their results in 8 athletes who underwent resection of tarsal coalitions. They found that 5 out of 6 athletes who had calcaneonavicular bars were able to return to play. Both athletes with talocalcaneal bars were also able to return to play following resection. Elkus74 examined 15 feet with 347
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Surgical treatment The most common procedures performed for tarsal coalition include resection of the coalition, selected arthrodesis, and triple arthrodesis. Previous reports have examined resection of tarsal coalitions in adolescent athletes. In Morgan and Crawford’s73 review of 12
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Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions
calcaneonavicular coalitions and 8 with talocalcaneal coalitions in a population of young athletes. All patients underwent resection of their coalitions with or without soft-tissue interposition. The majority of the patients had relief from pain (no numbers reported) with variable return of subtalar motion. The author did note that all 8 cases of talocalcaneal bar resection had improvement in motion, had decreased pain, and were able to return to athletic activity.
joint, sinus tarsi, and calcaneonavicular coalition. The coalition is resected in parallel cuts from each surface, avoiding convergence. The hindfoot is mobilized to test for adequate subtalar motion. Bone wax is generously packed into the bony surfaces. The extensor digitorum brevis is placed into the resection site and sutured in place. Closure is done in layers (Figs. 15-6 and 15-7).
TALOCALCANEAL COALITIONS CALCANEONAVICULAR COALITIONS The accepted treatment for calcaneonavicular coalitions is resection with soft-tissue interposition unless degenerative changes are present in the subtalar or midtarsal joints. Although talar beaking previously was thought to be evidence of degenerative changes, it is not a contraindication to resection.75 One contraindication to resection is the presence of a concomitant talocalcaneal coalition. Generally the bar should be resected during adolescence, but resection of bars in the adult population has been shown to be beneficial, as well.76 There is evidence that results are improved after resection of cartilaginous coalitions rather than bony bars.77 The reported outcomes following surgical excision of the coalition have been variable. Cohen et al.76 in 1996 reviewed their results when resecting coalitions in adults. They examined 12 patients, 77% of whom displayed degenerative changes before resection. All but two of the patients reported subjective relief of the preoperative symptoms. Gonzalez and Kumar77 reported on 75 feet in 48 patients with calcaneonavicular coalitions. Their results with resection and interposition with the extensor digitorum brevis muscle was good or excellent in 77% of the patients. The authors noted that their best results were in patients who had a cartilaginous coalition and who were younger than 16 years. In contrast, Andreasen78 reported results of 31 bar resections that were examined 10 to 22 years following surgery. He found 30% of the patients had mild pain and 26% had severe pain. A recurrence of the bar was seen in 67% of patients despite the use of interpositional muscle, and 96% of feet had osteoarthritic changes. Six patients required triple arthrodesis.
Technique of resection of calcaneonavicular coalition A 5- to 6-cm curvilinear incision is made just below the fibula, exposing the fascia overlying the extensor digitorum brevis. One should avoid branches of the superficial peroneal and sural nerves. The extensor digitorum brevis is reflected distally, exposing the calcaneocuboid
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Resection of the coalition also is the treatment of choice in patients with symptomatic talocalcaneal coalitions. Skeletally immature patients with smaller bars and no evidence of degenerative changes in the subtalar joint are most likely to benefit from resection.69 Contraindications to resection include patients with rigid flatfeet or degenerative changes of the subtalar and transverse tarsal joints. These patients are better served with a subtalar or triple arthrodesis. In carefully selected patients, generally 80% to 90% will report satisfactory results following a resection.79-81 The decision whether to resect the coalition or perform a fusion may be influenced by the size of the bar. Some feel that involvement of more than one half of the joint will preclude a successful resection.81 Wilde et al.82 reported unsatisfactory outcomes with middle coalition resection and fat interposition in the presence of middle facet coalition area greater than 50% of the area of the posterior facet. On the other hand, Kumar et al.80 did not find a correlation between the extent of middle facet coalition and the postoperative results in 18 feet on which resection was performed.
Technique of resection of talocalcaneal coalition A 6- to 7-cm linear incision is made just below the medial malleolus, just above the sustentaculum tali (Figs. 15-8, A and 15-9, A). Tenotomy scissors are used to dissect and identify the posterior tibial tendon, flexor digitorum longus, and tibial neurovascular bundle. The middle facet lies just under the flexor digitorum longus (FDL), often covered by minimal periosteum. The middle facet with coalition is identified and dissected, showing the extent of the coalition (Figs. 15-8, C and 15-9, B). Once the corners of the coalition are identified, excision is done using small straight osteotomes and rongeurs. The excised surfaces should be parallel to prevent contact and potential osseous fusion (Figs. 15-8, D and 15-9, C). Bone wax is placed generously on the excised surfaces, and Gelfoam is interposed. Other authors interpose fat from the surrounding tissue.76 Closure of the FDL sheath is included in the layered closure.
Talocalcaneal coalitions
Figure 15-6 Drawing demonstrating excision of calcaneonavicular coalition and interposition of extensor brevis. (A) Skin incision. (B) Exposure of the extensor brevis. (C) Reflection of the extensor brevis forward demonstrates the area of coalition. (D) Demonstration of the area of coalition to be resected. (E) Interposition of the extensor brevis muscles. (From Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 6, St Louis, 1992, CV Mosby. Used by permission.)
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CHAPTER 15
Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions
Figure 15-7 Calcaneonavicular coalition. (A) A 45-degree oblique view of the foot demonstrates the Calcaneonavicular coalition. (B) Postoperative 45-degree oblique view of the foot demonstrates adequate excision of the Calcaneonavicular coalition.
Figure 15-8 Excision of talocalcaneal coalition. (A) Skin incision. (B) Reflection of structures dorsally and plantarward to expose the area of coalition. (C) Outlining the coalition with needles. (D) Postexcision appearance of the coalition. (From Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 6, St Louis, 1992, CV Mosby. Used by permission.)
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References
Figure 15-9 (A) Incision marked on medial hindfoot. (B) Middle facet coalition with corners defined, flexor digitorum longus retracted inferiorly. (C) Coalition excised, flexor digitorum longus retracted superiorly.
8.
We would like to thank Thomas O. Clanton, MD, for contributions of pictures and figures to this chapter.
9. 10.
REFERENCES
11. 12.
1. Harper MC: The lateral ligamentous support of the subtalar joint, Foot Ankle 11:354, 1991. 2. Larsen E: Tendon transfer for lateral ankle and subtalar instability, Acta Orthop Scand 59:168, 1988. 3. Renstrom AH: Persistently painful sprained ankle, J Am Acad Orthop Surg 2:270, 1994. 4. Keefe DT, Haddad SL: Subtalar instability. Etiology, diagnosis, and management, Foot Ankle Clin 7:577, 2002. 5. Rubin G, Whitten M: The subtalar joint and the symptom of turning over on the ankle: a new method of evaluation utilizing tomography, Am J Orthop 4:16, 1962. 6. Brantigan JW, et al: Instability of the subtalar joint: diagnosis by stress tomography in three cases, J Bone Joint Surg 59A:321, 1977. 7. Chrisman OD, Snook GA: Reconstruction of lateral ligament tears of the ankle. An experimental study and clinical evaluation of seven
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patients treated by a new modification of the Elmslie procedure, J Bone Joint Surg 51A:904, 1969. Clanton TO, Berson L: Subtalar joint athletic injuries, Foot Ankle Clin 4:729, 1999. Thermann H, et al: Treatment algorithm for chronic ankle and subtalar instability, Foot Ankle Int 18:163, 1997. Laurin CA, et al: Talar and subtalar tilt: an experimental investigation, Can J Surg 11:270, 1968. Ishii T, et al: Subtalar stress radiography using forced dorsiflexion and supination, J Bone Joint Surg Br 78B:56, 1996. Heilman AE, et al: An anatomic study of subtalar instability, Foot Ankle 10:224, 1990. Harper MC: Stress radiographs in the diagnosis of lateral instability of the ankle and hindfoot, Foot Ankle 13:434, 1992. Louwerens JW, et al: Stress radiography of the talocrural and subtalar joints, Foot Ankle 16:148, 1995. Van Hellemondt FJ, et al: Stress radiography and stress examination of the talocrural and subtalar joint on helical computed tomography, Foot Ankle 18:482, 1997. Smith RW, Reischl SF: Treatment of acute lateral ankle ligament rupture in the athlete, Am J Sports Med 14:465, 1986. Wilkerson GB: Comparative biomechanical effects of the standard method of ankle taping and a taping method designed to enhance subtalar stability, Am J Sports Med 19:588, 1991. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby.
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19. Sammarco GJ, DiRaimondo CV: Surgical treatment of lateral ankle. instability syndrome, Am J Sports Med 16:501, 1988. 20. Sammarco GJ, Idusuyi OB: Reconstruction of the lateral ankle ligaments using split peroneus brevis tendon graft, Foot Ankle Int 20:97, 1999. 21. Leach RE, et al: Secondary reconstruction of the lateral ligaments of the ankle, Clin Orthop 160:201, 1981. 22. Gould N, Selligson D, Gassman J: Early and late repair of lateral ligaments of the ankle, Foot Ankle 1:84, 1980. 23. Schon LC, Clanton TO, Baxter DE: Reconstruction for subtalar instability: a review, Foot Ankle 11:319, 1991. 24. Solheim LF, Denstad TF, Roaos A: Chronic lateral instability of the ankle: a method of reconstruction using the Achilles tendon, Acta Orthop Scand 51:193, 1980. 25. Kato T: The diagnosis and treatment of instability of the subtalar joint, J Bone Joint Surg Br 77:400, 1995. 26. Pisani G: Chronic Laxity of the subtalar joint, Orthopedics 19:431, 1996. 27. Frey C, Feder KS: Arthroscopic evaluation of the subtalar joint: does sinus tarsi syndrome exist? Foot Ankle 20:185, 1999. 28. Meyer JM, Lagier R: Post-traumatic sinus tarsi syndrome. An anatomical and radiological study, Acta Orthop Scand 48:121, 1977. 29. O’Connor D: Sinus tarsi syndrome: a clinical entity, J Bone Joint Surg 40A:720, 1958. 30. Taillard W, et al: The sinus tarsi syndrome, Int Orthop 4:117, 1981. 31. Lektrakul N, et al: Tarsal sinus: arthrographic, MR imaging, MR arthrographic, and pathologic findings in cadavers and retrospective study data in patients with sinus tarsi syndrome, Radiology 219:802, 2001. 32. Klein MA, Spreitzer AM: MR imaging of the tarsal sinus and canal: normal anatomy, pathologic findings, and features of the sinus tarsi syndrome, Radiology 186:233, 1993. 33. Dozier TJ, et al: Sinus tarsi syndrome, J La State Med Soc 153:458, 2001. 34. Dufaurest P: Luxation du pied, en dehors, compliquee de l’issue de l’astragale a travers la capsule et les tegumens dechirees, J Med Chir Pharm 22:348, 1811. 35. Judcy P: Observation d’une luxation metatarsienne, Bull Fac Med Paris 11:81, 1811. 36. Broca P: Memoire sur les luxations sous-astragaliennes, Mem Soc Chir 3:566, 1853. 37. Malgaigne JF: Die Knochenbruche und Verrenkungen, Stuttgart, 1856, Reiger, p. 820. 38. Zimmer TJ, Johnson KA: Subtalar dislocations, Clin Orthop 238:190, 1989. 39. Grantham SA: Medial subtalar dislocation: five cases with a common etiology, J Trauma 4:845, 1964. 40. Goldner JL, et al: Severe open subtalar dislocations: long-term results, J Bone Joint Surg 77A:1075, 1995. 41. Ruiz Valdivieso T, de Miguel Vielba JA: Subtalar dislocation. A study of nineteen cases, Injury 2:83, 1996. 42. Merchan EC: Subtalar dislocations: long-term follow-up of 39 cases, Injury 23:97, 1992. 43. Bibbo C, et al: Injury characteristics and the clinical outcome of subtalar dislocations: a clinical and radiographic analysis of 25 cases, Foot Ankle 24:158, 2003. 44. DeLee JD, Curtis R: Subtalar dislocation of the foot, J Bone Joint Surg 64A:433, 1982. 45. Bohay DR, Manoli A: Occult fractures following subtalar joint injuries, Foot Ankle 17:164, 1996. 46. Bohay DR, Manoli A: Subtalar joint dislocations, Foot Ankle 16:803, 1995. 47. Haliburton RA, et al: Further experience with peritalar dislocation, Can J Surg 10:322, 1967.
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48. Heck BE, et al: Anatomical considerations of irreducible medial subtalar dislocation, Foot Ankle 17:103, 1996. 49. Leitner B: Obstacles to reduction in subtalar dislocations, J Bone Joint Surg 36:299, 1954. 50. Waldrop J, et al: Anatomical considerations of posterior tibialis tendon entrapment in irreducible lateral subtalar dislocation, Foot Ankle 13:458, 1992. 51. Meinhard BP, et al: Irreducible talar dislocation with entrapment by the tibialis posterior and the flexor digitorum longus tendons. A case report, Clin Orthop 286:222, 1993. 52. Tachdjian M: Pediatric orthopaedics, ed 2, Philadelphia, 1990, WB Saunders. 53. Pfitzner W: Die variationem im aufban des fusskelets, Morpho Arbeit 6:245, 1896. 54. Harris B: Anomalous structures in the developing human foot [Abstract], Anat Rec 121:399, 1955. 55. Wray JB, Herndon BN: Hereditary transmission of congenital coalition of the calcaneus to the navicular, J Bone Joint Surg 45:365, 1963. 56. Wynne-Davis R: Heritable disorders in orthopedics, Orthop Clin North Am 9:3, 1978. 57. Stormont DM, Peterson HA: The relative incidence of tarsal coalition, Clin Orthop 181:28, 1983. 58. Leonard MA: The inheritance of tarsal coalition and its relationship to spastic flat foot, J Bone Joint Surg 56B:520, 1974. 59. Mosier JM, Asher M: Tarsal coalitions and peroneal spastic flat foot: a review, J Bone Joint Surg 66A:976, 1984. 60. Olney B: Tarsal coalition. In Drennan JC, Ed, The child’s foot and ankle, New York, 1992, Raven Press. 61. Stuecker RD, Bennett JT: Tarsal coalition presenting as a pes cavovarus deformity: report of three cases and review of the literature, Foot Ankle 14:540, 1993. 62. Snyder RB, Lipscomb AB, Johnston RK: The relationship of tarsal coalitions to ankle sprains in athletes, Am J Sports Med 9:313, 1981. 63. Harris R: Rigid valgus foot due to talocalcaneal bridge, J Bone Joint Surg 37A:169, 1955. 64. Takakura Y, et al: Tarsal tunnel syndrome. Causes and results of operative treatment, J Bone Joint Surg Br 73B:125, 1991. 65. Varner KE, Michelson JD: Tarsal coalition in adults, Foot Ankle 21:669, 2000. 66. Oestreich AE, et al: The ‘‘anteater nose’’: a direct sign of calcaneonavicular coalition on the lateral radiograph, J Pediatr Orthop 7:709, 1987. 67. Beckly DE, Anderson PW, Pedegana DR: The radiology of the subtalar joint with special reference to talo-calcaneal coalition, Clin Radiol 26:333, 1975. 68. Kulik SA, Clanton TO: Tarsal coalition, Foot Ankle 17:286, 1996. 69. Hertzenberg JE, et al: Computerized tomography of talocalcaneal tarsal coalition: a clinical and anatomic study, Foot Ankle 6:273, 1986. 70. Weschler RJ, et al: Tarsal coalition: depiction and characterization with CT and MR imaging, Radiology 193:447, 1994. 71. Deutsch AL, Resnick D, Campbell G: Computed tomography and bone scintigraphy in the evaluation of tarsal coalition, Radiology 144:137, 1982. 72. Jayakumar S, Cowell HR: Rigid flatfoot, Clin Orthop 122:77, 1977. 73. Morgan RCJr, Crawford AH, et al: Surgical management of tarsal coalitions in adolescent athletes, Foot Ankle 7:183, 1986. 74. Elkus RA: Tarsal coalition in the young athlete, Am J Sports Med 14:477, 1986. 75. Swiontkowski MF, et al: Tarsal coalitions: long-term results of surgical treatment, J Pediatr Orthop 3:287, 1983. 76. Cohen BE, et al: Success of calcaneonavicular coalition resection in the adult population, Foot Ankle 17:569, 1996.
References 80. Kumar SJ, et al: Osseous and non-osseous coalition of the middle facet of the talocalcaneal joint, J Bone Joint Surg 74A:529, 1992. 81. Scranton PE Jr: Treatment of symptomatic talocalcaneal coalition, J Bone Joint Surg 69A:533, 1987. 82. Wilde PH, et al: Resection for symptomatic talocalcaneal coalition, J Bone Joint Surg 76B:797, 1994.
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77. Gonzalez P, Kumar SJ: Calcaneonavicular coalition treated by resection and interposition of the extensor digitorum brevis muscle, J Bone Joint Surg 72A:71, 1990. 78. Andreasen E: Calcaneonavicular coalition: late results of resection, Acta Orthop Scand 39:424, 1968. 79. McCormack TJ, et al: Talocalcaneal coalition resection: a 10-year follow-up, J Pediatr Orthop 17:13, 1997.
.........................................C H A P T E R 1 6 Diagnostic and operative ankle and subtalar joint arthroscopy C. Niek van Dijk, P.A.J. deLeeuw, and Rover Krips CHAPTER CONTENTS ...................... History of the technique
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Specific indications
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Indications and contraindications
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References
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Surgical technique
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Further reading
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HISTORY OF THE TECHNIQUE Arthroscopy has revolutionized the practice of orthopaedic surgery since the mid-1970s. After a long history of sporadic attempts at arthroscopy, technologic breakthroughs in Japan and several surgical pioneers in North America launched widespread interest in percutaneous joint surgery. Tagaki in 1939 described systematic arthroscopic assessment of the ankle joint.1 Watanabe published a series of 28 ankle arthroscopies in 1972, followed by Chen in 1976.2 In the 1980s, several publications followed.3,4 Over the last 15 years, arthroscopy of the ankle joint has become the most important diagnostic and therapeutic procedure for chronic and posttraumatic complaints of the ankle joint. Interest in ankle arthroscopy has increased steadily following successful clinical experience with arthroscopy of the knee and shoulder.5 This rapid rise in the popularity of foot and ankle arthroscopy is partly because other noninvasive techniques cannot adequately diagnose disorders in these joints. To operate in the central and posterior ankle, some type of distraction device is needed. Invasive external distraction was tried in the early 1980s. A noninvasive technique was first described by Yates and Grana in 1988.6 With the advent of better small-joint arthroscopes and instrumentation, and the production of more efficient noninvasive distraction devices, the development of tendoscopic surgery, and the introduction of a two portal technique for posterior ankle problems, ankle arthroscopy further developed to the current state. However, the dynamic nature of arthroscopy necessitates constant improvements that will continue to allow this field to
grow. Ankle arthroscopy has become an integral part of modern orthopaedic surgery. Arthroscopic procedures can be used most successfully when practiced with a firm understanding of their subtle refinements, limitations, and risks.
INDICATIONS AND CONTRAINDICATIONS The key point in the assessment of ankle joint pathology is the clinical diagnosis. By means of a clinical diagnosis, an indication is set for an arthroscopic intervention. Furthermore, the clinical diagnosis is essential for preoperative planning.7 The clinical diagnosis is based on history, symptoms and signs, and radiographic examination. Anterior problems include soft-tissue or bony impingement, synovitis, loose bodies, or ossicles. More centrally located complaints can originate from an osteochondral defect or arthrosis, whereas posterior problems can be caused by intra-articular pathology, such as posterior impingement syndrome (os trigonum); posttraumatic calcifications; loose bodies or synovitis; or by periarticular posterior ankle pathology, such as peroneal tendon, posterior tibial tendon, or flexor hallucis longus (FHL) pathology. In posterior ankle disorders, especially, differentiation from subtalar pathology is sometimes difficult. The relative contraindications for ankle arthroscopy include moderate degenerative joint disease with restricted range of motion, a significantly reduced joint space, severe edema, and tenuous vascular status.8
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
The absolute contraindications for ankle arthroscopy include absence of a clinical diagnosis, severe degenerative joint disease, and localized soft-tissue infection. However, if septic arthritis already is present, ankle arthroscopy is indicated, because it is a useful tool for drainage, debridement, and lavage of the joint.9
SURGICAL TECHNIQUE Operative setup ............................................................. The procedure generally is carried out as outpatient surgery under general anesthesia or epidural anesthesia. Patients can be placed in various positions. Most surgeons prefer the supine position with slight elevation of the ipsilateral buttock. A tourniquet is placed around the upper thigh. The heel of the affected foot rests on the very end of the operating table, thus making it possible for the surgeon to fully dorsiflex the ankle by leaning against the sole of the patient’s foot. For the treatment of posterior ankle problems, the patient is placed in prone position (Fig. 16-1). A tourniquet is applied and a small support is placed under the lower leg, making it possible to move the ankle freely. There are some important considerations in deciding whether to use dorsiflexion or traction for routine anterior ankle arthroscopy. When saline is introduced in the dorsiflexion position, the anterior working area ‘‘opens up’’ and any bony or soft-tissue impediment in front of the medial malleolus, in front of the lateral malleolus, at the talar neck, or at the distal tibia can be visualized and treated. For the treatment of anterior impingement lesions, synovitis, ossicles, and loose bodies, it therefore is beneficial to
perform the procedure without distraction. In this dorsiflexed position, the talus is concealed in the joint, thereby protecting the cartilage from potential iatrogenic damage. Loose bodies usually are located in the anterior compartment of the ankle joint. Dorsiflexion creates an anterior working area and makes removal easy.10 Distracting the joint makes it possible for the loose body to ‘‘fall’’ into the posterior aspect of the joint, thus making removal more difficult or impossible by an anterior approach. The same is true for the removal of ossicles and bony spurs by chisel or burr. Distraction of the joint results in tightening of the anterior capsule, thus making it more difficult to identify anterior osteophytes, ossicles, loose bodies, and soft-tissue impediments. Furthermore, when portals are created and instruments are introduced in the distracted position, this may result in iatrogenic cartilage damage at the talar dome.7 The main reason for inspection of the talar dome and tibial plafond is for treatment of an osteochondral defect. A clinical diagnosis must be established preoperatively using history, physical examination, and standard x-rays. In case of doubt about the existence or the exact location and size of a defect, a preoperative spiral computed tomography (CT) scan or magnetic resonance imaging (MRI) can be performed. Knowing the exact location of a defect makes it possible to decide preoperatively whether distraction will be necessary or whether the osteochondral defect can be approached in a forced plantarflexed position of the foot. In our experience, more than 90% of medial and lateral talar dome lesions can be treated in a hyperplantarflexed position.7 Distraction may be beneficial when an osteochondral defect is located in the posterior part of the medial or lateral talar dome or tibial plafond or when a soft-tissue impediment, ossicles, or an impregnated loose body is located in the joint space between fibula and tibia (intrinsic syndesmotic area).11,12 For posterior ankle problems, for example an osteochondral defect in the posterior quarter of the talar dome or in the posterior part of the tibial plafond, two-portal posterior ankle arthroscopy is an important alternative (Fig. 16-2).13
Arthroscopic equipment .............................................................
Figure 16-1 For posterior ankle arthroscopy, the patient is placed in prone position. A tourniquet is applied and a small support is placed under the lower leg, making it possible to move the ankle freely.
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A 4.0-mm and 2.7-mm arthroscope with 30-degrees obliquity can be used for ankle arthroscopy. The new small-diameter, short arthroscopes yield an excellent picture that is difficult to distinguish from a standard 4.0-mm scope. The small-diameter arthroscope sheet, however, cannot deliver the same amount of irrigation fluid per time as the standard sheet. This is an important drawback when motorized instruments are used because these cases must benefit from an adequate amount of irrigation fluid. For routine arthroscopic procedures such as anterior impingement syndrome, loose body removal, treatment of synovitis, and the vast majority of osteochondral defects, it is beneficial to use the
Surgical technique
4.0-mm arthroscope. A 2.7-mm arthroscope should be reserved for the treatment of osteochondral defects of the posterior third of the talar dome (when not approached by a posterior ankle arthroscopy), pathology of the articular part of the tibiofibular joint, such as a soft-tissue impediment or impregnated ossicles or loose bodies, or other posterior ankle problems that are treated by an anterior approach. Use of a 2.7-mm scope usually necessitates the creation of a third posterolateral portal to maintain adequate flow in the joint.
Irrigation Different fluids can be used for arthroscopic irrigation during ankle and foot arthroscopy. Lactated Ringer’s is the most commonly used fluid because it is physiologically compatible with articular cartilage and is rapidly reabsorbed if extravasated from the joint. Glycine and normal saline also can be used. When a 4-mm arthroscope is used, gravity inflow usually is adequate if the fluid is introduced through the arthroscope sheet. When a 2.7-mm arthroscope is used, the gravity inflow should be introduced through a separate (posterolateral) cannula. An alternative is to use an arthroscopic pumping device. Accessory instruments An 18-gauge spinal needle is used to distend the joint and to locate the anterolateral portal. The spinal needle allows precise positioning under direct vision of the portals. The probes used in ankle arthroscopy should be about 1.5 mm in diameter to reach the small recesses of the gutters and to lift up under loose articular cartilage. An angled tip is desirable to touch over the dome-shaped talus and flat tibia. Another important instrument is the grasper. For the removal of small, loose bodies in soft tissue, a flat-tipped grasping forceps
Portals for anterior ankle arthroscopy ............................................................. Portals provide an entry to visualize the structures of the ankle and foot. Proper portal placement is critical to performing good diagnostic and therapeutic arthroscopy.14 If the portals are positioned improperly, visualization can be impaired, making diagnosis and treatment more difficult. Two primary portals are used in routine ankle arthroscopy: the anteromedial and anterolateral portals. The anteromedial portal always is made first because it is easy to access. This is especially true with the ankle in hyperdorsiflexion. The exact point of entry in this position is easily reproducible, and the risk of neurovascular damage is minimal. Accessory anterior portals are located just in front of the tip of the medial or lateral malleolus. Some authors recommend routine placement of posterior portals in ankle arthroscopy. In these cases, a posterolateral portal is recommended. Because of the potential for serious complications, most authors feel that the posteromedial portal is contraindicated when performing anterior ankle arthroscopy.15
Anteromedial portal The anteromedial portal is placed just medial to the anterior tibial tendon at the joint line (Fig. 16-3). Care must be taken not to injure the saphenous vein and nerve transversing the ankle joint along the anterior edge of the medial malleolus. In the hyperdorsiflexed position, a local depression can be palpated. In the horizontal plane, this depression is located between the anterior tibial rim and the talus. The surgeon’s palpating thumb first detects the interval in the horizontal plane and subsequently locates the vertical position. In the vertical position, the anterior tibial tendon is the landmark. One should palpate the anterior tibial in the 357
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Figure 16-2 Two-portal posterior ankle arthroscopy is an important alternative for the treatment of posterior ankle problems.
with fine teeth can be used. For larger loose bodies and soft-tissue fragments, a cup-shaped, jaw-grasping forceps with serrated edges can be used. Small-joint basket forceps with different tip designs help to remove soft-tissue and chondral fragments. Various small-joint curettes, either straight or curved, are available. These instruments are particularly valuable for removing osteochondral lesions and trimming of articular cartilage edges. Small-joint osteotomes and chisels are available to remove osteophytes and ossicles and can facilitate tissue elevation. Sometimes a small periosteal elevator can be useful. Motorized instruments can excise larger volumes of tissue than conventional hand instruments and suction it quickly out of the joint. They also can be used for debridement of large osteochondral defects. A power burr is useful for abrading or excising hard bone fragments. Holes can be drilled in the subchondral bone to enhance vascularization and to stimulate the repair process.
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-3 Left ankle. The anteromedial portal is placed just medial to the anterior tibial tendon at the joint line. Care must be taken not to injure the saphenous vein and nerve transversing the ankle joint along the anterior edge of the medial malleolus.
dorsiflexed position. In this dorsiflexed position the anterior tibial tendon moves 1 cm lateral. The location of the anteromedial portal now can be marked onto the skin just medial from the anterior tibial tendon. By moving the ankle joint from the plantarflexed position to the dorsiflexed position, the talus can be felt to move in relation to the distal tibia. The surgeon’s thumb gets locked into this ‘‘soft spot’’ in the hyperdorsiflexed position. A small longitudinal incision is made through the skin only just medial from the anterior tibial tendon. Blunt dissection is performed with a mosquito clamp through the subcutaneous layer and through the capsule into the ankle joint. With the ankle in the forced dorsiflexed position, cartilage damage is avoided. In this forced dorsiflexed position, the arthroscope shaft with the blunt trocar is introduced. When the trocar is felt to contact the underlying bony ‘‘joint line,’’ the shaft with the blunt trocar is gently pushed further into the anterior working area in front of the ankle joint toward the lateral side. The anterior compartment is irrigated and inspected. The next portal to make is the anterolateral portal.
Anterolateral portal The anterolateral portal is the second standard anterior portal. It is placed just lateral to the tendon of the peroneus tertius at or slightly proximal to the joint line (Fig. 16-4). It is made under direct vision by introducing a spinal needle. In the horizontal plane, it is situated at the level of the joint line. In the vertical plane, the anterolateral portal is located lateral to the common extensor tendons and the peroneus tertius tendon. Care must be taken to avoid the superficial
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358
peroneal nerve because it runs subcutaneously. This subcutaneous nerve often can be palpated or visualized by placing the foot in forced hyperplantarflexion and supination. The lateral dorsocutaneous branch of the superficial peroneal nerve thus can be visualized. The intermediate dorsal cutaneous branch of the superficial peroneal nerve crosses the anterior aspect of the ankle joint superficial to the common extensor tendons. Damage to this branch can be avoided by staying lateral to the extensor tendons. Once the lateral branch is identified, its position can be marked with a marking pen on the skin. The location of the anterolateral portal may vary depending on the location of the lesion in the ankle joint. For the treatment of anteromedial ankle pathology, the anterolateral portal can be placed slightly above the level of the ankle joint and as close to the peroneal tertius tendon as possible. For the treatment of lateral pathology, the anterolateral portal is placed at the level of the joint line and more laterally. After a small skin incision has been made, the subcutaneous layer and capsule are divided bluntly with a mosquito clamp.
Accessory inferior anteromedial and anterolateral portals The lateral accessory portal is placed just below the anterior talofibular ligament. After introduction of a spinal needle, a skin incision is made in line with the anterior talofibular ligament. The bladeknife can be introduced
Figure 16-4 Left ankle. The anterolateral portal is placed just lateral to the tendon of the peroneus tertius at or slightly above the joint line.
Surgical technique
into the joint under direct vision. On the medial side (after locating the portal with the spinal needle), the incision is made in line with the fibers of the deltoid ligament. The knife can be introduced directly into the joint under direct vision.
Transtibial and transmalleolar portals A transmalleolar portal may be used for debridement and drilling of lesions of the talar dome. It is used most often in combination with ankle distraction. A special guide facilitates the placement of the portal and of the Kirschner wires that are used to drill the defect. Transtibial or transmalleolar drilling with a guiding system is especially useful for tibial plafond lesions. For the treatment of talar dome lesions, the transmalleolar portal has the disadvantage of causing damage to the cartilage of the medial malleolus opposite the osteochondral talar defect and therefore is not recommended to perform on a routine basis.
Portals for posterior and subtalar ankle arthroscopy
............................................................. The anatomic structures in the posterior ankle compartment are in close relation to each other. Operative treatment can use either a posterolateral or a posteromedial approach.13 Both imply the risk of damaging neurovascular structures. Posterolaterally, branches of the sural nerve and the lesser saphenous vein are at risk; posteromedially, the neurovascular bundle and its branches are at risk.14,15
Posterolateral portal The posterolateral portal is made at the level or slightly above the tip of the lateral malleolus, just lateral to the Achilles tendon (Fig. 16-5, A). After making a vertical
stab incision, the subcutaneous layer is split by a mosquito clamp. The mosquito clamp is directed anteriorly, pointing in the direction of the interdigital webspace between the first and second toe (Fig. 16-5, B). When the tip of the clamp touches the bone, it is exchanged for a 4.5-mm arthroscope shaft with a blunt trocar pointing in the same direction. By palpating the bone in the sagittal plane, the level of the ankle joint and subtalar joint most often can be distinguished because the prominent posterior talar process can be felt as a posterior prominence between both joints. It is not necessary to enter either joint capsule. The blunt trocar is situated extra-articularly at the level of the ankle joint. The blunt trocar is exchanged for a 30-degree, 4.0-mm arthroscope. The direction of view is lateral to prevent damage to the lens system.
Posteromedial portal This portal is made just medial to the Achilles tendon. In the horizontal plane, it is located at the same level as the posterolateral portal (Fig. 16-6). After the skin incision has been made, a mosquito clamp is introduced and directed toward the toward the arthroscope shaft, which already was introduced through the posterolateral portal. When the mosquito clamp touches the shaft of the arthroscope, the shaft is used as a guide to travel anterior in the direction of the ankle joint. All the way, the mosquito clamp must touch the arthroscope shaft until the mosquito clamp touches the bone. The arthroscope is pulled slightly backward and slides over the tip of the mosquito clamp until the tip of the mosquito clamp comes to view. The clamp is used to spread the extra-articular soft tissue in front of the tip of the camera. In situations in which scar tissue or adhesions are
Figure 16-5 (A) Right ankle. The posterolateral portal is made level to or slightly above the tip of the lateral malleolus just anteriorly to the Achilles tendon. (B) Left ankle. The mosquito clamp is directed toward the first interdigital webspace.
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Figure 16-6 Right ankle. The posteromedial portal is made just medial to the Achilles tendon. In the horizontal plane, it is located at the same level as the posterolateral portal.
present, the mosquito clamp is exchanged for a 5-mm, full-radius shaver. The fatty tissue overlying the joint capsule can be partially removed. At the level of the ankle joint, the posterior tibiofibular ligaments and the posterior talofibular ligament can be recognized. After removal of the very thin joint capsule of the subtalar joint, the posterior compartment of the subtalar joint can be visualized. The posterior talar process can be freed of scar tissue, and the FHL tendon can be identified. The FHL is an important landmark to prevent damage to the more medially located neurovascular bundle (Fig. 16-7). On the medial side, the tip of the medial malleolus and the deep portion of the deltoid ligament can be visualized. By opening the joint capsule from inside out at the level of the medial malleolus, the tendon sheath of the posterior tibial tendon can be opened and the arthroscope can be introduced into the tendon sheath. The posterior tibial (PT) tendon can be inspected. The same procedure can be followed for the flexor digitorum longus (FDL) (Fig. 16-8). With application of manual distraction to the os calcis, the posterior compartment of the ankle opens up and the arthroscope and shaver can be introduced into the posterior ankle compartment. A total synovectomy and/or capsulectomy can be performed. The talar dome can be inspected over almost its entire surface, as can the complete tibial plafond. An osteochondral defect or subchondral cystic lesion can be identified, debrided, and drilled. The posterior syndesmotic ligaments are inspected and, if hypertrophic, partially resected. Removal of a symptomatic os trigonum, a nonunion of a fracture of the posterior talar process, or a symptomatic large posterior talar prominence involves partial detachment of the posterior talofibular ligament and release of the flexor retinaculum, both of which attach
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Figure 16-7 Left ankle. After removal of the thin joint capsule, the posterior ankle and subtalar joint can be visualized. The posterior talar process can be freed of scar tissue and the flexor hallucis longus tendon can be identified. This is an important landmark to prevent damage to the more medially located neurovascular bundle.
Figure 16-8 Right ankle. By opening the joint capsule from inside out at the level of the medial malleolus, the tendon sheath of the posterior tibial tendon can be opened and the scope can be introduced into the tendon sheath of the posterior tibial tendon. This patient has a tendinitis of the posterior tibial tendon, recognized by the increased vascularity on and around the tendon. Higher up, a vincula is identified. The direction of the view is from distal to proximal.
Surgical technique
to the posterior talar prominence, and removal of the scar tissue on the posterior talar process. Removal of the pathologic bony fragment can be done by reduction from medial to lateral with a burr or by use of a 4-mm osteotome or a small rasp. When using the osteotome it is important not to start too far anterior to prevent damage to the subtalar joint. Release of the FHL involves detachment of the flexor retinaculum from the posterior talar process. Adhesions surrounding the flexor tendon can be removed. On the lateral side, the peroneal tendons can be inspected (Fig. 16-9). When a tight and thickened crural fascia is present, this can hinder the free movement of instruments. It can be helpful to enlarge the hole in the fascia by means of a punch or shaver. Bleeding is controlled by electrocautery at the end of the procedure.
Arthroscopic anatomy ............................................................. The ankle joint can be divided into anterior and posterior cavities, each of which can then be subdivided further into three compartments for methodologic inspection of the ankle joint. Ferkel15 developed a 21-point systematic examination (Table 16-1) of the anterior, central, and posterior ankle joint to increase the accuracy and reproducibility of the arthroscopic examination. For posterior ankle problems, Van Dijk et al.13 reported on a two-portal approach with the patient in the prone position, specifically for close
visualization of the posterior compartment of the ankle and subtalar joint. He developed a 14-point systematic examination for the hindfoot and posterior ankle joint (Table 16-2).
Table 16-1 the ankle
The 21-point arthroscopic examination of
Anterior: Deltoid ligament Medial gutter Medial talus Central talus and overhang Lateral talus Trifurcation of the talus, tibia, and fibula Lateral gutter Anterior gutter Central: Medial tibia and talus Central tibia and talus Lateral tibiofibular or talofibular articulation Posterior inferior tibiofibular ligament Transverse ligament Reflection of the flexor hallucis longus Posterior: Posteromedial gutter Posteromedial talus Posterocentral talus Posterolateral talus Posterior talofibular articulation Posterolateral gutter Posterior gutter From Ferkel, Fischer 199615
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Figure 16-9 Left ankle. During posterior ankle arthroscopy, the peroneal tendons can be inspected on the lateral side.
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Table 16-2 The 14-point hindfoot endoscopic examination 1. Lateral talocalcaneal articulation 2. Flexor hallucis longus retinaculum 3. Flexor hallucis longus tendon 4. Posterior talar process 5. Posterior talofibular ligament 6. Posterior tibiofibular ligament 7. Transverse tibiofibular ligament 8. Tip of the medial malleolus/medial malleolus 9. Posteromedial gutter 10. Posteromedial talus/tibia 11. Posterocentral talus/tibia 12. Posterolateral talus/tibia 13. Posterolateral gutter 14. Tip of lateral malleolus Additional (when indicated): Posterior tibial tendon Flexor digitorum tendon Peroneal tendons From Van Dijk CN, Scholten PE, Krips R: Arthroscopy 16:871, 2000.
Anterior ankle examination The anterior arthroscopic examination always is performed initially through the anteromedial portal and then through the anterolateral portal. The structures that can be visualized are the following (from medial to lateral): (1)The deep portion of the deltoid ligament as it arises from the tip of the medial malleolus and its fibers run vertically down to the medial trochlear surface of the talus. This is an area where ossicles may be hidden, and it should be evaluated carefully for pathology. (2) Also noted is the articular surface of the tip of the medial malleolus as it corresponds and articulates with the medial talar dome and the posterior recess and posterior ligaments. The medial gutter includes the area from the deltoid ligament to below the medial dome of
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the talus. Areas of articular damage here should be carefully noted. The tibia articulates with the medial dome of the talus. This is the medial corner of the ankle. In this region, the anterior articular margin of the tibia deviates from its more horizontal configuration centrally and laterally to a more convex configuration in the coronal plane. At this medial articular notch, the arthroscope may be maneuvered most easily into the central and posterior aspects of the joint without damaging the articular surfaces. The distal portion of the tibial lip directs slightly anteriorly in the sagittal plane. This portion of the tibia articulates within a depression in the talar surface and is called the sagittal groove. This groove lies between the medial and lateral shoulders of the talus and projects from anterior to posterior. At the area between the anterior tibial lip and the capsule is a periosteum-covered subchondral bone, the synovial recess. This extends from medial all the way to the lateral portion of the ankle. This is where tibial osteophytes develop and synovium and capsule become adherent at the margins of the osteophyte. More laterally, the trifurcation includes the distal lateral tibial plafond, the lateral dome, and the fibula and is bounded by the anterior inferior tibiofibular ligament superiorly. This relation is important in the ankle, because this is often the site of soft-tissue pathology. The syndesmotic or anterior inferior tibiofibular ligament runs at approximately a 45-degree angle from the lateral portion of the distal tibia to the fibula, just below the level of the lateral talus. The anterolateral talar dome also is the site of osteochondral lesions of the talus, and access into ankle joint usually is easy in this region. The lateral gutter is the space between the medial border of the fibular articulation and the lateral border of the talar articulation. It extends from below the anterior inferior tibiofibular ligament to the anterior talofibular ligament. This often is the site of chondromalacia and ossicles at the tip of the fibula within the ligament substance. The anterior talofibular ligament lies intracapsular and runs from the tip of the fibula to the inferior lateral portion of the talus. It can be easily reached for a shrinkage procedure in case of laxity in patients with chronic anterolateral ankle instability. The anterior gutter represents the capsular reflection anteriorly of the ankle as it inserts along the talar neck. There is a normal bare area proximal to the capsular insertion, similar to the area on the central portion of the distal tibia. A synovial recess also can be found at the anterior inferior aspect of the talar dome. In this area, anterior talar osteophytes may articulate or butt against osteophytes of the anterior tibial lip.10
Posterior ankle examination Using a posterolateral and posteromedial portal with the patient in the prone position, one first approaches
Surgical technique
the fatty tissue overlying the joint capsule (Fig. 16-10). This tissue can partially be removed. At the level of the ankle joint, the posterior tibiofibular ligaments and the posterior talofibular ligament can be recognized. After removal of the very thin joint capsule of the subtalar joint, the posterior compartment of the subtalar joint can be visualized. The posterior talar process can be freed of scar tissue and the FHL tendon identified. The FHL tendon is an important landmark to prevent damage to the more medially located neurovascular bundle. When manual distraction is applied to the os calcis, the posterior compartment of the ankle joint opens up and can be visualized. The arthroscope and instruments can be introduced into the posterior ankle compartment. Procedures such as a synovectomy and/ or capsulectomy of both ankle and subtalar joint can be performed. On the medial side, the tip of the medial malleolus, as well as the deep portion of the deltoid ligament, can be visualized. Opening the joint capsule from inside out at the level of the medial malleolus permits the tendon sheath of the posterior tibial tendon to be opened and the arthroscope to be introduced into the tendon sheath. The posterior tibial tendon can be inspected. The talar dome and nearly the entire surface of the complete tibial plafond can be inspected, as well. An osteochondral defect or subchondral cystic lesion can be identified, debrided, and drilled. The posterior syndesmotic ligaments are inspected and, if hypertrophic, partially resected. The intrinsic syndesmotic area and the posterior talofibular ligament can be inspected (Figs. 16-11 and 16-12). Removal of a symptomatic os trigonum or a nonunion of fracture of the posterior talar process involves partial detachment of the posterior
Figure 16-11 Left ankle. Removal of a symptomatic os trigonum (OT) or a nonunion of fracture of the posterior talar process involves partial detachment of the posterior talofibular ligament and release of the flexor retinaculum, both of which attach to the posterior talar prominence.
Figure 16-12 Left ankle. Removal of a symptomatic os trigonum (OT) involves partial detachment of the posterior talofibular ligament (PTFL) and release of the flexor retinaculum, both of which attach to the posterior talar prominence (see also Fig. 16-13).
talofibular ligament and release of the flexor retinaculum, both of which attach to the posterior talar prominence. Release of the FHL tendon involves detachment of the flexor retinaculum from the posterior talar process (Fig. 16-13). Adhesions surrounding the flexor tendon 363
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Figure 16-10 Right ankle. Using a posterolateral and posteromedial portal with the patient in the prone position, one first approaches the fatty tissue overlying the joint capsule. This tissue can be partially removed.
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
SPECIFIC INDICATIONS Anterior ankle impingement .............................................................
Figure 16-13 Left ankle. Release of the flexor hallucis longus retinaculum from the posterior talar process to remove a symptomatic os trigonum (OT) (see also Figs. 16-11 and 16-12).
can be removed. On the lateral side, the peroneal tendons can be inspected. A tight and thickened crural fascia can hinder the free movement of instruments; it can be helpful to enlarge the defect in the fascia by means of a punch or shaver.
Anterior ankle impingement syndrome is a clinical diagnosis characterized by anterior ankle pain with recognizable pain and a (slightly) limited dorsiflexion.10,16 Clinically, the patient complains of anterior joint pain made worse after activity such as walking up stairs or hills. Squatting or running is especially bothersome. Tenderness with recognition is localized over the anterior aspect of the ankle joint. Forced ankle dorsiflexion sometimes can provoke the complaints, but in most patients this test is negative. Plain radiographs may demonstrate anterior osteophytes. Additional oblique views (AMI views) can be helpful to demonstrate anteromedially located osteophytes (Fig. 16-14, A and B).16,17 In case of anterior ankle pain with negative x-ray findings, the most likely cause of the complaints is an anterior soft-tissue impediment.18 Congenital plicae within the ankle, posttraumatic scar tissue, adhesions, or ganglions all may act as a local soft-tissue impediment with local swelling and recognizable pain on palpation. Scoring systems for anterior impingement use the location (tibia or talus) and size of osteophytes as prognostic factors for postoperative success. Scranton et al.19 compared open resection with arthroscopic resection of painful anterior impingement spurs. They categorized ankle spurs from grades 1 through 4 according to the
Figure 16-14 (A) Plain lateral radiographs do not always demonstrate anterior located osteophytes, especially when they are located anteromedially. (B) Additional oblique views (AMI) in the same patient as in A now demonstrate anteromedially located osteophytes.
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Specific indications
size of spurs and degree of involvement of the ankle, and demonstrated that the treatment and recovery correlated with the grade. Grades 1, 2, and 3 spurs could be resected arthroscopically or by arthrotomy. Grade 4 spurs initially were not thought to be appropriate for arthroscopic resection. However, as experience has increased, grade 4 spurs also can be resected arthroscopically. The reproducibility of this classification system may be doubtful because the correlation was assessed with outcomes at short-term follow-up (10 weeks postoperatively). It has been determined that the degree of osteoarthritic changes influences the outcome of treatment. Osteophytes without joint space narrowing are not a manifestation of osteoarthrosis; subsequently a ‘‘normal’’ joint remains after removal of these spurs. A classification for anterior ankle impingement based on the degree of degeneration was developed (Table 16-3).10 The results at long-term follow-up show that the use of this osteoarthritic classification is more discriminating than the impingement classification of Scranton and McDermott as a predicting value for the outcome of arthroscopic surgery for anterior ankle impingement.10,19 Soft-tissue pathology accounts for about 30% to 50% of lesions seen in the ankle joint.18 The lesions usually involve the synovium, but the capsule or ligamentous tissues also may be affected. Soft-tissue impingement often is the primary cause of chronic ankle pain, usually after an ankle sprain. This can occur along the syndesmosis, the anterior gutter, or the syndesmotic interval between the tibia and fibula; underneath the ankle; or posteriorly in the syndesmosis and posterior gutter.20 Impingement of soft tissue often occurs in conjunction with bony impingement. Osteophytes can impinge into the capsule and synovium, resulting in an inflammatory reaction. The pain in a patient with bony impingement is most likely caused by this soft-tissue impingement and not by the bony impediments itself.10
In normal anatomy, the lower surface of the anterior tibia and the anterior part of the medial malleolus are covered with cartilage. The anterior joint capsule attaches onto the tibia above this cartilage rim, approximately 5 mm above the joint line.21 It is this nonweight-bearing anterior cartilage rim that undergoes the osteophytic transformation (Fig. 16-15). Damage to this anterior cartilage rim is known to occur in the majority of inversion traumas. Depending on the degree of damage, a repair reaction with cartilage proliferation, scar tissue formation, and calcification follows. Additional damage by recurrent instability or forced ankle movement will further this process. Recurrent direct (micro) trauma to this anteriorly located cartilage rim could be another important factor.21 Except for a thin subcutaneous layer, parts of the involved anterior cartilage rim (especially the anteromedial and anterolateral segments) are covered only by skin. Osteophytes are seen most commonly with a beak-like prominence of bone at the anterior lip of the tibia, usually associated with a corresponding area over the anterior neck of the talus. The talar abnormality may be a defect or an opposing osteophyte (‘‘kissing lesion’’). A common location for a soft-tissue impingement is the anterolateral gutter.22 Several studies report on patients with persistent pain and swelling over the
Table 16-3 Classification system for degenerative changes of the ankle
X-ray finding
1
Normal joint or subchondral sclerosis
2
Osteophytes without joint space narrowing
3
Joint space narrowing with or without osteophytes
4
(Sub) total disappearance or deformation of the joint space
From Van Dijk CN, Tol JL, Verheyen CCPM: Am J Sports Med 25:737, 1997.
Figure 16-15 Histologic sample of anterior joint capsule covering the anterior rim of the distal tibia and talus at the level of the ankle joint. In normal anatomy, the lower surface of the anterior tibia and the anterior part of the medial malleolus are covered with cartilage. The anterior joint capsule attaches onto the tibia above this cartilage rim, approximately 5 mm above the joint line.21 It is this nonweight-bearing anterior cartilage rim that undergoes the osteophytic transformation.
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CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
anterolateral aspect of the ankle after an inversion sprain. Arthrotomy of these ankles reveals hyalinized connective tissue extending into the joint from the anterior inferior portion of the talofibular ligament. This tissue is called a ‘‘meniscoid’’ lesion by some authors.23 Patients generally have a synovitis surrounding the anterior inferior tibiofibular ligament, both in front and behind, as well as synovitis of the anterior talofibular ligament. In addition, a small ossicle or loose body may be hidden in the soft tissues at the tip of the fibula. Rarely, an adhesive thick scar band, previously described as a meniscoid lesion, is present, extending from the anterolateral aspect of the distal tibia to the lateral gutter. After surgical reconstruction of the lateral ankle ligaments, soft-tissue impingement may be present between the reconstructed ligaments and the talus. In case of anterior and anteromedial located osteophytes, an additional soft-tissue impediment usually is present. During dorsiflexion, hypertrophic synovial tissue impinges between the osteophytes. Tol et al.21,24 concluded that the cause of pain is not the osteophyte itself but a soft-tissue impingement that occurs between the osteophytes. It can be hypothesized that removal of the soft-tissue impediment without removal of spurs would be sufficient. The presence of talar and tibial osteophytes, however, reduces the anterior joint space. After an arthroscopic intervention, a hematoma will be formed postoperatively that subsequently will develop into scar tissue. The scar tissue that fills the defect will act instantly as a new anterior soft-tissue impediment. It therefore is important to remove the osteophytes to enhance more anterior and anteromedial space and diminish the chance for a recurrence of symptoms.16,21,24 Visualization of the anterior ankle joint can be improved by bringing the ankle into a forced dorsiflexion position because in this position the anterior working area opens up. Distraction makes the anterior capsule more tense over the osteophyte, and its use therefore is not recommended.10 It is important to identify the anterior and superior borders of the osteophyte, and this often requires careful elevation or peeling of soft tissues from the confines of the osteophyte.
Surgical technique The patient is placed in a supine position with slight elevation of the ipsilateral buttock. The heel of the affected ankle rests on the very end of the operating table, thus making it possible for the surgeon to fully dorsiflex the ankle joint by leaning against the sole of the patient’s foot (Fig. 16-16). After making an anteromedial skin incision, the surgeon bluntly divides the subcutaneous layer with a hemostat. A 4-mm, 30-degree arthroscope routinely is used. The anterolateral portal is made under arthroscopic control. Additional portals just
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Figure 16-16 The heel of the affected ankle rests on the end of the operating table, thus making it possible for the surgeon to dorsiflex the ankle joint fully by leaning against the sole of the patient’s foot.
anterior to the tip of the lateral or medial malleolus are used only when indicated. Osteophytes are removed by a 4-mm chisel and burr. These spurs can be identified easily when the ankle is in a fully dorsiflexed position to prevent the anterior joint capsule from covering the osteophytes. Another advantage of the forced dorsiflexion position is the fact that the talus is concealed in the joint, thereby protecting the weight-bearing cartilage of the talus from potential iatrogenic damage. The contour of the anterior tibia is first identified by shaving away the tissue just superior to the osteophyte. An overcorrection of the medial malleolus generally is pursued by shaving some of it away after resection of the osteophyte.
Rehabilitation Postoperative rehabilitation consists of a compressive bandage and partial weight bearing for 3 to 5 days. The patient is instructed to actively dorsiflex his or her ankle and foot on awakening and to continue this exercise a few times every hour for the first 2 to 3 days after surgery.
Specific indications
Osteochondral defects An important cause of residual pain after an ankle sprain is an osteochondral lesion of the talus. It is defined as the separation of a fragment of articular cartilage, with or without subchondral bone. The incidence of an osteochondral lesion after an ankle sprain probably is
underestimated because these lesions often remain undetected. The incidence has been reported to be as high as 6.5% after ankle sprains. Osteochondral defects of the talus most often occur in young adults, with a nearly equal distribution between the sexes. In the acute situation, symptoms depend on the amount of damage to the periarticular tissues and the involvement of afferent pain fibers in the subchondral bone. Usually the lesion is located in the anterolateral or posteromedial aspect of the talar dome. Histologically the medial and lateral lesions are identical, but morphologically they differ. The lateral lesions are shallow and more wafer shaped, indicating a shear mechanism of injury. In contrast, medial lesions generally are deep, cup shaped, and located posteriorly, indicating a mechanism of torsional impact. From an etiologic point of view, trauma is the most common cause of osteochondral lesions of the talus, but idiopathic osteonecrosis often may be the underlying pathologic process. In the literature the latter has been associated with alcohol abuse, use of steroids, endocrine disorders, and some hereditary conditions. Although initial symptoms may be absent, in chronic cases most patients present with intermittent pain located deep in the ankle joint that increases on weight bearing. On physical examination, signs often are lacking. A discrete limitation of range of motion with some synovitis may be present. Local tenderness on palpation with recognition is absent in most cases. Because there are no specific pathognomonic signs or symptoms, it is essential that the examining physician and radiologist be aware that an osteochondral lesion can be present. The frequent absence of radiographic changes on conventional radiographs has led to the use of more sensitive methods for detection. A heel-rise view can be helpful to detect an osteochondral lesion. A recent prospective study of Verhagen26 demonstrated that with this additional view the chance of finding an osteochondral lesion of the talus with x-ray examination is doubled (Fig. 16-17). CT scan and MRI can be helpful for the diagnosis and preoperative planning. In the prospective study of Verhagen, there was no statistically significant difference between the sensitivity and specificity of CT and MRI in detecting an osteochondral lesion of the talus. Pritsch, Cheng, Ferkel, and Applegate developed an arthroscopic staging system that correlated well with the CT classification of Ferkel and Sgaglione (1994)27-29 and the MRI classification of Anderson et al. (1989).27-32 Recently, a new arthroscopic staging system was developed by Taranow et al.,33 who classified cartilage as viable and intact (stage A) or breached and nonviable (stage B). The bone component was determined as follows: (1) stage 1 is a subchondral compression or bone bruise, (2) stage 2 lesions are subchondral cysts and are not seen acutely (these develop from stage 367
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Synovitis Synovitis can be a noninflammatory, inflammatory, or septic process of the synovium, which is most characterized by joint swelling and tenderness. Synovitis can be caused by trauma or previous surgery. A generalized or localized synovitis can occur, most often with fibrous bands and adhesions. Synovitis accounts for approximately 30% of pathology seen in the ankle joint.15 Patients usually have complaints of aching, swelling, tenderness, and other signs of joint inflammation. A history of trauma or injury is more likely to cause a nonspecific type of synovitis, either localized or generalized; however, trauma also can trigger an underlying specific pathologic process. Radiographs often are negative. The clinical manifestation of soft-tissue lesions can be divided into the following: 1. Impingement, lesions with local pain and swelling. 2. Diffuse pain, swelling, calor, restriction of range of ankle motion in all directions. 3. Deep ankle pain without recognizable pain on palpation, no local swelling, and only minor restriction of range of motion. 4. Absence of symptoms. Synovitis of the ankle may be a difficult diagnostic problem. Even after careful history, physical examination, and diagnostic testing, the diagnosis may not be readily apparent. During arthroscopy, localized or generalized inflammation of the synovia can be present. It may contain hemosiderin or fibrin debris. Scarring, fibrosis, and adhesions often are seen in relation to the synovitis. In 1997, Cheng and Ferkel25 proposed the following classification system for synovial disorders: Congenital: plicae or congenital bands within the ankle; plicae, or shelves, have been demonstrated in the knee but are difficult to find in the ankle. Congenital bands are seen as an incidental finding when examining the ankle for other types of pathology Traumatic: sprains, fractures, and previous surgery Rheumatic: rheumatoid arthritis, pigmented villonodular synovitis, crystal synovitis, hemophilia, and synovial chondromatosis Infectious: bacterial and fungal Degenerative: primary and secondary Neuropathic: Charcot joint Miscellaneous: ganglions, arthrofibrosis
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-17 A heel-rise view (left) demonstrates a posteromedially located osteochondral defect. Because of the relative posterior location of the defect, a plain anterior-posterior view (right) is not able to demonstrate this lesion.
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1 lesions), (3) stage 3 lesions are partially separated or detached fragments in situ, and (4) stage 4 represents displaced fragments. The condition of the cartilage and bone together determines the type of surgical treatment. Despite the existence of these classification systems, few authors base their decision for a specific treatment on these systems. A meta-analysis of Tol et al.34 showed that the value of preoperative radiologic staging systems was of minor value in the preoperative planning because they hardly correlate with the perioperative findings. This demonstrates the shortcoming of preoperative radiologic staging systems as a guide for the treatment strategy. Perioperative staging of osteochondral defects therefore seems more appropriate. Eventually, the most rational way of preoperative assessment of osteochondral lesions is to determine whether they are symptomatic or asymptomatic.
Figure 16-18 From anterior to posterior the talar dome can be divided into four equal parts. When an osteochondral defect is located in one of the three anterior parts it can be reached by a routine anterior ankle arthroscopy. Soft-tissue distraction might be necessary. When the lesion is located in the most posterior quarter, it can be reached only by posterior ankle arthroscopy.
Surgical technique From anterior to posterior the talar dome can be divided into four equal parts (Fig. 16-18). When the osteochondral defect is located in one of the three ‘‘anterior’’ parts of the talar dome, it can be treated by a routine anterior ankle arthroscopy. When it is located in the most posterior quarter of the talar dome, the defect should be approached by a posterior ankle arthroscopy or by means of a medial malleolar osteotomy. The current treatment consists of removal of dead bone and overlying cartilage.34 After debridement, the subchondral sclerotic zone is perforated with a burr or K-wire or by microfracturing. Preoperatively, it is desirable to decide whether to use mechanical distraction in combination with a 2.7-mm arthroscope or to use a standard 4-mm arthroscope and to treat the osteochondral defects in
the anterior working area by forcing the ankle into full plantarflexion. The osteochondral defect in the posterior quarter of the talar dome is difficult to reach in the hyperplantarflexed position in patients having a diminished plantarflexion or in case of anterior osteophytes.33,35 Routinely the procedure is performed without distraction. The standard anteromedial and anterolateral approaches are created as described earlier. In an osteochondral defect located medially, the 4-mm arthroscope is moved over to the anterolateral portal and the instruments are introduced through the anteromedial portal. For an anterolateral defect, the arthroscope remains in the anteromedial portal and the instruments are introduced through the anterolateral portal. If osteophytes are present, they are removed first by chisel and/or burr. Synovitis located anterolaterally (in case of
Specific indications
an anterolateral defect) or anteromedially (in case of an anteromedial defect) is removed by a 4.5- or 5.5-mm synovator. The extent of removal of osteophytes and synovitis is checked by bringing the ankle into plantarflexion. It now should be possible to palpate and visualize the osteochondral defects (Fig. 16-19). If this is not the case, then a further synovectomy is performed in the dorsiflexed position. After sufficient synovectomy, it should be possible to identify the lesion in the forced plantarflexed position by palpating the cartilage with a probe. Not only can the lesion be palpated with a probe
Figure 16-19 An anterolateral located osteochondral defect of the talus. By bringing the ankle in full plantarflexion, the defect can be fully debrided. Completeness of the debridement can be checked by switching portals.
but it also should be possible to visualize at least the most anterior part of the lesion. It can be helpful to add soft-tissue distraction (Fig. 16-20, A and B).24 If possible, a 3.5- or 4.5-mm synovator is now introduced into the defect. After the defect has been debrided by the synovator or curette, the arthroscope is moved over to the portal opposite the defect (the anteromedial portal in case of an anteromedial osteochondral defect) to check the completeness of the debridement. The scope then is brought back to the opposite portal and further debridement is performed. It is important to remove all dead bone and overlying, unsupported, unstable cartilage. Every step in the debridement procedure should be checked by regularly switching portals. A precise and complete debridement, with removal of all loose fragments, thus can be performed. Introduction of the instruments and the arthroscope is performed with the ankle in the fully dorsiflexed position, thus preventing iatrogenic cartilage damage. After full debridement, the sclerotic zone is performed by microfracturing technique, or multiple drill holes are made with a 2-mm burr or a 1.6-mm K-wire. A Kwire has the advantage of flexibility, whereas a 2-mm drill can break more easily if the position of the ankle is changed during drilling. When a 2-mm drill is used, a drill sleeve is necessary to protect the tissue. In posteriorly located lesions for which an anterior approach is chosen, a noninvasive traction device that allows the surgeon to change quickly from the fully dorsiflexed position (introduction of the instruments) to the distraction position offers obvious advantages. The distraction device consists of a belt around the waist of the surgeon that is connected to a noninvasive distraction loop placed around the ankle. The amount of distraction can be adjusted by leaning more or less backward (see Fig. 16-20, B).
Figure 16-20 (A) A resterilizable soft-tissue distractor can be helpful to visualize lesions that are located more posteriorly in the ankle joint. (B) The amount of soft-tissue distraction can be adjusted by leaning more or less backward.
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Loose bodies and ossicles A loose body can be bony, chondral, or osteochondral. It arises from osteophytes or defects in the talus or tibia. Ossicles, broken osteophytes, and chondral or osteochondral fragments arising from defects in the talus or tibia all can be considered loose bodies in the ankle joint. Sometimes, such a loose body is attached with scar tissue to the capsule or other structures, and then it is called a ‘‘corpus liberum pendulans.’’15 A small, loose body may cause catching symptoms along with pain, swelling, and limitation of motion. Symptoms of internal derangement may resolve if a small loose body becomes fixed to the synovial lining, ceasing to cause joint irritation. A loose body may grow by proliferation of chondroblasts/osteoblasts or may shrink because of the action of chondroblasts/osteoclasts. The physical examination may not be very revealing, with vague areas of tenderness, possible limitation of motion, and catching. Rarely is a loose body palpable. As with all ankle problems, a careful physical examination must rule out extra-articular entities that can cause symptoms similar to intra-articular lesions. Peroneal subluxation, posterior tibial tendon attrition or rupture, tarsal tunnel syndrome, sinus tarsi syndrome, stress fracture, and tendinitis must be carefully excluded by both physical examination and ancillary studies. Plain radiographs usually reveal an osseous loose body, but chondral loose bodies are not visible on routine studies. A CT or MRI study is best suited to make the distinction between an intra-articular versus an extra-articular or intracapsular abnormality. The arthroscopic approach to loose bodies is straightforward. Loose bodies localized to the anterior compartment, particularly in patients with ligamentous laxity, can be approached with a routine setup using anteromedial and anterolateral portals. However, the posterior joint also should be examined for the presence of loose bodies, which can hide in the posterior recess of the joint.13,35 A posterolateral portal can be made. Posteriorly located loose bodies can be removed best by means of a two-portal posterior approach.
Posterior ankle impingement ............................................................. Posterior ankle syndrome is a pain syndrome. The patient experiences posterior ankle pain that is present mainly on forced plantarflexion. Posterior ankle impingement is caused by overuse or trauma.13 Distinction between these two disorders seems important because posterior impingement through overuse has a better prognosis. A posterior ankle impingement syndrome is found mainly in ballet dancers and runners. There are at least 10 specific causes for posterior ankle pain: os trigonum syndrome; posttraumatic
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calcifications, loose bodies, and bony avulsions; osteochondral defects; tendinitis of the FHL tendon; tendinitis of the posterior tibial tendon; tendinitis the peroneal tendons; tendinitis of the Achilles tendon; and ankle and subtalar arthrosis.13,35
Os trigonum syndrome The os trigonum is an inconsistently present accessory bone of the foot situated at the posterolateral aspect of the talus. It appears between the ages of 8 and 11 as a secondary center of ossification and usually fuses to the talus within 1 year after its appearance. When this ossification center remains separate from the talus it is referred to as the os trigonum. According to Sarrafian, the prevalence of this ossicle ranges from 1.7% to 7.7%.36 When fusion does occur and there is a large, intact posterolateral process, it is referred to as a fused os trigonum. Since Rosenmuller first described the os trigonum in 1804, there has been controversy concerning its origin.37 McDougall38 believed it to be a secondary ossification center of the talus, whereas other authors state that it is a nonnunited fracture of the posterolateral talar process. The os trigonum usually remains asymptomatic, but an otherwise normal os trigonum can become symptomatic during or after strenuous physical activities or following an injury to the ankle. Sometimes an acute trauma in plantarflexion may result in contusion, compression, or fracture of the os trigonum or posterior process of the talus. These injuries may cause an overload posttraumatic syndrome of the os trigonum. In this condition, the os trigonum becomes painful but appears undisrupted on the lateral x-rays (Fig. 16-21). On the other hand, chronic impingement of the posterior process of the talus against the tibia caused by chronic microtrauma or overuse by repeated hyperplantarflexion movements can lead to an inflammatory process of the os trigonum. It also can result in degenerative changes in the posterior capsule of the ankle joint, adjacent ligaments, tendon, and chondrosynovial surface. Clinically, the patient complains of pain during pushoff while running. The pain often is absent during walking on level ground but appears on uneven terrain. Usually pain is complained of posterolaterally in the ankle joint but sometimes it may be located in the posteromedial region. Physical examination can reveal the presence of moderate swelling on only the medial or on both sides of the Achilles tendon, with tenderness on palpation. A forced passive plantarflexion of ankle and foot will reproduce the recognizable symptoms. With this test the examiner performs repetitive, quick, passive forced plantarhyperflexion movements. The test can be repeated in slight exorotation or endorotation of the foot relative to the tibia. The investigator should apply this rotation movement on the point of maximal plantarflexion,
Specific indications
Figure 16-21 Posttraumatic syndrome of the os trigonum of the right ankle. Plain lateral x-rays (left) reveal an undisrupted os trigonum. Additional posteromedial impingement views (PIM) with the foot in 25-degrees external rotation in the same patient show that the os trigonum is disrupted.
excellent access to the posterior ankle compartment of the ankle joint. The posterior compartment of the ankle joint thus can be visualized, and the subtalar joint, os trigonum, and FHL can be inspected. After inspection, the posterior talofibular ligament must be detached from the posterior talar process. The superior border of the posterior talar process is cleaned with the shaver, after which the FHL tendon can be inspected (Fig. 1624). The flexor retinaculum can be cut. After this has been performed, the posterior talocalcaneal ligament must be cut. Finally, the os trigonum can be detached with a chisel or small osteotome and subsequently removed (Fig. 16-25).
Posttraumatic calcifications, loose bodies, and bony avulsions Calcifications, loose chondral or osteochondral fragments, and bony avulsions may result from major trauma to the ankle joint.15 When the fragments are located in the posterior compartment of the ankle, they are most likely the result of a hyperplantarflexion trauma or a combination of strong inversion, plantarflexion, and external rotation of the tibia. In either case, an unsuspected chondral or osteochondral lesion may occur and result in a loose body floating in the posterior compartment of the ankle or subtalar joint. Osteophytes of the posterior tibial rim, an os trigonum, and even part of the posterior talar process may 371
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thereby ‘‘grinding’’ the posterior talar process/os trigonum between the posterior tibial rim and calcaneus (Fig. 16-22). A negative test rules out a posterior impingement syndrome. A positive test in combination with pain on posterolateral palpation can be followed by a diagnostic infiltration. The infiltration is performed from the posterolateral position between the prominent posterior talar process and the posterior edge of the tibia. If the pain disappears on forced plantarflexion, the diagnosis is confirmed. After clinical examination, a routine lateral radiograph of the ankle should reveal an os trigonum. Bone scanning can effectively localize osseous injuries in and around the talus by demonstrating increased uptake in the posterior talar region but is not very specific. A CT scan enables the surgeon to determine the exact location, size, and shape of the ossicle and therefore is valuable for preoperative planning (Fig. 16-23, A and B). FHL tendinitis often is present in patients with a symptomatic os trigonum with pain located posteromedially. The FHL tendon can be palpated behind the medial malleolus. By asking the patient to flex the toes repetitively with the ankle in 10- to 20-degrees plantarflexion, the FHL tendon can be palpated in its gliding channel behind the medial malleolus. During palpation there may be crepitus and recognizable pain. A two-portal (posterolateral and posteromedial) approach with the patient in the prone position gives
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Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-22 Forced passive plantarflexion test. This test will reproduce the recognizable symptoms. The examiner performs repetitive, quick, forced passive plantarhyperflexion movements. The investigator should apply rotational movements on the point of maximal plantarflexion, thereby ‘‘grinding’’ the posterior talar process/os trigonum between the posterior tibial rim and calcaneus.
break off during a hyperplantarflexion trauma and act as a loose body. After a severe inversion trauma, the posterior talofibular ligament may avulse a bony fragment from posterior talar process and may cause posterior ankle impingement. Multiple loose cartilaginous or osteocartilaginous bodies also may form in synovial chondromatosis. A small, loose body may cause catching symptoms with joint motion along with pain. Plantarflexion may be limited and painful during the hyperplantarflexion test. Plain lateral radiographs usually reveal an osseous loose body, but when located posteromedially it may overproject. An additional posteromedial impingement view (PIM) with the foot in 25-degree external rotation relative to the tibia is helpful when there is suspicion for bony pathology in posteromedial compartment of the ankle joint (see Fig. 16-21). Lesions that appear on
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Figure 16-23 (A and B) A computed tomography scan enables the surgeon to determine the exact location, size, and shape of loose ossicles and is therefore valuable for preoperative planning. (A) A loose fragment posterolateral in the ankle joint on a sagittal reconstruction. (B) Loose fragments between the distal fibula and talus of the left ankle.
routine radiographs to be loose bodies may actually be intra-articular, intracapsular, or extra-articular in location, particularly in the posterior ankle joint compartment. The location of the lesions should be determined preoperatively to avoid embarrassment of performing an arthroscopic examination for loose body removal only to find the joint free of any abnormality. A CT scan is best suited to make the distinction between an
Specific indications
in this manner. However, when the lesion is located in the most posterior quarter, the lesion can be treated by posterior ankle arthroscopy. A preoperative CT scan with sagittal image reconstructions is important to determine the exact location of the lesion (Fig. 16-26). In case of a posteromedially located osteochondral defect, the FHL tendon should be inspected routinely. The tendon can be affected because of shredding of the tendon against the defect during flexion of the great toe while walking. When the tendon is affected, the flexor retinaculum should be cut and thus the tendon released and debrided.
Figure 16-24 Right ankle. Inspection of the flexor hallucis longus tendon in its channel. The view is from proximal to distal. See also Figs. 16-6 and 16-13.
Tendinitis of the FHL tendon Tendinitis of the FHL tendon is caused most often by posterior overuse and posttraumatic injuries in ballet dancers and soccer players.39 In the majority of cases it is a concomitant finding with other pathology, such as an os trigonum, loose bodies, bony avulsions, ankle and subtalar arthrosis, and their combinations. An unexpected but consequent finding that may cause FHL tendinitis is a posteriorly located osteochondral defect. The defect is located in the posterior quarter of the talar dome on the medial side. The tendinitis is maintained during the stance phase when walking. During this phase the ankle joint is in dorsiflexion. In this position the posterior talar dome is in closest contact with the tendon. The tendon, meanwhile, is moving in the opposite direction because the toes are actively flexed to start with the push-off phase. The tendon shreds against the
Figure 16-25 Removal of an os trigonum with a chisel. On the left the flexor hallucis longus tendon is located.
intra-articular abnormality versus an extra-articular or intracapsular abnormality and to determine the exact location in the posterior ankle joint compartment. Figure 16-26 A preoperative computed tomography (CT) scan with sagittal image reconstructions is important to determine the size and location of posterior located osteochondral defects. A sagittal CT reconstruction of a left ankle with an osteochondral defect that is located at the posterior end of the talar dome.
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Osteochondral defects In sagittal plane the talar dome can be divided into four equal quarters. When an osteochondral lesion is located in one of the anterior three quarters of the talar dome, it can be approached and treated by routine anterior ankle arthroscopy. The majority of the lesions can be treated
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-27 In a cadaver specimen it is shown that the flexor hallucis longus tendon shreds against the posterior part of the talus (often the place where osteochondral defects are located) during dorsiflexion (see text).
osteochondral defects and becomes irritated and inflamed (Fig. 16-27). In this way a posteriorly located osteochondral defect can cause an FHL tendinitis. In a consecutive series of patients with FHL tendinitis, the tendinitis was accompanied by os trigonum syndrome, bony avulsions, calcifications, and localized synovitis in 40 of 50 patients. In 7 patients the FHL tendinitis was combined with a posteromedial osteochondral defect, all located in the posterior quarter of the talar dome. Thus in only 3 patients did we find an isolated FHL tendinitis to be present. The pain of an FHL tendinitis is located posteromedially. The tendon can be palpated behind the medial malleolus. By asking the patient to flex the toes repetitively with the ankle in 10- to 20-degrees plantarflexion, the FHL tendon can be palpated in its gliding channel behind the medial malleolus. The tendon glides up and down under the palpating finger of the examiner. In case of stenosing tendinitis or chronic inflammation, there may be crepitus and recognizable pain. Sometimes a nodule in the tendon can be felt to move up and down under the palpating finger.40 During posterior ankle arthroscopy, the FHL tendon is an important landmark to prevent damage to the more medially located neurovascular bundle.13,35 When a tendinitis is present, it is treated by performing a release of the flexor retinaculum (Fig. 16-28). Adhesions surrounding the FHL tendon can be removed.
Tendinitis of the posterior tibial tendon The posterior tibial tendon plays an important role in normal hindfoot function. It plantarflexes and supinates
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the foot and thus prevents valgus deformity. Several authors have described a series of stages of posterior tibial tendon dysfunction as the disease progresses from peritendinitis to elongation and degeneration of the tibialis posterior tendon with fixed valgus deformation of the foot.39 Tenosynovitis is often seen in association with flatfoot deformity or a prominent navicular tubercle and, to a lesser extent, in association with psoriatic and rheumatoid arthritis. In the early stage of posterior tibial tendinitis, tenosynovectomy can be performed if conservative treatment fails. Postsurgery and postfracture adhesions and irregularity in the contour of the posterior aspect of the tibia/medial malleolus can account for a symptomatic posterior tibial tendon. Posttraumatic calcification in the posteromedial joint capsule can produce symptoms of posterior tibial tendinitis because of the close connection of joint capsule and posterior tibial tendon sheath in this region. In a cadaveric study, we found a consistent membranous mesotendineal structure between tendon and tendon sheath.39 This thin, vincula-like structure runs between the posterior tibial tendon and tendon sheath and attaches to the tendon sheath of the flexor digitorum tendon. It runs from the proximal end all the way with a free edge approximately 4 to 5 cm above the level of the posteromedial tip of the malleolus. After traumatic injury to the ankle, these mesotendineal structures may have clinical implications. The main portal for posterior tibial tendoscopy is located directly over the tendon, 2 cm distal to the posterior edge of the medial malleolus. The distal portal is made first, with an incision through the skin. The tendon sheath is penetrated by the arthroscope shaft with
Figure 16-28 Release of the flexor retinaculum in a left ankle. Adhesions surrounding the flexor hallucis longus tendon are removed.
Specific indications
a blunt trocar. A 2.7-mm arthroscope with an inclination angle of 30 degrees is introduced (Fig. 16-29). After a spinal needle is introduced under direct vision, an incision is made through the skin into the tendon sheath to create a proximal portal. Instruments such as shaver system can be introduced. Through the distal portal a complete overview can be obtained of the posterior tibial tendon, from its insertion (navicular bone) to approximately 6 cm above the level of the tip of the medial malleolus. The complete tendon sheath can be inspected by rotating the scope over the tendon. Special attention should be given to inspect the tendon sheath covering the deltoid ligament, the posterior medial malleolus surface, and the posterior joint capsule. More proximal, the free edge of the vincula is inspected. The posterior joint capsule can be palpated and removed with a shaver system. The arthroscope is placed from the distal portal between tendon and medial malleolus. The shaver comes down from the proximal portal. Once the arthrotomy is made, the arthroscope and instruments can be manipulated into the posteromedial compartment of the ankle joint. Synovectomy or loose body removal thus can be performed.
Tendinitis of the peroneal tendons Tenosynovitis of the peroneal tendons, (recurrent) dislocation, rupture, and snapping of one of the peroneal tendons account for most of the symptoms at the posterolateral side of the ankle joint.39,40 This disorder must be differentiated from fatigue fractures of the fibula, lesions of the lateral ligament complex, and posterolateral impingement (os trigonum syndrome). Peroneal
Figure 16-30 Left ankle. The main portal for peroneal tendoscopy is located directly over the tendons 2 cm distal to the posterior edge of the lateral malleolus. The distal portal is made first. A 2.7-mm scope can be introduced. The proximal portal is created under direct vision.
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Figure 16-29 Right ankle. The distal portal for posterior tibial tendoscopy is located directly over the tendon 2 cm distal to the posterior edge of the medial malleolus. A 2.7-mm arthroscope is introduced.
tendon disorders often are associated and secondary to chronic lateral ankle instability.41 Because the peroneal muscles act as lateral ankle stabilizers, more strain is placed on their tendons in the presence of chronic lateral instability, resulting in hypertrophic tendinopathy, tenosynovitis, and ultimately in (partial) tendon tears. The diagnosis may be difficult in patients with lateral ankle pain. Recurrent peroneal tendon dislocation and tenosynovitis can be established by clinical examination. In the case of subtotal tears of the peroneus brevis or longus tendon, supplemental investigations such as MRI or ultrasonography can be helpful for establishing the diagnosis. Postsurgery and postfracture adhesions and irregularities in the posterior aspect of the fibula where the gliding channel of the tendon is located can be responsible for symptoms in this region. The main portal for peroneal tendoscopy is located directly over the tendons, 2 cm distal to the posterior edge of the lateral malleolus. The distal portal is made first, with an incision through the skin. The tendon sheath is penetrated by the arthroscope shaft with a blunt trocar. A 2.7-mm arthroscope with an inclination angle of 30 degrees is introduced (Fig. 16-30). After a spinal needle is introduced under direct vision, an incision is made through the skin into the tendon sheath to create a proximal portal. Instruments such as shaver system can be introduced. Through the distal portal on the lateral side, a complete overview can be obtained of both peroneal tendons. The inspection starts approximately 6 cm proximal from the posterior tip of the lateral malleolus, where a thin membrane splits the tendon compartment into two chambers (Fig. 16-31). More distally, both tendons lie in one compartment. The complete compartment can be inspected by
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-31 Through the distal portal a complete overview can be obtained of both peroneal tendons. The inspection starts approximately 6 cm proximal from the posterior tip of the lateral malleolus where a thin membrane splits the tendon compartment into two chambers (1). More distally (2, 3) both tendons lie in one compartment.
rotating the endoscope over and between the two tendons. The vincula-like membrane by which both tendons are attached to the tendon sheath allows the arthroscope to rotate freely all around each tendon. The muscle fibers of the peroneus brevis can be recognized in the thin membrane up to the tip of the fibula. At this location both tendons cross the calcaneofibular ligament, which usually gives some fibers to the anterior talofibular ligament. Approximately 3 to 5 cm distal from the fibula the tendons cross each other and again get divided by a membrane and a bony prominence. With the tendoscopy a pathologic thickened vincula or tendon sheath can be released, adhesions can be removed, and a symptomatic prominent tubercle can be removed. A rupture of the peroneal longus or brevis tendon can be sutured. When a total synovectomy of the tendon sheath is to be performed, it is advisable to create a third portal more distal or more proximal from the previously described portals. In case of treatment for recurrent peroneal tendon dislocation, it is possible to deepen the groove of the peroneal tendons with a burr.42
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Tendinitis and paratendinitis in the Achilles tendon Overuse injuries of the Achilles tendon can be divided into insertional and noninsertional tendinitis. Because there is no evidence of inflammation in patients with ‘‘tendinitis,’’ the term tendinosis has been proposed.39,43 Noninsertional tendinitis can be divided into three subgroups: paratendinitis, paratendinitis þ tendinosis, and tendinosis. Paratendinitis is characterized by inflammation on only the lining of the tendon. With acute tendinitis there is diffuse swelling around the tendon. Most cases of isolated paratendinitis respond well to conservative treatment. In patients with paratendinitis plus tendinosis there is localized swelling, most often 4 to 7 cm above the insertion of the Achilles tendon (Fig. 16-32). On examination there is pain, particularly when the tendon is squeezed. Most often the pain is localized predominantly on the medial side. MRI demonstrates marked thickening of the tendon. In patients with Achilles tendinosis, fields of local degeneration in the tendon are present. With advanced tendinosis, the tendon elongates because of chronic degeneration and is no longer in functional continuity. There often is an increase in passive range of dorsiflexion. Heavy-load eccentric calf-muscle training has been demonstrated to be effective treatment for chronic Achilles þ paratendinitis. For operative treatment of paratendinitis, the diseased and thickened paratenon is excised. Operative treatment of chronic tendinosis consists of
Figure 16-32 Left ankle. In patients with paratendinitis and tendinosis there is localized swelling approximately 4 to 7 cm above the insertion of the Achilles tendon.
Specific indications
Figure 16-33 For peritendinitis of the Achilles tendon, the portals are created 2 cm distal and proximal of the lesion. After a spinal needle is introduced under direct vision, an incision is made at the location of the proximal portal.
Insertional tendonitis and retrocalcaneal bursitis Insertional tendonitis can be classified as retrocalcaneal bursitis, retrocalcaneal bursitis þ insertional tendonitis, and insertional tendonitis. Chronic retrocalcaneal bursitis is accompanied by deep pain and swelling of the posterior soft tissue just in front of the Achilles tendon (Fig. 16-34). The prominent bursa can be palpated medially and laterally from the tendon at its insertion. The lateral radiograph demonstrates the characteristic prominent superior calcaneal deformity. Operative treatment involves removal of the bursa and resection of the lateral and medial posterosuperior aspect of the calcaneus. Retrocalcaneal bursitis often is accompanied by midportion insertional tendinosis. Often a partial rupture of the midportion of the tendon is present at its insertion. When operative treatment for retrocalcaneal bursitis is indicated, debridement of the midportion of the Achilles insertion should be considered in case of a partial rupture.39 In case of insertional tendinosis, there is pain at the bone-tendon junction that worsens after exercise. The tenderness is specifically located directly posterior to the junction. Radiographic signs of ossification at the most distal extent of the insertion of the tendon (bone spur) are typical signs of insertional Achilles tendinosis. Most patients can be managed with nonoperative means, such as widening and deepening of the heel counter of the shoe. When operative treatment is indicated, the pathologic ossifications and spurs can best be approached by a central heel-splitting incision. Open surgery for insertional tendinitis with removal of the chronically inflamed bursa and the posterosuperior prominence of the calcaneus can be associated with a poor outcome. Open surgical treatment requires plaster immobilization to prevent equines malformation and to stimulate wound healing. Angermann and Hovgaard45 reported a cure rate of only 50% after open surgery for chronic retrocalcaneal bursitis. Endoscopic treatment offers the advantage of less morbidity, reduced postoperative pain, and outpatient treatment. Achillotendoscopy for retrocalcaneal bursitis is performed with the patient in the prone position. Two portals are created, medial and lateral to the Achilles tendon, at the level of the superior border of the os calcis. A 4-mm arthroscope with an inclination angle of 30 degrees is introduced through the posterolateral portal. A probe and subsequently a 5-mm, full-radius resector are introduced through the posteromedial portal. After removing of the bursa and inflamed soft tissue, the surgeon uses a full-radius resector and small acromionizer to remove the calcaneal prominence. 377
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debridement of the paratenon and removal of degenerative necrotic tissue. The thickened degenerative portion of the tendon is excised, and the defect is closed primarily. Revascularization is stimulated by making multiple longitudinal incisions into the tendon. Open surgery produces a guarded prognosis. In fact, Maffulli et al.44 reported poor results in more than 60% of patients. For peritendinitis of the Achilles tendon, the portals are created 2 cm proximal and 2 cm distal of the lesion (Fig. 16-33). The distal portal is made first: an incision is made through to the skin only. The crural fascia is penetrated by the arthroscope shaft with a blunt trocar, and a 2.7-mm arthroscope with an inclination angle of 30 degrees is introduced. After a spinal needle is introduced under direct vision, an incision is made at the location of the proximal portal. An instrument such as a probe or a small shaver is introduced. The pathologic paratenon is removed by use of the shaver. The Achilles tendon can be inspected by rotation of the scope over the tendon. The plantaris tendon can be recognized and released, or resected when indicated.
CHAPTER 16
Diagnostic and operative ankle and subtalar joint arthroscopy
Figure 16-34 (A) Achillotendoscopy: retrocalcaneal bursitis. (B) After removal of the bursa and inflamed soft tissue, the calcaneal prominence is removed with a full-radius resector and small acromionizer.
Subtalar joint arthroscopy, intraosseous talar cysts Subtalar arthroscopy was first described in 1985.46 The procedure may be applied as a diagnostic and therapeutic tool. As with any other joint, the subtalar joint should be compartmentalized and examined. Indications are the evaluation of subtalar instability, debridement of osteochondral lesions, and excision of avulsion fragments or loose bodies. The anterior subtalar joint consists of the anterior facet, middle facet, talonavicular joint, and spring ligament. The dividing axis through the subtalar joint consists of the sinus tarsi, tarsal canal, cervical ligament, talocalcaneal interosseous ligament, inferior extensor retinaculum, and fat pad. The posterior subtalar joint consists of the posterior facet that is 40 to 45 degrees lateral to the longitudinal axis of the foot, the capsule, the posterior recess, the lateral recess (thickened by the calcaneofibular ligament), and calcaneus. The patient may be positioned supine or laterally with a bolster under the foot at the edge of the table. A 1.9- to 2.7-mm arthroscope with 30-degree wide angle is used. Small joint shavers and burrs can be introduced. When needed, soft-tissue distraction can be performed. Four portals have been described.46 The anterior lateral portal is made in the sinus tarsi 2 cm anterior and 1 cm inferior to the tip of the lateral malleolus. Caution should be taken not to injure the superficial peroneal nerve. The inframalleolar portal is made anterior to the calcaneofibular ligament. Caution should be taken not to injure the peroneal tendons. The posterior lateral
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Figure 16-35 Subtalar joint arthroscopy: the posterior lateral portal is made approximately 1 cm posterior and 1 cm proximal to the tip of the fibula.
portal is made 1 cm posterior and 1 cm proximal to the tip of the fibula (Fig. 16-35). Caution should be taken not to injure the sural nerve, lesser saphenous vein, and peroneal tendons. The medial portal is made in the sinus tarsi approximately 2 cm anterior to the tip of the lateral malleolus. A blunt trocar is introduced through the deep fascia and guided gently through the tarsal canal to the medial skin surface. The foot is placed in equinus to relax the neurovascular structures.
Specific indications
An incision is made over the trocar. A blunt trocar is introduced from the medial portal. The joint is insufflated and the arthroscope is introduced to view the anterior lateral and posterior medial subtalar joint. Caution is taken to avoid the neurovascular structures, which are approximately 2.5 cm distal to the tip of the medial malleolus. A systematic examination of the subtalar joint is performed by varying the portal placement of the scope. An arthroscope in the anterior lateral portal enables evaluation of the sinus tarsi, interosseous ligament, cervical ligament, and lateral and posterior gutters. An arthroscope in the posterior lateral portal enables evaluation of the lateral gutter and lateral compartment. An arthroscope in the medial portal enables evaluation of the anterior lateral and posterior medial compartments. The major complications specific to this procedure are sural nerve injury at the posterior lateral portal, superficial peroneal nerve injury at the anterior lateral portal, and peroneal tendon disruption at the inframalleolar portal. The arthroscope may be placed inadvertently in the ankle joint or may penetrate the capsule of the ankle and enter the lateral ankle gutter. For this reason, fluoroscopic confirmation of position can be useful. Assessment of the posterior articulation of the subtalar joint can best be performed by means of a twoportal endoscopic approach of the hindfoot with the
patient in the prone position.13 The therapeutic indications include debridement of chondromalacia, excision of osteophytes, the removal of a loose body, lysis of adhesions with posttraumatic arthrofibrosis, and synovectomy. Intraosseous talar cysts can be approached through the subtalar joint.47 Retrograde curettage of these lesions with destruction of the surrounding zone of sclerosis, along with bone grafting, is our treatment of choice. Lesions with a communication to the subtalar joint can be treated with the patient in the prone position (see Fig. 16-1). For proper preoperative planning, a CT scan is indispensable. A shaver is introduced through the posteromedial portal. After identification of the FHL tendon, the posterior talar process is freed from its capsular attachments. The joint capsule of the subtalar joint is resected, and the opening of the cyst in the subtalar joint is identified by direct vision and palpation by means of a small probe (Fig. 16-36, A and B). With the endoscope in the posteromedial portal and the probe in place through the same posterolateral portal, the drill guide is introduced. The drill guide is parallel to the probe of which the curved tip is in place in the opening of the cyst in the subtalar joint. The drill guide is positioned onto the posterior talar process and a hole is drilled into the cystic lesion with a 4.5-mm drill (Figs. 16-37 and 16-38). The lesion is curetted and debrided with a
Figure 16-36 (A and B) A computed tomography (CT) scan is indispensable for proper preoperative planning. This CT scan shows an intraosseous cyst of the right talus that has communication with the subtalar joint.
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Figure 16-37 The opening of the cyst (see Fig. 16-36, A and B and text) in the subtalar joint is identified by direct vision and palpation by means of a small probe.
Figure 16-39 Cancellous bone obtained from the iliac crest is packed into the cystic lesion through a trocar.
two-portal endoscopic approach offers an excellent alternative to open techniques with obvious advantages. An arthrotomy or malleolar osteotomy is prevented. The articular origin of a cyst can be identified under direct arthroscopic vision. A second portal makes it possible to probe and subsequently treat the lesion by debridement, drilling, and transtrocar bone grafting. Excellent results at follow-up have been reported by using this technique.13,47
Figure 16-38 The drill guide is positioned, parallel to the probe, onto the posterior talar process. With a 4.5-mm drill, a hole is drilled into the cystic lesion.
closed-cup curette. The opening of the cyst is enlarged to 6.5 mm, and a 6.5-mm blunt trocar is introduced. Multiple drill holes are made through the cystic wall from inside the lesion with a K-wire (Fig. 16-38). Cancellous bone obtained from the iliac crest is packed into the cystic lesion through the trocar (Fig. 16-39). This
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Combined anterior and posterior ankle arthroscopy In case of combined anterior and posterior ankle pathology, anterior arthroscopy can be combined with posterior arthroscopy of ankle in the same operative setting. Indications are rheumatoid arthritis, pigmented villonodular synovitis, chondromatosis, or ankylosis. The patient first is placed in the prone position. A tourniquet is applied and a small support is placed under the lower leg. A two-portal endoscopic approach of the hindfoot is performed and the pathology treated. When the procedure has been finished and the portals closed and the wounded draped, a strap is placed around the foot, the knee is flexed approximately 90 degrees, and the strap is attached with a string to the ceiling of the operating room. The foot is now hanging upside down (Fig. 16-40). Next, the portals for the anterior ankle arthroscopy are made and synovectomy or capsulectomy is performed in the anterior ankle compartment. We have successfully performed this combined procedure with various indications in seven patients.
References
REFERENCES 1. Takagi K: The arthroscope: the second report, J Jpn Orthop Assn 14:441, 1939b. 2. Watanabe M, et al: Development of the Selfoc arthroscope, J Jpn Orthop Assoc 46:154, 1972. 3. Plank E: Die Arthroskopie des oberen Sprunggelenkes, Helfe zur Unfallheilkunde 131:245, 1978. 4. Andrews JR, Previte WJ, Carson WG: Arthroscopy of the ankle: technique and normal anatomy, Foot Ankle 6:29, 1985. 5. Johnson LL: Arthroscopic surgery: principles and practice, ed 3, St Louis, 1986, Mosby. 6. Yates CK, Grana WA: A simple distraction technique for ankle arthroscopy, Arthroscopy 4:103, 1988. 7. Van Dijk CN, Scholte D: Arthroscopy of the ankle joint, Arthroscopy 13:90, 1997. 8. Guhl JF: Ankle arthroscopy: pathology and surgical techniques, Thorofare, New York, 1987, Slack. 9. Myerson MS, Quill G: Ankle arthrodesis: a comparison of an arthroscopic and an open method of treatment, Clin Orthop 268:84, 1993. 10. Van Dijk CN, Tol JL, Verheyen CCPM: A prospective study of prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement, Am J Sports Med 25:737, 1997. 11. Cameron SE: Noninvasive distraction for ankle arthroscopy, Arthroscopy 13:366, 1997. 12. Van Dijk CN, Verhagen RAW, Tol JL: Technical note. Resterilizable non-invasive ankle distraction device, Arthroscopy 17:1, 2001. 13. Van Dijk CN, Scholten PE, Krips R: Technical note. A 2-portal endoscopic approach for diagnosis and treatment of posterior ankle pathology, Arthroscopy 16:871, 2000. 14. Ferkel RD, Guhl J, Buecken van K: Complications in ankle arthroscopy: analysis of the first 518 cases, Orthop Trans 16:727, 1993. 15. Ferkel RD: Arthroscopic surgery, In: The foot and ankle, Philadelphia, 1996, Lippincott-Raven. 16. Tol JL, et al: The anterior ankle impingement syndrome: diagnostic value of oblique radiographs, Foot Ankle Int 25:63, 2004.
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Figure 16-40 Combined anterior and posterior ankle arthroscopy. Posterior ankle examination is carried out with the patient in the prone position. Anterior ankle examination is carried out with the foot hanging upside down.
17. Van Dijk CN, et al: Oblique radiograph for the detection of bone spurs in anterior ankle impingement, Skeletal Radiol 31:214, 2002. 18. Akseki D, et al: The anterior inferior tibiofibular ligament and talar impingement: a cadaveric study, Knee Surg Sports Traumatol Arthrosc 10:321, 2002. 19. Scranton PE Jr, McDermott JE, Rogers JV: The relationship between chronic ankle instability and variations in mortise anatomy and impingement spurs, Foot Ankle Int 21:657, 2000. 20. Akseki D, et al: The distal fascicle of the anterior inferior tibiofibular ligament as a cause of anterolateral ankle impingement: results of arthroscopic resection, Acta Orthop Scand 70:478, 1999. 21. Tol JL, van Dijk CN: Etiology of the anterior ankle impingement syndrome: a descriptive anatomical study, Foot Ankle Int 25:382, 2004. 23. Renstrom PA: Persistently painful sprained ankle, J Am Acad Orthop Surg 2:270, 1994. 24. Tol JL, Verheyen CP, van Dijk CN: Arthroscopic treatment of anterior impingement in the ankle, J Bone Joint Surg Br 83:9, 2001. 25. Cheng JC, Ferkel RD: The role of arthroscopy in ankle and subtalar degenerative joint disease, Clin Orthop 349:65, 1998. 26. Verhagen RAW: Diagnostic guidelines for chronic ankle pain. From loose bodies to joint venture. Thesis, University of Amsterdam, Armsterdam, 2004. 30. Anderson IF, et al: Osteochondral fractures of the dome of the talus, J Bone Joint Surg Am 71:1143, 1989. 31. Cheng MS, Ferkel RD, Applegate GR: Osteochondral lesions of the talus: a radiological and surgical comparison, presented at the Annual Meeting of the Academy of Orthopaedic Surgeons, New Orleans, February 1995. 32. Ferkel RD, Sgaglione NA: Arthroscopic treatment of osteochondral lesions of the talus: long-term results, Orthop Trans 17:1011, 1994. 33. Taranow WS, et al: Retrograde drilling of osteochondral lesions of the medial talar dome, Foot Ankle Int 20:474, 1999. 34. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review, Foot Ankle Int 21:119, 2000. 35. Van Dijk CN: Hindfoot endoscopy, Sports Med Arthrosc Rev 8:365, 2000. 36. Abramowitz Y, et al: Outcome of resection of a symptomatic os trigonum, J Bone Joint Surg Am 85:1051, 2003. 37. Brodsky AE, Khalil MA: Talar compression syndrome, Am J Sports Med 14:472, 1986. 38. McDougall A: The os trigonum, J Bone Joint Surg Br 37:257, 1955. 39. Van Dijk CN, Scholten PE, Kort N: Tendoscopy (tendon sheath endoscopy) for overuse tendon injuries, Op Tech Sports Med 5:170, 1997. 40. Van Dijk CN: Hindfoot endoscopy for posterior ankle pain, Surg Tech Orthop Traumatol 55:219, 2001. 41. Van Dijk CN, Stibbe AB, Marti RK: Posterior ankle impingement. In Nyska M, Mann G, editors: The unstable ankle, Jerusalem, 2002, Human Kinetics. 42. Scholten PE, van Dijk CN: Tendoscopy of the peroneal tendons, Foot Ankle Clin 11:415–420, 2006. 43. Frey C: Arthroscoping the foot and ankle practice. In Guhl JF, editor: Foot and ankle arthroscopy, ed 2, Thorofare, NJ, 1993, Slack. 44. Maffulli N, et al: Surgical decompression of chronic central correlations of Achilles tendon, Am J Sports Med 27:747, 1999. 45. Angermann P, Hovgaard D: Chronic Achilles tendinopathy in athletic individuals: results of non-surgical treatment, Foot Ankle Int 20:304, 1999. 46. Dreeben SM: Subtalar arthroscopy techniques, Op Tech Sports Med 17:41, 1999.
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47. Scholten PE, et al: Treatment of a large intraosseous talar ganglion by means of hindfoot endoscopy, Arthroscopy 19:96, 2003.
FURTHER READING Canale ST, Belding RH: Osteochondral lesions of the talus, J Bone Joint Surg Am 62:97–102, 1980.
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Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP: Arthroscopic treatment of anterolateral impingement of the ankle, Am J Sports Med. 19:440–446, 1991. Loomer R, Fisher C, Lloyd-Smith R, Sisler J, Cooney T: Osteochondral lesions of the talus, Am J Sports Med. 21:13–19, 1993. Pritsch M, Horoshovski H, Farine I: Ankle arthroscopy, Clin Orthop 184:137–140, 1984.
.........................................C H A P T E R 1 7 Lesser-toe disorders Michael J. Coughlin, Jerry Speight Grimes, and Robert C. Schenck, Jr. CHAPTER CONTENTS ...................... Bunionettes
384
Claw toe
402
Intractable plantar keratoses
387
Metatarsophalangeal joint instability
403
Interdigital neuromas
392
Conclusion
408
Hard corns and soft corns
394
References
408
Hammertoes, mallet toes, and claw toes
397
Further reading
409
Metatarsalgia in the athlete can be a debilitating disorder leading to loss of competitiveness or even loss of the ability to participate in a recreational fashion. Forefoot disorders encompass lesser-toe abnormalities such as claw toes, hammertoes, mallet toes, and hard and soft corns. More proximally, problems can include intractable plantar keratosis (IPK), bunionettes, neuromas, and metatarsophalangeal (MTP) joint capsulitis and instability. For the athlete, repetitive activities can lead to repeated stress reactions in soft tissues, as well as bones and joint. Abrasions and repeated trauma over bony prominences can lead to callus formation and bursitis. Ideally, the goal should be to avoid the development of problems through the use of good footwear, proper training practices, and education. Many foot problems may develop despite prophylactic care and thus require the intervention of the orthopaedic surgeon either conservatively or surgically. When possible, nonsurgical treatment is preferred, usually leading to a rapid resumption of athletic activity. The complaint of pain in the forefoot must be differentiated to make a correct diagnosis. The accompanying algorithm (Fig. 17-1) may prove useful in determining the specific forefoot diagnosis when a patient complains of metatarsalgia. Most important is the exact location of pain. In addition, the physician should ask the following questions: Which specific activities increase symptoms? Which activities alleviate discomfort? Is the pain dorsal or plantar, medial or lateral? Is there an associated
neuritic symptom with the pain? Are enlarged exostoses or prominences associated with pain, swelling, or inflammation?
4 PEARL Location of Foot Pain When a patient complains of metatarsalgia, the initial concern on physical examination is the presence of an associated callosity. This can be seen laterally over the fifth metatarsal head with a bunionette formation. It can be localized to the plantar metatarsal region with an IPK. A callosity may develop over the dorsal distal interphalangeal (DIP) joint (a mallet toe) or the dorsal proximal interphalangeal (PIP) joint (hammertoe). On occasion a patient may complain of a callosity both overlying the PIP joint and beneath the associated metatarsal head. With a concomitant contracture of this toe, the diagnosis of a claw toe is made based on the basis of clinical findings.
Development of a callus between two toes (a soft corn) or over the lateral aspect of the fifth toe (a hard corn) can be extremely painful. When a patient complains of metatarsalgia but there is no callosity present, the patient should be examined carefully for neuritic symptoms. When such a scenario is present (along with other specific symptoms), the
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Figure 17-1 Algorithm. (From Coughlin MJ: J Bone Joint Surg 82B:781, 2000.)
diagnosis of an interdigital neuroma can be made. When neuritic symptoms are not present but symptomatic pain still is localized to the forefoot, suspicion of MTP joint capsulitis and/or instability should be considered. The presence of a positive drawer sign (dorsal plantar instability) or actual malalignment of the involved toe at the MTP joint aids in confirming the diagnosis of second toe instability or ‘‘cross-over toe.’’ Although this algorithm is not all-inclusive and much more enters into the specific diagnostic process than this flowsheet allows, it does offer a method of approaching the athlete with metatarsalgia. Sometimes symptoms overlap; frequently symptoms are vague, and repeated evaluation and physical and radiographic examinations are necessary to confirm a diagnosis. The cooperation of patients in defining their symptomatic complaints and in defining their problem through varying their athletic activity is highly important. Likewise, patient cooperation in modifying activities when conservative management is attempted is a critical factor in any successful treatment. When surgery is performed, patient cooperation in allowing adequate healing to occur before resuming athletic activity is instrumental not only in the recovery process but also in the avoidance of other associated problems or complications.
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4 PEARL Location of Foot Pain When evaluating forefoot pain, it often can be difficult to localize the exact location of a patient’s pain to make a correct diagnosis. Often, the physical examination is inconclusive, especially when the patient presents to clinic when asymptomatic. This is especially common in athletes, whose complaints often are activity related. To identify the location of pain, instruct the patient to repeat the offending activity, recreating the patient’s symptoms. The patient then is instructed to mark the spot with a felt tip marker pen. This ‘‘spot’’ will stay with the patient for the next clinical examination.
BUNIONETTES The development of inflammation, an enlarged bursa, or a callus over a prominent fifth metatarsal head may lead a physician to diagnose a bunionette (Fig. 17-2). Just as bunions can present with differing magnitude and different characteristics, so too can a bunionette.1 A bunionette may appear radiographically as an enlarged
Bunionettes
Figure 17-2 Bunionette with enlarged bursa. (From Mann RA, Coughlin MJ: In Surgery of the foot and ankle, St Louis, 1993, CV Mosby, p. 443.)
fifth metatarsal head (type I). A flare in the metaphysis may cause outbowing of the fifth metatarsal (type II), leading to symptoms, or a widened 4-5 intermetatarsal angle (type III) characteristic of a splayfoot may lead to pain and callus formation (Fig. 17-3).
Initially an athlete may complain of pain directly lateral over the fifth metatarsal head, but the examiner should be aware of plantar symptoms as well. Neuritic symptoms involving the fifth toe may occur because of pressure over the lateral digital nerve to the fifth toe. The athlete may note complaints of inflammation, blistering, ulceration, or infection. On physical examination, the aforementioned complaints usually are obvious. Significant callus formation may be observed on the lateral, plantar, or in a lateral plantar position overlying the fifth metatarsal head. Any pronation of the longitudinal arch should be noted, as well as any restriction in hindfoot motion. Radiographic evaluation may demonstrate an enlarged metatarsal head, outflaring of the fifth metatarsal metaphysis, or widening of the 4-5 intermetatarsal angle. Widening of the 4-5 angle is the most common. Abduction of the fifth toe in relation to the fifth metatarsal head also may be demonstrated.
Conservative treatment Early treatment involves attempting to relieve pressure on the underlying bony prominence. Stretching of shoes or obtaining shoes with a soft upper that is more forgiving will relieve overlying pressure. Seams or stitching directly over the bunionette should be avoided. Moleskin applied to a blister may promote healing and
Figure 17-3 (A) Bunionette with enlarged fifth metatarsal head. (B) Bunionette with bowing of metaphysic. (C) Bunionette with enlarged 4-5 intermetatarsal angle.
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protect the area while athletes continue their activities. Altering running and/or training activity also may diminish symptoms. Nonimpact activities such as stationary cycles or swimming can be integrated into the training program. A reduction in total miles per day and per week may be required. Trimming the callus may significantly relieve symptoms. Physicians may teach their patients how to pare the callus appropriately. The callus is shaved in thin layers with the scalpel parallel to the toe. A pumice stone also may be used to pare down the callus. A pumice stone is safer and often more acceptable to patients for home use than a scalpel. When athletic activity is significantly impaired after conservative efforts, surgical intervention may be contemplated (see Case Study 1). The type of osteotomy selected is dependent on the location of the callosity because specific osteotomies of the fifth metatarsal are oriented to redirect the metatarsal in different directions. Surgical intervention in treating forefoot callosities should be tailored to the patient. Extensive soft-tissue stripping, unsecured osteotomies, and multiple metatarsal osteotomies all should be avoided in athletes. Although a surgical procedure may relieve the painful callosity, athletic performance of the patient may be diminished and thus surgery may be considered unsuccessful. The two surgical procedures presented here fulfill the requirements of exposing the patient to less extensive surgery, use internal fixation, and appear better suited to athletes. Again, when possible, conservative treatment should be advocated by the treating physician until it obviously is incompatible with continued athletic function.
C A S E S T U D Y 1
A 30-year-old skier developed pain and swelling over the plantar lateral aspect of the fifth metatarsal head. An increased callosity was observed over the plantar lateral aspect of the bunionette. A painful, inflamed bursa developed during the middle of ski season that was partially relieved by grinding down the inner aspect of the ski boot overlying the bunionette. Likewise, the area overlying the fifth metatarsal head was relieved in the athlete’s everyday footwear by stretching the leather surface. On physical examination, a normal neurologic and vascular examination was noted. Prominence of the fifth metatarsal head was characterized by a callosity on both the plantar and lateral aspect. Radiographic evaluation demonstrated an enlarged fifth metatarsal lateral condyle (Fig. 17-4, A).
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Figure 17-4 Case study 1. (A) Bunionette preoperative x-rays. (B) Follow-up x-rays demonstrating correction. Conservative care, stretching of shoes, and padding all were recommended. At the end of ski season, the patient requested surgical treatment because of continued symptoms. An oblique osteotomy was performed and fixed with screws. At 8 weeks following surgery, the osteotomy was healed and the patient began progressive walking that evolved over the ensuing 2 months to jogging and sports activities. Figure 17-4, B shows the correction obtained. The patient skied the following season without symptoms.
Intractable plantar keratoses
Figure 17-5 An L-shaped capsular incision is used to approach the bunionette.
head. The osteotomy is fixed with one or two percutaneous 0.045 K-wires (Fig. 17-7). 6. Any remaining prominent metaphysis is shaved with the sagittal saw. A drill hole is placed in the dorsal proximal metaphysis, and the capsule is anchored with an interrupted suture. Remaining interrupted sutures are placed to reinforce the capsular repair (Fig. 17-8). 7. The skin is closed in a routine fashion. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a wooden-soled shoe. Athletic activity is increased as swelling and pain diminish. Radiographic confirmation of healing should be present before aggressive activity such as jogging, running, or jumping is commenced. In general, a patient can return to nonimpact activities at 2 months. Limited-impact activities such as jogging are permitted at 3 months. Full-contact/impact activities can be resumed at 4 months, depending on radiographic evidence of healing. In general, resolution of the symptomatic bunionette can be achieved with one of the above procedures for type I or type II bunionettes. With a splayfoot and a significantly wide 4-5 metatarsal angle, a diaphyseal midshaft osteotomy may be necessary to achieve more correction.6 More extensive procedures such as this should be reserved for athletes with significant limitations, because the extensive nature of this surgery may limit postoperative athletic expectations.
INTRACTABLE PLANTAR KERATOSES The development of a keratosis beneath one or more of the metatarsal heads is referred to as an intractable plantar keratosis or IPK. A callosity beneath the fifth metatarsal when associated with a bunionette already has been discussed. A callus may be a localized discrete lesion or a diffuse keratotic buildup (Fig. 17-9). Callus formation in athletes is not uncommon, and if asymptomatic rarely requires medical intervention. With significant buildup, painful symptoms may occur, requiring evaluation and treatment. A diffuse callus may be due to repetitive abrasion associated with athletic activity. It also may be associated with a long second metatarsal or a long second and third metatarsal. A discrete callus may occur beneath a single metatarsal head.7 It typically is associated with an enlarged fibular metatarsal condyle. It is important to distinguish this from a wart (Fig. 17-10). Although warts (plantar verrucae) typically are not found beneath a metatarsal head, on occasion they can occur in this region and thus must be differentiated from an IPK. Trimming of a wart will uncover end arterioles in 387
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Surgical treatment 1. The foot is cleansed and draped in the routine fashion. An Esmarch bandage is used to exsanguinate the foot. The ankle is padded carefully and the Esmarch is used as a tourniquet. 2. A longitudinal lateral incision is centered directly over the bunionette, extending from the midproximal phalanx to 1 cm above the metatarsal head. Care is taken to protect the neurovascular bundles. 3. The MTP capsule is detached on the dorsal and proximal aspect and turned downward, exposing the prominent lateral condyle (Fig. 17-5). 4. A sagittal saw is used to resect the lateral condyle in line with the diaphyseal shaft of the fifth metatarsal. (At this point, a decision must be made regarding the type of osteotomy to be performed. For a pure lateral callus, a chevron osteotomy is performed. For a combined plantar lateral callus, a distal oblique osteotomy is performed.) 5A. Chevron osteotomy2,3—A lateral to medial drill hole is placed in the center of the fifth metatarsal head, marking the apex of the chevron osteotomy. A 60-degree angled osteotomy based proximally is directed in a lateral to medial plane. The metatarsal head is translated medially and fixed with a percutaneous 0.045 K-wire (Fig. 17-6). 5B. Distal oblique osteotomy4,5—After exposing the metatarsal head and metaphysis, an oblique osteotomy is performed from a distal lateral to proximal medial direction. The metatarsal head is displaced medially and slightly proximally and is allowed to ‘‘raise up’’ approximately 3 mm to decrease plantar pressure beneath the fifth metatarsal
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Figure 17-6 (A) A drill hole is placed in the center of the metatarsal head and drilled in a lateral to medial direction. (B) A chevron-shaped osteotomy is based proximally with the apex at the drill hole. (C) Medial translation of the metatarsal head with K-wire fixation and shaving of the metaphyseal flare (shaded area denotes shaved bone in metaphysic).
the lesion characterized by punctuate hemorrhages. Evaluation of the athlete with an IPK involves determining the significance of the symptoms, length of duration, and association, if any, with specific athletic activity. A patient with minimal symptoms requires no treatment. Radiographic evaluation entails weight-bearing films with markers to determine the exact location of the IPK (a long metatarsal may be associated with an IPK; likewise a marker may be located directly beneath the fibular condyle of a metatarsal head).
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4 PEARL Pressure Points A Harris mat imprint is invaluable in identifying abnormal pressure points on the plantar surface of a patient’s foot. The patient is instructed to walk in a normal manner, stepping on the Harris mat. The test is repeated with the contralateral foot. Abnormal pressures are illustrated as unusually dark regions and will aid in making the correct diagnosis and appropriate treatment.
Intractable plantar keratoses
can transfer pressure to the metatarsal diaphysis and relieve symptoms (see Case Study 2). Custom or prefabricated orthotic devices also can aid in relieving symptoms. Athletes may alter their workout, change sporting activities, or change duration or intensity of the workout, all with gratifying results.
C A S E S T U D Y 2
Figure 17-8 L-shaped capsular closure. The dorsal proximal corner may be fixed with a drill hole in the metaphysic to anchor the repair.
Conservative treatment Conservative treatment revolves around paring the IPK and padding it to relieve the pressure (Fig. 17-11). A patient can be instructed to trim the lesion every 7 to 10 days, and this will significantly relieve discomfort. Placement of a metatarsal pad just proximal to the IPK
Surgical treatment: partial condylectomy8 1. The foot is cleansed and draped in a routine fashion. As Esmarch bandage is used to exsanguinate the foot. It is padded carefully at the ankle and used as a tourniquet. 2. A longitudinal incision is centered over the metatarsal head with a ‘‘hockey stick’’ extension distal into the adjacent interspace. (The extensor tendon may be released temporarily to aid exposure and is repaired at the conclusion of the procedure.) 3. The MTP joint capsule is released and the toe is flexed to 90 degrees at the MTP joint. 389
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Figure 17-7 Distal oblique osteotomy with K-wire fixation (shaded area denotes shaved bone in metaphysic).
A 50-year-old tennis player developed a painful callus beneath the second and third metatarsals. It was a diffusely thickened callus that began to limit his sports activities. On initial evaluation, the diffuse callus was trimmed and the patient instructed in how to care conservatively for the IPK. A pumice stone was used to pare the callus. The patient also obtained disposable scalpels to shave his thickened callosity. When he returned for further follow-up, radiographs demonstrated a long second and third metatarsal in relation to the adjacent metatarsals. A soft pad was placed in his shoe just proximal to the callosity. With the combination of shaving the callosity and padding it, symptoms were completely relieved and the patient returned to full sports activities. Later, a soft orthotic device was fabricated to relieve pressure beneath the second and third metatarsals. This convenient orthotic device can be moved from shoe to shoe and replaced the temporary soft pads that were used to alleviate his initial symptoms. When all methods of conservative treatment have been exhausted, surgical intervention may be considered. Caution is advised in considering any metatarsal osteotomy in a high-level athlete. The possibility of delayed union, nonunion, or malunion can significantly impair later athletic activity. The development of a transfer lesion beneath another metatarsal head is not uncommon. Multiple metatarsal osteotomies are to be discouraged. Likewise, floating metatarsal osteotomies without internal fixation have a high rate of malunion with resultant transfer lesions.
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Figure 17-9 (A) Discrete callus in a tennis player with an enlarged fibular condyle. (B) Diffuse callus in a runner. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
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Figure 17-10 A wart is characterized by punctate hemorrhages that are obvious when the callus is trimmed. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
Figure 17-11 Padding an intractable plantar keratosis often is successful treatment.
4. An osteotome is used to osteotomize 25% of the plantar condyle. Care is taken to avoid fracture to the metatarsal head (Fig. 17-12). The condyle is removed.
5. A 0.045 K-wire introduced at the MTP joint is driven distally out the tip of the toe. With the MTP joint reduced, the pin is driven in a retrograde fashion, stabilizing the joint.
Intractable plantar keratoses
Figure 17-12 (A) Plantar condylectomy for a discrete intractable plantar keratosis. (B) Interoperative view of plantar condylectomy (one fourth to one third of the plantar metatarsal head is excised).
6. The extensor tendon (if released) is repaired. The skin is closed in a routine fashion. 7. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a wooden-soled shoe. 8. At 3 weeks, the sutures and K-wire are removed. Athletic activity is permitted as swelling and pain decrease. The toe is protected for 6 weeks following surgery with taping immobilization. In general, a patient can return to nonimpact activities at 1 month. Limited-impact activities such as jogging are permitted at 6 weeks. Fullcontact/impact activities can be resumed at 3 months.
Figure 17-13 (A) Distal oblique osteotomy (dotted line shows proposed osteotomy site). (B) Following displacement and internal fixation with K-wire.
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Surgical treatment: metatarsal osteotomy 1. The foot is cleansed and draped in a routine fashion. An Esmarch bandage is used to exsanguinate the foot. It is carefully padded at the ankle and used as a tourniquet. 2. A dorsal longitudinal incision is centered over the involved metatarsal. 3A. If a distal oblique osteotomy9 is performed (Fig. 1713), the cut is directed in a vertical direction. The metatarsal head is displaced upward 3 mm10 and fixed with a 0.045 K-wire.
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Figure 17-14 Distal chevron osteotomy with internal fixation. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
Figure 17-15 Proximal closing wedge osteotomy with screw fixation. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
3B. If a vertical chevron osteotomy2 is performed (Fig. 17-14), the V-shaped osteotomy is directed in a vertical direction. (This is more stable side to side than a transverse osteotomy.) The metatarsal head is displaced upward 3 mm and fixed with a 0.045 K-wire. 3C. If a proximal transverse osteotomy11 is performed (Fig. 17-15), a dorsal based wedge is excised. The farther proximal the osteotomy is located, the more elevation is achieved with wedge removal. (Care must be taken not to overcorrect at the osteotomy site.) The wedge may be removed with a sagittal saw or with a small rongeur. Internal fixation is recommended. A screw, pin, or wire loop fixation is used. 4. The wound is closed in a routine fashion. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a wooden-soled shoe bearing weight on his or her heel. 5. Sutures are removed 3 weeks following surgery. Percutaneous K-wires are removed 3 to 4 weeks following surgery. The forefoot then is strapped with tape and gauze until symptoms remit. 6. Radiographic confirmation of union is important before aggressive athletic activity can be commenced. Athletic activity is permitted as swelling and pain diminish. In general, a patient can return to nonimpact
activities at 2 months. Limited-impact activities such as jogging are permitted at 3 months. Full-contact/impact activities can be resumed at 4 months based on radiographic healing. In general, with a partial plantar condylectomy, satisfactory results are attained for relieving the symptoms of a discrete, well-localized IPK.8 Likewise, a distal osteotomy9,11 may be efficacious for a similar lesion. A diffuse callus in the athlete probably is best treated with padding and shaving because a more extensive procedure involving a diaphyseal osteotomy12 may require prolonged healing time and place the athlete at greater risk for delayed healing, malunion, and transfer metatarsalgia. A proximal closing wedge osteotomy9 may be used to elevate a symptomatic long second or third metatarsal. Meticulous attention to the osteotomy and fastidious postoperative care are necessary to avoid complications.
INTERDIGITAL NEUROMAS An interdigital neuroma may be a source of ill-defined forefoot pain. Located in the second or third intermetatarsal space (IMS), a neuroma is rarely isolated to the first or fourth interspace. Rarely, in less than 3% of cases, do two neuromas occur in the same foot simultaneously.13
Interdigital neuromas
Typically an athlete initially describes ill-defined forefoot pain, often exacerbated with running or sports activities, which is relieved by rest or removal of a pair of shoes. Sometimes pain increases with intensity and/ or duration of sports activities. The physical examination includes educating patients regarding which symptoms to watch for. Although illdefined forefoot discomfort is common, the treating physician must help patients define the exact area of pain. With time and education, athletes may be able actually to pinpoint the exact area of pain from the dorsal and plantar aspect, usually in either the second or third interspace. Neuritic symptoms or numbness in either the second or third common digital nerve distribution may be observed. On physical examination, care is taken to observe for evidence of peripheral neuropathy or vascular insufficiency. Peripheral neuropathy is characterized by a loss of cutaneous, positional, and vibratory sensation. The Semmes-Weinstein 5.07 monofilament is the classic test for protective sensation. Vascular insufficiency is characterized by loss of distal hair, lack of pulses, dependent rubor, varicose veins, atrophic skin, and delayed capillary refill. The toes are examined for fixed deformity. Any callus or IPK is noted, and the adjacent MTP joints are evaluated for pain or instability (see section on MTP Instability). MTP capsular instability symptoms closely mimic those of an interdigital neuroma.14 Palpation of the involved interspace usually elicits pain. Grasping and compressing the transverse arch at the level of the metatarsal heads may elicit a click (Mulder’s sign),15 which occurs when the neuroma subluxates below the metatarsal head and transverse metatarsal ligament (TML).
Conservative treatment Early conservative treatment may alleviate symptoms in the athlete. With intermittent symptoms exacerbated by intense athletic activity or sports of significant duration, a change in the type of activity or its duration may completely relieve symptoms (i.e., a person who jogs 4 miles at a time and develops pain at 2.5 miles may jog for 2 miles and bicycle for 2 to 3 miles and be symptom free). Placing a small metatarsal pad just proximal to the symptomatic interspace may relieve symptoms. Change in athletic shoes also may alleviate pain. When conservative methods including the modification of sports activities have not relieved symptoms, surgical intervention may be considered.17-19 Surgical treatment: excision of interdigital neuroma 1. The foot is cleansed and draped in the usual fashion. An Esmarch bandage is used to exsanguinate the foot. The ankle is padded carefully and the Esmarch is used as a tourniquet. 2. A 3-cm dorsal incision is centered in the involved interspace. 3. The dissection is carried down to the transverse metatarsal ligament (TML) (Fig. 17-16). 4. A two- to three-prong Weitlaner retractor is used to distract the adjacent metatarsals and place the TML under tension.
4 PEARL Diagnosis of MTP Instability versus Interdigital Neuroma
Figure 17-16 Dorsal incision demonstrates a large interdigital neuroma. The transverse metatarsal ligament has been sectioned. (From Coughlin MJ: In Chapman M, editor: Operative orthopaedics, Philadelphia, 1993, JB Lippincott, p. 2289.)
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When a patient has difficulty isolating the location of pain, a 1% lidocaine injection may be used to determine the site of pain.16 During serial office visits 1 week apart, the physician may inject local anesthetic into the second IMS, then the third IMS, then the second MTP joint, and then the third MTP joint. Fluoroscopy and injectable contrast may be used to verify an intra-articular injection. It is important to use small volumes (1-3 ml) to prevent extravasation of anesthetic agent to adjacent structures. While anesthetized, the patient is asked to repeat the activity that causes the most discomfort, Within 1 or 2 hours the anesthetic wears off. When temporary relief is achieved with the injection, followed by recurrent symptoms, an anatomic diagnosis is confirmed.14
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5. The TML is sectioned only when necessary to expose the neuroma and common digital nerve. 6. The digital nerves distal to the bifurcation are severed at the level of distal webspace. The proximal stumps are tensioned. A nerve freer is used to dissect longitudinally to isolate the common digital nerve. Special attention is directed at freeing the plantar branches. With tension on the proximal nerve, a scalpel is used to transect the nerve as proximal as possible in the interspace. 7. The interspace is inspected for any other nerve tissue that may be a cause of pain. It is important to sever any adjacent capsular nerve branches that prevent proximal migration of the nerve stump. The retractor is removed, and the surgical wound is irrigated and closed in a routine fashion. 8. A gauze and tape dressing is applied and changed on a weekly basis, and the patient is allowed to ambulate in a postoperative shoe. 9. Suture removal is carried out 3 weeks following surgery, and a circumferential gauze and tape strapping is continued for 3 more weeks to allow adequate healing of the TML if it was sectioned (Fig. 17-17). Aggressive walking can be commenced 4 weeks following surgery, with increased activity as pain and swelling permit. Limited-impact activities such as jogging are permitted at 2 months. Full-contact/impact activities can be resumed at 3 months.
Figure 17-18 Hard corn with keratotic buildup. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
Patients can present with concurrent interdigital neuroma and MTP joint capsular instability. Isolated treatment of one of these conditions is unlikely to resolve the patient’s symptoms. Simultaneous interdigital neuroma resection and stabilization of the MTP joint results in better outcomes than isolated procedures.14 Techniques to address capsular instability are addressed later in this chapter.
HARD CORNS AND SOFT CORNS A hard corn (Fig. 17-18) develops over the lateral aspect of the fifth toe usually because of pressure of the shoe against an underlying exostosis or condyle on the fifth toe. Patients may complain of pain associated with a hypertrophic callus on the lateral aspect of the fifth toe. A soft corn (Fig. 17-19) develops between the toes because of pressure between two adjacent bony prominences. Patient may complain of exquisite pain; maceration sometimes occurs that resembles a mycotic infection. Desiccation of the lesion then may help to distinguish it from an infection.20 On physical examination, the obvious callosity occurs overlying a bony prominence. Radiographic evaluation may help to define the location of the lesion (Fig. 17-20). Figure 17-17 Strapping of the foot is continued for 6 weeks postoperatively to promote healing of the transverse metatarsal ligament.
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Conservative treatment Padding of the hard corn (Fig. 17-21) may alleviate discomfort. Stretching of shoes overlying the lesion may
Hard corns and soft corns
often eliminates compression between the two toes. Shaving of the callosity also may be indicated (see Case Study 3). When conservative measures have failed, surgical resection of the involved condyle may eliminate the prominence and alleviate the symptoms.
C A S E S T U D Y 3
Figure 17-19 A soft corn is demonstrated in the fourth webspace, mimicking a mycotic infection. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
A 40-year-old jogger developed exquisite pain beneath the fourth and fifth toes. He recognized maceration in the fourth webspace. It was unclear whether this was a fungus infection or a soft corn. On his initial orthopaedic evaluation, radiographs demonstrated impingement between the PIP joint of the fourth toe and DIP joint of the fifth toe. Initial treatment used rubbing alcohol applied with a cotton-tipped applicator three times a day to desiccate the area. Then lamb’s wool was placed between the toes to pad and alleviate pressure between the two prominent condyles. Later, a foam spacer was placed between the toes and the patient was allowed to resume all jogging activity. No surgery was performed.
Figure 17-20 Radiograph demonstrating the location of a soft corn. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
Figure 17-21 (A) An underlying exostosis combined with restrictive footwear leads to a hard corn. (B) A pad may be used to relieve pressure.
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decrease symptoms. Shaving of the callosity on a frequent basis may diminish the painful symptoms. With a soft corn, padding of one or both toes with either a foam spacer (Fig. 17-22) or tubular foam gauze
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Figure 17-22 A pad is used to relieve pressure in the webspace. (Courtesy Roger A. Mann, MD, and Michael J. Coughlin, MD.)
Figure 17-23 A dorsal incision is used for the condylectomy as the treatment for a hard corn.
Surgical treatment for hard corns21,33 1. The foot is cleansed and draped in the usual fashion. Often a digital anesthetic block is used, although a foot block also may be considered. 2. A dorsolateral longitudinal incision is centered over the prominent lateral condyle. 3. With sharp dissection, the capsular fibers are peeled off the condyle. 4. A rongeur is used to remove the prominent condyle, with care taken to leave enough articular surface to retain joint stability (Fig. 17-23). 5. The sharp, bony edges are beveled with a rongeur. 6. The capsule is closed with two or three interrupted absorbable sutures. 7. A percutaneous flexor tenotomy is performed at the MTP joint. 8. The skin is closed with a running skin closure. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a postoperative shoe. 9. Sutures are removed 3 weeks after surgery. The toe then is taped to the adjacent toe for 3 more weeks to promote stability and avoid injury. After suture removal, an increase in sports activity can be commenced. Walking and bicycling may be started when sutures are removed. Running may commence after swelling has diminished sufficiently to allow shoewear to fit adequately, typically 6 weeks.
Surgical treatment for soft corns33 1. The foot is cleansed and draped in the usual fashion. Often a digital anesthetic block is used, although a foot block also may be considered. 2. A decision is made whether to treat both lesions on adjacent toes or to treat only one. (With a significant lesion on one toe and a minor lesion on the corresponding toe, a surgical repair of the larger lesion usually will successfully eliminate the entire problem.) Whether one or both lesions are surgically treated remains the decision of the operating surgeon. 3. A dorsolateral longitudinal incision is centered over the prominent lateral condyle. This avoids an incision in the affected webspace. 4. With sharp dissection, the capsular fibers are peeled off the condyle. 5. A rongeur is used to remove the prominent condyle, with care taken to leave enough articular surface to retain joint stability (Fig. 17-24). 6. The sharp edges are beveled with a rongeur. 7. If a fixed contracture of the toes exists, a percutaneous tenotomy of the flexor tendon is performed. 8. The capsule is closed with an interrupted absorbable suture. 9. The skin is closed with a running skin closure. A gauze and tape dressing is applied and
Hammertoes, mallet toes, and claw toes
Figure 17-25 Hammertoe deformity. (From Coughlin MJ: Foot Ankle Int 21:94, 2000.)
changed on a weekly basis. The patient is allowed to ambulate in a wooden-soled postoperative shoe. 10. Sutures are removed 3 weeks after surgery. 11. A small gauze spacer is used between the toes for another 3 weeks until the surgical incisions have softened. After suture removal, walking and bicycling may be started. Running may commence after swelling has diminished successfully to allow shoewear to fit adequately, typically 6 weeks.
HAMMERTOES, MALLET TOES, AND CLAW TOES Deformities of the lesser toes include both flexible and fixed deformities. Typically callus formation occurs over bony prominences, and at times during athletic activity these areas may become inflamed and painful. A hammertoe (Fig. 17-25) is characterized by a flexion contracture at the PIP joint. Early on, it may present as a flexible deformity that in time may become fixed. With a mallet toe (Fig. 17-26), there is a flexion contracture at the DIP joint. Early on, it may present as a flexible deformity because of tightness of the flexor digitorum longus (FDL) tendon. With time it may become a fixed deformity. A callus may develop dorsally over the DIP joint because of pressure or abrasion from impacting against
the toe box. A callus may also develop at the tip of the toe because of pressure against the insole of the shoe. With a claw toe deformity, typically a flexion contracture develops at the PIP joint with hyperextension at the MTP joint. A callosity may develop over the PIP joint; with a long-standing contracture an IPK may develop beneath the metatarsal head. Early on, a flexible contracture may be passively correctable, although with time a fixed contracture may develop. Subjectively a patient typically complains of pain over a prominent callus on the involved toe; occasionally a painful callus will develop at the tip of the toe. On physical examination, the treating physician not only observes a keratotic buildup over the deformity but also examines the attitude of the toe. The flexibility or rigidity of the deformity may determine the particular surgical repair, should it be necessary. The presence of multiple toe deformities, contractures at adjacent joints, and neurologic deficits must be appreciated during the evaluation. With all of these lesser-toe deformities, an athlete may complain of blistering, callus formation, swelling, or pain because of a dynamic or static deformity. Occasionally an infection may develop in the overlying tissue.
Conservative treatment Conservative care includes relieving pressure over the painful area.22 The use of roomy shoewear often will relieve discomfort in the athlete. Padding often allows return to sports activity. Shaving of painful callosities may temporarily relieve keratotic buildup. Often conservative care will allow an athlete to continue activity, although decreasing the duration or intensity of the 397
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Figure 17-24 (A) A soft corn may develop over the base of the proximal phalanx. (B) Resection of the bony prominence.
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Figure 17-26 Mallet toe deformity.
workout or changing to a different sporting activity may be necessary on a temporary or permanent basis. When conservative measures do not allow acceptable athletic activity, surgical intervention may be necessary.
Surgical treatment: hammertoe repair23,28 1. The foot is cleansed and draped in the usual fashion. Usually a digital nerve block is used as an anesthetic. 2. A small Penrose drain may be used as a tourniquet (optional). 3. A dorsal elliptical or longitudinal skin incision is centered over the PIP joint. The incision is carried down to bone with excision of an ellipse of skin, extensor tendon, and capsule, exposing the condyles of the proximal phalanx. 4. The collateral ligaments of the PIP joints are severed, enabling the condyles to be delivered. 5. A bone-cutting forceps is used to osteotomize the proximal phalanx in the supracondylar region (Fig. 17-27). The sharp edges are beveled with a rongeur. 6. The articular surface of the middle phalanx is exposed, and a rongeur is used to remove the articular surface. 7. A 0.045 K-wire is introduced at the PIP joint and driven distally, exiting the tip of the toe. Then, with the toe reduced to the desired position, the K-wire is driven in a retrograde fashion, stabilizing
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the hammertoe repair. The pin is bent at the tip of the toe to prevent proximal migration. 8. A gauze and tape dressing is applied and changed on a weekly basis. The patient is permitted to ambulate in a bunion shoe. Sutures and K-wire are removed 3 weeks after surgery. 9. The patient then is instructed to tape the toe to an adjacent toe for an additional 4 weeks to protect it from injury. After the K-wire is removed, increased walking activity is permitted. Cycling may be allowed. Running or jogging usually is avoided until swelling has diminished (6 to 8 weeks). Often there will be 10 to 15 degrees of motion at the involved joint following adequate healing. Whether an arthrodesis occurs is not of significant concern. Fibrous ankylosis with a small amount of motion is equally acceptable. For a hammertoe that can be passively corrected and has no element of fixed contracture, a flexor tendon transfer may be used. The procedure is technically more difficult than a condylectomy but leaves the toe more flexible. The FDL tendon is transferred to the dorsum of the proximal phalanx. This procedure removes a deforming force and at the same time makes the FDL a plantarflexor of the proximal phalanx. Whether it is a dynamic transfer or a tenodesis is unclear, but it is a useful procedure for repair of the flexible hammertoe. This procedure also is used for a flexible claw toe and for the unstable MTP joint (both discussed later).
Hammertoes, mallet toes, and claw toes
Figure 17-27 Hammertoe repair. (From Coughlin MJ: Foot Ankle Int 21:94, 2000.)
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Surgical treatment: early flexible mallet toe repair37 1. The foot is cleansed and draped in the usual fashion. A digital block is used for anesthesia. (With an early mallet toe deformity, the toe can be corrected passively to neutral with pressure.) 2. A no. 11 scalpel blade is introduced on the plantar aspect of the DIP joint and the FDL tendon is released, and a K-wire is used to stabilize the DIP joint repair. 3. The incision is closed with an interrupted skin suture. 4. A gauze and tape dressing is applied, and the patient is allowed to ambulate in a postoperative shoe. 5. The sutures are removed 10 days after surgery. Athletic activity can be resumed rapidly following this procedure with little downtime. In general, a patient can begin to advance activities at 2 weeks. Full activities typically can be resumed by 4 weeks. When a fixed mallet toe is corrected, a procedure similar to that for hammertoe deformity is performed as is carried out for a hammertoe deformity. In this case the procedure is carried out at the DIP joint (Fig. 17-28).24 Surgical treatment: flexor tendon transfer25 1. The foot is cleansed and draped in the usual fashion. A foot block may be used for anesthesia. 2. The foot is exsanguinated with an Esmarch bandage. The ankle is padded carefully and the Esmarch is used as a tourniquet. 3. A 1-cm longitudinal incision is centered in the midline over the dorsum of the proximal phalanx. The dissection exposes the extensor digitorum longus tendon. Then with blunt dissection, with
Figure 17-29 The flexor digitorum longus is the largest of the tendons and is characterized by a midline raphe.
4.
5.
6. 7. 8.
9.
10.
Figure 17-28 Mallet toe repair. (A) Proposed resection. (B) K-wire fixation following condylectomy.
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11.
a mosquito clamp on either side of the proximal phalanx, a tunnel is created for transfer of each limb of the FDL tendon. The tunnel is created deep to the neurovascular bundles and superficial to the extensor expansion. On the plantar aspect of the toe, a transverse incision is made at the proximal plantarflexion crease of the toe. With blunt dissection, the long flexor tendon sheath is identified. A longitudinal incision is made in the tendon sheath and the flexor tendons are observed. The FDL tendon is the larger of the two tendons and is characterized by a midline raphe (Figs. 1729 and 17-33). Tension is placed on the FDL and a small plantar tenotomy puncture wound is made at the level of the DIP joint, releasing the FDL (Fig. 17-30). The FDL tendon then is withdrawn through the more proximal plantar wound and is split longitudinally along its median raphe (Fig. 17-31). Each limb of the FDL is passed on either side of the proximal phalanx. With the ankle held in neutral position, and the involved toe held in 10 degrees of plantarflexion, the tendon limbs are sutured to themselves with interrupted nonabsorbable suture (Fig. 17-32). Reinforcement sutures may be placed between the tendon and the extensor expansion. The toe then is inspected to ensure that proper alignment has been achieved. The tourniquet is released to ensure that it has not affected the tension of the repair. On occasion it is necessary to retension the repair, with tightening or loosening of one or both of the tendon limbs. The skin then is approximated in a routine fashion. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a postoperative shoe. Sutures are removed 3 weeks after surgery.
Hammertoes, mallet toes, and claw toes
Figure 17-30 (A) Lateral view of toe demonstrating long flexor tendon and other important tendons. (B) Long flexor tendon is demonstrated on the plantar aspect of the foot. (From Coughlin MJ: Orthopedics 10:63, 1987.)
Flexor digitorum longus is released distally. (From Coughlin MJ: Orthopedics 10:63, 1987.)
12. At 3 weeks, increased walking activity is permitted. Careful cycling also is an acceptable activity. Running, jogging, and aggressive sports should be avoided until swelling has subsided (6 to 8 weeks). The patient should be instructed to start passive manipulation of the
toe 4 weeks after surgery. The toe may become stiff because of immobilization, and frequent manipulation during this period increases the passive motion of the toe. Considerable active motion is sacrificed with the flexor tendon transfer. 401
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Figure 17-31
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Figure 17-32
Lesser-toe disorders
Flexor digitorum longus is transferred dorsally. (From Coughlin MJ: Orthopedics 10:63, 1987.)
Figure 17-33 Cross section of lesser toe at level of metatarsal head demonstrating flexor digitorum brevis and longus.
CLAW TOE A claw toe deformity may be flexible, semirigid, or fixed. Frequently it involves all of the toes on a foot. Although the etiology frequently is idiopathic, the treating physician should inspect the patient for other causes, such as spasticity, muscular dystrophy, spinal abnormality, and previous trauma (old fractured tibia, old compartment syndrome, and so forth).
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Many cases may be treated effectively with roomy footwear, padding, and pedicures; however, on occasion an athlete is so symptomatic that surgery is contemplated. Although claw toes frequently involve multiple toes, they have similarities with different stages in the development and treatment of hammertoe deformity. Early on, flexible claw toes (although multiple in nature) resemble flexible hammertoes. A flexor tendon transfer of the second, third, and fourth toes may achieve adequate realignment by releasing the contracted FDL tendon and depressing the proximal phalanx through the tendon transfer (see the section on Flexible Hammertoe Repair). Rarely is a flexor tendon transfer performed on the fifth toe. A flexor tenotomy occasionally is performed, although often the fifth toe is asymptomatic. As a claw toe becomes fixed, a patient may develop symptoms of a hammertoe, with callus formation overlying the PIP joint. Because of the fixed dorsiflexion contracture at the MTP joint, the toe buckles, depressing the metatarsal head. A plantar callus (IPK) may develop because of increased pressure beneath the metatarsal head. The treating physician must remember that the IPK usually is due to the contracted toe rather than to a prominent metatarsal condyle. Correction of the toe deformity often is associated with diminution or resolution of the plantar callosity. The fixed claw toe resembles a fixed hammertoe, although the claw toe also has a contracture at the MTP joint. A PIP joint contracture is repaired surgically
Metatarsophalangeal joint instability
combined with hammertoe repair, it is introduced at the PIP joint and driven distally, exiting the tip of the toe. It then is driven proximally through the proximal phalanx.) 6. The pin then is driven in a retrograde fashion, stabilizing the MTP joint. The pin is bent at the tip of the toe to prevent proximal migration. 7. The extensor tendon is repaired in a lengthened fashion, and the skin is closed in a routine fashion. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a postoperative shoe. 8. Three weeks following surgery, the K-wire and sutures are removed. The toe is taped in a corrected position for 4 to 6 weeks. After removal of the K-wire, increased activity is permitted. Walking, cycling, and swimming are allowed. It is wise to progress slowly, with the introduction of jogging and running, until adequate healing has occurred and swelling has subsided (6 to 8 weeks).
(Fig. 17-34) with a condylectomy of the proximal phalanx (see the section on Fixed Hammertoe Repair). Obviously, once the PIP joint contracture has been corrected, attention must be directed to the MTP joint contracture.
Surgical treatment: MTP soft-tissue arthroplasty24,25 1. The foot is cleansed in the usual fashion. An Esmarch bandage is used to exsanguinate the foot. The ankle is padded carefully and the Esmarch is used as a tourniquet. 2. An oblique or longitudinal incision is centered over the MTP joint. 3. The long extensor tendon is split longitudinally and Z-lengthened. 4. The medial, dorsal, and lateral capsule is completely released to allow reduction of the MTP joint. (This requires a significant release in a plantar direction of both collateral ligaments.) When a toe still does not reduce completely following an MTP release, there may be adhesions between the plantar capsule and the plantar metatarsal head. These usually can be released with a McGlanery elevator. The toe then should be easily reducible in a dorsal plantar plane. 5. A 0.062 K-wire is used to stabilize the repair. The pin is introduced at the MTP joint and driven in a distal direction exiting the tip of the toe. (When
METATARSOPHALANGEAL JOINT INSTABILITY Instability of the MTP joint can be an extremely difficult diagnosis to make, especially in the early stage, when there is a lack of clinical deformity. The second MTP joint is the most frequent location of instability because of the longer length of the second ray. In a report on athletes with second MTP instability, Coughlin26 reported 100% of the patients to have an elongated second metatarsal in relation to adjoining metatarsals. Most likely because of the stress of repeated and prolonged athletic activity, pain without deformity develops in the forefoot. The mechanism of instability generally is described as rupture or attenuation of the collateral ligaments and volar plate of the MTP joint.27 Typically an athlete initially describes ill-defined forefoot pain, often exacerbated by running and sports activities and relieved by rest. Sometimes pain increases with intensity and/or duration of sports activities. On physical examination, the treating physician initially must isolate the exact point of tenderness. With palpation, tenderness typically is elicited over the plantar, medial, or lateral MTP capsule. Usually pain is not so pronounced in the third or second intermetatarsal spaces (IMSs). Initially it may be difficult to differentiate second MTP pain from a second IMS neuroma. A critical differentiating finding, however, is that there are no neuritic symptoms in the second or third toes and no numbness associated with capsulitis or instability of the second MTP joint. (An IMS neuroma may occur along with MTP instability.) Capsulitis or inflammation of an MTP joint can be associated with systemic or localized arthritis. These 403
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Figure 17-34 (A) Claw toe deformity. (B) Following metatarsophalangeal joint release and extensor tenotomy and proximal interphalangeal joint arthroplasty.
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With time, the diagnosis becomes obvious as the toe deviates29,30 (Fig. 17-36). Initially, the toe deviates medially and with time dorsally, developing into a cross-over second-toe deformity. This development can be acute, although typically in athletes it occurs insidiously over several months. Radiographic evaluation involves routine anteriorposterior (AP) and lateral radiographs to determine whether there is widening of the joint space (effusion), narrowing (arthritis), or malalignment in relationship to the adjoining MTP joints (Fig. 17-37). Occasionally an arthrogram may be obtained, but this is not routinely performed.
Figure 17-35 A drawer sign is used to detect dorsal plantar instability.
conditions often involve other MTP joints, whereas without a preexisting inflammatory arthropathy only the second MTP joint usually is involved. A drawer sign28 (Fig. 17-35) typically is the diagnostic test most helpful in defining capsulitis and/or instability of the MTP joint. Grasping the involved toe between the fingers and stressing the MTP joint in a dorsal plantar direction can elicit exquisite pain, likely because of stress on the attenuated plantar capsule or collateral ligaments. (This finding is absent in an isolated interdigital neuroma.)
Conservative treatment Early conservative treatment relies on early diagnosis by the treating physician. Before deformity has developed at the second MTP joint, early MTP instability is best treated with taping the involved toe, padding, and a change in athletic activity. Taping requires stabilizing the toe to prevent dorsal plantarflexion excursion. Taping to an adjacent toe may be effective. A sling-type taping technique also may be effective (Fig. 17-38). An athlete may need to tape the involved toe for several months, although some athletes find it necessary to tape the toe only during sports activities. A metatarsal pad placed just proximal to the metatarsal head may alleviate pressure and relieve symptoms on the involved MTP capsule. Restructuring workouts and modifying athletic activity can be helpful in relieving pain. A runner may find that pain occurs only with greater than 2 miles of jogging and that shorter distances can be accomplished pain free. With unsuccessful resolution of discomfort, or insistence on a higher level of athletic activity, surgical intervention may be contemplated. What is presented is a
Figure 17-36 (A) Instability of the second metatarsophalangeal joint with a cross-over second toe may occur because of degeneration of the lateral collateral ligament. (B) Malalignment as demonstrated with a cross-over second toe.
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Metatarsophalangeal joint instability
step-by-step approach to MTP instability (see Case Study 4).
C A S E S T U D Y 4
Figure 17-37 Axial malalignment may be demonstrated on radiographic examination.
A 25-year-old, female aerobic instructor developed the onset of insidious but increasing pain in the area of her second MTP joint over 6 months. No specific injury was noted. She denied neuritic-type pain. She became unable to tolerate aerobic activity and then noted slight medial deviation of her second toe. On physical examination, she was noted to have normal sensation and no evidence of a neuroma. She had a negative Mulder sign. She had pain on palpation over the second MTP joint capsule. She had a positive drawer sign, and exquisite pain was elicited. Radiographic examination showed slight medial inclination of the second MTP joint. Initially the patient taped her second toe to the third toe for 3 months and was able to walk without pain. However, her pain resumed with aerobic activity. She requested surgical intervention. A medial MTP release, lateral capsular reefing, and flexor tendon transfer were performed. She then taped her toe to stabilize it for 6 weeks postoperatively.
Figure 17-38 Technique of taping toe. (From Coughlin MJ: Foot Ankle 8:29, 1087.)
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She resumed aggressive walking 6 weeks after surgery, jogging at 3 months, and aerobic instruction at 4 months. She achieved resolution of her pain and is very satisfied with her repair.
Surgical treatment: MTP instability For patients who fail conservative treatment, several surgical techniques exist. Selection of the appropriate technique depends on clinical assessment of the deformity. Synovitis and mild deviation the MTP joint is classified as a mild deformity and can be treated with capsular reefing. Dorsomedial deviation at the MTP joint or overlapping of the adjacent toe is considered moderate deformity and can be treated with capsular reefing and an flexor tendon transfer. This is the most likely situation for an athlete who does not respond to conservative treatment. This procedure is described in the following. Finally, complete dislocation at the MTP joint is a severe deformity that necessitates an osteotomy of the MTP joint.29 Surgical treatment: capsular reefing and flexor tendon transfer31 1. The foot is cleansed and draped in the routine fashion. The foot is exsanguinated with an Esmarch bandage. The ankle is padded carefully, and the Esmarch is used as an ankle tourniquet 2. A 2-cm dorsal midline incision is centered over the MTP joint. If hyperextension of the toe is present, the extensor digitorum longus tendon is lengthened and later repaired at the conclusion of the procedure. 3. The dorsal MTP capsule is released. With medial deviation of the phalanx, the medial capsule is completely released. In this case the lateral capsule then is reefed (Fig. 17-39) with two interrupted, 2-0 nonabsorbable sutures to realign the toe in a medial lateral plane. With lateral deviation, the lateral capsule is released and the medial capsule reefed. (This is quite uncommon.) 4. In the presence of remaining hyperextension of the MTP joint, or with remaining dorsal plantar
Figure 17-39 Technique of capsular reefing for repair of axial malalignment.
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instability, a flexor tendon transfer then is performed (see section earlier in this chapter). 5. The wound is closed in a routine fashion. A gauze and tape dressing is applied and changed on a weekly basis. The patient is allowed to ambulate in a wooden-soled shoe. 6. Sutures are removed 3 weeks after surgery. If a Kwire has been placed, it is removed at this time (Fig. 17-40). The toe is taped in appropriate position for 6 weeks postoperatively (see Fig. 17-38). The patient is permitted to do aggressive walking 6 weeks following surgery and may increase sporting activity as swelling diminishes and pain permits. Results with this type of approach are gratifying. Significant pain relief can be achieved, although Coughlin26 reported that several patients had to modify their athletic routine postoperatively. When possible, the successful conservative treatment of lesser-toe problems will allow rapid return to athletic activity with limited downtime. Surgical procedures on the lesser toes take time to heal, are prone to swell, and leave an element of stiffness at the involved joint, which may be of some concern to the athlete. Adequate preoperative counseling is important to identify areas of concern, problem areas of recovery, and patient expectations.
Surgical treatment: Weil osteotomy36,38 The Weil osteotomy is a shortening osteotomy that primarily benefits patients with painful instability associated with a long lesser toe. This osteotomy should be avoided in patients with a plantarflexed metatarsal because it does not dorsally displace the distal fragment.31 The relative stability of this osteotomy with weight bearing and the use of internal fixation make this an ideal osteotomy for the active patient. 1. The foot is cleansed and draped in the routine fashion. The foot is exsanguinated with an Esmarch bandage. The ankle is padded carefully, and the Esmarch is used as an ankle tourniquet. 2. A 3-cm incision is made in the adjacent IMS just proximal to the webspace. This allows access to adjacent metatarsals should more than one require attention. 3. The metatarsal head is exposed through a lateral capsular incision under the extensor tendon. The toe is plantarflexed, exposing the metatarsal head. 4. A narrow oscillating saw is used to make the osteotomy parallel to the weight-bearing surface of the foot. The osteotomy originates in the dorsal one fourth of the MTP joint (Fig. 17-41). 5. The distal fragment is displaced proximally until the metatarsal head is at the level of a line drawn from the MTP of the first and fourth rays. The fragment is fixed with one or two more fragment screws.
Metatarsophalangeal joint instability
Figure 17-40 (A) Clinical appearance of a cross-over toe deformity. (B) Radiographic appearance of a cross-over second toe. (C) Three-year follow-up demonstrating excellent alignment. (D) Three-year radiographic follow-up demonstrating excellent alignment. (From Coughlin MJ: Foot Ankle 8:29, 1987.)
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Figure 17-41 The Weil osteotomy. (From Trnka H: Foot Ankle 20:72, 1999.)
6. The overhanging bone is rongeured smooth. 7. The capsule is reefed if necessary as described previously. The capsule is repaired with absorbable sutures. 8. The patient is placed in a surgical shoe and allowed to weight bear with crutches.
CONCLUSION When correctly diagnosed and treated, forefoot disorders should not limit athletic endeavors. Although many of these conditions are treated nonoperatively, the orthopaedic surgeon often is the most appropriate practioner to identify the problem and direct treatment. When operative treatment is required, the patient should be able to resume activities at the previous level of competition.
REFERENCES 1. Coughlin MJ: Etiology and treatment of the bunionette deformity. In Greens WB, editor: American Academy of Orthopaedic Surgeons instructional course lectures, 39:1037-1048, AAOS-Chicago, p. 37, 1990. 2. Mann RA, Coughlin MJ: Bunionettes. In Video textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions.
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3. Throckmorton JK, Bradlee N: Transverse V sliding osteotomy: a new surgical procedure for the correction of Tailor’s bunion deformity, J Foot Surg 18:117, 1978. 4. Coughlin MJ: Bunionettes. In Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 6, St Louis, 1992, CV Mosby. 5. Sponsal KH: Bunionette correction by metatarsal osteotomy, Orthop Clin North Am 7:808, 1976. 6. Coughlin MJ: Treatment of bunionette deformity with longitudinal diaphyseal osteotomy with distal soft tissue repair, Foot Ankle 11:195, 1991. 7. Mann RA: Intractable plantar keratosis. In American Academy of Orthopaedic Surgeons instructional course lectures, Vol 33. St Louis, 1984, CV Mosby. 8. Mann RA, DuVries H: Intractable plantar keratosis, Orthop Clin North Am 4:67, 1973. 9. Pedowitz WJ: Distal oblique osteotomy for intractable plantar keratosis of he middle three metatarsals, Foot Ankle 9:7, 1988. 10. Dreeben SM, et al: Metatarsal osteotomy for primary metatarsalgia: radiographic and pedobarographic study, Foot Ankle 9:214, 1989. 11. Mann RA, Coughlin MJ: Intractable plantar keratoses. InVideo textbook of foot and ankle surgery, St Louis, 1991, Medical Video Productions. 12. Giannestras NJ: Shortening of the metatarsal shaft in the treatment of plantar keratosis, J Bone Joint Surg 49A:61, 1958. 13. Thompson FM, Deland JT: Occurrence of two interdigital neuromas in one foot, Foot Ankle Int 14:15, 1993. 14. Coughlin MJ, et al: Concurrent interdigital neuroma and MTP joint instability: long-term results of treatment, Foot Ankle Int 23:1018, 2002. 15. Mulder JD: The causative mechanism in Morton’s metatarsalgia, J Bone Joint Surg 33B:94, 1951.
Further reading 30. Coughlin MJ: When to suspect crossover second toe deformity, Musculo Skel Med 4:39, 1987. 31. O’Kane C, Kilmartin TE: The surgical management of central metatarsalgia, Foot Ankle Int 23:415, 2002.
FURTHER READING Coughlin MJ: Operative repair of the mallet toe, Foot Ankle 16(3):109-116, 1995. Coughlin MJ: Common causes of pain in the forefoot in adults, J Bone Joint Surg[Br] 82-B:781-790, 2000. Coughlin MJ: Lesser-toe abnormalities, J Bone Joint Surg [Am] 84A:1446-1469, 2002. Coughlin MJ, Dorris J, Polk E: Operative repair of the fixed hammertoe deformity, Foot Ankle Int 21:94-104, 2000. Coughlin MJ, Grimes JS: Geometric analysis of the Weil osteotomy, Foot Ankle Int 27:985-992, 2006. Coughlin MJ, Kennedy MP: Operative repair of fourth and fifth toe corns, Foot Ankle Int 24:147-157, 2003. Coughlin MJ, Pinsonneault T: Operative treatment of interdigital neuroma: a long-term follow-up study, J Bone Joint Surg [Am] 83A:1321-1328, 2001. Trnka HJ, Muhlbauer M, Reinhard Z, et al: Comparison of the results of the Weil and Helal osteotomies for the treatment of metatarsalgia secondary to dislocation of the lesser metatarsophalangeal joints, Foot Ankle Int 20:72-79, 1999.
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16. Coughlin MJ: Soft tissue afflictions. In Chapman M, editor: Operative orthopaedics, Philadelphia, 1988, JB Lippincott. 17. Betts LO: Morton’s metatarsalgia: neuritis of the fourth digital nerve, Med J Aust 1:514, 1940. 18. Mann RA, Reynolds JC: Interdigital neuroma: a critical clinical analysis, Foot Ankle 3:238, 1983. 19. Morton TG: A peculiar painful infection of the fourth metatarsophalangeal articulation, Am J Med Sci 71:37, 1876. 20. Mann RA, Coughlin MJ: Deformities of the lateral toes. In American Academy of Orthopaedic Surgeons instructional course lectures, 36:137-159, 1987. 21. Mann RA, Coughlin MJ: Lesser-toe deformities. In Jahss JM, editor: Disorders of the foot, ed 2, Philadelphia, 1991, WB Saunders. 22. Coughlin MJ: Mallet toes, hammer toes, claw toes, and corns— causes and treatment of lesser toe deformities, Postgrad Med 75:191, 1984. 23. Coughlin MJ: Lesser toe deformities, Orthopedics 10:63, 1987. 24. Coughlin MJ: Lesser toe abnormalities. In Chapman M. editor: Operative orthopaedics, Philadelphia, 1988, JB Lippincott. 25. Coughlin MJ, Mann RA: Lesser toe deformities. In Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, ed 6, St Louis, 1992, CV Mosby. 26. Coughlin MJ: Metatarsophalangeal joint instability in the athlete, Foot Ankle 14:309, 1993. 27. Haddad SL, et al: Results of flexor-to-extensor and extensor brevis tendon transfer for correction of the crossover second toe deformity, Foot Ankle Int 20:781, 1999. 28. Coughlin MJ: Subluxation and dislocation of the second metatarsophalangeal joint, Orthop Clin North Am 20:535, 1989. 29. Coughlin MJ: Cross-over second toe deformity, Foot Ankle 8:29, 1987.
.........................................C H A P T E R 1 8 Great-toe disorders Robert B. Anderson and Scott B. Shawen CHAPTER CONTENTS ...................... Introduction
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Specific entities of the great toe
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Anatomy
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Conclusion
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Biomechanics
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References
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INTRODUCTION Injuries to the hallux metatarsophalangeal (MTP) joint are not uncommon, particularly in the running athlete, and may result in chronic pain and deformity. Causes of hallux injuries range from soft-tissue disruption to overuse and degeneration. Trainers and physicians may fail to recognize the potential dysfunction of these injuries, thus providing inadequate care and protection from further injury. Long-term sequelae of even isolated soft-tissue injury include flexor hallucis longus (FHL) tendon tears, hallux valgus or varus, cock-up deformity with interphalangeal (IP) joint contracture, and degenerative joint disease, that is, hallux rigidus. Clanton and Ford1 found that foot injuries rank third behind ankle and knee injuries as the most common time-loss injury among university athletes. Of these foot injuries, a large proportion were sprains of the forefoot and, more specifically, the hallux MTP joint. In our practice, we have seen a number of professional athletes with a broad range of injuries to the great toe and base this chapter on our experiences. Great-toe injuries can lead to significant functional disability, especially when not recognized early. In the short term, these injuries can result in difficulties with push-off and running. Long-term sequelae include continued difficulty with pain and push-off strength, as well as progressive degeneration. Physicians involved in the treatment of foot and ankle injuries, especially those caring for athletes, must become familiar with the spectrum of injuries about the hallux MTP joint, the
conservative and operative treatments for these injuries, and the late sequelae encountered in these athletes.
ANATOMY To the surgeon responsible for the care of athletes with great-toe injuries, knowledge of the anatomy of the hallux MTP joint is paramount. In the simplest of terms, the motion of the joint consists of rolling, sliding, and compression. More specifically, the morphology of this joint allows for plantarflexion and dorsiflexion but very limited abduction and adduction. The fact that there is more than one center of motion contradicts the theory of a simple, hinged joint. Instead, the joint is a dynamic acetabulum or ‘‘hammock,’’ as described by Kelikian.2 The joint articulation provides little of the overall stability because of the shallow, glenoid-like cavity of the proximal phalanx. Most of the stability comes instead from the capsular-ligamentous-sesamoid complex, which is described in detail later. There are two sets of ligaments that contribute to the stability of the metatarsal (MT) head as it articulates with the proximal phalanx: the medial and lateral collateral ligaments and the metatarsosesamoid suspensory ligaments.3 The fan-shaped medial collateral ligament is composed of the medial MTP ligament and the medial metatarsosesamoid ligament (Fig. 18-1). The lateral collateral ligament is structured in a similar fashion.3 In addition to the collateral ligaments, the strong, fibrous plantar plate (see Fig. 18-1) also affords structural
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BIOMECHANICS
Figure 18-1 Medial diagrammatic representation of first metatarsophalangeal joint. (From Adelaar RS, editor: Disorders of the great toe, Rosemont, IL, 1997, American Academy of Orthopaedic Surgeons.)
support. The capsular ligamentous complex of the hallux MTP joint actually is a confluence of structures including the plantar plate, collateral ligaments, the flexor hallucis brevis, the adductor hallucis, and abductor hallucis tendons. This plantar plate is attached firmly to the base of the proximal phalanx and only loosely attached at the MT neck through the capsule.4 The split tendon of the flexor hallucis brevis runs along the plantar aspect of the hallux and envelops the sesamoids before inserting at the base of the proximal phalanx as the capsular-ligamentous complex (see Fig. 18-1). The two sesamoids are united by a thick, intersesamoid ligament and maintain the course of the FHL tendon. Adding to the stability of the hallux MTP joint are three other intrinsic muscles of the great toe. The extensor hallucis brevis originates at the fascia overlying the sinus tarsi and runs obliquely to attach into the extensor mechanism on the dorsum of the MTP joint. It functions primarily as an extensor of the hallux MTP joint. On the plantar aspect, the abductor and adductor hallucis tendons insert on the medial and lateral aspects of the hallux MTP joint, respectively. These tendons blend into the capsularligamentous complex, as well as the sesamoids, to provide additional structural support (Fig. 18-2).5 Not a simple, hinged joint. Most of the stability comes instead from the capsularligamentous-sesamoid complex. Capsular ligamentous complex: plantar plate, collateral ligaments, flexor hallucis brevis, adductor hallucis, and abductor hallucis tendons. Collateral ligaments have phalangeal and sesamoid insertions. Split tendon of the flexor hallucis brevis runs along the plantar aspect of the hallux and envelopes the sesamoids before inserting at the base of the proximal phalanx.
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The hallux MTP joint lies in an intricate balance of opposing tendons and ligaments. The anatomy outlined previously, especially with regard to the plantar plate, is important when considering the biomechanical demands placed on the first MTP joint. During normal gait, the great toe typically supports twice the load of the lesser toes and accommodates forces reaching 40% to 60% of body weight.6 During athletic activity, including jogging and running, the peak forces may approach two to three times body weight, and the forces increase to eightfold when a running jump is performed.7 The range of motion (ROM) in the normal foot has been studied extensively; it is noted to be highly variable and to decrease with aging. In the resting position, the first MTP joint is in a mean resting position of 16 degrees of dorsiflexion. The passive arc of motion was noted by Joseph to be from 3 to 43 degrees of plantarflexion and from 40 to 100 degrees of dorsiflexion.8 The mean passive MTP joint dorsiflexion during pushoff was 84 degrees. One study found that at least 60 degrees of dorsiflexion is considered normal in barefoot walking on a level surface.9 Athletes may accommodate up to 50% reduction in MTP joint motion resulting from acute injury to the plantar plate or hallux rigidus by various gait adjustments such as foot/leg external rotation, shortened stride, and increased ankle, knee, or hip motion.4 In addition, a stiff-soled shoe is capable of decreasing MTP joint dorsiflexion to 25 to 30 degrees without significantly affecting gait.9 The effects on the push-off power of the great toe following sesamoidectomy have been studied in vitro by Aper et al.10 They confirmed the importance of this seemingly insignificant bone to the function of the toe, particularly in the athlete, in whom even a small loss of power will affect overall performance. The study noted that the isolated excision of the tibial sesamoid
Figure 18-2 Twenty percent to 30% of the metatarsal head is removed, as well as the exostosis. (From Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby-Year Book.)
Specific entities of the great toe
SPECIFIC ENTITIES OF THE GREAT TOE Hallux rigidus Hallux rigidus is defined as a localized degeneration of the hallux MTP joint. It was first described as hallux flexus in 1887 by Davies-Colley.11 In his first description of this condition, he discussed a plantarflexed posture of phalanx relative to MT head. The actual term ‘‘hallux rigidus’’ was coined by Cotterill in 1888 and remains the most common term used today.12 Numerous papers have theorized the etiology and pathophysiology of hallux rigidus. One such theory is that of metatarsus elevatus, a term describing the dorsiflexed posture of the first ray in relationship to the foot and the subsequent plantarflexed posture of the hallux. This has been discussed by many authors, but the most current data indicate that the elevated posture of the first MT improves after dorsal decompression of the hallux MTP joint.13-16 Overuse and repetitive dorsiflexion forces, such as those occurring in a runner or kicker, may lead to chondral lesions and other occult injuries17 or to osteochondritis dissecans.2,18,19 It also may result as a sequelae to a turf-toe injury. Anatomic abnormalities that may lead to hallux rigidus include the flat or pronated foot,15,20,21 a long first MT or hallux,21 and a flat MT head.22 To this time the true potential etiologies for the development of hallux rigidus remain in question. Clinical grading from mild to severe (or I, II, and III) has been proposed by many authors. Grading depends on the severity of disease and is based on ROM, pain or crepitus with motion, the size of the dorsal osteophyte on the MT head, the presence of sesamoid involvement, and the radiographic alignment of the hallux (on anterior-posterior [AP] and lateral views). A radiographic classification scheme was created by Hattrup and Johnson in 1988.23 Their grade 1 is considered mild; the joint space is maintained and there is minimal spurring. Grade 2 is moderate disease in which the joint
space is narrow, bony proliferation is present on the MT head and phalanx, and there is subchondral sclerosis and/or cyst formation. Grade 3 is the severe type, with significant joint space narrowing and extensive bony proliferation that involves the entire periphery and includes loose bodies, a dorsal ossicle, or subchondral cyst formation. A more recent grading scheme, proposed by Coughlin and Shurnas,24 combines objective and subjective clinical data with radiographic findings (Grades 0 to 4). Treatment recommendations are made on the basis of grade severity. Symptoms with which the typical athlete may present include pain that is worse with push-off and more severe after increased activity (i.e., twice-a-day practice regimens), as well as swelling. Although there may be bilateral radiographic involvement, the patient almost always presents with unilateral symptoms. Swelling and the bony prominence itself may interfere with athletic shoewear (especially in soccer and football, sports in which athletes prefer tightly fitting shoewear). A dysesthesia in the dorsomedial cutaneous nerve can result from tight shoewear’s impinging on the bony prominence. Occasionally transfer lesions may develop. This presents as metatarsalgia secondary to the lack of hallux dorsiflexion, causing increased pressure on the lateral forefoot. In treating hallux rigidus in the athlete, one must consider the sporting activity and position played (i.e., a lineman who requires little hallux MTP dorsiflexion vs. a running back or wide receiver), shoewear requirement, and ROM of the entire foot and ankle. Even more minor or early-presenting cases can be problematic because some athletes create more forceful dorsiflexion, which can limit the function of the runner and incapacitate the dancer. Also important is the fact that if a bad joint is provided more motion, it may hurt more and degenerate more quickly. Nonoperative treatment options include the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and shoewear modifications. Shoes of adequate size and a more full-fitted toe box or increased depth are helpful and can be modified further with a balloon patch over bony prominences. Turf-toe inserts (Springlite, Otto Bock, Minneapolis, MN) that limit dorsiflexion and subsequent dorsal impingement are potentially useful but may limit performance in the elite runner. Rigid rocker soles function in the same manner as semirigid inserts and, although helpful in the general population, are not popular with the athlete because of the increased weight and excessive stiffness. Orthotic devices can unload the hallux MTP joint, but one must remember to increase the shoe size to accommodate for it. Taping techniques can limit dorsiflexion and provide pain relief. Application is the same as that for turf-toe; however, skin problems such as blistering can occur. Steroid 413
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equated to an 11% loss of flexor power, there was 19% loss for a fibular sesamoidectomy, and 32% when both are excised.10 Great toe supports twice the weight of each lesser toe. Hallux dorsiflexion during gait/running is 60 to 84 degrees. Up to 50% reduction in ROM can be accommodated through gait adjustments such as foot/leg external rotation, shortened stride, and increased ankle, knee, or hip motion. Sesamoidectomy: tibial excision results in 11% loss of flexor power, fibular 19% loss, and 32% when both are excised.
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injections must be given judiciously and perhaps only for ‘‘big game’’ situations. Repeated injections may accelerate the degenerative process.25 Surgery in the management of hallux rigidus is feasible, and there are many options. The decision to proceed with surgery requires a lengthy discussion with not only the athlete but the trainer and possibly the athlete’s agent. It must be emphasized to all parties that this is an arthritic process, there is no ‘‘cure,’’ and there is the potential for a lengthy rehabilitation with incomplete resolution of the symptoms. The physician must determine the following: What is causing the problem? Is it the bony prominence over the MT head and secondary shoewear irritation? Is there limited ROM? Are there biomechanical implications such as poor pushoff? Does the athlete suffer from transfer pain issues and other compensatory problems? Lastly, and most concerning, is there the presence of global pain and diffuse arthritis, especially in sesamoid-MT articulation? The most commonly performed surgical procedure in the management of hallux rigidus is a cheilectomy. This procedure can be defined in general as an excision of an irregular osseous rim that interferes with motion of a joint. In this particular instance it is the removal of the dorsal osteophyte of the MT head. As noted previously, the athlete should be counseled that the underlying condition is degenerative joint disease and that full symptom relief is not realistic. A cheilectomy may prolong the athletic life of the individual but probably does not slow the rate of joint degeneration. As a general rule, the dorsal ridge does not recur, but progressive narrowing of the joint is expected to occur. Indications for a cheilectomy include a lateral radiograph showing that reasonable space exists in the plantar one half of the MTP joint. There should be an absence of pain or crepitus with midrange motion and no sesamoid-MT pain or disease. This procedure allows for complete relief of dorsal impingement. It increases dorsiflexion by decreasing bulk of joint and subsequently relieving dorsal impingement pain. It also eliminates the source of painful shoe pressure. The true advantage of the cheilectomy is that ‘‘no bridges are burned,’’ and even in unsuccessful cases a salvage procedure is still technically possible. The technique has been described and popularized by Mann and Clanton.26 Their preference is a dorsal longitudinal incision centered over the hallux MTP joint. The joint capsule is incised on either side of the extensor hallucis longus (EHL) tendon and a complete synovectomy is performed. The joint is plantarflexed to permit inspection of the sesamoid articulation. Hamilton27 recommends mobilizing the sesamoids by blunt dissection, for they often are anchored by adhesions and limit dorsiflexion even after removal of impinging osteophytes. The amount of bone to be removed from
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the MT head is dictated by the size of the dorsal exostosis and the degree of articular cartilage destruction. If degeneration of articular cartilage is not significant and the main problem is the dorsal exostosis, then 20% to 30% of the dorsal aspect of the MT head is removed along with the exostosis (see Fig. 18-2). It is reasonable to be relatively aggressive with this resection, removing up to one third of the dorsal head to achieve improved motion. The cheilectomy should include removal of all osteophytes and a rounding of the MT head. The cheilectomy should achieve a minimum of 70 to 80 degrees of dorsiflexion because approximately one half of this will be lost in the postoperative period as a result of scar formation. It is Mann’s recommendation that if insufficient dorsiflexion is achieved after cheilectomy, then a proximal phalangeal osteotomy (Moberg) should be performed as described later. We have modified the cheilectomy technique through a medial approach. This allows for plantar debridement and release of plantar capsule and adhesions, thus improving dorsiflexion. In addition, the incision avoids the EHL tendon and the potential for tenodesis secondary to scar formation while still providing access to lateral osteophytes. We recommend a two-cut technique to avoid excessive resection of the MT head (Fig. 18-3). The first cut of the saw includes the dorsal exostosis and is made flush with the dorsal diaphysis. The
Figure 18-3 The first cut of the saw includes the dorsal exostosis and is made flush with the dorsal diaphysis. The subsequent cut removes the amount of articular surface necessary to achieve the desired dorsiflexion while eliminating the risk of excessive head removal that may jeopardize later arthrodesis. (From Adelaar RS, editor: Disorders of the great toe, Rosemont, IL, 1997, American Academy of Orthopaedic Surgeons.)
Specific entities of the great toe
of radiographic arthritis, but this did not correlate with symptoms. Three patients eventually required an arthrodesis. Phalangeal osteotomy has been advocated as a useful surgical adjuvant to a cheilectomy. This technique was first proposed by Bonney and Macnab in 1952.13 Kessel and Bonney19 described its use in 10 adolescents in 1958. Moberg is the name most commonly associated with the procedure, after his case series reported in 1979.33 The procedure involves a dorsal closing wedge osteotomy of the proximal third of the proximal phalanx. It relies on the principle that the arc of motion of the hallux MTP joint is translated to plantar aspect of head, thereby increasing functional motion. Basically it creates pseudodorsiflexion, which in turn places less stress on the hallux with push-off. Adequate plantarflexion of the joint is a prerequisite. Thomas and Smith34 also found that the procedure appeared to provide dorsal joint space decompression, as well, further relieving stress from the arthritic joint (Fig. 18-4). The indications for performing a Moberg osteotomy on the proximal phalanx includes grade I or II hallux rigidus, adolescent hallux rigidus, and the running athlete, perhaps regardless of grade. Most authors now recommend combining the procedure with a dorsal cheilectomy.32,34,35 The technique can be performed through a medial or dorsal incision, extending distally from the incision used for the cheilectomy of the hallux MTP joint. It is important to protect the dorsomedial and plantar medial cutaneous nerves to limit paresthesia and the potential for neuritis or neuroma. Longitudinal reflection of soft tissues at the proximal third of the phalanx is performed, maintaining capsular insertion. The FHL and
Figure 18-4 Space created by dorsiflexion osteotomy of the proximal phalanx. (From Thomas PJ, Smith RWL: Foot Ankle Int 20:4, 1999.)
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subsequent cut removes the amount of articular surface necessary to achieve the desired dorsiflexion while eliminating the risk of excessive head removal that may jeopardize later arthrodesis. Hamilton27 describes ‘‘radical cheilectomy’’ similar to the cheilectomy of Mann but also removing the dorsal portion of the base of the proximal phalanx, matching the resection performed on the MT head. This modification serves as an option for dancers with endstage disease and is similar to the Valenti28,29 procedure described later in this chapter. A cheilectomy affords a fairly rapid postoperative course and return to activity. The patient is allowed to weight bear immediately, typically in a rigid-soled healing sandal. ROM can be initiated by a therapist or trainer as soon as pain allows but not so aggressively as to create wound dehiscence. Sutures generally are removed at 10 days, at which time active and passive ROM should be conducted at least three to four times per day. Close monitoring is required to ensure that the motion within the hallux MTP joint is at a functional level, a minimum of 40 degrees of dorsiflexion. No significant athletic activities generally are allowed for 6 to 8 weeks following a cheilectomy, giving the joint time to mature following surgery. Athletes can continue to train by bicycling, swimming, running in water, and engaging in other activities that avoid significant impact against the MTP joint. The patient should appreciate that swelling may continue for many months but that maximal motion usually is achieved by 3 months. A number of authors have provided their results of cheilectomy. Mann and Clanton26 found that 22 of 31 patients had complete relief, 6 of 31 achieved considerable relief, and ROM increased an average of 20 degrees in 23 of 31 feet. Hattrup and Johnson30 reported that 53.4% were satisfactory and 27.6% unsatisfactory. Their failure rate increased from 15% with grade I radiographic changes to 37.5% with grade III changes. They concluded that cheilectomy is the procedure of choice in patients with hallux rigidus and grade I changes. Graves’31 experience showed little improvement in motion and stated that satisfaction with cheilectomy was more likely if the patient and the physician had reasonable expectations regarding outcome. He recommended careful patient selection. Myerson agreed that the procedure improves pain, not motion. Easley et al.32 reported on 57 patients (75 feet) with greater than 3-year follow-up (average 63 months). Their cheilectomy was performed via a medial approach by a single surgeon. American Orthopaedic Foot and Ankle Society (AOFAS) scores were 45 preoperative, 85 postoperative, and 90% satisfied. The average dorsiflexion improved from 19 degrees preoperative to 39 degrees postoperative. The majority of patients had worsening
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EHL tendons are protected as a dorsal closing wedge osteotomy is performed with a microsagittal saw approximately 3 to 5 mm distal to the MTP joint. In the adolescent, it is necessary to avoid the physis. Intraoperative fluoroscopy can be useful in confirming proper position of the osteotomy. The plantar cortex is maintained to allow for a ‘‘greenstick’’ effect with manual closure of the osteotomy. Generally 2 to 6 mm of dorsal cortex should be removed, with the actual amount determined by the degree of joint stiffness and amount of plantarflexion of the hallux available. The goal is to obtain 20 to 30 degrees of dorsiflexion relative to the first MT axis. The osteotomy should be stabilized with a suture, K-wire, screw, or staple. If combined with a cheilectomy, stable, internal fixation is mandatory to allow for the initiation of early motion (Fig. 18-5, A and B). The postoperative care is similar to that described for an isolated cheilectomy. Immediate full weight bearing is permitted in a hard-soled sandal, with passive dorsiflexion exercises begun at 1 to 2 weeks. In ranging the joint it is important to hold the entire toe as single unit. Plantarflexion exercises are delayed until 3 to 4 weeks postoperative. When a pin is present, removal is performed at 4 to 6 weeks, followed by transition to accommodative shoes. Published results of the proximal phalanx osteotomy include Moberg’s review of older individuals at short follow-up. Eight patients were noted to have satisfactory results. Citron and Neil36 evaluated 10 feet in 8 patients with 22-year follow-up (minimum 10 years) and identified 5 symptom free, others with progression of degenerative joint disease (DJD), and one requiring
Figure 18-5 (A) Dorsal cheilectomy and dorsiflexion osteotomy of the proximal phalanx. (B) The amount of correction after fixation. (From Thomas PJ, Smith RWL: Foot Ankle Int 20:4, 1999.)
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arthrodesis. The average postoperative motion was 43 degrees, 22 degrees being dorsiflexion, with late loss of plantarflexion noted. Asymptomatic compensatory hallux IP flexion contracture often was present. They felt that this osteotomy represented an especially good option in the adolescent. Thomas and Smith34 performed the osteotomy with a dorsal cheilectomy in 27 feet, 20 patients. At a follow-up average of 5.2 years, there was a 100% union rate, the average dorsiflexion increased 7 degrees, and 96% of patients were satisfied or satisfied with reservation. Complications of the Moberg osteotomy include nonunion or malunion, a problem avoided by using internal fixation and ‘‘greensticking’’ the plantar cortex to avoid gross instability. Injury to the FHL and EHL tendons can occur, as can neuritis or neuroma, although the latter typically is transient. The possibility of progressive arthritis of the hallux MTP joint is an outcome that must be discussed with the patient preoperatively. Decreased push-off power can occur and may be of concern in the athlete or dancer. Salvage for advanced degeneration or for a failed cheilectomy or osteotomy includes either arthrodesis or arthroplasty. Arthrodesis is best avoided in the ‘‘sprinting’’ athlete or dancer. If an arthrodesis must be performed, the toe tip should be at least 10 mm off the ground. Failure to meet this requirement will place significant stress on the distal hallux and IP joint. Slight shortening of the hallux also is of benefit, further lessening the potential of the athlete’s having to ‘‘vault’’ over the hallux during running activity. Resection arthroplasty, like that of a Keller, is reserved for the older individual. Capsular interposition is a modification of this procedure devised by Hamilton.37,38 In this procedure the proximal 5 to 10 mm of proximal phalanx is resected, followed by transection of the extensor hallucis brevis (EHB) tendon and dorsal capsule. This dorsal soft-tissue complex then is advanced to the plantar complex. Some authors release the flexor hallucis brevis (FHB) tendon from the base of the phalanx and suture this to the dorsal capsule. Temporary pin fixation is not necessary (Fig. 18-6, A and B). Our own experience with the procedure has noted good relief of pain from dorsal impingement and joint degeneration but a concerning loss of push-off strength. Similarly, the Valenti28,29 procedure is a salvage technique in which an angled resection on both sides of the joint is performed, preserving the plantar complex and overall length. The result is a ‘‘hinge’’ effect at the level of the joint (Fig. 18-7). Most recently, an ‘‘anchovy’’ interposition of the hallux MTP joint has been performed in those individuals failing a cheilectomy but needing to maintain hallux MTP motion. Conical resection on both sides of the joint is followed by insertion of a semitendinosus allograft rolled into an ‘‘anchovy.’’ We have used this
Specific entities of the great toe
Figure 18-6 (A) Interposition arthroplasty as described by Hamilton. (B) Pin fixation is not necessary. (From Hamilton WG, Hubbard CE: Foot Ankle Clin 5:663, 2000.)
technique on three patients, one a professional football player, with good short-term results. Coughlin and Shurnas39 recently reported on their experience with this technique in seven patients with excellent results. This case series demonstrates that this is a good surgical option in patients who otherwise would be treated with MTP arthrodesis. Implant arthroplasty has been advocated by some authors; the options described include a silastic double-stem hinge, titanium hemiarthroplasty, or total toe replacement. These implants are unlikely to hold up in the running athlete, and the surgeon is faced with a difficult revision should failure occur. It remains our recommendation to avoid this procedure in the athlete, career or recreational. Arthroscopic intervention for disorders of the hallux MTP joint has received some attention over recent years. It has been shown to be more of a diagnostic modality than a therapeutic one but may be a reasonable option for the removal of small dorsal osteophytes or loose bodies. It also may be used for debridement of an osteochondral defect on the MT head but is not indicated in advanced hallux rigidus. Van Dijk et al.40 performed a prospective study with 24 athletes and found that it was not favorable for hallux rigidus because of ‘‘scar fibrosis.’’ X-rays: AP and lateral weight-bearing foot. Multiple etiologies, occult trauma or overuse most common. Large dorsal soft-tissue and/or bony mass.
Sesamoid disorders There are many etiologies for sesamoid pain. The general term ‘‘sesamoiditis’’ is best considered a term for a symptom rather than a diagnosis. This term implies pain in the sesamoid region with negative radiographs and an equivocal magnetic resonance imaging (MRI). It represents a diagnosis of exclusion in which soft-tissue ailments such as bursitis or flexor tendinitis are considered and often is associated with a history of overuse or trauma.41,42 Fracture of the sesamoid, acute or stress, typically involves the tibial hallux sesamoid because of its larger size and greater propensity for weight-bearing forces. The classic radiographic appearance is a transverse fracture line, usually at the midwaist. It also can occur as the result of an MTP dislocation (Jahss Type II).5 Degenerative etiologies for pain in the sesamoid include chondromalacia, osteophytes, impingement, or plantar prominence. These particular problems may occur in an isolated fashion or in association with gout. Osteochondrosis has an unknown etiology but often is found as a late sequela to a crush injury or stress fracture. Avascular necrosis (AVN) also has been described, most often affecting the fibular hallux sesamoid. Painful fragmentation and cyst formation with flattening of the sesamoid can be seen in either AVN or osteochondrosis, with radiographic changes following symptoms by 6 to 12 months. Plantar prominence of a hallux sesamoid can occur with bursitis or with an intractable plantar keratosis. 417
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Figure 18-7 Resection of the dorsal metatarsal head as well as dorsal proximal phalanx. (From Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby-Year Book.)
Dysesthesia in the dorsomedial cutaneous nerve can result from tight shoewear impinging on the bony prominence. Nonoperative treatment: NSAIDs, large toe box shoes/balloon expansion, turf-toe plate, rocker bottom shoes. Surgical treatment: Cheilectomy if plantar joint space intact, Moberg phalanx osteotomy for running athletes, resection arthroplasty in elderly patients, and interpositional arthroplasty for complete joint destruction.
CHAPTER 18
Great-toe disorders
Osteomyelitis of the sesamoid can be the result of direct extension from a neuropathic ulcer or puncture wound but is unusual in the athlete.43 Tumors of the sesamoid seldom occur but are considered more likely in the fibular side than the tibial.5 Diagnostic evaluation begins with a complete history of the problem. The typical patient will relate pain localized to the plantar hallux MTP joint with weight bearing, worsened with sports and stair climbing, and often with no precipitating event. The clinical examination identifies the specific location of pain and tenderness. Plantarmedial signs relate to disorders of the tibial sesamoid, whereas direct plantar tenderness is indicative of fibular sesamoid pathology. In addition, the presence of swelling, warmth, and erythema should be documented. Joint motion and stability are assessed, noting restriction of motion secondary to pain or associated hallux rigidus. Vertical instability may follow a turf-toe or hyperextension injury. Sesamoid compression that produces pain and grind is consistent with metatarsosesamoid arthritis. It is mandatory that the radiographic evaluation of sesamoid disorders include standing AP and lateral foot views and axial or tangential sesamoid views. These views are adequate in assessing for focal arthrosis, plantar osteophytes, or bony prominences. The tangential sesamoid view is helpful for identifying fractures of tibial sesamoid. It is helpful to always place a marker (B-B) on the skin overlying the site of tenderness. This simple maneuver helps to differentiate which sesamoid is symptomatic, or may not correlate with a sesamoid location if there is a flexor tendon problem. A question that often arises is in the differentiation of a fracture versus bipartite sesamoid. A fracture has sharp, irregular borders on both sides of the separation, whereas a bipartite has smooth, cortical edges and a relatively total size larger than that of a single sesamoid. Contralateral AP radiographs may be useful in this differentiation as there is a reported 90% incidence of bilateral occurrence.44 Further diagnostic studies useful in the evaluation of sesamoid disorders include MRI, which helps to localize pathology while differentiating between bone and softtissue abnormality. It further assesses sesamoid viability, joint degeneration, and tendon continuity. A readily available tool that is sensitive yet inexpensive is the bone scan. Although there is a reported high rate of false positives, a three-phase study with pinhole images helps to identify the problematic sesamoid. Computed tomography (CT) imaging can be performed to delineate the degree of metatarsosesamoid arthrosis or to assess fracture healing. The nonoperative treatment of sesamoid disorders is general and begins with the RICE principle of rest, ice, compression, and elevation. Athletic activity and
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the training regimen are modified. Analgesics and antiinflammatory medication are useful adjuvants. A boot or cast is applied for the first week in more severe injuries. The cast can include a toe spica extension with the joint in mild plantarflexion, removing stress from the plantarly positioned sesamoids. Weight bearing is permitted as tolerated. Taping of the hallux, as one would for a turf-toe, provides compression and limits movement. This is found to be most helpful in milder injuries. As the patient or player returns to athletic or recreational activity, orthoses and shoewear modifications are mandatory. Off-the-shelf products, such as a Springlite turf-toe plate (Otto Bock, Minneapolis, MN) made of carbon fiber, in full or forefoot lengths, are useful in limiting dorsiflexion stresses. Custom-made devices can be fabricated with a Morton’s extension to limit hallux MTP motion. A dancer’s pad, MT pad, or arch support placed just proximal to the symptomatic sesamoid will assist in unloading weight-bearing pressures. Furthermore, the shoe itself can be stiffened with a plate incorporated into the sole. The patient should maintain low heel heights to minimize weight-bearing pressures. Turf shoes are modified by removing the cleat under the area of pain. Cortisone and/or anesthetic injections are not advised in any injury. An anesthetic injection alone may be used for localized pain in single-nerve distribution, but we would not completely anesthetize the toe or joint to enable an athlete to return to play. Surgeries for disorders of the sesamoid are directed to the pathology identified. The first problem to consider is the intractable plantar keratosis (IPK), attributable to the tibial hallux sesamoid. There are instances in which the plantar aspect of the sesamoid will develop a bony prominence, or osteophyte, and an overlying distinct callus will arise. This may occur in the presence of fat atrophy, and there may be an associated bursal component. Failure to improve with an orthosis to relieve pressure from this area may necessitate surgical decompression. The recommendation is for a plantar shaving of the tibial sesamoid via a plantar-medial approach. The periosteum overlying the sesamoid is reflected and the plantar 50% of the sesamoid is resected with a microsagittal saw. The FHL tendon is protected and the joint itself is not entered. The overlying soft tissues then are repaired so that the FHB tendon has been maintained in continuity, thus avoiding the risk of instability. The patient is allowed to weight bear to tolerance in the immediate postoperative period in a protective hard-sole boot or postoperative shoe. Return to regular shoewear and activity is expected over the following 6 to 8 weeks as pain and swelling subside. Fractures of the sesamoid can occur as acute events or can be stress induced. Acute fractures occur as a result of direct trauma, such as a forceful impact to the
Specific entities of the great toe
Osteochondrosis of the sesamoid may occur with progressive fragmentation. This process may occur insidiously or as the sequela of a stress fracture nonunion42 or osteonecrosis.47,48 Subchondral cysts may characterize early stages. Patients will present with chronic discomfort worsened by weight-bearing activity. Attempts can be made at nonoperative management using a period of rest and immobilization followed by orthotic management. However, a sesamoidectomy often is necessary in order for a return to recreational activities.42,47,48 Sesamoidectomy is the only option for the surgical management of a number of sesamoid disorders, including osteochondrosis, osteomyelitis, advanced degeneration, or the rare tumor. A tibial hallux sesamoidectomy is achieved through a medial or plantarmedial approach, avoiding the plantarmedial digital nerve. The sesamoid can be excised from within the joint or extra-articularly. As discussed for nonunions of the sesamoid, it often is helpful to assess the articular surfaces before excision; this can be accomplished by entering the joint along the superior border of the abductor hallucis tendon. By performing the excision through an extra-articular approach, the overlying FHB tendon can be repaired. A longitudinal incision and reflection of overlying soft tissues (subperiosteal) allows for full exposure of the sesamoid; the bone then can be shelled out circumferentially with a no. 69 Beaver blade. The defect then is repaired side to side with absorbable suture (i.e., 4-0 Vicryl). The surgeon must be aware of the proximity to the FHL tendon, protecting this structure during the dissection. Although rarely performed because of the risk of residual pain, partial sesamoid excisions can be considered if there is a small proximal or distal fragment. The abductor hallucis tendon can be transferred into large defects created by excision of bipartite or fractured sesamoids. This transfer is performed by dissecting the distal tendon off the capsule at the base of the proximal phalanx. A fasciotomy is performed proximally to allow for rerouting of the tendon to the plantar aspect of the joint, where it is sutured into the defect with absorbable material. A concomitant bunionectomy should be considered if significant hallux valgus is present at the time of tibial hallux sesamoidectomy, because a progressive deformity otherwise may develop.49 When performing a fibular hallux sesamoidectomy, the decision must be made whether to approach from dorsal or plantar surface. A dorsal approach is difficult unless there is a large intermetatarsal 1-2 angle with lateral subluxation of the sesamoid complex (i.e., bunion/ hallux valgus). A longitudinal first webspace incision is used in performing a dorsal-based excision. Following superficial dissection, a laminar spreader placed between the MT heads is helpful. This approach requires the release of the adductor hallucis tendon and other lateral soft-tissue structures. The sesamoid is shelled out of the 419
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forefoot region. Because of its larger size and greater propensity for weight bearing, the tibial sesamoid is more likely to be involved.44 These fractures generally heal with limitation of weight-bearing forces by use of such appliances as a cast (with a toe spica extension), boot or postoperative shoe. There have been anecdotal reports of internally fixing these midwaist fractures with small, dual-pitched screws,45 but this is technically demanding and may not provide significant benefit over traditional treatment methods. Stress fractures of the tibial hallux sesamoid have been noted to occur in athletes involved in repetitiveimpact exercises, such as long-distance running or aerobics. The diagnosis usually is made months after the onset of discomfort. By then the fracture likely has progressed to an established nonunion. Failure to improve the situation with orthoses designed to relieve pressure and limit excessive dorsiflexion through the joint may necessitate surgical intervention. Bone grafting of these tibial sesamoid nonunions has been performed successfully in an effort to avoid excision and the subsequent risk of losing push-off strength in the hallux.10 Indications for this bone graft procedure include a midwaist fracture location with minimal diastasis, preferably 1 to 2 mm. The articular surface of the sesamoid should be free of disease, and the two parts should not demonstrate gross motion between them. A plantarmedial incision is centered at the hallux MTP joint. The capsule is incised along the superior border of the abductor hallucis tendon, and the joint is examined. Should there be cartilage damage on the sesamoid or gross motion between the two halves, then sesamoidectomy is completed. Otherwise, an extra-articular approach to the sesamoid is performed with reflection of overlying periosteum but preserving the FHB tendon. The fibrous material of the nonunion is curettaged back to viable bone surfaces. Care is taken to avoid disruption of the overlying articular surface. Through the capsulotomy, a window is made in the medial cortex of the MT head, and a small amount of cancellous bone is harvested. This graft is packed into the nonunion defect created, and the overlying soft tissues are approximated with absorbable suture. There is no need for internal fixation because the two fragments should remain stable. The capsulotomy is repaired and the wound closed. Postoperatively, the patient is placed in a posterior splint with the distal portion enveloping the hallux itself. At 2 weeks the sutures are removed and a short-leg cast with a toe spica extension is applied. The patient is allowed to weight bear in such a device after 6 weeks, advancing to a shoe protected with a turf-toe plate at 8 weeks. A CT scan at 12 weeks should confirm union, and if accomplished, running is initiated with continued orthotic protection. We previously have reported on this technique in a series of 21 patients, 19 of which were successful.46
CHAPTER 18
Great-toe disorders
FHB tendon, taking care to avoid the neurovascular structures plantarly. The plantar-based approach to fibular sesamoidectomy is preferable in that the soft-tissue structures balancing the hallux MTP joint are not disrupted. In this approach, a curvilinear incision is placed over the palpable fibular sesamoid, but just off of the weight-bearing pad of hallux MTP joint itself. It is necessary to identify and protect the plantarlateral digital nerve (Fig. 18-8, A and B). Following the sesamoidectomy, the reflected periosteum and FHB tendon (lateral head) are repaired. Skin closure must carefully approximate the dermal edges to minimize hypertrophic scar formation. Postoperatively soft dressings are applied in such a manner as to maintain plantarflexion and either varus (tibial sesamoidectomy) or valgus (fibular sesamoidectomy). Weight bearing is allowed in a hard-soled sandal or short walker boot for a tibial sesamoidectomy, whereas nonweight-bearing or heel touch protection is recommended for a fibular sesamoidectomy performed through a plantar incision. With the latter, the patient is allowed to begin full weight bearing with the sutures in place at 2 weeks postoperatively. The sutures then are removed 1 week thereafter. Removable bunion splints help to maintain the desired hallux alignment between the second and sixth week. A gradual return to hard-soled shoes follows, using a turf-toe plate in athletic or training shoes. The results of sesamoidectomy have been provided by a number of authors. Inge and Ferguson50 reviewed 41 feet, 25 in which both sesamoids were excised. Complete pain relief was noted in 42%, whereas partial relief
was noted in 82% with single sesamoid excision and in 64% of those in whom both sesamoids were excised. Leventen51 found complete satisfaction in 18 of 23 sesamoidectomies. Mann et al.52 identified 19 of his 21 sesamoidectomies ‘‘improved,’’ but only 50% had complete pain relief and 66% had full motion. In this group, 1 of 13 tibial sesamoidectomies developed hallux valgus, 1 of 8 fibular sesamoidectomies developed hallux varus, and 12 patients developed ‘‘weakness.’’ We assessed 12 patients who underwent a fibular sesamoidectomy via a plantar approach and identified 9 who were very satisfied and 2 who were satisfied. In addition, all would do it again, and 11 of 12 returned to preinjury activity level, citing no complications (for example, scar, neuroma). Sesamoidectomy is a good procedure that provides reliable results. The surgeon and patient must be aware that there is the potential for biomechanical implications such as the loss of push-off strength. This is especially important in the running athlete or elite dancer and must be discussed before intervening surgically. X-rays: AP and lateral weight-bearing foot, axial/ tangential sesamoid views, skin marker over tenderness, contralateral views. MRI: differentiates soft-tissue from bone abnormality. Bone scan: high false-positive rate, use three-phase with pinhole images to isolate problem area. Fractures: tibial sesamoid more common. AVN: fibular sesamoid more common. Nonoperative treatment: NSAIDs, rest, boot/cast in more severe injuries, turf-toe plate, arch support, and/or MT pad. Surgical treatment: varies depending on diagnosis.
Figure 18-8 (A) A curvilinear incision is made just lateral to the fibular sesamoid, just off the weight-bearing pad of the hallux metatarsophalangeal joint. (B) Care must be taken to identify and protect the plantarlateral digital nerve. (Drawn by Robert B. Anderson, MD.)
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Specific entities of the great toe
Figure 18-9 An axial load applied to a foot fixed in equinus. As an impact or force is placed on the heel, the forefoot progresses into dorsiflexion, creating hyperextension at the hallux metatarsophalangeal joint. (From Adelaar RS, editor: Disorders of the great toe, Rosemont, IL, 1997, American Academy of Orthopaedic Surgeons.)
Figure 18-10 Valgus component to the hyperextension causing injury to the plantarmedial structures, resulting in a traumatic bunion. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:693, 2000.)
consistent with a medial collateral ligament tear, which was repaired. Like valgus injuries, varus injuries also are rare. Mullis and Miller59 reported on a basketball player with an injury to the hallux MTP joint 3 months before presentation. He had difficulty with running and was unable to return to sports participation. On physical examination, he was noted to have significant varus instability 421
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Turf-toe Since the term ‘‘turf-toe’’ was first used in the literature by Bowers and Martin54 in 1976, soft-tissue hyperextension injuries to the first MTP joint have received increasing attention from physicians, trainers, and athletes. Although these injuries have been grouped under the general heading of turf-toe, they actually represent a spectrum of injuries from the mild to the severe. In addition to the straight hyperextension injury of the first MTP joint, we now recognize there are variations that account for injury to specific anatomic structures in the capsular-ligamentous-sesamoid complex. The true incidence of turf-toe injuries is difficult to quantify. At major universities, these injuries rank number three behind knee and ankle injuries.1,55 When Coker et al.56 looked at the Arkansas football players, they found ankle injuries to be four times more common than hallux MTP joint injuries; however, the latter were more severe, accounting for a disproportionate number of missed practices and games. Over a 3-year period, 18 of their players had a hallux MTP joint injury, equating to six turf-toe injuries per year. At Rice University, over a 14-year period the average was 4.5 turf-toe injuries per year and included all sports.57 The mechanism of injury can be direct or indirect and requires a basic knowledge of that which is required of the great toe during athletics. When an athlete rises on the ball of the foot for such activities as initiating a jump, blocking, or running, the hallux MTP joint extends upward of 100 degrees. As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the MT head articular surface bears most of the load. As this plantar complex attenuates or ruptures, unrestricted dorsiflexion can lead to impaction of the proximal phalanx on the dorsal articular surface of the MT head. This leads to a spectrum of joint injuries from partial tearing of the plantar structures to frank dislocation. The typical scenario leading to this injury in the athlete involves an axial load on a foot fixed in equinus. As an impact or force is placed on the heel, the forefoot progresses into dorsiflexion, creating hyperextension at the hallux MTP joint (Fig. 18-9). However, not all turf-toe injuries are purely hyperextension. Numerous variations have been identified. For instance, a valgus component to the hyperextension of the hallux MTP joint results in injury to the plantarmedial ligamentous structures, occasionally to the tibial sesamoid, and the eventual development of a traumatic bunion with contracture of the lateral structures (Fig. 18-10). Douglas et al.58 reported the case of a soccer player who sustained a hallux MTP joint injury when he was slide-tackled during practice. He continued to complain of joint instability and he failed conservative measures. MRI and operative findings were
CHAPTER 18
Great-toe disorders
of the hallux MTP joint. Surgical findings included a torn conjoined tendon, lateral capsule, and lateral collateral ligament. The plantar structures were noted to be intact. All structures were repaired primarily, and the conjoined tendon was fixed to the base of the proximal phalanx through drill holes. Over the years many theories have been investigated as causative factors in hallux MTP joint injuries. By far, the two most common etiologic factors mentioned in the literature are the playing surface and flexibility of footwear. In a study by Rodeo et al.,60 80 active professional football players were surveyed, and of those with a turf-toe injury, 83% sustained the initial injury on artificial turf. Bowers and Martin54 addressed this relationship by studying the impact of AstroTurf on the West Virginia University’s football team. They coined the term ‘‘turf-toe’’ to describe injuries of the hallux MTP joint capsular-ligamentous complex sustained on artificial turf that previously had not been encountered on grass playing surfaces. The AstroTurf was alleged as a causative factor because of the hardness encountered with aging of the surface. However, Clanton and Ford1 and others investigated the relationship of turf-toe injuries to aging artificial turf and found no significant correlation. In the three seasons preceding the replacement of the artificial turf in Rice Stadium, there were 13 turf-toe injuries, versus 12 injuries in the three seasons following replacement with a more modern synthetic playing surface. Nigg and Segesser61 demonstrated an increased incidence of hallux MTP injuries on artificial turf and attributed this to the enhanced friction inherent in the surface. This may account for the forefoot’s becoming fixed to the artificial surface with applied external forces, causing hyperextension and resulting hallux MTP injury. Bowers and Martin,54 as well as Clanton and Ford,1 have postulated that the shoe-surface interface most likely is responsible for these injuries. The majority of injuries are encountered on artificial turf in athletes wearing flexible, soccer-style shoes. The abandonment of the traditional grass shoe for the lighter, more flexible, soccer-style shoe seems to have been a major contributing factor in the evolution of the turf-toe problem. The trainers and physicians at Rice University could not recall a single instance of a severe MTP joint sprain occurring in a football player wearing the traditional grass shoe during the 25 years before 1986. This is most likely the result of the steel plate incorporated into the sole of the shoe for the attachment of cleats, which has the secondary benefit of limiting forefoot motion.1,62,63 In the study by Rodeo et al.,60 shoe type was not associated with turf-toe injury in professional football players. However, the number of players wearing traditional grass cleats in this study was small (15 out of 80) and perhaps influenced the outcome.
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Some authors have suggested that hallux MTP joint ROM may play a role in turf-toe injuries. Many studies have looked specifically at this factor and concluded that there is no relationship between hallux MTP joint ROM and subsequent turf-toe injury.1,55,60 However, there may exist a relationship between increased ankle ROM and turf-toe injuries. In the study by Rodeo et al.,60 players with a turf-toe injury had mean ankle dorsiflexion of 13.3 degrees, versus 7.9 degrees for uninjured players, a statistically significant difference. It can be postulated that an increased ankle ROM places the hallux MTP joint at risk for hyperextension injuries. Still other causative factors contributing to turf-toe have been suggested. These include player position, weight, age, years of participation, pes planus, hallux interphalangeal degenerative joint disease, and a flattened first MT head.1,55,60 The data for these variables are largely inconclusive, and it is unlikely that any of these factors play a significant role in the etiology of turf-toe. Acute injuries to the hallux MTP joint have been classified into one of three general categories (Table 18-1).64 Hyperextension injuries usually can be differentiated from hyperflexion injuries by history and physical examination. The clinician should recognize that turftoe constitutes a broad spectrum of injury with marked variability in the extent of soft-tissue involvement. To plan treatment and predict return to activity, a clinical classification system has been devised (Table 18-2). The mechanism for each of these injuries was discussed previously. At the extremes of hyperextension, frank dislocation of the hallux MTP joint can be seen. To determine the extent of the injured structures in the hallux, the clinician must start by taking a history from the athlete. An exact determination of the events leading to the injury should be sought in each case. Reviewing the videotape of the game sometimes can aid in determining the mechanism. As with most athletic injuries, an examination of the involved extremity shortly after the injury is ideal. The examination should begin with observation of the hallux MTP joint for ecchymosis and swelling, with particular attention paid to the location. Palpation of the dorsal capsule, medial and lateral collateral ligaments and the plantar structures, including the sesamoid complex, should help the physician to elucidate the injured structures. The hallux MTP joint then can be placed through an ROM and compared with the opposite side. Abnormalities such as a mechanical block, hypermobility resulting from a plantar plate tear, or gross instability can be appreciated. Varus and valgus stress testing then should be performed and also compared with the contralateral side. A dorsoplantar drawer test (Lachman) of the MTP joint will test the integrity of the plantar capsular-ligamentous complex. Plantarflexion and dorsiflexion of the hallux
Specific entities of the great toe
Table 18-1
Classification of turf-toe
Type of injury
Grade
Description
Hyperextension (turf-toe)
I
Stretching of plantar complex Localized tenderness, minimal swelling, no ecchymosis
II
Partial tear Diffuse tenderness, moderate swelling, ecchymosis, restricted movement with pain
III
Frank tear Severe tenderness to palpation, marked swelling and ecchymosis, limited movement with pain, (þ) vertical Lachman’s if pain allows Possible associated injuries Medial/lateral injury Sesamoid fracture/bipartite diastasis Articular cartilage/subchondral bone bruise These may represent spontaneously reduced dislocations
Hyperflexion (sand toe)
Hyperflexion injury to hallux MTP or interphalangeal joint May also involve injury to additional MTP joints (lesser toes)
Dislocation
I
Dislocation of the hallux with the sesamoids No disruption of the intersesamoid ligament Frequently irreducible
IIA
Associated disruption of intersesamoid ligament Usually reducible
IIB
Associated transverse fracture of one or both of the sesamoids Usually reducible
IIC
Complete disruption of intersesamoid ligament, fracture of one of the sesamoids Usually reducible
MTP, metatarsophalangeal.
include capsular avulsions, sesamoid fractures, impaction fractures, diastasis of bipartite sesamoids, and proximal migration of the sesamoids. Recommended radiographs include a weight-bearing AP and lateral and a sesamoid axial view. A comparison AP view of the opposite foot is helpful. Prieskorn et al.65 found that patients with a complete plantar plate rupture had proximal migration 423
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MTP joint against resistance should be performed to check the integrity of the flexor and extensor tendons of the hallux. In reality, this detailed examination can be difficult in the acutely injured athlete because of pain. Following clinical evaluation, radiographic analysis is mandatory for all hyperextension injuries. In addition to the soft-tissue disruption, bony abnormalities may
CHAPTER 18
Table 18-2
Great-toe disorders
Clinical classification system
Grade
Objective findings
Activity level
Treatment
1
Localized plantar or medial tenderness
Continued athletic participation
Symptomatic
Loss of playing time for 3-14 days
Walking boot and crutches as needed
Loss of playing time for at least 4-6 weeks
Long-term immobilization in boot or cast versus surgical repair
Minimal swelling No ecchymosis 2
More diffuse and intense tenderness Mild to moderate swelling Mild to moderate ecchymosis
3
Severe and diffuse tenderness Marked swelling Moderate to severe ecchymosis Range of motion painful and limited
Figure 18-11 (A) Normal dorsiflexion lateral. (B) Forced dorsiflexion lateral demonstrating proximal migration of the sesamoids.
of the sesamoids. The easiest way to evaluate the radiograph is to compare the distal aspect of the sesamoidto-joint distance on the affected side with the unaffected side. The difference between sides should be within 3.0 mm (tibial) and 2.7 mm (fibular) 99.7% (3 SD) of the time. Looking at absolute numbers, if there was greater than 10.4 mm from the distal tip of the tibial sesamoid to the joint and greater than 13.3 mm from the distal tip of the fibular sesamoid to the joint, then there was a 99.7% chance of plantar plate rupture.
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In addition to the standard views, special views and studies may be indicated, depending on a clinician’s suspicion. Rodeo et al.66 have suggested a forced dorsiflexion lateral view (Fig. 18-11, A and B), which may delineate joint subluxation, sesamoid migration, or separation of a bipartite sesamoid. Stress radiographs may help to define complete disruption of the medial or lateral capsular-ligamentous complex. In addition, two oblique radiographs may be obtained. Other studies previously used in the diagnosis of turf-toe injuries
Specific entities of the great toe
Figure 18-12 Magnetic resonance imaging notes injury to bones and soft tissue. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:698, 2000.)
Figure 18-13 Example of a short-let walking cast with toe spica extension in slight plantarflexion. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:699, 2000.)
great toe, as well as shoewear modifications. The taping is designed to restrict hyperextension of the hallux MTP joint. Another technique used to restrict forefoot motion is the placement of an insole that includes a spring carbon-fiber steel plate in the forefoot region of the shoe. A custom insole with a Morton’s extension may be better suited for the high-performance athlete but generally requires a longer shoe with a wider toe box. Factory made turf-toe shoes are available that restrict forefoot bend, but most running athletes resist this treatment because of a perceived loss of mobility. Grade 2 injuries usually result in loss of playing time ranging from 3 to 14 days, followed by the same modalities as mentioned previously. The grade 3 injuries may result in loss of playing time of at least 4 to 6 weeks, often requiring long-term immobilization and examinations weekly. In athletes who experience continued 425
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include bone scintigraphy to rule out stress fractures or arthrography to document capsular tears. However, in our experience, MRI best defines soft-tissue injury and the presence of osseous and articular damage (Fig. 18-12). The use of a 1.5-Tesla MRI scanner with paired 3-inch–round phased array surface coils can be used to obtain proton density and T2-weighted images. These images, obtained in the coronal, axial, and sagittal planes, provide anatomic detail of the nature and extent of soft-tissue injuries in acute turf-toe injuries.65 We are liberal in performing this test because it assists in grading, identifies subtle injuries, provides timely decision making, and helps to formulate a prognosis. The treatment of all grades of turf-toe injuries in early stages is similar.67 Principles, which apply to most acute sprains of the musculoskeletal system, apply to the hallux MTP joint as well. Once the injury is recognized, immediate application of ice with a compressive-type dressing may aid in reducing swelling. Taping of the great toe in this acute stage is not recommended because swelling could lead to compromise of circulation. Clanton and Ford1 suggest using the RICE formula of rest, ice, compression, and elevation. In addition, an NSAID may be prescribed. In some cases, a walker boot or a short-leg cast with a toe spica in slight plantarflexion may be helpful to alleviate symptoms during the first week (Fig. 18-13). Early joint motion may begin within 3 to 5 days after initial injury if symptoms permit. At this point, a severity grading must be applied so the athlete can be advised regarding prognosis and the time necessary for rehabilitation before a return to competition. Athletes with a grade 1 injury usually are able to return to their sport with little or no loss of playing time. These athletes may benefit from taping of the
CHAPTER 18
Great-toe disorders
swelling and edema, modalities such as whirlpool and ultrasound with cold compression may be used as adjuncts to traditional therapy.68 In general, return to play is dictated by symptoms, preferably with the athlete demonstrating 50 to 60 degrees of painless passive dorsiflexion. However, this return to athletics is individualized, dependent on the player’s position, the level of discomfort, and healing potential. There is a paucity of literature on the surgical management of hallux MTP joint injuries. This stems from the general notion that surgical management rarely is indicated in the treatment of this disorder. However, when an athlete fails to respond to conservative modalities, the treating physician should be suspicious for pathology that requires surgical intervention. Indications for surgery include a cartilage flap or loose body within the hallux MTP joint, acute sesamoid fracture, separation of a bipartite sesamoid, proximal migration of the sesamoids, evidence of gross instability resulting in persistent pain or synovitis, and hallux rigidus. The study by Rodeo et al.63 revealed that four athletes were noted to have diastasis of a bipartite tibial sesamoid and underwent excision of the distal fragment with repair of the capsule. One of these four athletes underwent acute excision, and the other three after failed conservative management. All of these players returned to their preinjury level of competition. Our own experience in the repair or reconstruction of hyperextension injuries has been derived from a number of individuals who had sustained a turf-toe and subsequently were unable to perform athletically at their preinjury level. These athletes often complained of pain with running activity, along with the inability to cut from side to side. Clinical findings included malalignment of the hallux, traumatic and progressive bunion deformity, clawing of the great toe, diminished flexor strength, generalized joint synovitis, and advanced degeneration of the joint. Radiographic analysis often showed proximal migration of one or both sesamoids and cases of progressive diastasis of bipartite sesamoids (Fig. 18-14). MRI performed confirmed pathology through the plantar complex of this joint, often associated with injuries to the joint surface or FHL tendon. All the cases of proximal sesamoid migration associated with hyperextension injury have been associated with distal rupture. It appears that the sesamoids rupture distally and migrate proximally because of the preservation of the flexor tendons, along with the abductor and adductor tendons, and their ability to retract. Our surgical experience with this injury has included 12 professional and collegiate athletes. Five surgeries were performed acutely for proximal migration or diastasis of a bipartite sesamoid, whereas seven were performed for chronic injuries, which included two traumatic bunions and one hallux varus deformity.
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426
In the acute repair and reconstruction of these plantar complex injuries, exposure can be obtained through a medial, medial and plantar, or J-incision technique. Care is taken to avoid injury to the plantar medial digital nerve as it courses over the region at the tibial sesamoid. Plantarflexion of the joint can assist with plantar exposure of the joint. Once the defect has been identified in the plantar complex distal to the sesamoids, advancement and primary repair can be achieved with nonabsorbable sutures. Typically, sutures are placed into remnants of soft tissue on the base of the proximal phalanx. If found inadequate, then suture anchors or drill holes in the plantar lip of the proximal phalanx may be used. In cases of a progressive diastasis of a bipartite sesamoid, it is our recommendation to preserve one pole of the sesamoid if possible. Typically, the distal pole is excised and soft tissues are repaired through drill holes in the remaining proximal pole. Should both poles of this sesamoid be damaged, or if fragmentation of the sesamoid is encountered, complete sesamoidectomy may be necessary. In this instance, a large soft-tissue defect will result, leading to an incompetent FHB and potential loss of plantar restraints. We recommend that an abductor hallucis tendon transfer be performed (Fig. 18-15). This transfer will act not only dynamically, helping to restore flexion power to the hallux, but also as a plantar restraint to dorsiflexion forces. There are situations in which late reconstruction of these injuries is necessary, for example, when the athlete continues to perform despite injury or when the injury has been inadequately treated and protected. In these situations the sesamoids may migrate well proximal, a problem often associated with hallux valgus, varus, or cock-up deformity. Reconstruction may include attempts at distal advancement of the sesamoids with soft-tissue reconstruction. This requires significant mobilization of the soft tissues proximal to the sesamoids, necessitating fasciotomies or fractional lengthenings of the flexor hallucis brevis and abductor hallucis muscles. Joint debridement and cheilectomy may be necessary in cases of associated synovitis and osteochondral injury. Reconstruction of traumatic bunion deformities necessitates not only reconstruction of the plantar medial soft tissues but also a release of the lateral soft-tissue contractures. The reconstruction of the claw toe deformity that occurs as a late sequela to hyperextension injuries is difficult. If the deformity is passively correctable at both the hallux MTP and IP joint levels, a flexor-to-extensor tendon transfer can be performed successfully. This transfer can be achieved either by splitting the flexor tendon and reapproximating dorsally into the extensor hood, as described by Girdlestone-Taylor, or by transferring directly through a drill hole into the base of
Specific entities of the great toe
Figure 18-14 (A) Anterior-posterior (AP) radiographs of a professional football player following a turf-toe injury. Note the diastasis of the tibial sesamoid. (B) AP radiograph repeated 1 year later demonstrating progression of diastasis, which was associated with early clawing of the toe. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:701, 2000.)
plantarflexion for a period of 7 to 10 days. At that time the athlete is initiated on protective, passive plantarflexion under the direct guidance of the athletic trainer or physical therapist. We avoid active and passive dorsiflexion and active plantarflexion maneuvers. When at rest, the toe is protected with a bunion splint using a plantar Velcro restraint and a removable posterior splint or cast boot. Nonweight-bearing ambulation is continued for a period of 4 weeks. ROM of the hallux is increased gradually at that time, along with protected ambulation in a cast boot. At 2 months postoperative, the patient is placed into an accommodative athletic shoe with the protection of an insole plate that limits dorsiflexion. Active ROM is instituted, and by 3 to 4 months postoperative, the patient is allowed to return to contact activity with the continued protection of 427
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the proximal phalanx (Fig. 18-16). Occasionally, a claw toe deformity will include a fixed contracture of the IP joint. This situation can be addressed through hallux IP arthrodesis and a flexor-to-extensor tendon transfer, as described previously. The postoperative management of athletes undergoing surgical reconstruction of hyperextension injuries is difficult because of the delicate balance between softtissue protection and early ROM. First, it is important to avoid placing the hallux in greater than 10 degrees of plantarflexion, either through surgical reconstruction techniques or with postoperative external immobilization modes. Excessive plantarflexion to this joint may become fixed and difficult to compensate for in the running athlete. Our protocol includes external immobilization in approximately 5 to 10 degrees of
CHAPTER 18
Great-toe disorders
Figure 18-15 Technique of abductor hallucis tendon transfer for reconstruction of hallux metatarsophalangeal joint. (A) Abductor hallucis tendon dissected from underlying capsule and immobilized proximally. (B) Plantar defect following sesamoid excision. (C) Transfer of abductor hallucis tendon completed with attachment to proximal phalanx. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:703, 2000.)
taping techniques and shoewear modifications. We have found that it takes approximately 6 to 12 months before the athlete can perform at the preinjury level of function. Late sequelae of turf-toe injuries may occur after conservative management or, less commonly, after surgical treatment has been rendered. Coker et al.55 reported on nine athletes who had sustained a hyperextension injury. The most commonly reported late sequelae were joint stiffness and pain with athletic activity. Clanton et al.,57 in their study of 20 athletes with turf-toe injury and 5 years of follow-up, noted a 50% incidence of persistent symptoms. Other late sequelae include cock-up deformity, hallux valgus, hallux rigidus, arthrofibrosis, loose bodies, and loss of push-off strength. Turf-toe constitutes a broad spectrum of injury with marked variability in the extent of soft-tissue involvement. Hyperextension injury to the plantar capsularligamentous-sesamoid complex.
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Can have varus or valgus component to injury pattern. Note ecchymosis, hypermobility, and varus/valgus on physical examination. X-rays: weight-bearing AP and lateral with contralateral views, sesamoid view, forced dorsiflexion lateral with contralateral view. Note sesamoid-to-joint distance. MRI: coronal, axial, and sagittal planes. May identify subtle injuries. Treatment: rest, ice, compression, elevation. Return to activity depends on severity of injury (see Table 18-2). Shoe modifications and/or turf-toe insert to prevent hallux hyperextension. Surgical indications include a cartilage flap or loose body within the hallux MTP joint, sesamoid fracture, separation of a bipartite sesamoid, proximal migration of the sesamoids, evidence of gross instability resulting in persistent pain or synovitis, and hallux rigidus.
Specific entities of the great toe
A
B
K-Wire for Fixation
C
D
Figure 18-16 (A-D) Technique for reconstruction of a claw-toe deformity that is passively correctable. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:706, 2000.)
transverse MT ligament or intersesamoid ligament may be required.71 If the joint is unstable after reduction, stabilization with a Kirschner wire is recommended; this can be removed after 3 to 4 weeks.71 Type II injuries are subclassified into types IIA and IIB (Fig. 18-17). In type IIA dislocations, the intersesamoid ligament is disrupted and radiographs reveal widening of the space between sesamoids and dislocation of the MT head into or through the sesamoid split. Type IIB injuries produce a transverse fracture through one (usually tibial) or both sesamoids. In the situation of a single sesamoid fracture, the proximal fragment remains aligned with the intact sesamoid, and the distal fragment often becomes a loose body in the joint, usually requiring surgical removal. In addition to these types described by Jahss,69 Copeland and Kanat72 defined a type IIC that is a combination of both IIA and IIB. The type IIC dislocation represents both a complete disruption of the intersesamoid ligament and a transverse fracture of either sesamoid (Table 18-3). 429
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Dislocations of the hallux MTP joint Frank dislocation of the hallux MTP joint most likely represents the extreme along the spectrum of hyperextension injuries. Dislocation in the dorsal direction is by far most common, yet plantar and lateral dislocations have been described. Jahss classified dislocation of the hallux MTP joint into two types.69 In the type I dislocation, the MT head buttonholes through the weak capsular tissue proximal to the sesamoids. The distal plantar plate, sesamoids, and intersesamoid ligament remain intact and attached to the phalanx distally. This intact complex comes to lie just dorsal to the MT head, with the flexor hallucis brevis tendon dorsally translated. A closed reduction in the emergency department always should be attempted under local anesthesia. However, this injury typically is irreducible and requires an open reduction of the MTP joint through a dorsal approach.70 If reduction cannot be obtained by reducing the sesamoids with an elevator, release of the adductor tendon and the deep
CHAPTER 18
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Great-toe disorders
Figure 18-17 Dislocations. (A and B) Anterior-posterior (AP) and lateral radiograph of a type IIA hallux metatarsophalangeal (MTP) dislocation. (C and D) AP and lateral radiograph of a type IIB hallux MTP dislocation. (From Watson TS, Anderson RB, Davis WH: Foot Ankle Clin 5:710, 2000.)
Conclusion
Dislocation type
Radiographic findings
I
No widening between sesamoids on AP view
IIA
Wide separation between sesamoids on AP view
IIB
Fracture of sesamoid (usually tibial)
IIC
Combination of type IIA and type IIB
AP, Anterior-posterior.
Differentiating between type I and type II dislocations is important because operative intervention typically is required for type I but not for type II dislocations. The general reduction maneuver is performed by placing gentle distraction with hyperextension on the MTP joint. If the joint is reducible, it typically is stable and is placed into a cast or hard-soled shoe for 3 to 4 weeks. A postreduction radiograph is required to confirm an anatomic reduction or to rule out the presence of any loose bodies.73 Occasionally, gross instability will follow a type II dislocation, particularly when a fracture of the sesamoid(s) has occurred. In this instance, the patient will experience pain with push-off and hallux rigidus type symptoms. A positive drawer sign is elicited, along with signs of generalized synovitis. Surgical correction in this setting includes plantar reconstruction to restore a restraint to dorsiflexion forces. Specifically, sesamoidectomy and abductor hallucis tendon transfer may be indicated. In the case of late clawing, an FHL transfer should be considered, as described previously. Most extreme hyperextension injury with two main types (see Table 18-1). Type I: MT head buttonholes through intact plantar complex and likely irreducible. Surgical intervention to release blocks to reduction. Usually stable but may require K-wire fixation. Type II: three subtypes with injury to the plantar complex. Usually reducible, may require delayed reconstruction.
Hyperflexion injuries of the hallux MTP joint As stated previously, turf-toe injuries involve primarily a hyperextension injury to the hallux MTP joint with a
possible varus or, more commonly, a valgus component. Rodeo et al.,60 in their report on turf-toe injuries in professional football players, concluded that 12% of the players had a hyperflexion injury to this joint. Hyperflexion injuries clearly do not fit into the classification system for turf-toe. In fact, the mechanism and pathology are much different, and these injuries should not be grouped together. Frey et al.74 reported on a series of professional beach volleyball players with a hyperplantarflexion injury to the hallux MTP joint, an injury referred to as ‘‘sand toe.’’ This injury can result in significant functional disability noted with push-off, forward drive, running, and jumping. Although described in volleyball players, it also can be seen in football players, soccer players, and dancers. The hyperflexion injury occurs when the weight of the body lands on a neutral or slightly plantarflexed hallux MTP joint. Frey et al.74 reported on 12 volleyball players, 11 of whom had sustained an injury to the hallux MTP joint. The treatment for this injury mainly is conservative: taping, rest, ice, and NSAIDs. Once the inflammation has resolved, the athlete should undergo a rehabilitation program that includes strengthening of the intrinsic and extrinsic muscles of the foot. However, the time to recovery was, on average, 6 months (range 1-12 months). The most common problem after injury was loss of dorsiflexion of 25% to 50% at the hallux MTP joint, as well as residual pain. No toe deformities were noted. The authors attribute the loss of motion to capsular damage, synovitis, and arthrofibrosis. Whether or not arthroscopic debridement would benefit these athletes remains a question for future study. Different mechanism and injury pattern than turf-toe. Often referred to as sand toe. Treatment normally nonoperative with rest, ice, and NSAIDs. Rehabilitation after inflammation subsides with intrinsic/extrinsic strengthening. Motion loss of from 25% to 50% is common.
CONCLUSION The great toe and its articulations are of paramount importance to the athlete. Great forces are transferred through this area with running, jumping, changing direction, and landing. Minor injuries can affect the ability even to walk or stand. A complete knowledge of the anatomy, forces involved, and treatment regimens are paramount when treating patients with these disorders.
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Table 18-3 Radiographic findings in hallux metatarsophalangeal joint dislocations
CHAPTER 18
Great-toe disorders
REFERENCES 1. Clanton TO, Ford JJ: Turf toe injury, Clin Sports Med 13:731, 1994. 2. Kelikian H: Hallux valgus: allied deformities of the forefoot and metatarsalgia, Philadelphia, 1965, WB Saunders. 3. Sarrafian SK editor, Anatomy of the foot and ankle: descriptive, topographic, functional, ed 2, Philadelphia, 1993, JB Lippincott. 4. Bowman MW: Athletic injuries to the great toe MP joint. In Adelaar RS, editor: Disorders of the great toe, Rosemont, IL, 1997, AAOS. 5. Jahss MH: The sesamoids of the hallux, Clin Orthop 57:88, 1981. 6. Stokes IA, et al: Forces under the hallux valgus foot before and after surgery, Clin Orthop 142:64, 1979. 7. Nigg BM: Biomechanical aspects of running. In Nigg BM, editor: Biomechanics of running shoes, Champaign, IL, 1986, Human Kinetics. 8. Joseph J: Range of movement of the great toe in men, J Bone Joint Surg Am 36:450, 1954. 9. Bojsen-Moller F, Lamoreux L: Significance of free-dorsiflexion of the toes in walking, Acta Orthop Scand 50:471, 1979. 10. Aper RL, Saltzman CL, Brown TD: The effect of hallux sesamoid excision on the flexor hallucis longus moment arm, Clin Orthop 325:209-217, 1996. 11. Davies-Colley M: Contraction of the metatarsophalangeal joint of the great toe, Br Med J 1:728, 1887. 12. Cotterill JM: Condition of stiff great toe in adolescents, Edinburgh Med J 33:459, 1887. 13. Bonney G, MacNab I: Hallux valgus and hallux rigidus: a critical survey of operative results, J Bone Joint Surg Br 34:366, 1952. 14. Horton GA, Park YW, Myerson MS: Role of metatarsus primus elevatus in the pathogenesis of hallux rigidus, Foot Ankle Int 20:777, 1999. 15. Jack EA: The aetiology of hallux rigidus, Br J Orthop Surg 27:492, 1940. 16. Lambrinudi C: Metatarsus primus elevatus, Proc R Soc Med 31:1273, 1938. 17. McMaster MJ: The pathogenesis of hallux rigidus, J Bone Joint Surg Br 60:82, 1978. 18. Goodfellow J: Aetiology of hallux rigidus, Proc R Soc Med 59:821, 1966. 19. Kessel L, Bonney G: Hallux rigidus in the adolescent, J Bone Joint Surg Br 40:668, 1958. 20. Jansen M: Hallux valgus, rigidus, and malleus, J Orthop Surg 3:87, 1921. 21. Nilsonne H: Hallux rigidus and its treatment, Acta Orthop Scand 1:295, 1930. 22. DuVries HL, editor: Surgery of the foot, St Louis, 1959, Mosby. 23. Hattrup SJ, Johnson KA: Hallux rigidus: a review, Adv Orthop Surg 9:259, 1986. 24. Coughlin MJ, Shurnas PJ: Hallux rigidus: grading and long-term results of operative treatment, J Bone Joint Surg Am 85:2072, 2003. 25. Thompson FM, et al, editors: Surgery of the foot and ankle, ed 6, St Louis, 1993, Mosby-Year Book. 26. Mann RA, Clanton TO: Hallux rigidus: treatment by cheilectomy, J Bone Joint Surg Am 70:400, 1988. 27. Hamilton WG: Foot and ankle injuries in dancers, Clin Sports Med 7:143, 1988. 28. Kurtz DH, et al: The Valenti procedure for hallux limitus: a longterm follow-up and analysis, J Foot Ankle Surg 38:123, 1999. 29. Saxena A: The Valenti procedure for hallux limitus/rigidus, J Foot Ankle Surg 34:485, 1995. 30. Hattrup SJ, Johnson KA: Subjective results of hallux rigidus following treatment with cheilectomy, Clin Orthop 226:182, 1988.
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31. Graves SC: Personal communication, 1997. 32. Easley ME, Anderson RB, Davis WH: Intermediate to long-term follow-up of medial-approach dorsal cheilectomy for hallux rigidus, Foot Ankle Int 20:147, 1999. 33. Moberg E: A simple operation for hallux rigidus, Clin Orthop 142:55, 1979. 34. Thomas PJ, Smith RW: Proximal phalanx osteotomy for the surgical treatment of hallux rigidus, Foot Ankle Int 20:3, 1999. 35. Makwana NK: Osteotomy of the hallux proximal phalanx, Foot Ankle Clin 6:455, 2001. 36. Citron N, Neil M: Dorsal wedge osteotomy of the proximal phalanx for hallux rigidus. Long-term results, J Bone Joint Surg Br 69:835, 1987. 37. Hamilton WG, Hubbard CE: Hallux rigidus. Excisional arthroplasty, Foot Ankle Clin 5:663, 2000. 38. Hamilton WG, et al: Capsular interposition arthroplasty for severe hallux rigidus, Foot Ankle Int 18:68, 1997. 39. Coughlin MJ, Shurnas PJ: Soft-tissue arthroplasty for hallux rigidus, Foot Ankle Int 24:661, 2003. 40. van Dijk CN, Veenstra KM, Nuesch BC: Arthroscopic surgery of the metatarsophalangeal first joint, Arthroscopy 14:851, 1998. 41. Coughlin MJ: Sesamoid pain: causes and surgical treatment. In Green WB, editor: Instructional course lectures 39, Park Ridge, IL, 1990, American Academy of Orthopaedic Surgeons, 2000. 42. McBryde AM Jr, Anderson RB: Sesamoid foot problems in the athlete, Clin Sports Med 7:51, 1988. 43. Rowe MM: Osteomyelitis of metatarsal sesamoid, Br Med J 2:1071, 1963. 44. Zinman H, Keret D, Reis ND: Fracture of the medial sesamoid bone of the hallux, J Trauma 21:581, 1981. 45. Riley J, Selner M: Internal fixation of a displaced tibial sesamoid fracture, J Am Podiatr Med Assoc 91:536, 2001. 46. Anderson RB, McBryde AM Jr: Autogenous bone grafting of hallux sesamoid nonunions, Foot Ankle Int 18:293, 1997. 47. Ilfeld FW, Rosen V: Osteochondritis of the first metatarsal sesamoid: report of three cases, Clin Orthop 85:38, 1972. 48. Kliman ME, et al: Osteochondritis of the hallux sesamoid bones, Foot Ankle 14:435, 1993. 49. Rahn KA, Jacobsen KS: Pseudomonas osteomyelitis of the metatarsal sesamoid bones, Am J Orthop 26:365-367, 1997. 50. Inge GAL, Ferguson AB: Surgery of the sesamoid bones of the great toe, Arch Surg 27:466, 1933. 51. Leventen EO: Sesamoid disorders and treatment. An update. Clin Orthop, 269:236, 1991. 52. Mann RA, et al: Sesamoidectomy of the great toe, American Orthopaedic Foot and Ankle Society, Las Vegas, NV, 1985. 53. Anderson RB, Milia MJ, Davis WH: Plantar approach for isolated fibular hallux sesamoidectomy, American Orthopaedic Foot and Ankle Society, San Diego, CA, 2001. 54. Bowers KD Jr, Martin RB: Turf-toe: a shoe-surface related football injury, Med Sci Sports Exerc 8:81, 1976. 55. Coker TP, Arnold JA, Weber DL: Traumatic lesions of the metatarsophalangeal joint of the great toe in athletes, Am J Sports Med 6:326, 1978. 56. Coker TP, Arnold JA, Weber DL: Traumatic lesions of the metatarsophalangeal joint of the great toe in athletes, J Ark Med Soc 74:309, 1978. 57. Clanton TO, Butler JE, Eggert A: Injuries to the metatarsophalangeal joints in athletes, Foot Ankle 7:162, 1986. 58. Douglas DP, et al: Rupture of the medial collateral ligament of the first metatarsophalangeal joint in a professional soccer player, J Foot Ankle Surg 36:388, 1997. 59. Mullis DL, Miller WE: A disabling sports injury of the great toe, Foot Ankle 1:22, 1980.
References 68. Sammarco GJ: How I manage turf toe, Physician Sportsmed 16:113, 1988. 69. Jahss MH: Traumatic dislocations of the first metatarsophalangeal joint, Foot Ankle 1:15, 1980. 70. Lewis AG, DeLee JC: Type-I complex dislocation of the first metatarsophalangeal joint: open reduction through a dorsal approach, J Bone Joint Surg Br 66:1120, 1984. 71. Yu ED, Garfin SR: Closed dorsal dislocation of the metatarsophalangeal joint of the great toe. A surgical approach and case report, Clin Orthop 185:237, 1984. 72. Copeland CL, Kanat IO: A new classification for traumatic dislocations of the first metatarsophalangeal joint. Type IIC, J Foot Surg 30:234, 1991. 73. Schenck RC Jr, Heckman JD: Fractures and dislocations of the forefoot: operative and nonoperative treatment, J Am Acad Orthop Surg 3:70, 1995. 74. Frey C, et al: Plantarflexion injury to the metatarsophalangeal joint (‘‘sand toe’’), Foot Ankle Int 17:576, 1996.
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60. Rodeo SA, et al: Turf-toe: an analysis of metatarsophalangeal joint sprains in professional football players, Am J Sports Med 18:280, 1990. 61. Nigg BM, Segesser B: The influence of playing surfaces on the load of the locomotor system and on football and tennis injuries, Sports Med 5:375, 1988. 62. Jones DC, Reiner MR: Turf toe, Foot Ankle Clin 4:911, 1999. 63. Rodeo SA, et al: Diastasis of bipartite sesamoids of the first metatarsophalangeal joint, Foot Ankle 14:425, 1993. 64. Watson TS, Anderson RB, Davis WH: Periarticular injuries to the hallux metatarsophalangeal joint in athletes, Foot Ankle Clin 5:687, 2000. 65. Prieskorn D, Graves SC, Smith RA: Morphometric analysis of the plantar plate apparatus of the first metatarsophalangeal joint, Foot Ankle 14:204, 1993. 66. Tewes DP, et al: MRI findings of acute turf toe: a case report and review of anatomy, Clin Orthop 304:200, 1994. 67. Anderson RB: Turf toe injuries of the hallux metatarsophalangeal joint, Tech Foot Ankle Surg 1:102, 2002.
.........................................C H A P T E R 1 9 Bunion deformity in elite athletes Roger Mann CHAPTER CONTENTS ...................... Introduction
435
Radiographic evaluation
439
Biomechanics of the first metatarsophalangeal joint
435
Decision making
439
Types of hallux valgus deformity
435
Surgical procedures
441
Conservative management
436
Postoperative management
443
Physical examination
438
Further reading
443
INTRODUCTION The hallux valgus deformity in the athlete is no different from the deformity in the nonathlete, but it becomes almost a philosophical question because a foot is to an athlete what a hand is to a musician. Its function must be respected because without it, the athlete, whether a ballerina or lineman, may not be able to perform at an acceptable level. In most cases, unless the athlete’s career is jeopardized by his or her hallux valgus deformity, surgical correction probably should not be undertaken for fear that a less than perfect result may jeopardize the athlete’s career.
BIOMECHANICS OF THE FIRST METATARSOPHALANGEAL JOINT The main function of the first metatarsophalangeal joint is to stabilize the longitudinal arch through the windlass mechanism. Anatomically the windlass mechanism consists of the plantar fascia inserting into the base of the proximal phalanx via the plantar plate (Fig. 19-1). As the windlass mechanism becomes functional in the last half of stance by the dorsiflexion of the proximal phalanx on the metatarsal head, the metatarsals are depressed as weight is transferred to the toes. The effect of the windlass mechanism is greatest for the hallux and least for the small toe. Secondarily the windlass mechanism elevates
the longitudinal arch and aids in inversion of the calcaneus (Fig. 19-2). When a hallux valgus deformity develops and lateral subluxation of the proximal phalanx on the metatarsal head occurs, the sesamoid sling is no longer beneath the first metatarsal head; therefore the windlass mechanism becomes less functional (Fig. 19-3). This is because when dorsiflexion of the phalanx occurs, plantarflexion of the metatarsal and weight transfer to the hallux are diminished resulting in progressive loss of the stability of the longitudinal arch. As it progresses, this loss of stability weakens the medial longitudinal arch, resulting in weight transfer from the first metatarsal to the second. This subsequently can result in excessive fatigue of the foot and possibly callus formation beneath the second metatarsal. This combination of effects results in diminished performance in the athlete, although it could be tolerated by the nonathlete.
TYPES OF HALLUX VALGUS DEFORMITY The hallux valgus deformity can be divided into two basic groups—persons with a congruent joint and those with a noncongruent or subluxed joint. In those with the congruent deformity, the windlass mechanism is not disrupted, and therefore the stability of the foot is not a problem (Fig. 19-4, A). In these individuals, the main disability is a large medial eminence, which results in chafing against their shoe. In the noncongruent deformity, there is progressive subluxation of the
CHAPTER 19
Bunion deformity in elite athletes
Figure 19-1 Plantar aponeurosis. (A) Cross section. (B) Division of plantar aponeurosis around flexor tendons. (C) Components of plantar pad and its insertion into the base of the phalanx. (D) Extension of toes draws plantar pad over metatarsal head, pushing them into plantarflexion. (From Mann RA: In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby.)
Figure 19-2 Dynamic function of plantar aponeurosis (A) foot at rest. (B) Dorsiflexion of metatarsophalangeal joints activates windlass mechanism, bringing about elevation of the longitudinal arch, plantarflexion of metatarsal heads, and inversion of heel. This produces stability of the longitudinal arch of the foot. (From Mann RA: In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, ed 7, St Louis, 1999, Mosby.)
metatarsophalangeal joint that leads to instability and weight transfer (Fig. 19-4, B). In these individuals, the problem is more than an enlarged medial eminence because of the instability that occurs. If the enlarged medial eminence results in sufficient disability for the athlete and he or she can no longer function at the level needed to participate in his or her sport, a hallux valgus repair can be considered.
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CONSERVATIVE MANAGEMENT Conservative management of the athlete with a hallux valgus deformity begins with specifically pinpointing the area of maximal pain because our conservative management must be directed toward relieving that problem. Generally, pain is over the medial eminence and
Conservative management
Figure 19-3 Severe hallux valgus deformity with subluxed metatarsophalangeal joint. A deformity of this severity significantly alters the function of the plantar aponeurosis, giving rise to progressive instability of the longitudinal arch. Although this is tolerated by the nonathlete, it may present a significant disability for the athletic individual.
not infrequently where the dorsal medial cutaneous nerve crosses over the bony medial eminence. First, the size of the shoe must be evaluated carefully in relation to the foot. Next, the pattern of the seams that cross over the medial eminence must be evaluated, because, although leather will give way to pressure from the medial eminence, the stitching will not. Sometimes just altering the seams that cross over the bony prominence will result in a great deal of relief. If it appears that the shoe is of adequate size, then the area over the painful spot can be relieved by having the shoe enlarged over this area. This is particularly useful in the athlete who requires a rigid boot, such as a skier, hockey player, rollerblader, and so forth. Even the ballet slipper can be expanded to a certain extent to relieve the pressure over the medial eminence. The shoe itself could be stiffened to decrease stress across the first metatarsophalangeal joint if the patient’s athletic performance would not be diminished. Obviously a lineman can tolerate a stiffer shoe than a ballerina or gymnast. As a general rule, an orthotic device per se will not do anything to relieve the problems associated with a hallux valgus deformity unless there is sesamoid pain or a transfer lesion beneath the second metatarsophalangeal joint.
Figure 19-4 (A) Radiograph of a congruent metatarsophalangeal joint. There is no lateral subluxation of the proximal phalanx on the metatarsal head. This maintains the function of the plantar aponeurosis and hence the stability of the foot. (B) An incongruent metatarsophalangeal joint has lateral subluxation of the proximal phalanx on the metatarsal head. This creates an unstable situation, progressive in nature, giving rise to decreased function of the plantar aponeurosis and increasing instability of the medial longitudinal arch.
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Bunion deformity in elite athletes
One must be careful when using an orthotic device because it will take up a certain amount of volume in the shoe and as a result may aggravate the patient’s problem rather than relieve it. An orthotic device will not prevent a bunion from occurring. If the hallux valgus deformity has progressed to the point at which a transfer lesion is occurring beneath the second metatarsal head, then some type of an orthotic device to relieve the pressure will be useful. One must keep in mind, however, that whenever something is added to a shoe it takes up volume; if the shoe is already small, this can aggravate the problem. A change in shoewear may be necessary if an orthotic device is to be used. Sometimes when an individual has a large medial eminence that is painful, there is tendency to place a pad over the involved area, with the thought that this will relieve pressure, but in actuality doing this increases the pressure. The person should be advised to cut out an area in the pad so that pressure is taken off of the medial eminence rather than applied to it.
PHYSICAL EXAMINATION The physical examination begins with the patient standing so that the clinician can observe the overall posture of the foot, deformity of the first metatarsophalangeal joint and the alignment of the lesser toes. In athletes,
the spectrum of hallux valgus deformities and the shape of the foot are extremely variable. One could be evaluating a National Basketball Association (NBA) player who often has a large, rather flat foot, with multiple lessertoe deformities as well as the hallux valgus or a ballerina with a moderate to severe hallux valgus deformity associated with multiple lesser toe deformities because of pressure from the dancing shoes. Obviously, there is the entire spectrum in between these types of athletes. During the physical examination, the patient should be asked to put his or her finger on the area that causes the most pain, and in this way the clinician is directed to the place at which the most attention must be focused. With the patient sitting, the clinician should determine the range of motion of the ankle, subtalar, and transverse tarsal joint, as well as the posture of the forefoot in relation to the hindfoot. To determine gastrocnemius tightness, the overall tightness of the Achilles tendon should be evaluated with the knee both flexed and extended. The range of motion of the first metatarsophalangeal joint must be observed carefully, and any crepitation or dorsal impingement should be noted. During this procedure, one is observing the total range of motion, whether or not there is an element of hallux rigidus present, which may be the source of the patient’s pain, rather than the deformity itself. One also should see how much passive correction of the deformity can be achieved because this provides insight regarding the degree of correction possible. The clinician palpates the
Figure 19-5 Subluxation of the tibial sesamoid beneath the first metatarsal head. As a result of this alignment, there often is pain beneath the metatarsal head because the sesamoid rides against the cresta on the plantar aspect of the metatarsal.
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Decision making
Figure 19-6 Radiographic analysis of a hallux valgus (HV) deformity (A). Hallux valgus angle should be less than 15 degrees, and the intermetatarsal (IM) angle less than 8 degrees. (B) The distal metatarsal articular angle (DMAA) should be less than 10 degrees of lateral deviation. (C) An increased DMAA may result in a clinical situation in which there is a hallux valgus deformity without subluxation of the metatarsophalangeal joint. To correct this problem, a distal metatarsal osteotomy, carrying out a medial closing wedge osteotomy to realign the articular surface, will be necessary. One cannot correct the hallux valgus deformity with an increased DMAA without realigning the metatarsal head because stiffness of the joint will result.
RADIOGRAPHIC EVALUATION Radiographic evaluation is carried out by obtaining weight-bearing anterior-posterior (AP), lateral, and
oblique x-rays. For accurate evaluation of a foot, the radiograph must be weight bearing. The measurements obtained are the same as those used for evaluation of other patients with hallux valgus deformity: hallux valgus angle, intermetatarsal angle, joint congruency, distal metatarsal articular angle (DMAA), and evidence of arthrosis (Fig. 19-6). One should determine whether the first metatarsophalangeal joint is congruent or incongruent, identify osteophyte formation around the first metatarsophalangeal joint, observe the sesamoids and their location in relation to the cresta, and observe the alignment of the lesser metatarsophalangeal joints.
DECISION MAKING If the decision is made to carry out correction of the hallux valgus deformity, the operative procedure must be selected carefully. In the patient who has primarily an enlarged medial eminence with a congruent metatarsophalangeal joint, the distal soft-tissue procedure alone can provide satisfactory correction. In this situation, the main problem is the enlarged medial eminence, with no subluxation of the metatarsophalangeal joint, so that little or no correction is required. In this case the hallux valgus angle would be less than 30 degrees and the intermetatarsal angle less than 11 degrees. If the 439
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sesamoid area, looking for the possibility that the problem may be due to a fractured or collapsed sesamoid. At times the sesamoid pain is due to the sesamoid’s being positioned beneath the cresta (Fig. 19-5). Occasionally, particularly in the ballerina or the younger gymnast, one may encounter avascular necrosis of a sesamoid (usually fibular) as the source of the discomfort. The clinician examines the plantar aspect of the foot, looking for the possibility of transfer lesions, which would occur if the person had an advanced hallux valgus deformity. The lesser toes must be evaluated by checking the range of motion of the metatarsophalangeal joint and the stability of the lesser metatarsophalangeal joints. Sometimes with a severe hallux valgus deformity there can be instability and possible subluxation of the second metatarsophalangeal joint. The presence of hammertoes or mallet toes also must be observed carefully to determine whether or not these are painful. The neurovascular status of the foot should be checked, but this obviously is rarely a problem in the athletic population.
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Bunion deformity in elite athletes
intermetatarsal angle is much more than 11 degrees, the possibility of a recurrence will be significant because complete correction of the IM angle probably cannot be achieved. The athlete who is large and has a large foot often has an extremely ‘‘stiff’’ foot. By a stiff foot we mean one that is quite rigid so that the arc
of motion of the metatarsophalangeal joints is limited to no more than 45 to 50 degrees. In a foot such as this, obtaining correction of the bunion deformity can be technically difficult; and for the soft-tissue procedure to succeed, an osteotomy must be performed (Fig. 19-7).
Figure 19-7 (A) Preoperative and postoperative radiographs demonstrating a satisfactory reduction of a moderate severe hallux valgus deformity using a distal soft-tissue procedure and proximal crescentic osteotomy. (B) A somewhat less than optimal result following a distal soft-tissue procedure and proximal osteotomy in a male with a very ‘‘stiff’’ foot, which made complete reduction of the deformity not possible. The problem with an incomplete correction is that it has a greater possibility of recurrence than one that is completely corrected, and the incompletely reduced sesamoid may be a source of plantar pain.
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Surgical procedures
The chevron procedure can be used if there is a very large medial eminence, a somewhat larger deformity of the intermetatarsal angle, up to 13 degrees, but the hallux valgus angle should not be more than 30 degrees. The chevron can be used with a mildly subluxed or incongruent joint or may be useful if the patient has an increased DMAA that requires correction. It is important to keep in mind, however, that if the sesamoids have subluxed they often are not corrected by the chevron procedure itself; and, if the sesamoid lies beneath the cresta, this may be a source of pain in the future. Lastly, the patient with a subluxed metatarsophalangeal joint and an increased intermetatarsal angle will require a correction with a distal soft-tissue procedure and proximal metatarsal osteotomy. In patients with a subluxed metatarsophalangeal joint, complete correction should be obtained; otherwise the metatarsophalangeal joint may be painful because the sesamoids have not been completely reduced, resulting in pain beneath the cresta. The error that sometimes is made when trying to correct a hallux valgus deformity is to correct the deformity incompletely by using a procedure that does not adequately correct both the bony and the soft-tissue components of the deformity. It is critical that a partial correction be avoided if an early recurrence is to be prevented. This is never a good event for the patient or doctor; but, in the case of the athlete, when there has been downtime from his or her profession and the problem recurs, the result is an extremely difficult situation.
of the head then is identified with a K-wire, after which a chevron cut is made. It is important that the blade not pass too far laterally after it passes the lateral cortex to protect the blood supply laterally. The chevron osteotomy then is displaced in a lateral direction approximately one quarter to one third of the width of the head, depending on the severity of the deformity. If the DMAA is a problem, then possibly a medial closing wedge-type of procedure can be carried out. The osteotomy site is stabilized with either a pin or screw and the capsule is plicated (Fig. 19-8). Postoperatively the patient is then kept in a dressing and postoperative shoe for approximately 6 to 8 weeks. If adequate stabilization of the capital fragment has been achieved, the patient probably could start stationary bicycle riding about 2 weeks after the surgical procedure to maintain cardiovascular fitness.
The distal soft-tissue procedure and proximal osteotomy This procedure is used for the incongruent (subluxed) metatarsophalangeal joint with a hallux valgus deformity of more than 30 degrees and an intermetatarsal angle more than 13 degrees. The principle of this procedure is to carry out a complete distal release of the deformity and then to carry out some type of a proximal metatarsal osteotomy. The type of metatarsal osteotomy used depends on the surgeon. I prefer the proximal crescentic
SURGICAL PROCEDURES It is beyond the scope of this chapter to present in detail surgical procedures that could be used to treat the hallux valgus deformity. Only a brief description of the procedures is discussed, and more details of the surgery can be found in standard foot and ankle textbooks.
Figure 19-8 Preoperative and postoperative radiograph demonstrating a chevron procedure. (continued)
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The chevron procedure The chevron procedure, as stated previously, is for the patient who primarily has a congruent metatarsophalangeal joint with a large medial eminence as the main source of discomfort. The chevron procedure should not be used in the athletic population to correct a joint that has more than 1 to 2 mm of incongruency (subluxation). The operation is carried out through a medial approach, which is carried down to the joint capsule. With this type of approach, the dorsomedial cutaneous nerve is not endangered, as it is when a dorsal approach is used. The joint capsule is opened, and the medial eminence then is removed starting at the sagittal sulcus and then angled in a medial direction (not in line with the metatarsal shaft) to obtain as wide a base as possible for the osteotomy site. The center
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Bunion deformity in elite athletes
Figure 19-8 cont’d
osteotomy; others prefer a proximal chevron or a short oblique. The principle involved is that the intermetatarsal angle must be corrected along with the distal softtissue procedure to obtain a correction that will stand the test of time.
The distal soft-tissue procedure is carried out through a dorsal incision in the first webspace, releasing the adductor tendon, the sesamoid sling, and the transverse metatarsal ligament. The lateral joint capsule also is released from its insertion into the metatarsal head.
Figure 19-9 Preoperative and postoperative radiograph demonstrating correction following a distal soft-tissue procedure and proximal metatarsal osteotomy.
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Further reading
At the same time that the hallux valgus deformity is corrected, any existing symptomatic hammertoes can be corrected, if necessary. If there is a dislocation of the second metatarsophalangeal joint, I think that this can be treated with a distal metatarsal osteotomy to decompress the joint and permit adequate reduction of the deformity to occur.
POSTOPERATIVE MANAGEMENT No matter what bunion procedure is carried out, the foot obviously is weakened by the procedure; and it is important that, after the dressings are removed, the patient undergoes a period of physical therapy to regain the range of motion of the metatarsophalangeal joint. I believe that one should wait at least 1 month before allowing the athlete to return to impact-type activities to allow the bones and soft tissues to mature adequately.
FURTHER READING Coughlin MJ: The chevron procedure, Contemp Orthop 23(1):45, 1991. Coughlin MJ: Hallux valgus in the athlete, Sports Med Arthrosc Rev 2:326, 1994. Coughlin MJ, Mann RA: Adult hallux valgus. In Coughlin MJ, Mann RA, Saltzman C, editors: Surgery of the foot and ankle, ed 7, St Louis, 2007, Mosby, Chap. 6. Mann RA, Rudicel S, Graves SC: Hallux valgus repair utilizing a distal soft tissue procedure and proximal metatarsal osteotomy, a long term follow-up, J Bone Joint Surg 74:124, 1992.
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The second incision is made on the medial side of the metatarsophalangeal joint where it is carried down to the joint capsule. Care is taken to retract the dorsal and plantarmedial cutaneous nerves. A capsulotomy then is performed, and a segment of the joint capsule is removed. The enlarged medial eminence is removed, starting 2 mm medial to the sagittal sulcus and removing the fragment in line with the medial aspect of the first metatarsal. This is different from the resection made for the chevron procedure. A third incision is used to carry out the proximal crescentic osteotomy. This is a dorsal approach, starting approximately at the midshaft of the metatarsal and carried just proximal to the metatarsocuneiform joint. The osteotomy site is carried out approximately 1 cm distal to the metatarsocuneiform joint, and a screw is used for fixation. The postoperative immobilization is carried out by using a Kling and adhesive dressing, which holds the toe in proper alignment for a period of 8 weeks (Fig. 19-9). The patient is permitted to ambulate in a postoperative shoe during this period. If one feels that the osteotomy site is sufficiently stable, cardiovascular training on a stationary bicycle can be started after approximately 2 weeks. I do not feel that a metarsocuneiform joint arthrodesis should be carried out in the active athlete. I think that this procedure carries with it too much morbidity, and the possibility exists of both nonunion at the fusion site and the fusion site spilling over into the second metatarsocuneiform area, which would further stiffen the foot. Although this is tolerated by the nonathlete, I do not think it is a good idea in the athletic population.
.........................................C H A P T E R 2 0 Chronic leg pain Peter H. Edwards, Jr. and Peter B. Maurus CHAPTER CONTENTS ...................... Introduction
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Popliteal artery entrapment syndrome
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Medial tibial stress syndrome
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Operative
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Stress fractures
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Summary
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Chronic exertional compartment syndrome
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References
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Nerve entrapment
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INTRODUCTION As the general population in the United States has become more active, orthopaedists have observed an increase in the incidence of sports-related injuries. Nonspecific complaints of pain in the foot, ankle, calf, or shin are often reported, with shin pain as the most common presentation.1,2 Evaluation of leg pain not only requires knowledge of the anatomy and biomechanics of the lower extremity but also an understanding of the pathology of the injury. Conducting a thorough history and physical examination and appropriately interpreting diagnostic tests are essential to the establishment of an accurate diagnosis. In addition, specific details regarding physical activity, including training regimens, surface conditions, and shoewear must be determined, because these factors also play a significant role in the diagnosis. Because several etiologies may present with similar characteristics, patients must be evaluated for multiple conditions.3 The differential diagnosis of chronic leg pain includes the following conditions: bony or softtissue tumors, chronic exertional compartment syndrome (ECS), claudication, isolated leg trauma, medial tibial stress syndrome (MTSS), muscle strains, nerve entrapment, popliteal artery entrapment syndrome (PAES), radiculopathy, referred pain from meniscal pathology, stress fractures, and tendinitis. Despite this wide range of diagnoses, several studies demonstrate that certain conditions are more prevalent among athletes, in particular.1,4-6 In a retrospective review of 72
track and field athletes with athletic-related injuries, 28% of injuries were due to overuse of the leg.4 Furthermore, chronic exertional shin pain accounts for approximately 10% to 15% of all running injuries and may be responsible for approximately 60% of all leg pain syndromes.1 In another retrospective study of 150 patients with exercise-induced leg pain, chronic ECS was the most prevalent cause of pain, representing 33% of cases; stress fractures and MTSS accounted for 25% and 13% of cases, respectively.6 Conversely, in our experience MTSS has been more prevalent than either chronic ECS or stress fractures. This chapter focuses on common causes of chronic leg pain in athletes, including MTSS, stress fractures, chronic ECS, nerve entrapment, and PAES. The incidence, pathology, clinical presentation, and treatment options are discussed for each condition.
MEDIAL TIBIAL STRESS SYNDROME ‘‘Shin splits’’ is a nonspecific diagnosis of posteromedial leg pain commonly used to describe not only MTSS but also a wide variety of other lower leg pain conditions, including chronic ECS, fascial hernia, muscle strains, periostitis, and stress fractures.2,3,5,7-9 One of the most common sites of overuse pain is the distal one third of the medial border of the tibia.9-12 Several terms, including medial tibial syndrome, MTSS, tibial stress syndrome, posterior tibial syndrome, soleus syndrome, and periostitis have been proposed to link this common clinical presentation to a specific condition.2,11-19 Medial
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Chronic leg pain
tibial stress syndrome may be the most accurate of these terms, however, because it describes both the location and the likely pathophysiology of the syndrome.5,11,12,20 MTSS typically is observed in runners and individuals involved in jumping activities such as basketball and volleyball.3,8,11,18,21,22 In our experience it also represents the most common cause of chronic leg pain. Both biologic and biomechanical factors have been reported as possible causes of MTSS.10-12 Although the tibialis posterior muscle historically has been implicated as the source of this condition,9,16,22-24 a recent study of 50 cadaveric legs revealed that the tibial posterior muscle was more lateral, indicating that this muscle was not a likely source of MTSS.10 Other recent studies have identified the soleus, flexor digitorum longus (FDL), and crural fascia as sources of the pain.10,15,25 More specifically, a three-phase bone scan study of 10 patients with MTSS demonstrated low-grade uptake along a diffuse region of the posteromedial tibia, suggesting that the condition is related to the soleus muscle.15 During running, heel strike occurs in relative supination, with pronation of the foot increasing until midstance.11,17,26 Because the soleus is the primary plantarflexor and invertor of the foot, it has been theorized that the medial portion of this muscle contracts eccentrically as the foot pronates (Fig. 20-1).17 The repetitive eccentric contraction that occurs in hyperpronating athletes may explain the increased incidence of MTSS observed in such athletes.5,9,11,14,17,25,27-29 In addition, hyperpronation is a compensatory mechanism that occur in patients with hindfoot and forefoot varus,25,26 tibia vara,26 tight Achilles tendon,26,28,29 and tight gastrocnemius and soleus muscles;26 therefore such patients also are at increased risk for developing MTSS.
History The most common complaint associated with MTSS is a recurring, dull ache localized over the distal one-third posteromedial cortex of the tibia (Case Study 1). In our experience, MTSS tends to occur late in the sport season after prolonged activity, whereas stress fractures tend to occur early in an athletic season as stresses increase rapidly. Early in the development of MTSS, patients may experience pain at the beginning of a workout or run but feel a relief of symptoms with continued activity, only to be followed by a recurrence of pain either at the conclusion of the activity or some time afterward. Pain usually is alleviated with rest and generally does not occur at night. However, as this condition progresses, pain may occur throughout training or during low activity, such as walking, and possibly may continue during rest.
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Figure 20-1 (A) During running, the medial portion of the soleus contracts eccentrically as the foot pronates. Hyperpronating athletes, in particular, are at an increased risk for developing medial tibial stress syndrome (MTSS). (B) The source of pain is at the origin of the flexor digitorum longus (FDL) and soleus fascial bridge on the posteromedial aspect of the tibia.
Physical examination The pathognomonic physical finding in MTSS is palpable tenderness along the posteromedial edge of the distal one third of the tibia. In rare cases, erythema or localized swelling over the medial tibia also may be observed. Although studies have reported conflicting ranges of motion associated with MTSS, in theory, hypermobile pronating feet are at increased risk of MTSS. Therefore evaluation for foot pronation or subtalar varus also is recommended. Abnormal pulse, diffuse swelling, firm compartments, neurologic deficits, and vibratory pain are not associated with this syndrome. Diagnostic studies Roentgenograms generally are normal in patients with MTSS3,7,11,17,30 but are recommended to rule out abnormalities associated with other conditions such as stress fractures and tumors.3,11,12 A three-phase bone scan is warranted to rule out stress fractures if a conservative treatment program does not alleviate pain. This type of bone scan is a valuable diagnostic tool used to differentiate between MTSS and stress fractures, because each condition has a distinct scintigraphic pattern.7,9,11,15,17,31,32 A bone scan demonstrating
Medial tibial stress syndrome
a longitudinal and diffuse pattern in the distal one third of the tibia is indicative of MTSS (Fig. 20-2).9,11,15,32 In general, only delayed images are positive in cases of MTSS, whereas both early and delayed images demonstrate uptake in cases of stress fracture.11,15 In addition, magnetic resonance imaging (MRI) is another diagnostic tool for MTSS recommended by some authors.11,31 However, we believe that MRI has a limited role in the evaluation of MTSS because of its higher cost compared with other imaging options7 and its difficulty in delineating MTSS from stress fractures.
Treatment ............................................................. Conservative The recommended management of MTSS is multimodal, consisting of rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and ice.3,12 Physical therapy modalities such as iontophoresis and ultrasound also may be used.3,12 Initially, rest or a decrease in training for 2 to 3 weeks is suggested and may be curative without further workup.12 Cardiovascular conditioning may be maintained during this period with swimming, upper body weightlifting, and deep-water running.11,12 Stationary biking is another option but should be performed with the heel on the pedal, a precaution that will diminish
Operative Fasciotomies of the posterior compartments of the tibia are possible treatment options in patients with intractable MTSS.6,11,14,34,36 In these rare cases, fasciotomies may alleviate the pull of the soleus and deep compartment muscles on the corresponding fascial insertions.6,11,14,34,36 However, in our experience, conservative management alone has been successful in treating MTSS cases, eliminating the need for surgical intervention.
4 PEARL MTSS pain actually may subside during workout but will recur following cessation of activity. Conversely, pain associated with chronic ECS and PAES does not subside during activity and tends to remain until activity is completed. Pain is localized to the distal one third of the tibia in MTSS but is usually more proximal in the typical stress fracture.
C A S E S T U D Y 1
A 16-year-old, female, cross-country runner presented for evaluation of progressive right leg pain. Over the preceding 3 weeks, training intensity had been increased
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Figure 20-2 Classic bone scan demonstrating the increased linear uptake along the posteromedial aspect of the tibia in the delayed phase indicative of medial tibial stress syndrome (MTSS). The linear uptake is most commonly observed in the distal one third of the leg; however, in this specific case, the location is slightly more proximal.
muscular stress transmission to the leg. NSAIDs often are prescribed to relieve pain11,12 and to decrease possible inflammation. Ice may be used to further reduce swelling and inflammation.12,31 Addressing biomechanical abnormalities is also recommended.12,33,34 For example, excessive pronation may be corrected with the use of custom or off-the-shelf orthotics.33 Physical therapy modalities, including massage, electrical stimulation, iontophoresis, and ultrasound also have been used.10,31,35 If pain is present with walking or at rest, range-of-motion boots and/or walkers are used. In rare cases, crutches may be necessary. If the patient has not experienced pain during conservative treatment, a gradual return to training may be initiated. Warm-up and cool-down routines, including stretching, are advised with each workout to prevent recurrence of symptoms. If the patient remains asymptomatic, progression of training is recommended at increments of 10% to 25% for 3 to 6 weeks.11 If symptoms return, activity should cease for at least 2 weeks before training is resumed at a lower intensity and duration.
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Chronic leg pain
in preparation for a season-ending tournament. During that time, increasing pain developed over the distal medial leg. Initially, pain was present only at the conclusion of training but progressed to include soreness on first arising in the morning and with daily activities, forcing the patient to decrease training. She denied constitutional symptoms, history of trauma, or recent shoewear change. Physical examination was remarkable only for tenderness along the posteromedial cortex of the distal one third of the tibia. Plain radiographs were normal. On the basis of a clinical diagnosis of MTSS, conservative treatment, consisting of cessation of training for 2 weeks, NSAIDs, and ice, was recommended. At the 2-week follow-up, only minor improvement had been achieved and the patient remained in significant pain. Consequently, a range-of-motion boot was implemented and a bone scan was ordered to rule out a possible stress fracture. Because the bone scan was negative, as indicated by a diffuse uptake in the delayed phase, the patient remained in the range-of-motion boot for an additional 4 weeks. After this period, activities of daily living were conducted without pain, permitting a gradual return to training over the ensuing 6 weeks.
STRESS FRACTURES Repetitive loading caused by overuse or overloading of the lower leg results in microtrauma to the bone that eventually may lead to stress fracture.6,35,37-39 Stress fractures of the tibia are more frequent3,11,37,40-44 and more problematic to treat than those of the fibula. Fibula stress fractures tend to heal more rapidly and generally do not require adjunctive therapy.41,43 The focus of this section is on tibial stress fractures because most fibula stress fractures occur about the ankle and are covered elsewhere. Most fractures of the tibia occur in the proximal metaphyseal or upper diaphyseal regions,35,44,45 whereas tibial fractures that are longitudinal in nature46-49 or occurring in the midanterior region9,35,37,38,50,51 are less prevalent. Athletes, in particular, are subject to stress fractures of the leg. Specific stress fractures also are related to certain types of activities. For example, the more common posteromedial stress fracture usually is associated with running activities.11,35,46 Conversely, midanterior tibial cortex stress fractures often are associated with dancers and athletes involved in cutting and jumping activities.35,38,50-54 Risk factors for developing a stress fracture include excessive training, training errors, biomechanical variants, and menstrual irregularities with corresponding changes in bone density.9,11,40,42,46,55,56 Excessive training, particularly common early in the athlete’s season,
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causes overuse or overloading, which may result in stress fracture.6,35,46 In addition, overlapping of sport seasons, which often occurs when teenage athletes participate in multiple sports, also may lead to an overuse scenario. Training errors, including changes in training surface, shoewear, and technique often result in overloading, which may result in stress fracture.6,35,37 Weather and seasonal differences affect surface conditions for many outdoor sport activities and may increase the risk of stress fracture. For example, dry conditions and the fall season are both associated with hard ground surfaces, which result in an overloading environment for soccer players. Simple measures, such as watering soccer fields when the ground is hard, may reduce the risk of stress fracture and other injuries by minimizing loading conditions. Biomechanical factors, such as cavus feet, leglength inequality, and muscular imbalance also may increase the risk of developing a stress fracture.9,11,40,44 Finally, low body weight and menstrual abnormalities in female runners have been associated with an increased incidence of stress fractures.39,40,42,55 The cause of stress fractures is multifactorial in nature and often results from an imbalance of natural bone formation and resorption cycle because of repetitive loading.37,44,51,56 One theory proposed to explain the mechanism of stress fracture suggests that muscle fatigue results in the transmission of excessive forces to the underlying bone, ultimately leading to stress fracture.20,37,44,51,55 Another hypothesis asserts that simple, repetitive weight bearing leads to a concentrated rhythmic muscle action, which causes excessive transmission of forces beyond the threshold of bone, thereby resulting in fracture.20,37,44,51,57 Forces from large posterior muscle groups, in particular, may cause increased tension on the anterior cortex of the tibia, possibly leading to the problematic midanterior tibial stress fracture.51
History Pain associated with tibial stress fractures is more proximal than that caused by MTSS (Case Study 2). Although pain typically is localized to the fracture site, diffuse pain also may occur. Stress fracture pain will develop gradually, occurring initially as a mild ache following a specific amount of exercise and then subsiding. As the condition progresses, pain may become severe and occur during earlier stages of exercise and after cessation of activity. In rare cases, night pain also is possible. Any complaints of constitutional symptoms, including fever and fatigue, should raise concern of a possible tumor or infectious process. In addition to obtaining a history of pain and symptoms, training and activity also should be investigated to identify possible errors that may increase the risk of stress fracture. Recent changes in activity level, such as increased quantity or intensity of training, modifications
Stress fractures
in training surface, shoewear alterations, and technique should be noted. Inquiries regarding diet also should be conducted because the presence of eating disorders increases the risk for stress fracture. Furthermore, obtaining menstrual histories of female athletes also is pertinent because oligomenorrhea and delayed menarche both increase the risk of stress fracture. Finally, a review of systems is suggested to assess general health, medications, and personal habits to identify any additional factors possibly influencing bone health.
Diagnostic studies A clinical diagnosis of stress fracture often may be made solely on the basis of the history and physical examination,37,56 but diagnostic imaging may confirm the diagnosis or assist in identifying the stress fracture in questionable cases. Plain roentgenograms should be performed as the first imaging step but may be negative, because radiographic abnormalities often are not observed until 2 to 3 weeks after the onset of symptoms.3,37,44,46 Radiographic abnormalities may appear as a faint periosteal reaction, a fluffy area of callus, or a cortical lucency.39 If radiographic examination demonstrates the presence of a stress fracture, no further imaging is necessary. A three-phase bone scan is indicated when suspicion of stress fracture remains despite negative radiographs.39,46 The specific scintigraphic pattern of a stress fracture demonstrates focal uptake in the area of fracture (Fig. 20-3).37,58 MRI, another diagnostic option, differentiates among fracture, tumor, and infection and also localizes the pathology.31,44,46,56,59 However, because a diagnosis often may be determined by plain radiograph or bone scan, both of which are more cost effective than an MRI, we reserve MRI for special cases, including a history of allergic response to dye, an aversion to needles, or an atypical presentation. An MRI also is useful in differentiating between longitudinal stress fractures and MTSS, the more commonly observed overuse injury, because bone scans of these conditions
Figure 20-3 Bilateral bone scan demonstrating normal scintigraphy (left) versus the focal uptake pattern of a typical tibial stress fracture (right).
demonstrate identical diffuse uptake in the distal one third of the tibia (Case Study 3). In addition to its diagnostic capabilities, imaging also assists in differentiating among the various types of stress fractures. For example, radiographs depicting a small lucency or a ‘‘dreaded black line’’ in the midanterior cortex of the tibia are indicative of a midanterior cortex tibial stress fracture (Fig. 20-4, A).35,46 Because of the relatively avascular nature of this portion of the tibia, a bone scan initially may be interpreted as negative, but closer examination will depict an area of decreased uptake at the fracture site.46,54 If this type of fracture is not initially diagnosed and treated, a complete fracture may result. Conversely, plain radiographs of longitudinal tibial stress fractures often are normal, whereas bone scans will demonstrate increased uptake in the lower tibia.60
Treatment ............................................................. Conservative Conservative treatment for stress fracture is focused on pain relief and protection from further injury.39,46 Improvement in muscular strength and endurance, continuation of cardiovascular fitness, and management of biomechanical factors also are important. Relative rest, possibly with weight-bearing restriction, is recommended for a minimum of 2 to 4 weeks. Mild analgesics or NSAIDs also may be prescribed in conjunction with physical therapy modalities, such as ice or cross training.38,46 Cardiovascular fitness should be maintained with cycling, swimming, deep-water running, or other 449
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Physical examination On gross physical examination, the leg will appear normal. Compartments should be soft and the posteromedial aspect of the middle to distal one third of the tibia should not be tender. Joint range of motion usually is normal, but gait analysis may reveal biomechanical risk factors. Neurovascular examination typically is normal in the absence of any associated abnormalities. Palpation will reveal tenderness localized to the fracture site. In addition, erythema or localized swelling also may be noted. An ultrasound or a tuning fork will produce vibratory pain over the site of the stress fracture. In long-standing fractures, a palpable bony thickening may be present.
CHAPTER 20
Chronic leg pain
Figure 20-4 (A and B) Preoperative radiographs of a male runner who presented with a midanterior cortex tibial stress fracture, also referred to as a ‘‘dreaded black line,’’ which is visible in the lateral radiograph (B). (C and D) Because of the severity of the fracture, intramedullary nailing was required. As demonstrated in the 2-month postoperative radiographs, the fracture healed completely without the need for bone grafting.
nonloading activities.39,44,46,58 Upper body strength training is recommended to maintain muscle mass and is not likely to jeopardize fracture healing.44 Bracing or casting may be required for 3 to 12 weeks to immobilize the fracture adequately in severe cases or if pain is not relieved after the initial 2- to 4-week rest period.33,61 Because prompt return to activity is a priority for elite athletes, electrical stimulation is highly recommended. Electrical stimulation also has been effective in healing nonunioned traumatic fractures.35,46,50,51 Contributing factors, such as training errors, improper shoewear, and muscle imbalance that were identified in the history and physical examination also must be addressed.6,39,44 Training regimens should be individualized for each patient. Treatment plans for athletes with eating disorders or females with menstrual irregularities should involve dietary counseling and/or estrogen replacement therapy to accelerate healing and to prevent future problems.37,46 Shoes should be examined for signs of wear and inadequate support and also must be replaced every 500 km.38,46 If necessary, appropriate orthotics should be implemented. Return to activity should be gradual and individualized according to symptoms, with an emphasis on progress only when activity is accomplished without pain.44,46 It must be stressed that activity should cease if any pain occurs and should not be reattempted until the pain is alleviated.46,58 In addition, once the pain is
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alleviated, the patient must return to the lower loading activity and not advance until each successive activity has been accomplished without pain. A period of rest also must be implemented between activities before advancing to a higher loading activity. Although athletes may resume full training in 8 to 16 weeks, patients must be aware that a prolonged recovery period may be required for more severe stress fractures.51,54 Midanterior cortex tibial stress fractures, in particular, require a significant period of rehabilitation.3,38,46,50,51,58 Despite this prolonged rehabilitation, conservative treatment is similar to that for other tibial stress fractures and includes avoidance of activity, bracing or casting, and possible electrical stimulation.46,51,54
Operative Although most stress fractures heal successfully with conservative treatment, surgery may be warranted for severe stress fractures, such as midanterior or longitudinal tibial stress fractures, or for chronic nonunions of proximal medial stress fractures.38,50,51,54 Intramedullary nailing has yielded promising results in high-demand patients with problematic stress fractures.38,50,51,54 Our experience with intramedullary nailing also has been positive and involves the treatment of three midanterior tibial stress fractures, all of which healed completely without the need for bone grafting (Fig. 20-4, B).
Stress fractures
Vibration from a tuning fork or ultrasound will produce pain corresponding to the stress fracture site but will not elicit pain in cases of MTSS or chronic ECS. If a stress fracture is suspected on the basis of the history and physical examination despite negative plain radiographs, additional imaging, such as a three-phase bone scan, is recommended to confirm the diagnosis. Pain and swelling in the subcutaneous border of the tibia is indicative of a midanterior tibial stress fracture, which requires careful radiographic evaluation to confirm the presence of the subtle ‘‘dreaded black line.’’ If diagnosis remains questionable, a three-phase bone scan demonstrating a focal area of decreased uptake in the anterior tibial cortex will confirm the diagnosis.
C A S E S T U D Y 2
A 16-year-old, female soccer player related a 3-week history of anterior tibial pain localized approximately 7 cm below the tibial tubercle. Initially, pain was mild and occurred only with prolonged training. When the patient continued her training intensity, the pain progressed to the point at which training became difficult and persisted with daily activities; however, the patient did not seek treatment at this time. Before her final game, the patient stated that her pain was so severe she was unsure whether she should could continue to play. Despite constant pain, the patient competed in the final game and experienced a noncontact tibial fracture while running. Roentgenograms confirmed the presence of a tibial fracture with an intact fibular that was located at the anterior tibial cortex approximately 7 cm below the tibial tubercle, corresponding to the site of a presumed existing stress fracture. Conservative treatment was recommended and involved long-leg casting for 3 months. Because of minimal bone healing, determined by radiographic evaluation, long-leg casting continued and pulsed electromagnetic stimulation was added for 1 month. Following the use of the long-leg cast, a long-leg fracture brace was used with continued pulsed electromagnetic stimulation. After 6 months of conservative treatment, aching continued at the fracture site on weight-bearing ambulation. Subsequent plain radiographs and computed tomography (CT) scan indicated small areas of spot weld healing but a largely inadequate bridging callus. Consequently, operative treatment involving reamed intermedullary nailing of the tibia without fibular osteotomy was performed. Approximately 4 months following surgery the fracture was completely healed, and, by 8 months postsurgery the patient returned to playing soccer.
C A S E S T U D Y 3
A 47-year-old woman who regularly walks for cardiovascular fitness presented with complaints of left lower-leg pain. The patient described a ‘‘deep-aching’’ pain in the lower one third of her leg. Over the past 3 months, pain increased with continuation of the patient’s walking program and began to occur at night, eventually resulting in limitation of activity. Her medical history was significant for osteoporosis and systemic lupus erythematosus, which was treated with multiple medications. Neurovascular and physical examinations were grossly normal. No swelling was observed, but palpation revealed mild tenderness along the distal tibia. Plain radiographs did not reveal the presence of a fracture or periosteal reaction. An MRI was ordered to differentiate between the suspected longitudinal stress fracture and possible MTSS and subsequently demonstrated a longitudinal stress fracture in the tibial metaphysis with surrounding bone edema (Fig. 20-5). Conservative treatment involving a range-of-motion boot and nonweight-bearing ambulation was recommended. Six weeks following treatment, plain radiographs demonstrated a slight callus formation, indicative of the healing process. As a result, the patient was instructed to progress from partial to full weight-bearing ambulation over a 4-week period. Full weight-bearing ambulation in a range-of-motion boot
Figure 20-5 Magnetic resonance imaging portraying the longitudinal signal change in the distal tibia typical of a longitudinal tibial stress fracture.
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4 PEARL
CHAPTER 20
Chronic leg pain
continued for an additional 4 weeks, with subsequent introduction of a regular shoe. At 41/2 months, the patient resumed her walking program with a gradual increase in mileage.
Anterior compartment Deep peroneal nerve
Superficial peroneal nerve Saphenous nerve
Fibula
CHRONIC EXERTIONAL COMPARTMENT SYNDROME Chronic ECS of the lower leg generally is induced by exercise that impairs neuromuscular function within the involved compartment and is characterized by pain and swelling.62,63 This syndrome is classified into two forms: acute, the more severe form requiring immediate surgical intervention, and chronic.62,64-72 Acute ECS, commonly caused by trauma, occurs when intracompartmental pressure is elevated to such a degree that immediate decompression is necessary to prevent intracompartmental necrosis.62,64,65,69 Conversely, the chronic form of ECS develops when exercise sufficiently raises intracompartmental pressure to produce small vessel compromise, which subsequently causes ischemia and pain,66,68,73 but not to the degree exhibited in the acute form.62,65 Athletes exhibiting chronic ECS who continue or increase training are at greater risk of developing acute ECS.65,67,71 Chronic ECS often presents in bilateral form in young athletes with equal incidence in males and females and typically is observed in runners or participants in sports involving ball or puck.3,8,63,74-76 Anterior chronic ECS is more common than the lateral and posterior forms of this syndrome (Fig. 206).3,8,30,63,66,74,76-78 Although symptoms of chronic ECS, such as pain, muscle weakness, numbness, and swelling are general, the onset and subsidence patterns are specific to the condition.64-66,74 Symptoms resolve after activity is discontinued but generally return at the same interval or intensity at the next training session.3,8 Although the etiology of chronic ECS is not as well understood as that of the acute form, raised intracompartmental pressure resulting in relative ischemia of the involved muscles is likely the pathophysiologic mechanism producing this condition.1,63,69,70,74,75,79 Repeated muscle contractions during exercise cause an increase in muscle volume by as much as 20% because of fiber swelling and increased intracompartmental blood volume.62,65,66,74,78 The resulting increase in compartmental pressures is transient and typically will normalize within 5 minutes of completing exercise in asymptomatic people.66,76,80,81 In chronic ECS, however, intracompartmental pressures may remain abnormally high for 20 minutes or longer after exercise before returning to normal.64,77,82
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Tibia
Lateral compartment
Tibial nerve Deep posterior compartment
Superficial posterior compartment
Figure 20-6 Cross-sectional view demonstrating the compartments of the lower leg and associated anatomy.
Several theories have been proposed to explain tissue ischemia, the main symptom of chronic ECS. The first theory suggests that increased compartmental pressure during exercise causes arterial spasm, which results in decreased arterial inflow.74,83 An alternative hypothesis asserts that transmural pressure disturbances produce arteriolar or venous collapse, which subsequently leads to ischemia.74,83-85 Finally, and perhaps more pertinent to athletes, venous obstruction recently has been advocated as a possible cause of tissue ischemia.64,65,69,74 According to this theory, eccentric exercise results in myofiber damage, which causes release of proteinbound ions into the compartment. Such repetitive eccentric contractions therefore cause not only an increase in ion concentration within the compartment but also a subsequent increase in osmotic pressure. This resulting arteriovenous gradient, in which venous pressure is increased and arterial blood flow is decreased, consequently leads to tissue ischemia.64,65,69,74 The association between repetitive eccentric contraction in the anterior compartment of runners and the increased incidence of chronic ECS in the anterior compartment lends support to this theory.63,65,66,74,76,77,86,87
History Patients experiencing chronic ECS may complain of cramping, burning, or pain over the involved compartment(s) with exercise (Case Study 4). Pain associated with anterior chronic ECS may not be limited to the compartment but also may radiate to the ankle and foot. The most characteristic symptom of chronic ECS is pain occurring at a fixed point in the patient activity. The pain will become progressive with continued exercise
Chronic exertional compartment syndrome
or increased intensity but often will dissipate or cease with rest, usually within 20 minutes of completion of activity. Although this pattern of pain relief is observed in the majority of athletes with chronic ECS, it is not unusual for pain to ensue for a longer period. In extreme cases, pain may be constant. In addition, patients with anterior and deep posterior compartment syndromes occasionally describe paresthesia in the dorsum of the foot or in the instep, respectively. In severe cases, transient footdrop may occur.
Physical examination Results of physical and neurocirculatory examinations in patients exhibiting chronic ECS are normal before exercise. Because pre-exercise examinations may not yield insight into the condition, examinations also must be conducted after the patient has performed the exercise that initiates the symptoms. Following exercise, a sensation of increased fullness, swelling, tension, or increased leg girth may be produced in the involved compartments. The leg also may be tender over the involved muscles. This diffuse muscular tenderness must be distinguished from that associated with superficial nerve entrapment, which usually is focal at the site of entrapment. In cases of severe chronic ECS, muscle weakness and paresthesia to a light touch may be observed. Pulses, however, will remain normal in all cases of chronic ECS.
Figure 20-7 (A) Hand-held compartmental pressure measurement device (Stryker Instruments, Kalamazoo, Mich.). (B) To ensure accurate compartmental pressure measurements, the patient should be placed in a supine position with the knee extended.
in a supine position with the knee extended and the ankle in neutral dorsiflexion (Fig. 20-7, B). The needle tip location and depth of penetration must be controlled to obtain reliable measurements.88 Pressure measurements are taken before exercise and at 1 minute and 5 minutes following exercise. If 5-minute measurements are borderline, 15-minute compartmental pressure measurements are obtained following exercise. We use the compartmental pressure measurement guidelines to establish a diagnosis of chronic ECS and are supported by other surgeons, as summarized in Table 20-1.65,76,81 Pressures usually return to normal within 3 to 5 minutes after exercise in patients without this condition.20 If elevated pressures continue for 5 to 10 minutes, chronic ECS is diagnosed. 453
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Diagnostic studies In addition to physical examination, diagnostic testing, such as radiographs, bone scans, electrophysiologic testing, and MRI/magnetic resonance angiography (MRA) may assist in differentiating other possible lower leg conditions from chronic ECS. Radiographs typically are normal in cases of chronic ECS. Although rarely positive in chronic ECS, bone scans also should be obtained to eliminate MTSS and stress fracture diagnoses. Electrophysiologic testing generally is not necessary but may be beneficial in documenting the extent of motor loss in patients with footdrop. An MRI/MRA is recommended only when symptoms are accompanied by a visible or palpable mass in the leg or when clinical evidence suggests possible popliteal artery compression. The most useful diagnostic tool to confirm chronic ECS is compartmental pressure testing.3,20,87 Although many authors advocate performing pressure tests before,20,65,81,88 during,19,20,79,88-92 and after exercise,20,65,88,93 we prefer pre-exercise and postexercise testing only and do not recommend that measurements be obtained during exercise because of technical difficulties and the unreliability of measurements. The slitcatheter technique, which we use, involves the injection of small amounts of local anesthetic into the skin using an 18-gauge needle and a hand-held compartmental measurement device (Fig. 20-7, A). Patients are placed
CHAPTER 20
Table 20-1
Chronic leg pain
Compartmental pressure measurement guidelines for establishing chronic exertional compartment syndrome
Source
Pre-exercise
1-min postexercise
5-min postexercise
15-min postexercise
Edwards PH, Myerson MS65
15 mm Hg
30 mm Hg
20 mm Hg
N/A
Pedowitz RA, et al.76
15 mm Hg
30 mm Hg
20 mm Hg
N/A
Rorabeck CH82
15 mm Hg
N/A
N/A
15 mm Hg
Treatment ............................................................. Conservative Although some authors solely advocate surgical management for the treatment of chronic ECS, we recommend beginning with nonoperative treatment to address the extrinsic and intrinsic factors that contribute to the condition.8 Modification of extrinsic factors, including training surface, shoe design, and training intensity may decrease the symptoms of chronic ECS. Muscle imbalance, flexibility, and limb alignments are intrinsic factors that may be addressed with either strengthening and stretching exercises or orthoses. A short-leg cast used for approximately 4 weeks may cause atrophy of the leg musculature that in turn may alleviate symptoms. Biomechanical abnormalities also should be addressed and corrected, usually with an orthotic, before training is resumed. Because identifying and modifying all risk factors contributing to chronic ECS is difficult, many athletes may continue to have symptoms of chronic ECS on resumption of activity and may be unable to return to competition.73 In such cases, an operative approach may be warranted to enable return to the previous level of intensity. Operative The surgical technique for treating chronic ECS involves decreasing intracompartmental pressure, as depicted in Fig. 20-8.6,72,74,86 Fasciotomy generally is recommended if symptoms persist for at least 3 months and produces favorable results, especially in the anterior and lateral forms of the condition.36,63,65,68,73-75,77,81,88,93-95 Care must be taken to identify and protect the superficial peroneal nerve. In case of concomitant superficial peroneal nerve entrapment, release of any fascial tethering or compression also may be performed. To prevent postoperative fascial scarring, early passive and active rangeof-motion exercises are implemented and weight-bearing ambulation as tolerated is permitted within 2 weeks following surgery.65,74,77 Patients may begin exercise on a stationary bicycle at 2 weeks postoperatively, followed
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by isokinetic strengthening exercise 3 to 4 weeks after surgery. Running may be initiated 5 to 6 weeks postoperatively, with speed and agility drills added during the eighth week.65,74 Athletes generally return to full sports participation within 8 to 12 weeks following surgery.
4 PEARL Patients are able to predict the time of symptom onset. The physical examination typically is normal at rest. For the most accurate diagnosis, it is imperative to perform compartmental pressure testing after activity that initiates symptoms.
C A S E S T U D Y 4
A 15-year-old, female soccer player presented with complaints of bilateral leg pain during activity. The patient had been diagnosed with chronic ECS approximately 1 year ago and underwent bilateral fasciotomies of four compartments at another facility. After her initial postoperative rehabilitation, pain recurred on exercise. A second bilateral fasciotomy of four compartments was performed, followed by recurrence of symptoms. Presently, pain developed approximately 15 minutes after beginning soccer practice and increased until activity ceased. The current evaluation revealed a normal examination at rest, with well-healed surgical incisions. It was noted that the medial incision was quite proximal. Compartmental pressure measurements after provocative exercise confirmed bilateral compartment syndrome, based on pre-exercise and 1-minute and 15-minute postexercise readings. The 1-minute and 15-minute postexercise measurements were greater (continued on page 456)
Chronic exertional compartment syndrome
i
Soleus fascial bridge ii
iii
Tibia
Saphenous nerve and vein
A Superficial peroneal nerve i
ii
B
iii
iv
Intermuscular septum
Figure 20-8 (A) Fasciotomy technique for decompression of superficial and deep posterior compartments used for the treatment of chronic exertional compartment syndrome (ECS). i, A longitudinal incision is created on the posteromedial aspect of the leg. ii, The tibial posterior border is exposed, allowing full visibility of the saphenous vein and nerve. iii, The soleus bridge is released providing exposure of the posterior compartments. iv, The affected compartment is incised, using scissors or a fasciotome to extend the fasciotomies proximally and distally. (B) Fasciotomy technique for decompression of anterior and lateral compartments used for the treatment of chronic ECS. i, A longitudinal incision is created on the anterolateral aspect of the leg, midway between the tibia and fibula. ii, Following exposure of the fascia, a transverse incision is created. iii, The intermuscular septum is identified to assist in locating the superficial peroneal nerve. Care must be taken to avoid the superficial branch of the peroneal nerve, which crosses laterally to anteriorly approximately 10 cm above the ankle. iv, The appropriate compartment is incised, using scissors or a fasciotome to extend the fasciotomies proximally and distally.
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Chronic leg pain
than 21 mm and 17 mm Hg, respectively, in all compartments. Edwards performed a third surgery involving bilateral fasciotomies of four compartments. Because of the proximal position of the medial incision and the suspicion that the soleus bridge previously was unreleased, a new 10-cm medial incision was created to be used in addition to the previous midleg lateral incisions. The soleus bridge subsequently was released. Recurrent scarring of the anterior and lateral fasciotomy incisions was noted, and repeat extensile releases were completed. The patient recovered fully and returned to full activity at 12 weeks postoperatively, including twice-daily soccer practice.
NERVE ENTRAPMENT Lower extremity nerve entrapment is a mechanical irritation of a peripheral nerve caused by impingement.96,97 The common peroneal, superficial peroneal, and saphenous nerves are the most at risk for entrapment, which may produce neurogenic leg pain in the athlete (Fig. 20-9).98-103 Trauma is a primary cause of all three forms of entrapment.100,103 Superficial peroneal nerve entrapment also is observed in dancers and athletes in a wide variety of sports, including bodybuilding, horse racing, running, soccer, and tennis.96,98,100,103 Common peroneal nerve entrapment often is associated with repetitive exercises involving inversion and eversion, which often occur in running and cycling.96,99,100 External compressive sources, such as tight plaster casts and anterior cruciate ligament (ACL) braces, and internal compressive sources, including osteophytes or proximal tibiofibular joint ganglion cysts, also may cause common peroneal nerve entrapment.100,103,104 Knee surgery also may cause common peroneal and saphenous nerve entrapments,100,105 the latter of which also may result from inflammatory conditions such as thrombophlebitis.105 Superficial peroneal nerve entrapment, caused by either trauma or fascia hernias, is the most common type of nerve entrapment that we have observed. Although the causes of nerve entrapment are well established, the mechanism responsible for this syndrome is unknown.99,102 Certain factors, however, predispose nerves to entrapment. Nerves coursing through soft tissues are particularly at risk for entrapment. Nerves branching near joints also are at increased risk for entrapment because joints are associated with a high volume of movement and are common sites of trauma.97,104 Additionally, nerves, as opposed to circulatory and lymphatic vessels, are susceptible to
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Figure 20-9 Common sites of nerve entrapment in the lower extremity. (A) Common peroneal nerve entrapment occurs as the nerve wraps around the head of the fibula and exits the peroneal tunnel. (B) Entrapment of the superficial branch of the peroneal nerve typically occurs as it pierces the deep fascia of the lateral or anterior compartments of the leg. (C) A common site of saphenous nerve entrapment occurs where the nerve branches, approximately 15 cm proximal to the medial malleolus.
impingement because of inherent inelasticity.97 Because nerves lack independent movement, impact or compression from either trauma or internal pressure may cause entrapment.
History Patients suffering from nerve entrapment of the lower extremity typically present with pain that is aggravated with continued exercise. Common peroneal nerve entrapment pain is located in the region of nerve compression and is referred to the lateral leg and foot. In contrast, pain associated with superficial peroneal nerve entrapment involves the lateral calf and/or dorsum of the foot (Case Study 5). Saphenous nerve entrapment often occurs just above the medial malleolus, leading to local pain and referred pain to the dorsum of the foot medially (Case Study 6). Numbness, often described as a burning sensation, also may be observed with all
Nerve entrapment
Physical examination The lower back, hips, and ankle joints should be examined to confirm that an overriding neurologic condition is not present. Fascial hernia also should be ruled out. Range of motion of all leg joints and stability of the knee and ankle should be assessed. Compression or percussion of the nerve is the hallmark test used to determine a diagnosis of nerve entrapment. A tingling sensation along the nerve or at its exit from the fascia is indicative of entrapment syndrome. Tingling typically will be elicited at the level of the fibular neck radiating distally in common peroneal nerve entrapment. Alternatively, in superficial nerve entrapment, tingling will occur 7 cm to 12 cm above the lateral malleolus, whereas tingling will radiate from just above the medial malleolus and more distally on the medial foot in saphenous nerve entrapment. Diagnostic studies Roentgenograms, MRI, compartmental pressure tests, electromyography (EMG), nerve conduction, and/or nerve block are possible diagnostic tests conducted to confirm the diagnosis of nerve entrapment.100,101,106 Radiographs typically are normal in nerve entrapment syndromes but assist in identifying possible compressing bony lesions and in excluding stress fractures and bone tumors.101,106 An MRI is recommended if a pressure-causing mass is suspected. Compartmental pressure tests may be conducted to distinguish between chronic ECS and nerve entrapments,98,101,106 because elevated compartment pressures are indicative of chronic ECS. To differentiate between common and superficial peroneal nerve entrapments and to locate the anatomic point of compression, EMG and nerveconduction studies are recommended and should be performed before and after exercise.100,101 A nerveconduction velocity of less than 40 m/sec is considered abnormal and is indicative of nerve entrapment of the lower extremity.107 If superficial nerve entrapment is suspected on the basis of any of the aforementioned diagnostic tests, a nerve block should be performed. The anesthetic should be injected where the Tinel’s sign is the strongest or at the location corresponding to maximal pain on pressure. Immediate pain relief following injection is suggestive of nerve entrapment.96,97,102,103,105
Treatment ............................................................. Conservative Conservative treatment for nerve entrapment includes modification of precipitating activity, biomechanical correction, physiotherapy, and/or soft-tissue massage.98,100,103 NSAIDs used in conjunction with tricyclic medications such as amitriptyline and, occasionally, gabapentin may alleviate the pain and associated swelling of all three forms of nerve entrapment.103 Iontophoresis is another option that we prefer because of its less invasive nature in comparison with a nerve block. However, nerve blocks may be necessary if iontophoresis fails. Because constrictive clothing and/or devices, including ACL braces or patellar tendinitis straps, place additional stress on the nerves, the use of these devices is not recommended during treatment.100,103 Operative Although common peroneal and saphenous nerve entrapments often are successfully treated by conservative measures, superficial peroneal nerve entrapment typically requires surgical treatment.100,103 If surgery is warranted, fasciotomy is performed to expose the nerve, and, if necessary, is followed by external neurolysis.98-100,105,106 In our experience, however, fasciotomy alone typically is sufficient. In common peroneal nerve entrapment, resection of osteophytes, ganglion cysts, or other obstructions may be necessary before neurolysis is performed.100,103 In rare cases of trauma-induced saphenous nerve entrapment, neuroectomy may be required.10,102,105 Because of the increased risks associated with neurologic surgical procedures, including neuromas and reflex sympathetic dystrophy, surgical treatment requires a thorough knowledge of the peripheral neuroanatomy.103 To minimize such risks, the nerve should be manipulated as little as possible and the surrounding soft tissue should be relatively undisturbed.103 Activity may be increased gradually on wound healing.
4 PEARL A careful history and physical examination should be conducted to rule out referred pain or an overriding neurologic condition. A positive Tinel’s sign is highly suggestive of nerve entrapment. If physical examination and all diagnostic tests, including compartmental pressure measurements, are normal, nerve compression often is the source of the pain. The fascial exit of the superficial peroneal nerve is variable, ranging from approximately 7.5 cm to 12.5 cm from the tip of the lateral malleolus.
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compressive neuropathies. In addition, some patients may experience localized swelling. Diffuse swelling, on the other hand, is indicative of chronic ECS or a systemic problem. Finally, motor weakness, such as footdrop, typically is observed late in common peroneal nerve entrapment.
CHAPTER 20
Chronic leg pain
C A S E S T U D Y 5
A 30-year-old, male runner presented with complaints of lateral leg pain and foot numbness. The symptoms progressed after he began an aggressive running program during the prior year. The pain was described as sharp and tingling and typically occurred over the mid to distal aspect of his lateral leg during running. He denied a history of injury. On physical examination, a small prominence of soft tissue was noted over the painful area. ‘‘Lightning-like’’ sensations and paresthesias corresponding to the superficial branch of the peroneal nerve were elicited on percussion. Gross neurovascular examination, including sensation, otherwise was normal. After conservative treatment, including failed iontophoresis, a fasciotomy was performed to release the nerve. Postoperatively, activity gradually was increased, with resumption of training at 6 weeks.
C A S E S T U D Y 6
A 52-year-old, avid golfer presented with a 3-month history of distal medial leg pain. The pain increased with activity and radiated to the dorsum of the foot. Initially, pain was mild but progressed to the point at which the patient was unable to complete a round of golf without significant pain. NSAIDs and ice were implemented without improvement. Although the patient initially denied a history of trauma, on further inquiry, he recalled that he had hit his distal tibia approximately about the medial malleolus on his daughter’s bicycle 3 months before the present complaint. Physical examination revealed full range of motion, with no swelling or cutaneous changes about the distal third of the leg. In addition, no tenderness was observed over the medial distal tibial cortex, and a vibratory test was negative. However, a positive Tinel’s sign over the saphenous nerve above the medial malleolus was elicited, reproducing the distal-radiating pain. On the basis of these clinical findings and the traumatic nature of the injury, a diagnosis of posttraumatic saphenous neuritis was established. Conservative treatment comprising NSAIDs, ice, and iontophoresis was prescribed. Symptoms improved markedly at 2 weeks following treatment and completely resolved by 4 weeks, enabling the patient to return to regular activity.
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POPLITEAL ARTERY ENTRAPMENT SYNDROME PAES is more common in athletes than in the general population, especially as a result of increased participation in competitive sports.6,108 This condition results from an abnormal relationship between the popliteal artery and the surrounding myofascial structures (Fig. 20-10), producing calf pain on exertion.6,108-111 PAES is progressive and, in more severe cases, may result in occlusion of the popliteal because of compression from the medial head of the gastrocnemius muscle.6,108 Although PAES is a possible diagnosis in any athlete with calf pain and intermittent claudication, it is predominantly observed in males under the age of 30.6,108-110,112-122 This condition typically occurs unilaterally6,111,114,117,118,121,123 but may be observed bilaterally at an incidence as high as 67%.108,109,114,116,123 PAES often results from high-intensity exercise with excessive dorsiflexion and plantarflexion of the ankle, which commonly occurs in football, basketball, soccer, and running.6,108,111 Two forms of PAES, anatomic and functional, have been suggested to explain the mechanism of this condition.6,108,109,114 In anatomic PAES, an abnormal relationship between the popliteal artery and the surrounding myofascial structure occurs during embryonic development as the medial head of the gastrocnemius muscle migrates medially and cranially. The popliteal artery becomes entrapped during this migration and subsequently is swept medially with the gastrocnemius. Rignault et al. proposed the functional theory after observing no anatomic abnormalities within the popliteal fossa during surgical exploration.108,124 According to this theory, muscle contraction, particularly active plantarflexion of the ankle, compresses the artery between muscle and the underlying bone. This functional theory was further substantiated by Turnipseed and Pozniak,125 who also provided an explanation for claudication by suggesting involvement of the popliteal nerve. It was hypothesized that entrapment may be due to compression of the popliteal neurovascular bundle against the lateral condyle of the femur.125 Repetitive muscle contraction from plantarflexion causes trauma on the popliteal nerve, resulting in the subsequent neuromuscular form of claudication.125
History PAES should be considered in the differential diagnosis of healthy young patients presenting with complaints of intermittent pain typically involving the foot and leg (Case Study 7). Pain, described as a deep ache or cramping, generally is posterior in location and typically occurs
Popliteal artery entrapment syndrome
Figure 20-10 Normal course of the popliteal artery versus possible aberrant pathways involving the medial head of the gastrocnemius muscle that cause popliteal artery entrapment syndrome (PAES) (popliteal artery ¼ dark, popliteal vein ¼ striped, tibial nerve ¼ white). (A) Normal course of the popliteal artery in which the artery and vein course distally between the heads of the gastrocnemius muscle, over the popliteus muscle, and beneath the soleus muscle. (B) The popliteal artery deviates medially, wraps around the medial head of the gastrocnemius muscle, and then resumes the normal distal course. (C) The popliteal artery deviates medially, wraps around the medial head of the gastrocnemius muscle, and abnormally courses beneath the popliteus muscle, consequently becoming entrapped. (D) The popliteal artery courses normally but is compressed by the medial head of the gastrocnemius muscle, which is positioned laterally to its normal insertion. (E) The popliteal artery courses normally but is entrapped between the medial head and an accessory tail of the gastrocnemius muscle. (Modified from Rich NM, et al: Arch Surg 114:1377, 1979.)
...........
459
CHAPTER 20
Chronic leg pain
after vigorous exercise. It is important to note, however, that claudication may be atypical early in the course of this condition, because it may occur with walking and not with prolonged leg exercise. Symptoms occurring less frequently include numbness, tingling, or coolness of the foot; these symptoms may be relieved by changing leg positions.
activity is the only suggested form of conservative treatment. Because this is not a viable option for many athletes, a surgical approach may be warranted.6,130
Physical examination Physical examination often is normal at rest in PAES cases, especially if the artery is still patent. Compartments may be soft, and palpation of the bone and soft tissues may not elicit tenderness. Bilateral pulses should be examined to determine whether reduction in pulse volume exists between limbs. The pulse should be palpated with the ankle in passive dorsiflexion or active plantarflexion with the knee in extension because this maneuver places tension on the gastrocnemius muscle and will lead to extrinsic compression of the popliteal artery. On auscultation, a bruit may be heard after provocative exercise, but the significance of this observation is unclear because it also may be observed in a normal athlete.
To prevent long-term arterial damage, early operative treatment is recommended if PAES recurs following resumption of activity.110,127,128,131 The principles involved in surgical treatment of PAES include releasing the entrapped nerve and restoring normal arterial flow. If the physical examination did not indicate evidence of arterial damage, a myotomy is performed with the release of the offending fibrous band.108,110,128 However, if the condition is more advanced and involves popliteal endofibrosis or arteriosclerosis, endarterectomy and vein-patch angioplasty is recommended.110,118,128 In cases of complete occlusion, a saphenous vein-bypass graft is required.110,118,123,128
Diagnostic studies Doppler sonography is recommended when PAES is suspected.6,108,123,126 Pulses should be measured in a neutral position and also while the leg is maneuvered toward knee hyperextension and ankle dorsiflexion.6,111,119,126 Obliteration of the pulse or reduction in pulse pressure after exercise is suggestive of PAES.6,108,110,116,120,127 If Doppler sonography indicates PAES, arteriography is recommended to confirm the diagnosis.108,113,119,128 Often referred to as the ‘‘gold standard test’’ of PAES, arteriography is an invasive procedure involving radiographic imaging after injection of a radiopaque material into the suspected arterial segment.108,118,120 Because arteriography may be normal in PAES when the ankle is in the neutral position and the knee is extended, it is important to repeat the studies bilaterally after exercise or with the ankle in positions of provocation, because extrinsic arterial obstruction may be demonstrated with ankle plantarflexion.6,112,119,122,127-129 MRI/MRA also may be beneficial in evaluating PAES.128,129 Compartmental pressure measurement testing and three-phase bone scans are recommended to rule out chronic ECS and stress fractures, respectively.
Treatment ............................................................. Conservative Because PAES typically recurs on activity and may lead to long-term arterial damage if untreated, avoidance of
...........
460
OPERATIVE
4 PEARL The knee may be warm on palpation because of increased collateral circulation. Bilateral pulses with provocation should be examined to determine whether reduction in pulse volume between limbs exists. If PAES is suspected on the basis of Doppler sonography, arteriography should be performed to confirm the diagnosis.
C A S E S T U D Y 7
A 19-year-old, female, competitive soccer player presented with complaints of bilateral leg pain. Pain, described as a dull ache in the posterior aspect of both legs, began during workouts. The pain continued to intensify until cessation of activity was required. However, the pain resolved after a short rest period of 5 to 10 minutes. This pattern of intense pain during activity followed by relief after rest continued without progression with every successive practice and competition. The initial physical examination did not reveal any abnormalities, as demonstrated by soft compartments, no
Operative
Figure 20-12 Intraoperative photograph illustrates the abnormal pathway of the popliteal artery as it courses medially to the head of the gastrocnemius and anteriorly to the popliteus muscle indicative of popliteal artery entrapment syndrome (PAES). (Image courtesy Paul Cook MD, Riverside Methodist Hospital, Columbus, Ohio.)
461
...........
Figure 20-11 Arteriograms obtained following provocative active plantarflexion and passive dorsiflexion with a straight leg, demonstrating normal flow (A) compared with the decreased flow (B) associated with popliteal artery entrapment syndrome (PAES). (Images courtesy Louis J. Unverferth, MD, Riverside Methodist Hospital, Columbus, Ohio.)
tenderness on palpation, and normal neurovascular findings. Radiographs and resting compartmental pressure measurements were normal. In an attempt to reproduce the patient’s symptoms, the patient was instructed to exercise and subsequently returned with complaints of posterior calf pain and mild tenderness on deep palpation of the calf. During this symptomatic period, neurovascular examination and compartmental pressure measurements remained normal. A subsequent three-phase bone scan and MRI also were normal. As a result, conservative treatment consisting of rest was implemented for 1 month. The patient returned for evaluation because of continued symptoms, but the physical examination remained normal. Compartmental pressures were reevaluated at pre-exercise and postexercise intervals and remained within normal limits. Examination of pedal pulses demonstrated normal dorsalis pedis and posterior tibial artery pulses. However, when this measurement was repeated with active plantarflexion or passive dorsiflexion with a straight leg, loss of all pulses was observed bilaterally. To confirm a diagnosis of PAES, an arteriogram with provocative maneuvers was performed and demonstrated loss of flow at both popliteal arteries (Fig. 20-11). Because the patient desired to continue competitive soccer, she elected to undergo surgical release of the entrapped popliteal artery. Surgical inspection revealed a popliteal artery coursing medially to the head of the gastrocnemius muscle and anteriorly to the popliteus muscle belly (Fig. 20-12). These areas of entrapment then were released. After wound healing, the patient gradually increased activity over a 6-week period and returned to competitive soccer 3 months postoperatively.
CHAPTER 20
Chronic leg pain
SUMMARY The most common conditions involving lower leg pain in athletes are MTSS, stress fractures, chronic ECS, nerve entrapment, and PAES. Similarities of symptoms among these conditions make diagnosis difficult. The challenge for the sports medicine specialist is to differentiate among these similarities to establish an accurate diagnosis. Although pain is the hallmark symptom in all of these conditions, subtleties exist in the location and occurrence of pain among the various conditions. Therefore determining whether the pain is generalized or localized and isolating the onset and diminishment of pain will assist in determining the appropriate
Table 20-2
diagnosis, as summarized in Table 20-2. Keys to making an accurate diagnosis include conducting a thorough history, performing an exhaustive physical examination (Table 20-3), and using the appropriate diagnostic tools to distinguish further among these conditions (Table 204). Once a diagnosis is established, the preferred treatment is conservative management, consisting of rest from activity and modification of extrinsic and intrinsic factors. Treatment should be individualized according to the patient’s symptoms and involve gradual rehabilitation and return to activity. Although a conservative approach typically is successful, surgical intervention may be required for cases in which conservative treatment has failed or for diagnoses of nerve entrapment and PAES.
Pain locations of the common lower-leg conditions
Leg condition
Localized or generalized
Location of pain
MTSS
Generalized
Posteromedial distal 1/3
Stress fracture
Localized
Bony tenderness above distal 1/3
Chronic ECS
Generalized
Involved compartments with exercise
Nerve entrapment
Localized
Fascial exit site
PAES
Generalized
Posterior with exercise
ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome.
Table 20-3
Physical examination observations of common lower-leg conditions
MTSS
Stress fracture
Chronic ECS
Nerve entrapment
Edema/ warmth
Posteromedial distal 1/3
Over site
No
No
Possible around knee
Paresthesias
No
No
Rarely
Often
Rarely
Pedal pulse
Normal
Normal
Normal
Normal
Pedal pulses with provocation
Palpation tenderness
Posteromedial distal 1/3
At site
Involved compartment(s) with exercise
Possible at site of compression
Posterior with exercise
ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome.
...........
462
PAES
Diagnostic studies useful in distinguishing among common lower-leg conditions*
Diagnostic study
MTSS
Stress fracture
Chronic ECS
Nerve entrapment
Roentgenograms
Recommended
Recommended
Recommended
Recommended
Not recommended
Normal
Periosteal reaction/early callus after 10-14 days
Normal
Normal
N/A
Recommended
Recommended
Not routinely recommended
Not recommended
Not routinely recommended
Linear uptake
Focal uptake
Normal
N/A
Normal
Not routinely recommended
Not routinely recommended
Not routinely recommended
Not routinely recommended
Not recommended
Signal changes
Bone edema
Normal
Normal
N/A
Not recommended
Not recommended
Not recommended
Not recommended
Recommended
N/A
N/A
N/A
N/A
Flow with provocation
Not recommended
Not recommended
Recommended
Not routinely recommended
Not routinely recommended
N/A
N/A
15 mm Hg at rest; >20mm Hg 5-min postexercise
Normal
Normal
Not recommended
Not recommended
Not recommended
Not recommended
Recommended
N/A
N/A
N/A
N/A
Obstruction with provocation
Bone scan
MRI
MRI/MRA
Compartmental pressure test
Arteriography
PAES
Summary
ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome. *The upper portion for each diagnostic study represents our recommendation; the lower portion indicates the results corresponding to the diagnosis.
463
............
Table 20-4
CHAPTER 20
Chronic leg pain
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Chronic leg pain
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.........................................C H A P T E R 2 1 Foot and ankle injuries in dancers John G. Kennedy, Christopher W. Hodgkins, Jean-Alain Columbier, and William G. Hamilton CHAPTER CONTENTS ...................... Introduction
469
Anterior ankle
477
Metatarsophalangeal joint
470
Posterior ankle
477
Great hallux interphalangeal joint
472
Achilles tendon
479
Lesser metatarsophalangeal joints
472
Heel pain
480
Metatarsal injuries
473
Leg pain
481
The medial ankle
474
Summary
482
Lateral ankle
475
References
482
INTRODUCTION Ballet has all the elements of the arts in its makeup— drama, poetry, literature, painting, sculpture, design, music, and, of course, dance. Dancers, both male and female, are the physical means by which the choreographer sculpts a composition of expressive motion. The grace and art of the ballet performance belie the great physical strain on the body as a whole and the foot and ankle in particular. From an early age the dancer must learn to be an artist, gymnast, and athlete. Most ballet dancers train for a minimum of 10 years before attaining the skill set necessary to join a corps de ballet. Very few dancers develop into soloists and fewer still attain the role of principle ballerina. Throughout this time of training, the body is placed under great strain, and it is by a process of natural selection that those dancers who are flexible and technically proficient survive the rigors of training to advance further. Female dancers spend a considerable time en pointe, or on the points of the toes (Fig. 21-1), whereas male dancers tend not to dance on their toes and spend much of their time in turning, lifting, and holding ballet dancers. As such, male and female dancers tend to present with distinct injuries. In addition to the myriad of physical injuries related to female dancers that follows, female
dancers also are prone to the triad of anorexia, amenorrhea, and osteoporosis. This unfortunate triad stems from the significant pressure on dancers to weigh less and less. The most disturbing data suggest that female dancers weigh more than 15% below the ideal weight for height. This has metabolic consequences leading to stress fractures and slower union rates in injured female dancers.1 In contradistinction, male dancers have fewer metabolic problems but are prone to overuse injuries from repetitive motion and to stress fractures from the sudden deceleration of large leaps, vole´, saute´, or jete´. Dancer’s feet are the instruments on which their art depends. They require, in addition to an extraordinary flexibility and strength, a particular anatomic profile. Over time a dancer’s foot will evolve and only the strongest will survive. Dancers’ feet typically are ‘‘intrinsic plus:’’ they have narrow metatarsal width with straight toes. (Intrinsic-minus feet have wider metatarsal splaying and clawing of the toes.2) Apart from muscle strength, dancers’ feet require great flexibility. In the releve´ position (Fig. 21-2) the ankle is in a vertical position—90 degrees of plantarflexion of the ankle-foot complex. The dancer also requires 90 to 100 degrees of dorsiflexion in the first metatarsophalangeal (MTP) joint to go from releve´ to en pointe. These are extraordinary ranges of motion and can only be achieved with years of practice, which mold the young ballet dancer’s
CHAPTER 21
Foot and ankle injuries in dancers
to the first and fifth metatarsal. However, dancers do not have the same problems associated with transfer metatarsalgia as does the general population with this foot configuration. 2. Egyptian foot. Long first ray relative to the central metatarsals. This can predispose the first MTP joint to degenerative arthrosis or hallux rigidus. 3. Simian foot. Metatarsus primavarus with hypermobile first ray that causes transfer metatarsalgia to central metatarsal heads. 4. Peasant foot. Uniform metatarsal length, giving broad, square foot. Its stability makes it an ideal platform for dancing. 5. Model’s foot. This foot is long and slender with a taper exaggerated cascade from first to fifth metatarsal head. As such, it bears weight unevenly on demi-pointe and is a poor foot for dance. The following is a review of the more common dance injuries and problems in the foot and ankle. Figure 21-1 Illustration of the en pointe stance.
METATARSOPHALANGEAL JOINT Bunions Although dancing has been said to play a role in the pathogenesis of bunions, it is unlikely that this is the case. Dancers, like the rest of the population, can be either resistant or prone to develop bunions.7 In those dancers that are prone to develop bunions, it is imperative to delay surgical intervention for as long as possible. Bunion surgery adversely affects dorsiflexion of the first MTP joint, a critical motion in dancers. Most bunions can be treated with conservative methods, including toe spacers and horseshoe pads. The senior author has seen several aspiring young dancers whose careers were ended by well-meaning bunion surgery. If a bunion is precluding the dancer from activity and surgery is warranted, then a chevron osteotomy can provide pain relief and stability without compromising motion.
Figure 21-2
Illustration of the releve´ stance (demi-pointe).
bones during the bone growth phase.3-5 As a result of endless practice barres, class, and training, dancers’ feet tend to be cavus and have thickened metatarsals to support when en demi-pointe. Calluses abound secondary to pressure demands on the skin. In general, five types of dancer’s feet have been described:6 1. Grecian (also known as Morton) foot has a relatively long second and third metatarsal in relation
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Hallux rigidus Any restriction to full dorsiflexion of the first MTP joint will prevent the dancer from performing releve´. Many dancers can accommodate by rolling out onto the lateral border of the foot, a process known as ‘‘sickling.’’ The treatment of hallux rigidus depends on the grade of the disease (Fig. 21-3). In grade I disease, the joint is preserved and marginal osteophytes can be resected, with excellent outcome expected. In grade II disease, the joint is involved, with minor cartilage destruction evident as joint space narrowing on plain radiograph. Treatment involves resection of marginal osteophytes (cheilectomy). In addition, the
Metatarsophalangeal joint
Illustration of hallux rigidus.
dorsal one third of the metatarsal head is resected.8 Intraoperative dorsiflexion of the hallux greatly overestimates the degree of motion that can be expected following surgery. Just over half of what is achieved at the time of surgery will be evident in the postoperative follow-up examination. It is important that dancers understand that, although surgery will make the condition better, the joint will never be normal. In addition, the length of recovery time must be discussed with the dancer, because a full functional recovery often takes 6 months. To improve functional motion following surgery, a dorsally based closing osteotomy can be used (Moberg). This procedure improves dorsiflexion but at the expense of plantarflexion, and the dancer should be warned of this. In some cases we also can use a shortening scarf osteotomy to decompress the MTP joint and allow reestablishment of the mobility. Grade III hallux rigidus presents with dorsal and lateral osteophytes in addition to clear degenerative arthrosis on both sides of the joint. Arthrodesis, an acceptable surgical option in the general population, is not feasible in a career dancer. To preserve motion, a capsular arthroplasty can be performed with reproducible outcomes9 (Fig. 21-4, A and B). It is important to select these patients carefully because transfer metatarsalgia is common in those patients with a foreshortened first ray.
Injuries to the sesamoid bones ............................................................. The sesamoid bones lie within the substance of the flexor hallucis brevis tendons. They are commonly injured in dancers, particularly in those who fail to perform a plie´ on landing, absorbing the energy of the landing through partially flexed knees. Without such absorption built into a dancer’s technique, sudden deceleration with high impact of the sesamoid bones predisposes to injury.
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Figure 21-3
Sesamoiditis The differential diagnosis of sesamoiditis is lengthy and requires careful history taking and clinical examination. Magnetic resonance imaging (MRI) aids diagnosis. The following is a list of differentials: Stress fracture of the sesamoid bone, Avulsion fracture or sprain of the proximal pole of the sesamoid, Sprain of the distal pole, Sprain of a bipartite sesamoid, Arthrosis of the sesamoid metatarsal articulation, and Preradiographic osteonecrosis of the sesamoids. Several mechanisms are responsible for producing sesamoiditis in dancers. Most of theses can be treated with a felt pad around the sesamoid for relief (‘‘dancer’s pad’’). In general, symptoms resolve without any additional interventions although this may take up to 6 months for full resolution. In those cases requiring further diagnostic testing, a bone scan or MRI can be useful. The medial sesamoid is often bipartite, with rounded edges on plain radiograph, distinguishing it from a recent fracture. In those cases with recalcitrant pain, surgery is warranted. A medial-based incision can locate the medial sesamoid; however, a plantar incision is always needed for a lateral sesamoid. Partial excision is preferred to prevent varus or valgus malalignment. Surgery should be reserved for those patients with symptoms persisting for at least 6 months following initial treatment. Other conditions may mimic sesamoiditis, including instability, bursitis, and nerve entrapment: 1. Sesamoid instability. Rarely, the medial collateral ligament of the tibial sesamoid is torn, causing a clear ‘‘clunk’’ as the sesamoid dislocates laterally when the dancer releve´s. Repair of the medial collateral ligament usually requires release of the lateral ligament as an adjunct. The medial ligament may be frayed or not repairable end to end. In this case, local soft tissue is used to supplement the repair. Care must be taken not to overtighten the medial aspect of the joint and disrupt MTP joint motion. 2. Sesamoid bursitis. Swelling and inflammation within the sesamoid bursa may mimic sesamoiditis. However, careful clinical examination usually can identify a symptomatic bursa when present. Treatment consists of a well-directed local corticosteroid injection to the bursa. Bursitis still may take some time to resolve, and it can be complicated by a fibrous scar that causes repeated symptoms. In such cases, a bursectomy can be performed through a careful plantar incision. Care should be taken in identifying the proper digital nerve, and a precise and meticulous skin closure is critical to a good outcome.
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Foot and ankle injuries in dancers
Extensor hallucis brevis Extensor hallucis longus
Flexor hallucis brevis
Capsule
Flexor hallucis longus
A Figure 21-4 (A) Diagrammatic representation of an interpositional arthroplasty of the first metatarsophalangeal joint. (B) Intraoperative photograph of an interpositional graft in situ.
3. Joplin’s neuroma. Entrapment of the proper digital nerve, adjacent to and, rarely, under the tibial sesamoid, will cause symptoms similar to sesamoiditis. Joplin’s neuroma, however, will display a characteristic nerve compression sign with palpation. In those cases recalcitrant to conservative therapy, neurolysis and transposition of the nerve are required.
Lateral proper digital nerve entrapment The lateral proper digital nerve may be compressed under the deep transverse ligament, causing pain in the great toe on the lateral side. Because of the position of the nerve, a compression test cannot be performed. Diagnosis is made with a selective local anesthetic injection to the nerve. Surgical resection of the transverse ligament is curative.
GREAT HALLUX INTERPHALANGEAL JOINT In young ballet dancers, hyperflexion of the great toe interphalangeal joint (IPJ) can occur when attempting en pointe. Here, weight is distributed over the nail and dorsum of the toe in the pointe shoe. Hyperextension of the great toe IPJ also occurs, usually to compensate for lack of motion in adjacent joints. Rarely does this need surgical intervention, despite radiologic appearances, because the joint is quite accommodating and typically asymptomatic. In those who do complain of symptoms, lambs wool wrapping can help to alleviate the discomfort problem.
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LESSER METATARSOPHALANGEAL JOINTS Metatarsalgia is uncommon in dancers, and when it is encountered the differential diagnosis must include MTP instability and Freiberg’s infraction.
MTP instability As the dancer releve´s the phalanx subluxes dorsally, pushing the metatarsal head plantarward and causing pain. In the demi-pointe position, excessive loads are transmitted through the second and third MTP joints. Clinical examination will elicit a translation in the anterior-posterior (AP) plane that is in excess of the adjacent joints.10 Treatment initially is directed at taping to neighboring toes and stress-relieving padding. Surgical correction includes a very limited resection arthroplasty with a plantar condylectomy. Alternately, a limited Weil osteotomy may be used with screw fixation. Motion is begun early. Scarring at the plantar aspect of the wound facilitates tightening of the redundant plantar plate. Dislocation of the MTP joints Acute injuries should be reduced and immobilized until soft-tissue healing can occur. In cases of delayed diagnosis, reduction often is impossible secondary to scarring and the risk of neurovascular stretching. In such instances, a resection arthroplasty or Weil osteotomy reducing the length of the metatarsal will facilitate reduction. Freiberg’s infraction Dancers have a propensity to develop Freiberg’s infraction equal to that of the general population. In general,
Metatarsal injuries
Preoperative and postoperative radiographs of Freiberg’s infraction.
conventional radiography lags behind clinical symptoms by up to 6 months (Fig. 21-5). Bone scan or MRI facilitate early diagnosis. Four types of infraction occur: Type I: A localized osteonecrosis of the metatarsal head that heals by creeping substitution. No cartilage defect is seen. Type II: Following metatarsal head osteonecrosis, the structural support of the head is lost. New bone formation occurs but is not sufficient to prevent collapse of the head. The articular cartilage is preserved; however, osteophytes on the dorsal lip limit dorsiflexion. Surgical debridement is curative, with exostectomy of the dorsal ridge to facilitate dorsiflexion. Type III: In addition to metatarsal head collapse, the articular cartilage is destroyed. Surgical management includes excision of the dead bone and cartilage and osteophyte resection. The plantar aspect of the joint usually is intact and can be left alone. Type IV: A rare entity with several heads involved. May represent a congenital epiphyseal dysplasia rather than a true infraction.
Idiopathic MTP synovitis Characterized by the appearance of a ‘‘sausage toe,’’ this clinical entity is associated with MTP joint laxity and instability. Anti-inflammatory medication and taping
may provide benefit. If surgical exploration is required, a very limited resection arthroplasty with a plantar condylectomy is used. Alternately a limited Weil osteotomy is performed if the ray is long and plantarflexed relative to adjacent metatarsals. Scarring at the plantar aspect of the wound causes the plantar plate to tighten by scarring fibrosis. Motion is encouraged early to facilitate the flexibility needed by the dancer. This is a fine balance between flexibility and instability.
METATARSAL INJURIES Second metatarsal base stress fracture Most high-level dancers have a mild cavus foot, and despite the mechanical advantages this creates vis-a`-vis technique, the rigidity of the foot places high stresses on the bones on impact.11 In those dancers who start their careers early in life, the metatarsals hypertrophy and the cortices broaden to accommodate the increased stresses placed on them. In certain cases, however, stress fractures occur despite cortical hypertrophy because the repeated microtrauma of dancing exceeds the reparative capacity of the bone. Because of the cuneiforms’ Roman arch configuration, the second metatarsal sits wedged between the medial and lateral cuneiform bones. This causes a relative rigidity to the second ray and consequently a potential site for a 473
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Figure 21-5
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Foot and ankle injuries in dancers
Figure 21-7
Figure 21-6 Stress fracture of the second metatarsal neck.
stress fracture. In fact, this is the most common site for a stress fracture in the dancer’s foot, and when a patient complains of pain and tenderness in the base of the second metatarsal, it should be regarded as a stress fracture until proven otherwise (Fig. 21-6). Conventional radiographs may not show the fracture, but a bone scan or MRI will confirm clinical suspicion in such instances. As the second metatarsal hypertrophies from years of pressure in the demi-pointe position, it may have the appearance of a healing fracture. Again, MRI can be useful in determining the true diagnosis. Acute injuries require a cam walker for up to 6 weeks to allow time for the fracture to consolidate. Cast immobilization usually is not required, provided that the dancer can be trusted to keep the cam walker in place as prescribed. Rarely, a fracture may progress to a delayed union, and in these cases a small ultrasound bone stimulator can be used to accelerate healing.
Fifth metatarsal fractures 1. Spiral diaphyseal fracture of the fifth metatarsal. These fractures occur when the dancer rolls over onto the lateral border of the foot from a demipointe position.12 The fracture invariably heals but may take several months to heal sufficiently to allow further dance. 2. Jones fracture of the proximal diaphysis. This is a difficult fracture to treat in a dancer because it requires extensive time in a nonweight-bearing cast (Fig. 21-7). Nonunions are rare in a nonweight-bearing cast despite the tenuous blood supply. Weight-bearing casts, on the other hand, have a greater risk of nonunion. Should nonunion
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Jones fracture.
occur, a single screw down the diaphysis is required. This may or may not need to catch the medial cortex, depending on the grip of the screw within the diaphysis. Bone graft may be used as an adjunct to help osteosynthesis. If the screw is removed, the fracture has a significant risk of recurring. 3. Avulsion fracture of the fifth metatarsal. Usually caused by sudden inversion of the foot, the peroneus brevis attachment is avulsed, in addition to the lateral band of the plantar fascia and the abductor digiti minimi. In general this injury can be treated with immobilization and rarely requires surgical intervention, because a fibrous union will invariably occur even in the presence of significant distraction of the fragments. In a skeletally immature dancer, this apophysis will not have ossified and the fracture will not be visible on plain radiographs. The diagnosis must be made clinically. The treatment is similar.
Bunionettes Pain over bunionettes usually can be diminished with soft padding or Micropore adhesive tape to reduce friction and callus formation. Surgical resection usually is reserved for a retired dancer because the time to recovery from the procedure is extensive.
THE MEDIAL ANKLE Although posterior tibial tendon pathology is relatively common in other sports, it is rare in dancers. The reasons for this are multiple. Typically a dancer’s foot is cavus, which tends to protect him or her from tibialis posterior pathology in comparison to a more planus foot. Also, when a dancer is in equines, the posterior
Lateral ankle
Figure 21-8 Magnetic resonance imaging (MRI) scan demonstrating coronal (A) and sagittal (B) views of an osteochondral defect (OCD) in the talus.
Medial ankle sprains Medial ankle sprains occur infrequently and are associated with a pronated foot landing off balance. If the foot is in plantarflexion, the anterior deltoid is maximally affected, and the tension is greatest in the deltoid in this position. Similarly, when the foot is flat on the ground and hyperpronated, the tear will occur in the midportion of the deltoid. An accessory bone, the os subtibiale, can be found in the substance of the deltoid. When injured, it may manifest as a trigger point of pain when ligamentous healing should be complete. A local injection of steroid is all that is required to treat this symptom. Chronic strain of the deltoid from poor form in rolling in (pronation) of the foot is a common overuse injury in dancers. Chronic strain of the anterior aspect of the deltoid ligament, anchored to the capsule of the talonavicular joint, may predispose the ankle to chronic rotatory instability. Recalcitrant medial ankle pain also may be caused by osteochondritis dissecans of the talus following a sprain. Clinical suspicion warrants further investigation with
computed tomography (CT) or MRI, which will demonstrate the extent of the lesion (Fig. 21-8, A and B). The size of the osteochondral lesion determines the most appropriate treatment. Microfracture treatment, chondrocyte transplant, allograft implants, and osteochondral grafting are available techniques. Osteochondral autologous transplant surgery (OATS) is indicated for large lesions with cartilage collapse or deficit and extensive underlying bone necrosis. The lesion is cored out of the talus and filled with osteochondral autograft, commonly from a nonweight-bearing location in the lateral femoral condyle (Fig. 21-9, A and B).
LATERAL ANKLE Lateral ankle sprain The most common injury in dancers involves the lateral ligament ankle stabilizers.13 The anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL) are stressed at different ankle positions. The ATFL sprains in a plantarflexed and inverted foot, whereas the CFL is more prone to injury when the foot is dorsiflexed. 475
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tibial tendon is relatively shortened as the subtalar joint is inverted.
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Figure 21-9 (A) Talus after ‘‘coring’’ of the osteochondral defect (OCD). (B) Talus following implantation of the autologous osteochondral graft.
Three grades of tears commonly are seen: Grade I: Partial tear, usually of the ATFL. This is a stable injury, requiring rest, ice, compression, and elevation for 48 hours. Thereafter, motion is encouraged with a light compressive bandage. Dancers can begin light workouts at 48 hours with the aid of a brace or Aircast. Initially, therapy should concentrate on range of motion. After 4 or 5 days, dancers begin to wean out of the brace and initiate proprioception, balance, and peroneal strengthening exercises. Grade II: Complete tear of the ATFL, occasionally including the CFL as well. A positive drawer sign but negative talar tilt are observed. Treatment is immobilization in a cam walker or Aircast for up to 6 weeks. Initially, physical therapy should focus on regaining appropriate range of motion. Thereafter, a triple-phase rehabilitation program including peroneal strengthening, balance, and proprioceptive training should be initiated early. Grade III: Unstable injury. Both the ATFL and the CFL are injured. In addition, the drawer sign and talar tilt are positive. Treatment traditionally is immobilization for up to 4 months. In a professional dancer, primary repair is preferred, and the Brostrom-Gould usually can be performed 1 week following the injury with predictable results and return of function.14 Regardless of the treatment used, attention must be paid to reestablishing a functionally stable joint. A comprehensive literature evaluation and meta-analysis showed that early functional treatment produced the fastest recovery
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of ankle mobility and earliest return to activity without affecting mechanical stability.15 Closed chain balance and proprioception activities, along with peroneal muscle strengthening, will improve the neuromuscular control of the ankle. A therapist must be familiar with the modalities needed to achieve these goals to optimize outcomes in these dancers. Residual symptoms following lateral ankle sprains in dancers may be secondary to: 1. Avulsion fracture of the tip of the fibula, 2. Accessory ossicle or os subfibularae, 3. Os calcis fracture or avulsion of extensor digitorum brevis, 4. Fractured os peroneum, 5. Fractured lateral process of talus, 6. Cuboid subluxation, 7. Soft tissue entrapment, 8. Sinus tarsi syndrome, 9. Fractured os trigonum or Shepherd’s fracture, 10. Syndesmotic disruption, 11. Maisonneuve injury, 12. Anterolateral gutter scarring or Ferkel’s phenomenon, 13. Talar irritation from a slip of the ATFL inserting at the extreme tip of the fibula or the Bassett’s ligament, 14. Peroneal tendon dislocation or subluxation, 15. Functional ankle instability, or 16. Impingement of a lateral branch of the deep peroneal nerve (LBDPN).
Posterior ankle
LBDPN Impingement Persistent dorsolateral foot pain following ankle sprain is common. It often is attributed to chronic ligament dysfunction, sinus tarsi syndrome, anterior tarsal tunnel syndrome, or functional ankle instability. The pain is triggered most commonly in a plantarflexed and inverted position. In those cases recalcitrant to a rehabilitation program, an impingement of an LBDPN over the anterolateral corner of the talus (Fig. 21-10) or underneath the extensor digitorum brevis (EDB) muscle should be sought. Diagnosis is confirmed with persistent pain, exclusion of the above differentials, a positive Tinel’s sign over the anterolateral talus, and response to a localized subcutaneous anesthetic injection. Shoewear modification can often alleviate any external compression. However specifically guided injections and ultimately release of the EDB is often necessary.16
ANTERIOR ANKLE The cavus foot is ideal for dancers in that plantarflexion is maximal. However, this is at the expense of dorsiflexion, which is limited. The most common form of anterior impingement typically is seen in male dancers who perform high jumps and deep plie´s (bravura). Impingement of the anterior lip of the tibia against the talus causes the cambial layer of the periosteum to produce reactive bone formation and osteophytes or ‘‘kissing lesions.’’17 This is a continuous cycle as more bone forms, and eventually motion is significantly restricted.
Figure 21-11
Radiograph of tibiotalar osteophytes.
Three main types of lesions are seen (Fig. 21-11): 1. Anterior tibial lip, 2. Talar neck, or 3. A combination of both. Treatment of type I is resection using the arthroscope. Type II and III lesions often may require an anterior arthrotomy. Attention always should be directed to the medial joint whether using an arthroscopic approach or a formal arthrotomy. A medial impingement exostosis on the talus that impinges on the medial malleolus can be found and resected.
POSTERIOR ANKLE Ideally, more than 100 degrees of plantarflexion should occur at the foot-ankle complex in a professional ballet dancer. Much of this has to be accomplished by the subtalar joint, and subtalar motion is facilitated by the turned-out position of mild forefoot pronation and abduction. Any form of tarsal coalition, whether fibrous or bony, will prevent the subtalar joint from supplementing the ankle joint in full equinus. Consequently, most dancers with subtalar coalitions do not reach professional grade.
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Figure 21-10 Illustration of branching pattern of the lateral branch of the deep peroneal nerve (LBDPN).
Posterior impingement syndrome The posterior tubercle of the talus varies greatly in size. In posterior impingement syndrome, either a large posterior tubercle or an os trigonum (Fig. 21-12, A through C) is caught between the posterior lip of the tibia and the os
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Figure 21-12 (A) Radiograph of an os trigonum. (B) Radiograph of an os trigonum in releve´. (C) Illustration of os trigonum posterior impingement.
calcis when the dancer is in releve´.18 A simple clinical sign, the forced plantarflexion sign, confirms the diagnosis when pain is produced by full plantarflexion at the back of the ankle. The syndrome is usually a result
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of an os trigonum impinging the soft tissue rather than the bone itself. The differential diagnosis includes Achilles tendinitis, peroneal tendinitis, or heel pain.
Achilles tendon
The os trigonum is present in up to 10% of the population and is bilateral 50% of the time. Anatomically, the os trigonum represents the nonfused lateral process of the talus. This forms the lateral border of a fibro-osseous tunnel, the medial border being the medial talar tubercle. Through this tunnel runs the flexor hallucis longus. Most cases of an os trigonum are asymptomatic in the general population, and this is also true in dancers. However, in dancers this condition often is operated on unnecessarily. For this reason, a diagnostic injection of local anesthesia is mandatory before any surgical intervention. If there is no subsequent pain relief, one must seek an alternative diagnosis such as: 1. Flexor hallucis tendinitis (FHL) tendinitis, 2. Peroneal tendinitis, 3. Hairline or stress fracture of the posterior process, 4. Localized coalition, or 5. Osteoid osteoma. Treatment of an os trigonum generally is nonsurgical. Once a diagnosis has been confirmed by local anesthetic injection, the next step is rest and activity modification. Local steroid can give dramatic relief of symptoms that often is long lasting or permanent. When surgery is required, either a posteromedial or posterolateral approach can be used. In cases in which it is suspected that there is an associated FHL tendinitis, a posteromedial approach is preferred so that tenolysis can be performed safely. Posterior impingement also may occur following a lateral ligament sprain. With lateral ligamentous laxity, the talus slips forward and the posterior lip of the tibia impinges on the os calcis. Treating the lateral ligament instability usually addresses this form of impingement. A pseudomeniscus, with or without an os trigonum, causes another, less common, form of posterior impingement. This embryologic remnant, similar to a plica, can cause symptoms of locking and pain following a tear in its substance.
As the largest tendon in the body, the Achilles tendon incurs forces up to six times body weight during running and jumping.1 Therefore the tendon is commonly injured in dancers either from repetitive overload or excess stress applied by poor technique. Although a common site of injury in dancers, the tendon is rarely ruptured in this group of athletes.
Flexor hallucis longus tendinitis This entity has become known as ‘‘dancer’s tendinitis.’’19 As the tendon passes between the fibro-osseous tunnel at the back of the talus, it runs deep to the sustentaculum tali. Within this pulley system it can become inflamed and cause irritation and swelling. When the tendon has a partial tear or becomes swollen at a particular area, it may cause triggering (Fig. 21-13). This condition is known as hallux saltans.12 When the tendon becomes completely stuck down within the pulley system, a pseudohallux rigidus can be seen. Treatment of this condition requires a compliant patient to rest. Anti-inflammatories are a useful
Peritendinitis of the achilles tendon The Achilles tendon has no real synovial sheath and is surrounded by a peritendon, which can become inflamed from overuse or from the tight ribbons of ballet shoes. The peritendinitis is classically seen as a diffuse swelling along the Achilles tendon. When the tendon itself is inflamed, it presents as a discrete swelling along the tendon. Treatment of peritendinitis requires rest. A cam walker with a heel-raise insert worn for 23 hours/day should be worn for at least 2 weeks. This can break the cycle of inflammation and prevent the next step in the continuum of pathology—inflammation of the tendon itself.
Figure 21-13
Flexor hallucis longus tendinosis.
adjunct. Local steroid injections should be avoided whenever possible. When the condition is recurrent or disabling surgical, tenolysis is warranted. Three areas of FHL tendinitis typically are found. The most common location is behind the medial malleolus. It also may be found at the knot of Henry, or at the base of the first metatarsal where the tendon passes beneath the sesamoid bones.
ACHILLES TENDON
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Tendinitis of the achilles tendon Tendinitis is caused by microtears of the collagen fibers on the surface or in the substance of the tendon. The most common form of tendinitis occurs at the isthmus of the tendon and involves a localized swelling of the pseudosheath. This may be felt clinically as crepitus when the tendon is stretched and relaxed—the so-called painful arc sign. Chronic tendinitis can be felt as multiple nodules on the surface of the tendon. More severe strains result in a classic fusiform swelling of the tendon. This is slow to heal and carries a guarded prognosis. Treatment requires rest initially, usually in a cam walker with a heel-raise insert for up to 6 weeks. This should be worn continuously, including bed, for the first 2 to 3 weeks. Failure to comply with strict immobilization initially can result in prolonged symptomatology and rupture of the tendon. Treatment can be supplemented with anti-inflammatory medication. Rehabilitation consists of stretching exercises and a gradual strengthening program. In more chronic cases, use of an overnight splint to assist with a prolonged stretch in a dorsiflexed position can be helpful. Orthotic prescription may be considered to help correct any structural imbalances in the foot. A ‘‘stretch box’’ is a useful tool to prevent injury that is used by many ballet schools. This allows dorsiflexion of the ankle with stretching of the Achilles tendon before and between performances. However, dancers must exercise caution to avoid stretching the Achilles tendon too aggressively, causing more tears and thereby worsening the condition. Certain factors can predispose to tendinitis in dancers: 1. Cavus foot with associated Haglund’s disease (Fig. 21-14), with tendinitis of the Achilles overlying the retrocalcaneal bursa. Cavus feet are common in this population, because they afford the dancer a distinct anatomic advantage. For this reason, any
2. 3. 4. 5.
prominence at the posterosuperior aspect of the os calcis can cause irritation of the tendon. This may necessitate resection of the prominence (Fig. 21-15). ‘‘Rolling in’’ or pronation of the foot. ‘‘Ribbon burn’’ from tight toe ribbon at the back of the leg. Congenitally thin tendon is predisposed to overload injury. Tight heel cord.
Rupture of the achilles tendon Achilles tendon ruptures are rare in female athletes and more common in male dancers older than 30 years. Typically a tear presents as a sharp pain of sudden onset and an inability to walk on the toes. A Thompson test is the best clinical diagnostic test. Feeling for a defect along the tendon usually is diagnostic; however, an intact peritendon filled with hematoma may mimic an intact tendon. Ultrasound can confirm the diagnosis with a high degree of sensitivity and specificity. Treatment is dependent on the requirements of the patient. Cast immobilization is associated with up to 30% rate of rerupture and will allow up to 80% normal strength and function. Operative intervention has the advantage of restoring the physiologic length and thus optimizing functional outcome. This requires up to a full year of treatment and rehabilitation before the dancer can return to preinjury levels of dance. Newer techniques of limited open incisions with percutaneous suturing facilitate early motion and reduce the risk of associated skin problems.20 Correct tensioning of the repair is critical to outcome regardless of the technique used. Pseudotumor of the calf An accessory soleus muscle can present as a slowly enlarging mass on the medial side of the calf. It generally is painless, usually presenting as a feeling of tightness. Surgical division of the muscle sheath will generally relieve the symptoms.
HEEL PAIN
Figure 21-14
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Cavus foot with Haglund’s deformity.
1. Heel spurs syndrome: The spur usually is not the cause of heel pain, despite often-impressive radiographic evidence. The plantar fascia is not intimately attached to the spur, giving rise to the flexor digitorum brevis. A silicone heel can give symptomatic relief in a dancer who has point tenderness in this area. 2. Plantar fasciitis: Pain on the medial aspect of the fascia origin is the most common presentation. Stretching of the fascia before rehearsing or
Leg pain
Preoperative (A) and intraoperative (B) radio-graphs of Haglund’s deformity.
performing can reduce the incidence of this injury. Also, using a firm rubber ball for rolling into the plantar fascia while weight bearing helps to loosen the fascia and make it more pliable. 3. Plantar calcaneal bursitis: Found beneath the calcaneus, this condition usually can be diagnosed clinically; however, ultrasound can confirm the diagnosis. 4. Baxter’s nerve neurapraxia: The first branch of the lateral plantar nerve or nerve to abductor digiti minimi may be trapped under the deep fascia of the abductor hallucis.21 This is exacerbated when the dancer ‘‘rolls in’’ or pronates. Although the cause is a neurapraxia of the lateral branch of the plantar nerve, the condition is painful on the medial aspect of the heel, adjacent to the medial calcaneal tuberosity. A local anesthetic directed into the area may make the diagnosis. Surgical resection of the fascia yields excellent outcomes.
LEG PAIN The three primary conditions in dancers that predispose to leg pain include shin splints, stress fracture, and compartment syndrome.
Shin splints (medial tibial stress syndrome) ‘‘Shin splints’’ is a generic term often used to describe both traction periostitis and stress fractures. It has gained credence in the general population to describe generalized leg pain. A more useful nomenclature is medial tibial stress syndrome (MTSS). For the purposes of this discussion, MTSS describes a traction periostitis alone. This condition is associated with a diffuse anteromedial or posteromedial tibial pain. Typically the pain is
in the distal one third of the tibia. It can be differentiated from stress fracture, which has localized point tenderness and usually is in the middiaphysis of the tibia and distal one third of the fibula. Typically, MTSS occurs at the beginning of the season after a prolonged period of inactivity. Stress fractures typically are from repetitive trauma and occur usually in mid to late dance season. Posterior MTSS is most common in dancers and arises at the origin of the flexor digitorum longus (FDL), and not from the tibialis posterior, which arises from the interosseous membrane. Anterior MTSS, not as common in dancers, represents a periostitis at the origin of the tibialis anterior muscle. Soleus syndrome, pain at the posteromedial aspect of the medial malleolus, is caused by an abnormal slip of soleus muscle. Treatment is a decrease in activity, cross training, and isometric exercises in addition to well-cushioned shoes. Rarely, a fasciotomy of the soleus insertion may be required.
Stress fractures Prolonged biomechanical imbalances and increased repetitive loads beyond the body’s reparative capacity typify the causes of stress fractures. Thus these injuries generally occur at the end of the dancer’s season, in contradistinction to MTSS, which occurs at the beginning. In the initial phases radiographic evidence may be slim, and the best method of confirming a clinical suspicion is a bone scan or MRI. Delayed subtle periosteal reaction occasionally can be seen (Fig. 21-16). In chronic stress fractures, conventional radiographs may reveal the ‘‘dreaded black line’’ seen on the anterior aspect of the tibia. This represents granulation tissue in a slowly healing fracture. The line is an indicator that the fracture will be slow to heal, requiring at least 6 to 481
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Figure 21-15
CHAPTER 21
Foot and ankle injuries in dancers
a high tarsal tunnel syndrome should be made before embarking on a fasciotomy in a dancer.
SUMMARY
Figure 21-16
Tibial stress fracture.
8 months. In a competitive dancer this is an extremely long period. A drilling procedure may be used to accelerate healing and can be performed using a small drill percutaneously with the aid of a FluoroScan, if available. The drill is used to penetrate the anterior cortex and stimulate neovascularization and callus formation. Return to activity is titrated against radiographic healing of the stress fracture line. Since the introduction of Balanchine method of dance, which emphasizes fluid motion, the number of stress fractures has reduced. This is in contrast to the rapid deceleration motion seen in the Bravura technique.
Compartment syndrome When the pressure within an enclosed fascial compartment exceeds the pressure required to perfuse the muscle with blood, the muscles and enclosed structures may become compromised. This can lead to pain initially and may reach the point of muscle ischemia in more severe cases. In dance, the blood volume to the exercising muscle can increase up to 20%, thereby exceeding the physiologic pressure within the muscle compartments. Most cases of exertional compartment syndrome involve the anterior compartment or the deep posterior compartment. Normal resting compartment pressures range from 0 to 8 mm Hg. During exercise this can increase to 50 mm Hg. Following exercise, this pressure should fall to 15 mm Hg within 15 minutes. Treatment of exertional compartment syndrome usually is conservative, with anti-inflammatory medication and shoe modification, as well as activity modification. Rarely, a fasciotomy is required. Careful attention to ruling out
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Classical ballet offers a graceful and beautiful spectacle. This beauty comes at great physical, psychological, and economic cost to the ballet dancer.22 It is estimated that up to 95% of dancers employed for greater than 1 year will suffer a significant injury. Most of these physical injuries occur to the foot and ankle in female ballet dancers.23 Many of these injuries are as a result of dancing on the point of the toe. This form of dancing was first performed by Genevieve Gosselin in 1818 at the Paris Opera house. The illusion of weightlessness and the grace implied in en pointe dancing was further enhanced by the great dancers Taglioni and the immortal Istomina. Since their time, the beauty, romance, and grace of en pointe have been enjoyed by dancers all over the world. Unfortunately, the ‘‘cruel little slipper’’ that is the en pointe shoe, as well as the physical demands of the dance itself, have left many dancers with significant injuries and permanent deformities. It must be emphasized that, when the orthopaedist examines a ballet dancer, the entire kinetic chain requires close inspection. Isolated injuries to the foot and ankle may precipitate additional injuries farther up the kinetic chain as a compensatory response to the injury or inadequate and improper rehabilitation.24 Apart from the physical examination, a careful history and biochemical profile should be investigated in those dancers showing any signs of the aforementioned dancer’s triad: anorexia, amenorrhea, and osteoporosis.25 In addition to the biomechanical examination and biochemical evaluation, the orthopaedist should be cognizant of the psychosocial aspects of a dancer’s makeup. Dancers, in general, regard injury and pain as a way of life and are reluctant to present to health care professionals for fear of long-term immobilization and eventual unemployment.22,26 As an advocate for the dancer as an athlete, the clinician should be aware of these concerns and strive to provide an accurate diagnosis and expeditious treatment strategy.
REFERENCES 1. Warren M, et al: Scoliosis and fractures in young ballet dancers: relationship to delayed menarchal age and amenorrhea, N Engl J Med 314:1338, 1986. 2. Hamilton WG: Surgical anatomy of the foot and ankle, Ciba Clin Symp 37(3):1, 1985. 3. Hamilton WG: Physical prerequisites for ballet dancers, J Musculoskel Med 13:61, 1986.
References 16. Kennedy JG, Brunner JB, Bohne WH, et al: Clinical importance of the lateral branch of the deep peroneal nerve, Clin Orthop Relat Res 459(Jun):222-228, 2007. 17. Kleiger B: Anterior tibiotalar impingement syndromes in dancers, Foot Ankle 3:69, 1982. 18. Hamilton WG: Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the os trigonum in ballet dancers, Foot Ankle 3:74, 1982. 19. Hamilton WG: ‘‘Dancer’s tendinitis’’ of the FHL tendon Read before the 2nd annual meeting of the American Orthopedic Society of Sports Medicine, Durango, Colo, 1976, July 11-14. 20. Assal M, et al: Limited open repair of Achilles tendon ruptures: a technique with a new instrument and findings of a prospective multicenter study, J Bone Joint Surg Am 84:161, 2002. 21. Baxter DE, Pfeffer GB: Treatment of chronic heel pain by surgical release of the first branch of the lateral plantar nerve, Clin Orthop 279:229, 1992. 22. Kelman BB: Occupational hazards in female ballet dancers. Advocate for a forgotten population, AAOHN J 48:430, 2000. 23. Nilsson C, et al: The injury panorama in a Swedish professional ballet company, Knee Surg Sports Traumatol Arthrosc 9:242, 2001. 24. Macintyre J, Joy E: Foot and ankle injuries in dance, Clin Sports Med 19:351, 2000. 25. Warren MP, et al: Osteopenia in exercise-associated amenorrhea using ballet dancers as a model: a longitudinal study, J Clin Endocrinol Metab 87:3162, 2002. 26. Turner BS, Wainwright SP: Corps do ballet: the case of the injured ballet dancer, Social Health Illn 25:269, 2002.
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4. Hamilton WG: Ballet. In Reider B, editor: The school-age athlete, Philadelphia, 1991, WB Saunders. 5. Hamilton WG, et al: A profile of the musculoskeletal characteristics of elite professional ballet dancers, Am J Sports Med 20:267, 1992. 6. Viladot A: Patologia del Antepie, Barcelona, 1957, Ediciones Toray. 7. Einarsdottir H, Troell S, Wykman A: Hallux valgus in ballet dancers: a myth? Foot Ankle Int 16:92, 1995. 8. Mann RA, Clanton TO: Hallux rigidus: treatment by cheilectomy, J Bone Joint Surg Am 70:400, 1988. 9. Hamilton WG, O’Malley MJ, Thompson FM: Capsular interposition arthroplasty for severe hallux rigidus, Foot Ankle Int 18:68, 1997. 10. Thompson FM, Hamilton WG: Problems of the second metatarsophalangeal joint, Orthopedics 10:83, 1987. 11. O’Malley MJ, Hamilton WG, Munyak J: Stress fractures at the base of the second metatarsal in ballet dancers, Foot Ankle Int 17:89, 1996. 12. Hamilton WG: Foot and ankle injuries in dancers, Clin Sports Med 7:143, 1988. 13. Hamilton WG: Sprained ankles in ballet dancers, Foot Ankle 3:99, 1982. 14. Hamilton WG, Thompson FM, Snow SW: The Brostrom/Gould repair for lateral ankle instability, Foot Ankle 14:1, 1993. (Published erratum appears in Foot Ankle 14:180, 1993.) 15. Lynch SA, Renstrom PA: Treatment of acute lateral ankle ligament rupture in the athlete. Conservative versus surgical treatment, Sports Med 27:61, 1999.
.........................................C H A P T E R 2 2 An international perspective on the foot and ankle in sports A. Personal perspective on foot and ankle sports conditions S. Giannini and F. Vannini CHAPTER CONTENTS ...................... A. Personal perspective on foot and ankle sports conditions
485
E. Foot and ankle injuries caused by traditional Japanese martial arts
507
Ankle instability
486
Judo
507
Osteochondral lesions of the talar dome
487
Sumo
508
Achilles tendon lesions
488
Kendo
509
Plantar fasciitis
489
Lisfranc sprains
490
References
491
Further reading
492
B. Treatment of Achilles tendon ruptures
492
F. Foot and ankle problems caused by some traditional Chinese habits and sports
511
G. Foot and ankle sports injuries in Korea
514
Introduction
514
Ssireum (Korean traditional wrestling)
514
Taekwon-do (Korean martial arts)
515
Basketball, soccer, rugby, and baseball
516
Accessory navicular syndrome
516
Introduction
492
Diagnostics
492
Treatment
493
Rehabilitation
497
Conclusion
497
Foot/ankle injuries in surf lifesaving
517
References
498
References
519
Further reading
519
C. Foot and ankle injuries in United Arab Emirates sports
D. Nerve injuries complicating inversion ankle sprains
H. Australian foot and ankle conditions in sport
516
498 I. Soccer: hallux osteochondral lesion and rupture of the Achilles tendon
519
Hallux osteochondral lesion in beach soccer players
520
Neglected rupture of the Achilles tendon
521
References
522
502
Anatomy
502
Clinical picture
503
Treatment
503
References
506
Further reading
507
J. Footballer’s (soccer) ankle in Venezuela Clinical evaluation
522 523
CHAPTER 22
An international perspective on the foot and ankle in sports
Additional studies
524
Biology
527
Treatment
524
Principles of tendinopathy management
529
Complications
526
Surgical management
530
References
526
Discussion
532
Conclusion
532
References
532
K. The biologic perspective of sports disorders affecting foot and ankle Introduction
527 527
ANKLE INSTABILITY The lateral ligamentous complex of the ankle may be the most commonly damaged structure in sport injuries.1,2 Garrik3 reported a frequency of 45% in basketball practice, 31% in soccer, and 25% in volleyball. Primary repair of the ligaments was previously recommended; nonoperative treatment also has been recently recommended.2,4 However, despite adequate primary functional treatment, some patients develop chronic instability. In 20% of the cases, ligamentous reconstruction is required.5 Indications for ligament reconstruction are mechanical and functional instability and failure of rehabilitative treatment. The goal of surgical treatment is to improve stability and proprioceptive sensation maintaining complete range of motion (ROM). Ankle instability surgery has been divided into an anatomic repair consisting of imbrications of the local tissue of the lateral ligamentous complex and an ankle-ligament reconstruction involving tendon grafts. A nonanatomic tenodesis results in stiffness of the operated ankle, prolonging recovery and decreasing sport6 because of the incorrect orientation of the reconstructed ligaments.
Because of these considerations, our choice technique is a modified Brostrom with a reinforced flap when the local tissues are strong enough. Otherwise an ‘‘anatomic reconstruction’’ is performed with a tendon graft using the plantaris. When no plantaris is available, a tibialis posterior hemisection harvested from a cadaver is used.
Surgical technique 1 The anatomic reconstruction has been described previously by Brostrom4 and consists of the direct suture of the stumps of residual tissue. In our experience, to reinforce the reconstructed ligaments a periosteal flap should be harvested from the anterolateral aspect of the fibula and turned down and sutured as talofibular ligament or split in two and used also to reinforce the calcaneofibular ligament (Fig. 22A-1). Surgical technique 2 When the residual tissues are not strong enough to permit direct suture or after failure, we perform a reconstruction of the talofibular and calcaneofibular ligaments using the plantaris, if present, or a cadaveric tibialis posterior graft. The tendon is fixed through a transosseous tunnel or with an anchor on the neck of the talus.
Figure 22A-1 To reinforce the reconstructed ligaments, a periosteal flap should be harvested from the anterolateral aspect of the fibula and turned down and sutured as talofibular ligament or split in two and used also to reinforce the calcaneofibular ligament.
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Osteochondral lesions of the talar dome
A tunnel is created through the anterior aspect of the lateral malleolus where the talofibular is inserted and the tendon is passed in and sutured to the periosteum. In case of an associated calcaneofibular lesion, the tendon will be passed through the apex of the lateral malleolus and be sutured on the lateral wall of the calcaneus (Fig. 22A-2). We pay particular attention to reconstruct the ligament with a proper length, direction, and tightness similar to those of the healthy anatomic complex to obtain an isometry of the new ligaments permitting a physiologic ROM and avoiding stiffness.7 In a 1983 study, Giannini et al.8 concluded that 67% of ankle sprains in sports activity were in athletes with cavus foot. Because of this observation, in cases with a cavus foot associated with a varus of the calcaneus, evaluated as reducible according to the Coleman test,9 a mini-invasive dorsiflexion metatarsal osteotomy (see Fig. 22A-2) associated with the ligamentous reconstruction is indicated. This procedure will rebalance the foot, helping to prevent further sprains and improving function.
OSTEOCHONDRAL LESIONS OF THE TALAR DOME Osteochondral lesions of the talar dome are very common in sports activity as a consequence of ankle
sprains.10,11 Procedures for the treatment of osteochondral lesions of the talus including debridement of the joint, shaving of fibrillated cartilage, and resection or perforation of subchondral bone in the last decade have been performed arthroscopically with low morbidity. These surgeries are not effective in lesions larger than 1.5 cm2 and have not been histologically effective in restoring the hyaline cartilage.12–20 Autologous chondrocyte transplantation (ACT) has proved to be capable of restoring the articular hyaline cartilage surface, including defects larger than 2 cm2 (Figs. 22A-3, 22A-4, and 22A-5).17 In the past, this practice required a medial or lateral malleolar osteotomy, and, although there were good clinical and histologic results, the technique was quite invasive and technically demanding.17 Recently, advancement in tissue engineering permitted the development of absorbable synthetic scaffolds, permitting a completely arthroscopic technique through the traditional anteromedial and anterolateral approaches. Because of this improvement, it appears to be reasonable, mostly in the young athletes, to extend the indications of ACT even in smaller lesions traditionally treated with microfractures.
Surgical technique The first step requires ankle arthroscopy with cartilage harvesting for cell culture, performed directly from the
Figure 22A-2 (A) A tunnel is performed through the anterior aspect of the lateral malleolus where the talofibular is inserted. The tendon is passed and sutured to the periosteum. In case of an associated calcaneofibular lesion, the tendon will be passed through the apex of the lateral malleolus and be sutured on the lateral wall of the calcaneus. (B) A bone procedure such as a dorsiflexion metatarsal osteotomy may be performed to correct the associated cavus deformity of the foot.
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CHAPTER 22
Figure 22A-3 type II.
An international perspective on the foot and ankle in sports
Immunohistochemical staining for collagen
Figure 22A-5 detection.
Alcian blue staining for proteoglycans
The Hyalograft-C scaffold, made of hyaluronic acid, is sized and prepared in the right shape and placed on the positioner (Fig. 22A-6). Through an appropriate cannula, the self-adhesive scaffold is positioned to cover the lesion (Fig. 22A-7). Immediate daily continuous passive motion (CPM) for 6 to 8 hours begins after surgery and continues for a period of 6 weeks. Touchdown (20%-30%) crutch walking is permitted for 6 weeks. After 6 weeks, progressive increased weight bearing and active ROM are permitted. Full weight bearing will be allowed at 8 weeks. Return to cutting, turning, or jumping sport is permitted only after 1 year.
ACHILLES TENDON LESIONS
Figure 22A-4 Immunohistochemical staining for proteoglycans.
affected joint using the osteochondral fragment. After 30 days, a second step ankle arthroscopy through traditional anteromedial and anterolateral accesses is performed. The focus of the lesion is carefully shaved, and care is taken to reach the healthy cartilage.
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Achilles tendon lesions in soccer are 31% to 34% of all traumas, according to Lanzetta et al.21 The Achilles tendon rupture usually is caused in soccer by direct or indirect trauma during jumping, cutting, or turning.22 Predisposing factors in the soccer player are due to an overuse of the calcaneal-Achilles-plantar system, possibility of preexisting tendinopathy, or corticosteroid injections. The clinical presentation is variable. Pain may be mild for the preexisting degeneration of the tendon because functionality may be performed by the retromalleolar pronator and supinator muscles with different percentages, making the clinical evidence less clear. Rerupture occurs
Plantar fasciitis
tissue, and disturbance of sensation,23,24 our choice is surgical repair with a mini-invasive technique. The advantages of mini-invasive surgery are less surgical trauma, better quality of reparative scar tissue, avoidance of damage to the local vascularity, faster recovery, and return to sport activity. Indications for the mini-invasive treatment are lesions from 6 to 8 cm from the calcaneal insertion and no more than 6 days after the rupture.
Figure 22A-6 The Hyalograft-C (FIDIA s.r.l. Abano PD, Italy) scaffold, made of hyaluronic acid, is sized and prepared in the right shape and placed on the positioner.
Surgical technique The Achilles tendon repair system (Fig. 22A-8) permits a suture of the tendon through a 1.5-cm incision. Both stumps of the ruptured tendon are identified. The instrument is introduced in the closed position, under the paratenon, in a proximal direction. When the tendon lies between the two branches of the instrument, the sutures are passed, and the end of each is held with a small clamp to keep the sutures separate from each other. When the instrument is withdrawn, the sutures slide to a peritendinous position. Afterward, the same sequence is performed on the distal stump, and the tendon reduction is performed under visual control. Postoperative treatment consists of a boot worn for 8 weeks. Mobilization is permitted only in plantarflexion from the first to the sixth week, after which complete ROM is achieved. Partial weight bearing (15 kg) is permitted with the boot in plantarflexion for 3 weeks. Partial weight bearing (15 kg) is permitted with the boot at 90 degrees for 3 weeks. Total weight bearing is permitted with boot ROM from 10 degrees plantarflexion to 10 degrees dorsiflexion for 2 weeks.
PLANTAR FASCIITIS
in 10% to 30% of high-performance active patients with nonoperative treatment;23-25 therefore surgery generally is recommended. Because formal open procedures have been associated with a high rate of complications related to poor wound healing, deep infection, adhesion of scar
489
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Figure 22A-7 Arthroscopic view showing the self-adhesive scaffold positioned to cover the lesion.
Plantar fasciitis is common in high-performance athletes, mostly runners and basketball and volleyball players because of the high stress concentrated at the fascia insertion in running and jumping.26 Commonly cited risk factors for plantar fasciitis are the flat or cavus foot, a tight Achilles tendon, the type of training shoes worn, and errors in the training routine.27 Anti-inflammatory medications may be helpful in providing symptomatic relief. Some improvement is possible with the use of a shoe insert providing 1 cm height at the hindfoot and daily stretching exercises of the Achilles tendon-plantar fascia complex. A safe and effective nonoperative treatment that we feel should be considered before surgery is the application of low-energy shock waves at the fascia insertion (three applications of 2100 impulses of low-energy shock waves), usually providing good results.28 If the
CHAPTER 22
Figure 22A-8
An international perspective on the foot and ankle in sports
The Achilles tendon repair system permitting a suture of the tendon through a 1.5-cm incision.
fasciitis does not respond to the nonoperative treatment, in a minimum of 4 months for a professional athlete, surgical treatment should be attempted. Because the open technique has a high failure rate, with 15.5% of the patients reporting dissatisfaction,29 we prefer the use of a percutaneous fasciotomy. It is important to note that this technique does require surgical experience and may be associated with complications.
Surgical technique A 14-mm K-wire is inserted manually in the medial aspect of the foot to identify the level of the insertion of the fascia. The fasciotomy is performed with a tenotomy blade while the foot is maintained in dorsiflexion and the fascia is probed externally with a finger (Fig. 22A-9). This method reduces the formation of scars and provides for a fast recovery at a low cost. Surgery should be followed by early ROM, stretching exercises, and ankle dorsiflexion. An orthosis that maintains the foot and ankle in 10 degrees of ankle dorsiflexion should be worn during the night for the first 3 weeks.
LISFRANC SPRAINS Injuries to the Lisfranc ligament complex in the general population are uncommon and typically occur as a result of high-velocity and indirect trauma that causes an obvious displacement and disruption of the tarsometatarsal anatomy.30 Low-velocity Lisfranc sprains also can occur
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Figure 22A-9 The fasciotomy is performed with a tenotomy, maintaining the foot in dorsal hyperflexion and probing the fascia with a finger.
after an indirect trauma when the foot is plantarflexed and slightly rotated. This is a frequent condition in soccer players. Lisfranc sprains represent a spectrum of injuries to the Lisfranc ligament complex, from partial sprains with no displacement to complete tears with frank diastasis31 (Fig. 22A-10). Although the nondisplaced injuries often heal uneventfully, patients with displacement should undergo a closed reduction and internal fixation with cannulated screws.
References
Postoperatively, a nonweight-bearing boot is maintained for 4 weeks, followed by 4 weeks of boot with progressive weight bearing. Screw removal occurs from 14 to 24 weeks. Return to sport activity should be permitted after a functional rehabilitation program, usually after 4 months.
REFERENCES
Figure 22A-11 Under C-arm control, percutaneous guidewires and cannulated screw are used to maintain the reduction.
Surgical technique A percutaneously placed large bone clamp is used to assist the reduction. Under C-arm control, percutaneous guidewires are inserted, followed by placement of cannulated screws (Fig. 22A-11).
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Figure 22A-10 Lisfranc sprains resulting in a frank diastasis.
1. Burks RT, Morgan J: Anatomy of the lateral ankle ligaments, Am J Sports Med 22:72, 1994. 2. Kannus P Renstom P: Current concepts review. Treatment for acute tears of lateral ligaments of the ankle: operation, cast or early controlled mobilization, J Bone Joint Surg Am 73:305, 1991. 3. Garrick JM: The frequency of injuries, mechanism of injury and epidemiology of ankle sprains, Am J Sports Med 5:241, 1977. 4. Brostrom VI: Sprained ankles: surgical treatment of chronic ligament ruptures, Acta Chir Scand 243:551, 1966. 5. Renstrom PA: Persistently painful sprained ankle, J Am Acad Orthop Surg 2:270, 1994. 6. Baumhauer JF, O’Brien T: Surgical considerations in the treatment of ankle instability, J Athl Train 37:458, 2002. 7. Leardini A, et al: A geometric model of the human ankle joint, J Biomech 32:585, 1999. 8. Giannini S, et al: Nostri orientamenti sul trattamento degli esiti delle fratture-lussazioni della Lisfranc, Chir del piede 17:169, 1983. 9. Coleman SS, Chestnut WJ: A simple test for hindfoot flexibility in the cavus varus foot, Clin Orthop 123:60, 1977. 10. Schenck R, Goodnight JM: Osteochondritis dissecans: current concepts review, J Bone Joint Surg 78A:439, 1996. 11. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review, Foot Ankle Int 21:119, 2000. 12. Alexander AH, Lichtman DM: Surgical treatment of transchondral talar-dome fractures (osteochondritis dissecans), J Bone Joint Surg 62A:646, 1980. 13. Altman RD, et al: Preliminary observations of chondral abrasion in a canine model, Ann Rheum Dis 51:1056, 1992. 14. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation, N Engl J Med 331:889, 1994. 15. Buckwalter JA, Lohmander S: Operative treatment of osteoarthrosis: current concepts review, J Bone Joint Surg 76A:1405, 1994. 16. Buckwalter JA, Mow VC, Ratcliffe A: Restoration of injured or degenerated articular cartilage, J Am Acad Orthop Surg 2:192, 1994. 17. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint, Foot Ankle 22:513, 2001. 18. Hangody L, et al: Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients, Foot Ankle 22:552, 2001. 19. Homminga GN, et al: Perichondral grafting for cartilage lesions of the knee, J Bone Joint Surg 72B:1003, 1989. 20. Kumai T, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus, J Bone Joint Surg 81A:1229, 1999. 21. Lanzetta A, Meani E, Tinti G: Le lesioni dell’Achilleo nella pratica sportiva: considerazioni etiopatogenetiche e indicazioni terapeutiche, Ital J Sport Traumatol 3:113, 1989. 22. Hattrup SJ, Johnson KA: A review of ruptures of the Achilles tendon, Foot Ankle 6:34, 1985.
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An international perspective on the foot and ankle in sports
23. Carden DG, et al: Rupture of the calcaneal tendon. The early and late management, J Bone Joint Surg Br 69:416, 1987. 24. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature, Am J Sports Med 21:791, 1993. 25. Roberts C, et al: Dynamised cast management of Achilles tendon ruptures, Injury 32:423, 2001. 26. Snider MP, Clancy WG, Mc Beath AA: Plantar fascia release for chronic plantar fasciitis in runners, Am J Sports Med 11:215, 1983. 27. Warren BL: Plantar fasciitis in runners. Treatment and prevention, Sports Med 10:338, 1990. 28. Rompe JD, et al: Shock wave application for chronic plantar fasciitis in running athletes. A prospective, randomized, placebo-controlled trial, Am J Sports Med 31:268, 2003.
29. Clanton TO, DeLee JC: Osteochondritis dissecans: history, pathophysiology and current treatment concepts, Clin Orthop 167:51, 1982. 30. Mantas JP, Burks RT: Lisfranc injuries in the athlete, Clin Sports Med 13:719, 1994. 31. Nunley JA, Vertullo CJ: Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete, Am J Sports Med 30:871, 2002.
FURTHER READING Davies MS, Weiss GA, Saxaby TS: Plantar fasciitis: how successful is surgical intervention? Foot Ankle Int 20(12):803-807, 1999.
B. Treatment of Achilles tendon ruptures Hajo Thermann and Christoph Becher
INTRODUCTION The rapidly growing trend for participation in recreational and competitive sport is accompanied by an increase of overuse syndromes. In the foot and ankle, the incidence of Achilles tendon rupture and subsequent problems has increased significantly in recent decades.1-3 In Germany the incidence of acute Achilles tendon rupture is estimated to be 15,000 cases/year.3 The rupture usually does not occur at the time of top-level sporting activities. Most studies show a peak between the ages of 30 and 45 years.4-9 The patient collective has a remarkably large portion of leisure-time athletes and patients with sedentary occupations.10 The portion of injuries in track-and-fields athletics is cited as only 10%. These are mostly young patients who sustained a tendon rupture as a result of an incompletely treated achillodynia or an enormous training workload.9 In the future, an increasing number of older patients (older than 50 years) will sustain Achilles tendon rupture as strenuous sports activities become more and more common in this age group. Of all the tendons of the human body, the Achilles tendon seems to be the most susceptible to degenerative changes. The male-to-female ratio of persons with Achilles tendon rupture ranges between 5:1 and 10:1 in most studies, and on average the men are older.9,11 According to the literature and our experience, Achilles tendon ruptures occur most often (in 80% to 90% of cases) 2 to 6 cm proximal to the calcaneal insertion.9 The incidence of proximal ruptures distal to the musculotendineal
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transition is 10% to 15% and is caused by degenerative changes. Ruptures near the calcaneal insertion are rare and mostly are found in hyperpronators with a heel spur (Haglund’s heel). In contrast to impulsive injury mechanism in tendinous ruptures, bony avulsions usually are caused by continuously increasing tension and strength or direct impact.9 The rupture mechanism usually is a consequence of an indirect loading and traction mechanism, such as a push-off with the foot in plantarflexion and simultaneous knee extension or a sudden, unexpected dorsiflexion of the ankle with powerful contraction of the calf muscles.9 Direct impact, such as a kick or hit on the tensed tendon, accounts for only 1% to 10% of ruptures.11,12 The degenerative and the mechanical theory of etiopathogenesis of Achilles tendon rupture face each other. Aseptic inflammations (tendinitis, paratendinosis) and reduced vascular supply lead to degenerative changes with cell loss and disorders of mucopolysaccharide content, even to fatty, mucoid, or calcifying degeneration.13 Repetitive or single stresses result in minor microtrauma. Low temperature and fatigue of athletes (lactic acid) lead to decreased maximal load resistance.9 If regenerative healing processes cannot keep pace, the sum of microtrauma leads to rupture.
DIAGNOSTICS The typical characteristic of a tendon rupture is a hit or whiplash-like sudden pain. Ruptures happening in
Treatment
contact sports often are perceived as a hit by an ax or a bar. A crack or a popping sound often is heard. A palpable gap and a positive Thompson test are the first clinical signs of an acute Achilles tendon rupture. Because of hematoma, these signs are not always visible but usually are palpable. The strength of plantarflexion typically is decreased or completely lost, resulting in an inability of heel rise and weak rolling of the foot with stalking landing of the leg and an externally rotated foot. A remaining plantarflexion does not indicate an intact tendon because extrinsic flexors such as the plantaris muscle also are able to produce this movement. Although most Achilles tendon ruptures can be diagnosed clinically, evaluation by ultrasonography and magnetic resonance imaging (MRI) enables a definitive diagnosis and is decisive for the choice of treatment (Figs. 22B-1 and 22B-2). Ultrasonographic appearance of acute Achilles tendon rupture shows broad variations. The most common signs are interruption of continuity and demarked tendon stumps. Hypoechogenic accumulations of liquid at the rupture site and loss of the typical parallel hyperechogenic reflex patterns are depicted regularly by experienced examiners. Because some ruptures do not show a visible diastase of the stumps from the hematoma, dynamic examination in dorsiflexion and plantarflexion is essential. Even if there is no visible gap, a spreading of fine parallel echoes, corresponding to a loss of cross-wise network of elastic fibers, reveals a rupture. Inflammatory tendinosis with edematous dissolution of the structures must be differentiated. Disrupted or retracted soleus fibers, which are detected mostly in toplevel athletes, are significant for the choice of treatment and especially for the surgical technique. Although this can be detected by ultrasonography, MRI shows a better
Figure 22B-2 Ultrasonography of an acute Achilles tendon rupture. Interrupted continuity and demarked tendon stumps (arrows).
validity.9 The soleus muscle must be examined with sagittal and axial scans. Furthermore the differentiation of rupture area and tendon ends enables an exact determination of the diastase and distance to the calcaneal insertion.
TREATMENT Conservative treatment Primary conservative immobilizing treatment and postoperative aftercare in a cast are not justified concerning the disadvantages of muscle atrophy and loss of coordination and proprioception. The concept of primary functional treatment considers the ultrasound or MRI morphology as a basis for treatment strategy. The ultrasonographic or MRI depiction of complete adaptation of tendon ends in 20-degrees plantarflexion is required. The validity of this method, compared with operative treatment, could be proven in a series of more than 550 patients using a high-shaft shoe, comparable to a modified boxer boot (Variostabil, Orthotech, Germany)*14 (Fig. 22B-3). Indication for primary functional treatment independent of the ultrasonographic or MRI findings should be preferred in the elder nonactive patient or in patients with altered operative risk or reduced capacity for tissue regeneration (e.g., after organ transplantation surgery, systemic corticosteroid treatment, diabetes).15 Operative treatment Issues that comprise the decision for operative treatment include the following:
*Available from Orthotech GmbH, 82131 Gauting, Germany (www. orthotech-gmbh.de).
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Figure 22B-1 T1-weighted magnetic resonance imaging (MRI) sagittal. Complete rupture of the Achilles tendon with diastase of the tendon stumps.
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Figure 22B-3
An international perspective on the foot and ankle in sports
The Variostabil boot (Orthotech GmbH, 82131 Gauting, Germany; www.orthotech-gmbh.de).
Patients with dubious compliance for primary functional treatment. Patients who insist on or feel safer with a surgical procedure. Patients in whom no adaptation of the tendon stumps was found sonographically or on MRI. Patients with a demonstrable disruption of the soleus muscle. Patients such as top athletes for whom surgery is intended to prevent medial gastrocnemius atrophy. Patients with distal ruptures (2 cm) near the calcaneal insertion. It generally is possible to appose the tendon stumps within 3 weeks of rupture. In older ruptures the tendon ends usually are retracted and need reconstructive modalities.
Techniques In acute Achilles tendon ruptures, simple end-to-end or three-bundle sutures have been the methods of choice to date (Fig. 22B-4). In recent years in the United States the suture technique by Krackow (Fig. 22B-5) has become popular because it provides strong mechanical stability that allows early functional rehabilitation.16,17 A biomechanical study by Watson et al.,17 however, proved the weak stability of the suture realized by the different open techniques and questioned the advantages of the open surgical treatment. The combination of the advantages of the biology of tendon healing from the primary functional treatment along with minimally invasive surgery to stabilize the
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Figure 22B-4 End-to-end suture technique according to Bunnel-Mason.
tendon stumps adaptation for the first healing period is addressed by the percutaneous technique described by Buchgraber and Pa¨ ssler18 (Fig. 22B-6). Using only five small incisions, a 1.3-mm polydioxanone suture (PDS) is guided percutaneously by means of an awl. It connects the proximal tendon with the calcaneal insertion and crosses the
Treatment
The lace technique by Segesser pays special attention to the rotation of radiating tendon bundles, as described by Cummins. With his technique he provides an adequate reinsertion of the medial gastrocnemius and soleus fibers, which often are disrupted or retracted in Achilles tendon ruptures in top-level athletes (Fig. 22B-7). For rehabilitation, functional aftertreatment in the Variostabil boot is an essential part of an optimal outcome.
The suture technique according to Krackow.
rupture site, thereby acting as an internal fixator. To tighten the cord into the tendon, multiple dorsiflexions of the foot are performed. Another advantage of this technique is the remaining integrity of the paratendon, which is important for the healing process. To prevent the potential risk of injuring the sural nerve, an endoscopically assisted percutaneous technique with a 2.8-mm arthroscope can be used. 9
Figure 22B-6
Treatment of chronic ruptures The problem of chronic rupture is retraction of the tendon stumps with the lack of an efficient regenerate. Sometimes a primary reconstruction is possible, but in most cases reconstructive techniques are indispensable.
¨ssler. The percutaneous technique described by Buchgraber and Pa
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Figure 22B-5
Treatment of reruptures In the treatment of reruptures there are two options. If an adaptation of the tendon stumps is seen in plantarflexion either sonographically or by MRI, a simple percutaneous suture can be performed. In cases with a tendon gapping, a shortening of the gastroc-soleus-Achilles complex with adhesions is probable. This happens in the majority of delayed cases. In these circumstances, a small medial incision (4-5 cm) at the former incision is made. Then the gastro-soleus complex is released distally (Fig. 22B-8). A normal subcutaneous suture is performed and serves as an ‘‘internal fixator’’ of the ruptures tendon. In addition, classic Krakow sutures are applied for the tendon stumps (Fig. 22B-9). The aftertreatment has the same protocol with the Variostabil boot.
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Figure 22B-7
The lace technique by Segesser.
Figure 22B-8 complex.
Digital distal release of the gastro-soleus
The decision for the correct reconstructive technique depends on the amount of insufficient tissue. Therefore evaluation by MRI is mandatory. Defects of 2 to 5 cm arethe indication for reconstruction with a modified ‘‘two flaps technique,’’ first described by Thermann in
Figure 22B-10 The modified ‘‘two flaps technique.’’
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Figure 22B-9 Subcutaneous suture in addition to Krackow’s technique in the treatment of reruptures.
the year 2000. For reconstruction, two flaps of the aponeurosis of the triceps surae muscle are used. In the first step, the muscle is released proximal by a medial incision, followed by the preparation of the two flaps
Conclusion
Figure 22B-11 The transfer of the flexor hallucis longus tendon or the peroneus brevis tendon. In both techniques, the distal and proximal stumps are sewn together with the transferred tendon.
REHABILITATION The Variostabil boot plays a major role in rehabilitation and regaining of functional performance. The general concept is to prevent stress at the rupture site while having axial loading, which promotes a safe and powerful tendon healing. This boot has a plastic tongue to prevent dorsiflexion; the lateral shaft-stabilization reduces torsion, and the reducible heel pad allows a gradual adjustment of 20 degrees from plantarflexion to neutral position. Its
functional potential regarding gastrocnemius activities was proved by electromyography, which showed comparable amplitudes to the uninjured side after 3 months.15 With the fitted boot the patient is allowed to perform full weight bearing and to continue the previously begun isometric exercises. The patient wears the boot for 6 weeks, day and night (or alternatively uses a night splint to protect the tendon) and for the following 2 weeks only during the daytime. After 3 weeks the patient is allowed to exercise on a stationary bike, but only with little application of power. In ambitious patients, a physiotherapeutic treatment with well-dosed strengthening exercises (isometric exercises, isokinetic bicycle), proprioceptive neuromuscular facilitation (PNF), and coordination exercises in the boot is allowed after 4 weeks. In addition, ultrasound application (1 Hz) and cryotherapy are performed to enhance tendon regeneration. From the sixth week on, leg-press training is begun in the boot. After 8 weeks, an ultrasonographic control evaluates the restoration of continuity and tendon regeneration. After an appropriate tendon regeneration has been achieved (8 to 12 weeks MRI or sonography control), the treatment in the boot is discontinued. A small heel lift in the normal shoe is recommended for a further 6 to 8 weeks. Jogging is allowed after 3 months if coordination and muscle power are appropriate.
CONCLUSION The goal of treatment today is not only the restoration of the tendon continuity but also the regaining of the former activity level at the earliest possible time. This is achievable by the appropriate surgical technique and also depends on the adequate aftertreatment and rehabilitation protocol. 497
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from the medial and lateral part of the aponeurosis. Essential for the modification is the turning down and 180-degree rotation of the medial flap approximately 1.5 cm proximal to the corresponding lateral part. This offset considerably facilitates the skin closure later. After fixing the flaps medially and laterally at the distal stump, suturing is performed continuously with a 3.0-mm PDS cord in a ‘‘tubulation technique,’’ thus creating a ‘‘neotendon’’ as a consequence (Fig. 22B10). The neotendon should be stretched in a manner that forces a slight plantarflexion. For wound healing, a cleaved cast is applied, followed by rehabilitation in the Variostabil boot for 8 weeks according to primary functional treatment.9,19 Reconstruction of larger defects requires a transfer of the flexor hallucis longus tendon20 or the peroneus brevis tendon.21 In both techniques the distal and proximal stump are sewn together with the transferred tendon. Also, the neotendon should be adequately stretched to put the foot in an equine position (Fig. 22B-11). Because the peroneal tendon is not ‘‘in phase,’’ there are only very limited indications for this procedure. Rehabilitation protocol corresponds to the ‘‘two flaps technique.’’
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REFERENCES 1. Christensen J: Rupture of Achilles’ tendon, Acta Chir Scand 106:50, 1953. 2. Scho¨nbauer HR: Diseases of the Achilles’ tendon, Wien Klin Wochenschr 14(suppl 1):23, 1986. 3. Thermann H: Treatment of Achilles’ tendon ruptures, Foot Ankle Clin 4:773, 1999. 4. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature, Am J Sports Med 21:791, 1993. 5. Inglis AE, Sculco TP: Surgical repair of ruptures of the tendo Achillis, Clin Orthop 156:160, 1981. 6. Jakobs D, et al: Comparison of conservative and operative treatment of Achilles’ tendon rupture, Am J Sports Med 3:107, 1978. 7. Lo IK, et al: Operative versus nonoperative treatment of acute Achilles tendon ruptures: a quantitative review, Clin J Sport Med 7:207, 1997. 8. Nistor L: Surgical and non-surgical treatment of Achilles tendon rupture. A prospective randomized study, J Bone Joint Surg Am 63:394, 1981. 9. Thermann H: [Treatment of Achilles tendon rupture], Unfallchirurg 101:299, 1998. 10. Jozsa L, et al: The role of recreational sport activity in Achilles tendon rupture. A clinical, pathoanatomical, and sociological study of 292 cases, Am J Sports Med 17:338, 1989. 11. Riede D: Therapy and late results of subcutaneous Achilles’ tendon rupture, Beitr Orthop Traumatol 6:328, 1972.
12. Arner O, Lindholm A: Subcutaneous rupture of the Achilles tendon; a study of 92 cases, Acta Chir Scand 116(suppl 239):1, 1959. 13. Kannus P, Jozsa L: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients, J Bone Joint Surg Am 73:1507, 1991. 14. Thermann H, Zwipp H, Tscherne H: [Functional treatment concept of acute rupture of the Achilles tendon. 2 years results of a prospective randomized study], Unfallchirurg 98: 21, 1995. 15. Thermann H: [Rupture of the Achilles tendon–conservative functional treatment], Z Orthop Ihre Grenzgeb 136:20, 1998. 16. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation, Am J Sports Med 23: 392, 1995. 17. Watson TW, et al: The strength of Achilles tendon repair: an in vitro study of the biomechanical behavior in human cadaver tendons, Foot Ankle Int 16:191, 1995. 18. Buchgraber A, Pa¨ssler HH: Percutaneous repair of Achilles tendon rupture. Immobilization versus functional postoperative treatment, Clin Orthop 341:113, 1997. 19. Lindholm A: A new method of operation in subcutaneous rupture of the Achilles tendon, Acta Chir Scand 117:261, 1959. 20. Monroe MT, et al: Plantarflexion torque following reconstruction of Achilles tendinosis or rupture with flexor hallucis longus augmentation, Foot Ankle Int 21:324, 2000. 21. Trillat A, et al: [Treatment of former rupture of the Achilles tendon (transfer-plasty of the lateral peroneus brevis)], Lyon Chir 63:603, 1967.
C. Foot and ankle injuries in United Arab Emirates sports M. Kazim
The United Arab Emirates (UAE) has a desert climate and is situated directly on the Persian Gulf. This unique geography lends itself to a truly wide variety of sporting activities among the residents. Water sports such as water skiing, wakeboarding, and kite surfing are hugely popular. Other sports such as soccer, rugby, tennis, and squash are commonplace. In the desert, sand boarding and motor sports command the winter months. Most of the common injuries seen elsewhere are encountered but with some unique scenarios. Certain niche sports are found in the UAE. For example, falcons are trained to hunt prey. This involves long periods of bonding and progressive conditioning of the predator bird. To accomplish this, the owner often has to run rapidly to tend to his falcon, and in the soft sand this is better accomplished barefoot.
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Figure 22C-1 A unique sport in the UAE is hunting prey with falcons. The sandals keep the foot high off the ground to prevent entry of pebbles. They are discarded when running in soft sand.
Foot and ankle injuries in united arab emirates sports
On the harder desert plain, the hunter seen here with the falcon (A) uses enclosed shoes (B).
Sandals typically are worn (Fig. 22C-1) to keep the foot high off the ground to prevent entry of pebbles but are discarded when running in soft sand. Still, minor stub and barb injuries are common. Because the terrain underfoot is soft, the barbs or other objects have little force for any penetration. When training the falcons on the harder desert plain, one wears enclosed shoes (Figs. 22C-2 and 22C-3) to prevent the entry of foreign objects. Also, ankle sprains (mostly lateral) tend to be relatively minor on the sand because the surface is not firm and thus is very forgiving during inversion. Arabs have a long tradition with horses. In the UAE, horse racing (speed and marathon) and polo are two sports in which injuries are relatively common. Most tend to be in the upper extremities from falls, but foot and ankle injuries also occur. The prolonged ‘‘heel down’’ position in the saddle can lead to impingement syndromes of the anterior chamber of the ankle, requiring removal of any kissing osteophytes or soft tissues. Because these are mostly symptomatic early in their development, arthroscopic debridement is very successful, with arthrotomy rarely being required. Minor crush injuries of the foot and ankle occur as the horses collide during play, but
serious crush injuries from hooves are surprisingly uncommon in the UAE. This could possibly be from the combination of a high standard of horsemanship and well-trained thoroughbreds that are used in the sport. Motocross has its share of injuries because dirt bikes are ridden in the sand at high speeds. Riders are required to wear body armor and protective footwear (Fig. 22C-4). However, unlike hard dirt terrain that causes a violent plantarflexion force of short duration, sand produces a more moderate force of longer duration. This leads to sprains of the anterior structures, with relatively frequent anterior capsular tears. Conservative care with walker-type removable braces allows rapid return to riding. Occasionally, more severe problems such as Lisfranc injuries and subluxations or dislocations of the talocrural joint occur. When surgical reconstruction is warranted, rigid internal fixation is used, possibly including the repair of a deltoid ligament avulsion and concomitant syndesmosis stabilization (Fig. 22C-5). Long-distance bike riding is now becoming popular in the UAE. A relatively common problem seen in these cyclists is Morton’s neuroma. This happens despite appropriate shoewear and possibly results from a combination of the high heat and humidity causing edema of 499
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Figure 22C-2
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Figure 22C-3
An international perspective on the foot and ankle in sports
Another example of the falcon trainer (A) with typical shoewear (B) used for hard desert terrain (C).
the foot. Conservative care with metatarsal pads and a wider toe box to accommodate the forefoot is very successful. In the UAE, we emphasize rapid rehabilitation and return to sports. Fast-track programs and hydrotherapy
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for management of foot and ankle injuries provide an early start to the recovery process, with weight bearing as soon as safely possible. Rapid progression to strengthening and proprioceptive feedback exercises has been beneficial to returning the player quickly to his or her sport.
Foot and ankle injuries in united arab emirates sports
Figure 22C-4 A popular winter sport is motocross. The rider wears body armor and protective footwear to minimize injury. (A) The rider here is preparing to land on a dune following a jump. (B) The rider cuts across the soft and at times unstable sand and is susceptible to ankle and leg trauma.
Figure 22C-5 (A) This syndesmotic injury was noted on a stress view of the ankle. (B) Two syndesmotic screws close the tibiofibular space and suture anchors stabilize the deltoid tear.
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D. Nerve injuries complicating inversion ankle sprains E. Melamed and C. Zinman
Inversion, plantarflexion, and twisting forces put the ankle ligaments and bones under tension and strain that eventually may cause them to fail, culminating in ankle sprain and fractures. Diagnostic workup in the athlete usually is directed to rule out fractures, assess the severity of the ankle ligaments injury, and tailor treatment and rehabilitation to ensure healing of the ligaments in the desired length and strength. The proprioceptive mechanism and peroneal muscle strength also must be addressed to ensure safe return to sporting activities. Inversion injury imposes stretch and stress also on the more superficial structures, the nerves and integument. Skin swelling and hematoma formation are caused by injury to the skin and its lymphatics, small venules, and capillaries (in addition to bleeding from the torn ligaments) and is a sin qua non of ankle sprain. It usually resolves with time and is not a reason for concern to the treating physician or coach. However, there often is less awareness of the existence and importance of stretch to the nerves.1 Overall, the superficial peroneal nerve (SPN) is the most commonly injured nerve in ankle sprain as well as ankle fractures. The spectrum of injury to the SPN runs from mild (hardly noticeable stretch resulting in mild numbness, dysesthesia, or transient burning sensation in the distribution of that nerve) to severe allodynia, sudomotor changes, severe spontaneous pain, and paresis involving whole or large parts of the foot and ankle. These changes may evolve rapidly into a florid pain syndrome, reflex sympathetic dystrophy (RSD) by the older nomenclature or complex regional pain syndrome (CRPS) type 2 by the new one. In this section we briefly review the anatomy of the SPN, the pathomechanics and pathology of its stretch injury, and the myriad of symptomatology, focusing on early diagnosis of injury to the nerve. We equip the reader with some useful tips regarding early institution of therapy for these individuals by the primary care sport physician or orthopaedist. We review the algorithm and treatment options for the more severe cases.
ANATOMY The peroneal branch of the sciatic nerve separates from the tibial one at the popliteal fossa, where it takes a more
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lateral course. It emerges from underneath the biceps tendon near its insertion to fibula head and courses around the neck of the fibula, where it divides to the SPN and deep peroneal nerves (DPN). The SPN travels in the lateral compartment underneath the peroneus longus and exits the crural fascia to become subcutaneous about 10 to 15 cm proximal to the tip of the lateral malleolus in most cases.2,3 There are variations, however, in the exit mode, some of which carry special clinical relevance. The nerve can have a low exit point (5 cm from the tip in 2% and 7.5 cm in 5%).4 It also may penetrate into the anterior compartment first and then through the crural fascia. The SPN bifurcates to main two branches, the intermediate dorsal cutaneous nerve, supplying the dorsolateral aspect of the foot, and the dorsomedial cutaneous branch, which innervates the skin on the medial aspect of the dorsal forefoot and the hallux. Occasionally it also supplies the second toe and some cross innervation with the DPN in the first webspace.3
Pathoanatomy of nerve injury with ankle sprain Normal excursion of the peroneal nerve during ankle inversion is about 4 cm.5 This excursion is transferred and shared by the whole nerve up to the level of the common peroneal nerve through several gliding mechanisms. Severe ankle inversion may stretch the nerve beyond its physiologic capability to withstand stretch and gliding.6 Anatomic variations and preexisting conditions may hamper the gliding mechanisms and predispose to more severe injury.7 The exit level is important because if there is impedance to nerve gliding through the fascial hiatus and the exit is low, the same stretch is imposed on a shorter nerve segment. Even with a normal exit, overstretching because of severe inversion-plantarflexion may result in nerve damage. Typically a combination of the two will result in a more severe injury. Nerves that penetrate to the anterior compartment before emerging through the fascia cruris also are prone to stretch injury.8 We postulate other possible mechanisms that may contribute to gliding impedance and that have not been studied. The ‘‘acute on chronic entrapment’’ means that because of chronic entrapment there is fibrosis, thickening, or other changes in the fascial opening that impede gliding. In the case of severe sprain and extreme nerve stretch, the excursion of the nerve is relatively slow
Treatment
CLINICAL PICTURE Symptoms related to nerve injury in association with ankle sprain or inversion injury vary according to the severity of nerve damage. They often are masked by the associated mechanical derangement. The clinician may tend to ascribe the symptoms and pain to the mechanical ligamentous or bony injury and miss the opportunity to initiate early treatment, which in the severe cases may prevent deterioration to florid pain syndrome.
In general, we divide the clinical presentation of nerve injuries after ankle sprain to three groups on the basis of their myriad of symptoms and severity. Group 1 represents those with mild traction neuritis. They typically have mild numbness and/or allodynia. Their pain level is moderate (visual analogue score [VAS] score usually 4–7). The nerve is tender to palpation, percussion, and inversion. These patients usually heal well within 1 to 2 months. Patients in group 2 have significant symptoms and signs of neuritis. Pathologically there is perineural fibrosis, scarring, or intraneural microscopic changes. They may well have entrapment of the nerve in the fascial hiatus. They either have constant pain (usually burning, tingling, or electric shooters), which exacerbates with activities, or they may have only provoked pain. The nerve may look and feel thickened. Plantarflexion of the foot and fourth toe causes the nerve to be more prominent, and usually there is tenderness to percussion along the course of the nerve. Further plantarflexion and inversion is unpleasant and aggravates the athlete’s symptoms. Occasionally the tenderness will be confined to the exit site of the nerve from the fascia at the distal anterolateral aspect of the leg. In such cases entrapment is the probable diagnosis and the prognosis is favorable after surgical decompression. Group 3 was composed of patients with neuropathic pain whose pain and symptoms are beyond the distribution of the injured SPN. These patients suffer from increased general activity of the pain system and actually may have CRPS type 2.15 Their pain score is high (VAS 7–10). They have spontaneous and provoked pain in which pain often is worse at night. It is characterized by a burning quality, deep ache, or electric shooters. There often is diffuse swelling from the toes to the distal leg, transient color and temperature (vasomotor) changes, and sudomotor disturbances, which may manifest as edema and hyperhydrosis or dry skin. The skin often is swollen and shiny. Allodynia (pain in response to nonpainful stimuli, e.g., light touch) is common. Sensation typically is disturbed beyond the territory of the injured nerve. Weight bearing is limited and often impossible. The prognosis for these patients typically is grave. We assume that early intervention with pain treatment may halt the progression to florid pain syndrome in many of these patients. The role of early surgical intervention has not been established yet, but certainly in some of the cases it is justified.
TREATMENT Nonsurgical treatment ............................................................. As a routine, nonsurgical treatment should be used first. In some of the cases, however, nonoperative modalities 503
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in the canal. The excessive stretch is loaded mainly on the distal part of the nerve. We assume that muscle swelling and increased intracompartmental pressure created during rigorous athletic activity9 presses the nerve against the fascia cruris and impedes nerve gliding through the hiatus. Another hypothesis is the ‘‘intraperoneal entrapment.’’ During acute inversion the nerve glides distally. At the same time, rigorous contraction of the peroneal muscles may compress and entrap the SPN, which courses between them. The contracting muscles pull the nerve proximally, in the opposite direction, thus increasing the stretch on the nerve. There may be damage to the subcutaneous tissue because of shearing and ruptures of subcutaneous fat, small blood vessels, and lymphatics. Scarring will ensue, and the areolar tissue, which allows the nerve to glide smoothly, will lose its pliability. The clinical relevance of this phenomenon per se may be the experience of pain on inversion (sometimes even at night because of the plantarflexed-inversion position of the foot at sleep) and/or chronic, occasional subclinical entrapment, which may manifest itself only in a future sprain episode. Quite often the picture is mixed, with intraneural, perineural, and nerve bed changes. Histologically, in the severe cases stretching injury to nerve will result in perineural tears, which may lead to intraneural and perineural fibrosis.10,11 In cases in which we had to resect the nerve following inversion ankle injury, we saw on histology laceration and discontinuation of nerve fibers. In one extreme case we observed fatty degeneration with marked thickening of the nerve. Macroscopically the picture varies from a nerve that appears normal to a thickened one. The fascial exit site may show frank cicatrization. Extensive scarring may be seen at the nerve bed at the dorsum of the foot, which interferes with nerve gliding (Fig. 22D-1). New evidence sheds light on the role of inflammation in the pathology and perpetuation of nerve pain with the development of pain syndromes.12-14 Although the importance of the inflammatory mechanism is not completely clear, and the research was focused on patients with CRPS, the available data suffice to justify the addition of anti-inflammatory agents to the treatment protocol.
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Figure 22D-1 A 22-year-old sustained an ankle sprain 3 years before surgery. She developed pain in the distribution of the superficial peroneal nerve (SPN) that worsened with walking and at night. SPN block relived 80% of her pain. She was not improved with nonsurgical therapy. At surgery to release the nerve, dense scarring was found along the course of the nerve (A-C). A stepwise release was carried out (B and C). Nerve release and dissection must continue proximally to the exit point of the nerve from the peroneal muscle compartment (C). The nerve is freed distally until unscarred nerve can be seen (in this case far beyond the bifurcation to its two main branches. At completion of release, the fascia has been opened and the nerve can be seen emerging freely from the muscular compartment (D). The patient felt complete relief immediately after surgery, but over the course of the next year worsened to some extent. Two years after surgery she has mild pain on daily activities but does not take pain medications. She can perform limited sport activities.
will not be effective, and occasionally, delaying surgery has its own risks. For example, traction injury to the SPN, which flares out the adjacent nerves and the pain system with evolving CRPS, may be treated best with early nerve release or transection. In such cases, a short course of aggressive medical treatment may need to be followed by early surgery. Nonsurgical means include oral medications, topical applications, repeated nerve blocks, physical therapy, and pain modalities. More complicated pharmaceutic interventions, sympathetic or epidural blocks, or spinal cord stimulation can be performed by physiatrists and pain specialists.
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Oral medications We prescribe pain medications, which affect the various modalities of the altered pain pathways. Such treatment may include a combination of acetaminophen (or dipyrone), nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., celecoxib, rofecoxib, etodolac, diclofenac), nerve pain medication that is usually either antidepressants or antiepileptics, and tramadol (Ultram; Ortho-McNeil, Inc., Raritan, NJ) and/or narcotic medications.16,17 The selection of treatment modality is determined mainly according to the severity and intensity of symptoms. The relationship between the type of pain and
Treatment
Carbamazepine (Tegretol; Novartis Pharmaceuticals, East Hanover, NJ) is an antiepileptic medication with known antineuralgic effect. For many physicians this is the drug of choice for neuralgic pain. The dose for that indication usually is 400 to 800 mg/day. The initial dose is 100 mg twice a day, and it can be increased in 200-mg daily increments. Timonil (carbamazepine sustained release; Desitin Pharmaceuticals, Hamburg, Germany) is a prolonged-release version, manufactured in 300-mg tablets that can be divided to quarters. One quarter of a tablet daily is taken initially and the dose is increased by another quarter every week. Drowsiness, dizziness, and blurred vision are the main side effects. Discontinuation should be implemented gradually. Gabapentin (Neurontin; Pfizer, New York, NY), also an antiepileptic drug, may be the most effective medication available for neuropathic pain, with fewer side effects and good tolerability. Its main limitation is high cost, and in many countries it is not approved yet for peripheral neuritic pain. The initial dose is 300 mg once a day, increased every 3 days by 300 mg to 300 mg four times a day (e.g., change from once to twice to three and four times a day, with every change made after 3 days of getting used to the new dosage). Higher doses may be required, but we recommend in such cases that the patient be seen by a pain specialist or a physiatrist.
Topical preparations Few topical preparations are available. Capsaicin (Zostrix; Rodlen Laboratories, Health Care Products, Amityville, NY) is an active ingredient of red pepper that causes substance P depletion, thus interrupting nerve transmission at the peripheral level. It is applied on the tender regions (or along the course of the nerve if it is tender) three or four times daily. The main side effect is burning sensation at the site of application. If severe, this sensation can be relieved by preventive lidocaine application (EMLA cream) before applying Zostrix. It may take a few days to 1 month before Zostrix exerts its analgesic effect. Once the burning sensation has decreased, one can change from the low to the higher potency (0.075%). Another alternative is the lidocaine patch (Lidoderm; Endo Pharmaceuticals, Chadds Ford, PA), which is applied once daily and releases the local anesthetic in a controlled mode. Topical NSAID preparations may have a role in mild cases but we have not seen great benefit in cases of neuropathic pain. In the United States, Custom Meds (Inverness, FL) a custom compounding company, formulates nearly all of the previously mentioned medications into an absorbable, topically applied gel. The formulations, combinations of various doses of medications, can be applied to the affected area with good results. 505
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specific drug selection is not so clear. In the mild to moderate cases an ascending prescription attitude can be adapted. In this approach either a new or additional medication or higher dose of a given one is added gradually as needed. Simple pain medication (e.g., acetaminophen or dipyrone) is sufficient in group 1 or mild group 2 cases. (Dipyrone is an antianalgesic and antipyretic but not an anti-inflammatory medication; it is approved for use in many parts of the world but not in United States because of the rare incidence of agranulocytosis). An NSAID is prescribed concomitantly or subsequently. If pain is refractory to these medications, or in the presence of neuropathic symptoms (allodynia, burning sensation), nerve pain medication is added. Nerve pain medications usually are either antidepressants or antiepileptics. Their role is to decrease the spontaneous nerve activity and reset the correct pain threshold. Typically, the dose is increased gradually. The next step is a more potent pain medication. Tramadol is a weak m receptor agonist and N-methyl-D-aspartate (NMDA) receptor inhibitor. Although it is not regulated as a narcotic medication, it resembles narcotics in its affinity to m receptors and in having (uncommon) addictive potential. Narcotics can be prescribed for severe or refractory cases. In common use is oxycodone, which is available in a controlled-release preparation (daily every 8–12 hours) or in combination with aspirin (Percodan; Endo Pharmaceuticals, Chadds Ford, PA) or acetaminophen (Percocet; Endo Pharmaceuticals, Chadds Ford, PA). OxyContin (sustained-release oxycodone; Purdue Pharma L.P., Stamford, CT) usually is prescribed at 10 mg twice a day initially, and the dose can be increased to 20 mg twice a day. If a higher dose is needed, we recommend urgent referral to pain clinic. It is worthwhile for the orthopaedist or sport physician to have in his or her armamentarium two or three nerve pain medications. Our first choice drug is amitriptyline (Elavil; AstraZeneca Pharmaceuticals LP, Wilmington, DE), which is a tricyclic antidepressant, 10 mg daily at night. The goal and treatment rationale should be discussed with the patient; otherwise he or she may not comply. The patients typically will read on the package that this is an antidepressant therapy and are reluctant to take the medicine, unless they had received the needed explanation. The dose may be increased in weekly intervals to 20 (two 10-mg pills), 25, 35, and 50 mg. The main side effect is sedation, which may be beneficial in case of night pain. The patient should be warned against driving or performing tasks that mandate alertness. Other common side effects are dry mouth, blurred vision, and constipation. Because of the relative low doses (in comparison with that required for depression) the side effects usually are not severe, and approximately three quarters of patients can tolerate the drug.
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An international perspective on the foot and ankle in sports
Nerve blocks Nerve block with local anesthetic often is essential to confirm the diagnosis. In some patients the block has a therapeutic effect with symptomatic improvement that outlasts the pharmacologic effect of the local anesthetic. The physiologic basis for this phenomenon is not completely clear. There is cessation of bombardment of the central nervous system with painful impulses that may affect the central sensitization of the pain system. We combine a short-acting local anesthetic (e.g., lidocaine) with a longer-acting one. Bupivacaine is a longacting local anesthetic with average effect of 6 to 12 hours. The main hazard is inadvertent intravenous injection, which may cause lethal arrhythmia (ventricular fibrillation). Alternatively, the addition of adrenaline may double its duration. Ropivacaine (Naropin; AstraZeneca Pharmaceuticals LP, Wilmington, DE) has a local anesthetic effect for nearly 24-hours and has the benefit of a good safety profile. Its main disadvantage is high cost. When performing a nerve block we generally use a 25-gauge needle to minimize the additional risk of inadvertent damage to the nerve. We estimate that up to one third of patients will respond favorably to repeated nerve block. If the patient experiences a beneficial effect that lasts several days, there is a role for repeated nerve blocks.
Surgical treatment ............................................................. If nonsurgical means fail to achieve the desired effect, surgery may be contemplated. In general, entrapment of the SPN at its exit site from the compartment will respond favorably to surgical release of the fascia. The surgical findings will dictate whether fascial release will be sufficient and will help to establish the prognosis. In cases in which adhesions are found, release of the nerve should provide immediate relief. If there is a thick scar bed, the risk that new adhesions will form is significant. In the case of intrasubstance damage to the nerve, a nerve release probably is not going to help. In addition, it is important to consider and to inform the patient that there is an element of unpredictability in the response of nerve to surgery (and insult). This is particularly true if resection of a diseased nerve is indicated. In this case, there is considerable risk for temporary and even permanent pain exacerbation, often in adjacent nerves.
Type of surgery selected As a rule, the choice of surgery follows Schon’s algorithm of surgical treatment for nerve pain.18 The common surgeries are nerve release, revision nerve release (with or without containment), nerve resection (usually with burial of the nerve stump), and peripheral nerve stimulation (PNS).
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Neurolysis of the nerve often is successful in the case of entrapment. The crural fascia is opened 3 to 5 cm from the original exit site. Smooth excursion of the nerve is checked intraoperatively. The surgeon observes that there also is free movement of the nerve in the fatty tissue more distally. If the fat and nerve seem normal, there is no need to extend the surgical incision distally. In case of adhesion bands, the nerve is freed as far distally as needed, usually beyond the division to its two main branches (Fig. 22D-1). Scar tissue may be formed around the nerve. Dense adhesions imply damage to the nerve bed and increase the likelihood of rescarring. The typical result will be temporary relief with worsening of symptoms beginning after 6 weeks. In the milder cases, new adhesions may be formed up to 1 or 2 years from surgery. If there is no relief after surgery, either an incomplete release or an intrasubstance nerve lesion is the cause. The nerve may have looked normal or grossly disturbed. If there are no adhesions or entrapment, intranerve damage is the probable cause. The surgeon then should consider whether to resect the nerve. If the symptoms are severe (VAS score 8–10), the nerve probably should be resected. We bury the stump in the fibula and have not experienced stump tenderness.19 Loss of sensation on the dorsum of the foot usually is unpleasant but tolerable. If there is a flare-up of the pain in adjacent nerves and the patient shows signs of CRPS, then more aggressive management is indicated. If nerve resection fails to relieve pain and the pain is confined to the specific nerve distribution, PNS is the next step.20,21 In this procedure an electrode is implanted on the nerve and is connected to an internal pacemaker that can stimulate the nerve. Stimulation of the nerve generates nonpainful stimuli that ‘‘close the gate’’ to painful impulses and thus relieve the pain. The surgery involves a wake-up test after the nerve is isolated and the wound anesthetized. During this portion of the implantation, the patient is reversed from anesthesia and the 4-electrode lead is placed in various locations around the nerve until pain relief is achieved. If the test is favorable, the patient is placed under anesthesia to permit tunneling of the wires and insertion of the pacemaker device in the thigh. In severe cases, some surgeons advocate considering the combination of concomitant nerve resection and PNS. In a long-term follow-up study (3–16 years), good results (more then 50% relief of pain with abstinence from analgesic medications) were reported by 36 out of 46 patients (78%).20
REFERENCES 1. Nitz AJ, Dobner JJ, Kersey D: Nerve injuries and grade II and III ankle sprains, Am J Sports Med 13:177, 1985.
Judo 2. Blair JM, Botte MJ: Surgical anatomy of the superficial peroneal nerve in the ankle and foot, Clin Orthop 305:229, 1994. 3. Saraffian SK:In Anatomy of the foot and ankle: descriptive, topographic, functional, ed 2, Philadelphia, 1993, Lippincott. 4. Horwitz NT: Normal anatomy and variations of the peripheral nerves of the leg and foot, Arch Surg 36:626, 1938. 5. Kleinrensik GJ, et al: lowered motor conduction velocity of the peroneal nerve after inversion trauma, Med Dci Sports Exerc 26:887, 1994. 6. Millesi H, Zoch G, Rath T: The gliding apparatus of peripheral nerve and its clinical significance, Ann Chir Main Memb Super 9(2):87, 1990. 7. Styf J, Morberg P: The superficial peroneal tunnel syndrome. Results of treatment by decompression, J Bone Joint Surg 79B:801, 1997. 8. Acus RW 3rd, Flanagan JP: Perineural fibrosis of superficial peroneal nerve complicating ankle sprain: a case report, Foot Ankle 11:233, 1991. 9. Styf JR, Korner LM: Chronic anterior compartment syndrome of the leg, J Bone Joint Surg 68A:1338, 1986. 10. Kwan MK, et al: Strain, stress and stretch of peripheral nerve. Rabbit experiments in vitro and in vivo, Acta Orthop Scand 63:267, 1992. 11. Lundborg G: Structure and function of the intra-neural microvessels as related to trauma, edema formation and nerve function, J Bone Joint Surg 57A:938, 1975. 12. Bennet GJ: Are the complex regional pain syndromes due to neurogenic inflammation? Neurology 57:2161, 2001. 13. Oyen WJ, et al: Reflex sympathetic dystrophy of the hand: an excessive inflammatory response? Pain 55:151, 1993.
14. Weber M, et al: Facilitated neurogenic inflammation in complex regional pain syndrome, Pain 91:251, 2001. 15. Stanton-Hicks M, et al: Reflex sympathetic dystrophy: changing concepts and taxonomy, Pain 63:127, 1995. 16. McQuay HJ, et al: A systematic review of antidepressants in neuropathic pain, Pain 68:217, 1996. 17. Monfared H, Sferra JJ, Mekhail N: The medical management of chronic pain, Foot Ankle Clin North Am 9:373, 2004. 18. Schon CL, Easley ME: Chronic pain. In Myerson MS, editor: Foot and ankle disorders, vol 2. Philadelphia, 2000, WB Saunders. 19. Melamed EA, Schon LC: Deep burial of resected nerve in bone—a simple technique, Foot Ankle Int 23:952, 2002. 20. Eisenberg E, Waisbrod H, Gebershagen HU: long term peripheral nerve stimulation for painful nerve injuries, Clin J Pain 20:143, 2004. 21. Schon LC, et al: Prelimunary results of peripheral nerve stimulation for intractable, lower extremity nerve pain, Pain Med 1:195, 2000.
FURTHER READING Schon LC, Easley ME: Chronic Pain. In Myerson MS, editor: Foot and ankle disorders, London, England, 2000, WB Saunders. Styf J: Entrapment of the superficial perineal nerve, J Bone Joint Surg 71B:131, 1989.
E. Foot and ankle injuries caused by traditional Japanese martial arts Yasuhito Tanaka
JUDO Because judo is an Olympic sport, the number of people who practice judo is increasing worldwide. A judo contest is a fight between two contestants who wear judo suits and fight on tatami (straw) mats. The first contestant to score a full point (‘‘ippon’’) wins. A contestant can score a full point by throwing the opponent on his or her back, holding the opponent for 30 seconds, or making the opponent concede. Injuries almost always are caused by throwing moves. Many judo injuries occur in the lower extremities, particularly at the knees, ankles, and feet. Because mild foot injuries are so common, those who sustain them rarely seek treatment at a medical institution. 507
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In Japan, there are many forms of traditional martial arts that are still actively practiced today. This chapter explains in detail foot and ankle injuries associated with the three most popular martial arts: judo, sumo, and kendo. Although the origin of these martial arts is not known, the earliest known mention of their basic forms is found in Japanese documents written during the eighth century. In the last half of the nineteenth century, the modern rules for these martial arts were established, and people began to practice them as sports. Because these martial arts are practiced barefoot, there is a high incidence of ankle and foot injuries among their practitioners. However, because playing surfaces and styles of competition differ markedly among these three martial arts, they are associated with different foot injuries.
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Figure 22E-1 Many judo injuries occur in the lower extremities. During ‘‘Ohsoto-gari,’’ a throwing technique, the foot and ankle assume an equinovarus position. Inversion sprain can occur in the foot of a defense (arrow).
The most common foot injury is ankle sprain; about half of all judo practitioners suffer an ankle sprain at some point (Fig. 22E-1). Severe inversion sprains typically are accompanied by osteochondral fracture of the talar dome. Also, ankle instability persists in many cases, and many people who practice judo for a long period develop osteoarthritis of the ankle. Also, when a strong external force is applied, a malleolar fracture occurs, but plafond fractures and talar fractures are rare. The incidence of toe injury is high among judo practitioners. Turf-toe is a well-known injury associated with sports played on turf, such as American football. Most cases of turf-toe are caused by excessive dorsiflexion of the great toe. When a foot sweep is attempted in judo, the sweeping foot is in the equinovarus position and is swung horizontally. If the sweeping foot gets caught in the seams of the tatami mats or on the opponent’s foot,
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Figure 22E-2 The great toe is easily plantarflexed (arrow) (‘‘tatami toe’’). Tatami (straw) mats typically are used as a floor covering in judo.
the metatarsophalangeal joint of the great toe is excessively plantarflexed (Fig. 22E-2). Although this generally causes sprain without a fracture, severe bending can cause a chip fracture. This type of toe injury is sufficiently unique to judo to merit its own name (perhaps ‘‘tatami toe’’). If accompanied by osteochondral damage to the metatarsophalangeal joint of the great toe, osteoarthritis can lead to hallux rigidus. Although toe injuries most often affect the great toe, sometimes they can affect the lesser toe.
SUMO Sumo is a sport in which two wrestlers fight on a round ring that is made of packed earth and has a diameter of about 4 m. Sumo wrestlers wear nothing but a loincloth belt. In each bout, two wrestlers initially face each other from
Kendo
behind two parallel lines at the center of the ring. Once the bout begins, they collide violently, like guards and tackles in American football. The loser is the first wrestler to touch the ring with any part of the body other than the bottom of the feet or the first wrestler to go out of the ring. Sumo wrestlers try to push each other out of the ring, and heavy body weight confers an advantage in this pushing. Consequently, sumo wrestlers intentionally try to achieve and maintain a heavy body weight. Although the most common clinical problem associated with sumo is lumbar pain, injuries in the lower extremities account for more than half of all injuries associated with sumo. Ankle and foot injuries account for about 15% of all sumo-related injuries. It might seem that this is a low percentage for a sport that is practiced barefoot. The reason for this low percentage is the manner in which sumo wrestlers move, by shuffling their feet instead of lifting their feet off the ground (Fig. 22E-3). In sumo, the friction between the ground and the soles of the feet is important in keeping a wrestler in position. If either foot comes off the ground for even a short time, the wrestler easily can be pushed out of the ring. Thus shuffling helps to prevent a wrestler from being pushed out of the ring. During shuffling, the knees are bent in the valgus position, the lower legs are abducted, and the feet are pronated. As a result, sumo training strengthens the peroneal muscles, thus lowering the incidence of inversion sprain. Furthermore, even if a sprain occurs, it usually does not cause persistent ankle instability. Foot shuffling and squatting with knees spread apart are the basic movements of sumo, and during these
movements the ankles are dorsally flexed. Thus in competition, the ankle often is dorsally flexed (Fig. 22E-4). Furthermore, when a wrestler braces against being pushed out of the ring, the ankles are in excessive dorsiflexion. On the anterior surface of the ankle, the tibia often collides with the neck of the talus, causing impingement exostosis. Because this condition exists in most sumo wrestlers, and not many sumo wrestlers have ankle instability, its onset must involve collision. Because sumo wrestlers are heavy and collisions are violent, there is a high incidence of bone fracture around the ankle. Pronation-external rotation-type malleolar fracture is common because the lower leg is abducted and the foot is pronated, unlike the case in sports that are played with a ball. However, despite their severity, rehabilitation of such injuries is faster than for soft-tissue injury. Severe toe injuries are less common than severe ankle injuries. Unlike judo, sumo does not involve many moves in which a foot in the equinovarus position is swept sideways. However, lacerations of the skin on the plantar side of the first metatarsophalangeal joint are very common. Some sumo wrestlers prevent such lacerations by taping their toes or wearing Japanese thick-soled socks (‘‘tabi’’) (Fig. 22E-3).
KENDO Japanese swords are the symbol of the Samurai culture. Unlike Western swords, Japanese swords are held using both hands. Kendo is a sport modeled after samurai sword fighting, using bamboo swords resembling Samurai swords. Practitioners wear protective pads on the face (‘‘men’’), belly (‘‘do’’), and forearm (‘‘kote’’). A point 509
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Figure 22E-3 Exercise of shuffling. Keeping the feet on the ground improves stability in this sport, which evolves around collisions and pushing. The knees are bent in the valgus position, the lower legs are abducted, and the feet are pronated. The playing surface is packed earth. Sumo wrestlers tape their toes and wear ‘‘tabi’’ to prevent lacerations on the soles of their feet.
Figure 22E-4 The ankles often are dorsally flexed in a bout. The incidence of anterior ankle impingement exostoses is high in sumo wrestlers.
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Figure 22E-6 An offense hit on a face guard (‘‘men’’). The right leg goes forward during a lunge. Excessive force is loaded on the left Achilles tendon during the sport. The incidence of Achilles tendon injuries is high relative to the other martial arts.
Figure 22E-5 A starting posture of kendo is demonstrated. Note that the sport is practiced barefoot on a wooden floor. The right leg is in front of the left. Weight is kept on the forefoot.
is scored when a bamboo sword cleanly hits one of the protective pads. A kendo practitioner holds a bamboo sword using both hands, with the right hand in front of the left hand, somewhat like a right-handed baseball player holding a bat. The two competitors face each other so that the tips of their bamboo swords are lightly touching (Fig. 22E-5). Right- and left-handed practitioners take the same stance. The right foot is placed in front, while the left foot stays back. Competitors put their weight on the front half of each foot and slightly lift the heels so that they can move very quickly. Kendo is generally a safe sport, with a low incidence of fracture, but mild toe injuries are quite common. Beginners often complain of heel pain. Because kendo is practiced barefoot on a wooden floor, there is great impact on the feet during kendo moves. About 40% of kendo practitioners develop hemoglobinuria because red blood cells in the skin and subcutaneous tissue of
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the sole are destroyed by the impact of the heel hitting the floor. Some kendo practitioners develop a condition called ‘‘black heel,’’ which is characterized by ecchymosis on the sole of the feet. Usually, heel pads are used to treat this condition. In kendo, the most common severe injury is rupture of the Achilles tendon. This injury almost always occurs in the left leg, because of the positions of the legs in the kendo stance (Fig. 22E-6). During kendo moves, a great amount of force is applied to the left leg. When the body pushes forward, the triceps muscle of the calf is tensed, and the Achilles tendon can rupture if there is a delay in plantarflexion of the ankle. In most sports, rupture of the Achilles tendon is rare among young people, but among kendo practitioners, this injury is somewhat common in high school students. This supports the theory that a great amount of force is applied to the Achilles tendon in the left leg when the body pushes forward in kendo. Rupture of the Achilles tendon is rare among beginners but is more common among skilled practitioners. Most of those who sustain this injury chose to undergo surgery, and rehabilitation takes 6 to 12 months.
Kendo
F. Foot and ankle problems caused by some traditional Chinese habits and sports Xu Xiangyang and Zhu Yuan
There are some traditional sports that are still popular in China, such as shuttlecock kicking, rope skipping, and Chinese ‘‘wushu,’’ often called kung fu. Although Chinese wushu is changing to be more competitive, most of the time traditional Chinese sports are pursued for health purposes and personal fulfillment. Thus there are infrequent opportunities for competitive athletics among the general public. Still it is not unusual to see foot and ankle injuries caused by these traditional
‘‘Wushu,’’ a popular traditional sport.
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Figure 22F-1
Chinese sports in clinic, usually a soft-tissue injury without a major fracture (Fig. 22F-1). The frequent reasons for foot and ankle injury stem from the players performing a trick when they kick the shuttlecock and/or skip rope. Coupled with uneven ground, this is a typical setup for an accident. Although some players did this well when they were young, their mental capabilities may be greater than their physical competence in their later years. Furthermore, injury
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An international perspective on the foot and ankle in sports
Figure 22F-2
‘‘Wushu,’’ a popular traditional sport.
Figure 22F-3
‘‘Wushu,’’ a popular traditional sport.
may occur as a result of increasing body weight, decreasing strength of their ligaments, or declining general fitness. Chronic injury is seen in Chinese wushu when the player continues to practice wushu exercises for decades after a primary injury that occurred when he or she was younger. There are many different kinds of foot and ankle injuries caused by these traditional Chinese sports. They include ankle sprain, fifth metatarsal base avulsion fracture, medial and lateral malleolus fracture, Achilles tendon rupture, diastasis of syndesmosis, metatarsophalangeal joint capsular injury, and instability of the ankle.
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Figure 22F-4
Shuttlecock kicking.
Most of the time we manage these kinds of injuries with traditional Chinese medicine unless we find the injury unstable or prone to sequelae. There are some special, traditional treatments for soft-tissue injuries of the ankle joint in China that have a long history. These include acupuncture needles, Chinese herb ointment, fomentation, and foot massage. Ice, Chinese herb ointment, and sometimes a splint are the usual management for soft- tissue injury in the early stage of trauma. Chinese herb ointment can effectively decrease the swelling and dissipate the sludge (edema, etc.) quickly. Fomentation, needles, and massage,
Kendo
Figure 22F-5
Rope skipping.
Figure 22F-6
Chinese herb ointments and their original materials.
of ‘‘Bi,’’ or pain, caused by a localized disruption to the flow of Qi. The traditional Chinese explanation for soft-tissue injury is that the channel running through the damaged tissue has been physically disrupted, resulting in local pain, a disease of Bi. To treat the pain, the integrity of the channel and the flow of vital energy through the channel must be restored. This can be achieved by the selective use of points on the damaged channel, thereby restoring the flow of Qi and relieves the pain. 513
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accompanied by functional exercises, are the treatments for subacute injury. Needles and massage are important components of restoring balance to the person’s vital energy channels, which form the basis behind traditional Chinese medicine. The channels are a system of conduits throughout the body that carry and distribute Qi, or vital energy. Disease is present when the flow of vital energy through the channels is disrupted. This may occur when the integrity of the channels themselves is damaged by a sprain or strain. The Chinese describe this as a disease
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Figure 22F-7
An international perspective on the foot and ankle in sports
Foot massage.
The foot plantar surface is an important place for the body because there are many points of channels, which represent many internal organs. Therefore foot massage not only treats the injury of foot but also can treat diseases anywhere in the body. In China, foot massage hygiene is looked on as a good method for preventing and treating diseases and is popular throughout the whole country. Foot massage is used to stimulate the points of the channels that can activate the gates of the body, which are opened and closed to adjust circulation in the channels. Foot massage has four functions: (1) it can enhance the blood circulation, so as to accelerate the metabolism of the body; (2) it can regulate the nervous system; because there are many nerves endings in the foot,
Figure 22F-8 Foot massage.
one can stimulate the reflex zone of the foot to regulate the corresponding tissues and organs; (3) it can mobilize Qi, moisture, and blood and invigorate proper function of the muscles, nerves, vessels, glands, and organs; and (4) it brings the efficacy of release and relaxation. Generally, foot and ankle soft-tissue injury can be cured with Chinese traditional medicine in 2 to 3 weeks. Even if there is instability of the ankle, most patients can get good results after these treatments. Only a few patients need surgery for ligament repair. Certainly, if there is a relatively severe fracture of the ankle and foot, surgery or casting is necessary. In general, foot massage is the mainstay of treatment and is used for healthy care as well.
G. Foot and ankle sports injuries in Korea Hong-Geun Jung, Kyung-Tai Lee, and Yong-Wook Park
INTRODUCTION Overall, foot and ankle sports injuries in Korea are similar to those in the rest of the world, because most of the sports that are played at present, such as soccer, basketball, and baseball originated in non-Asian countries. Distinct sports injuries occurring during some of popular Korean traditional sports and martial arts, such as ssireum and taekwon-do, are reviewed.
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Furthermore, we present some specific injuries that seem to show a higher incidence in Korea.
SSIREUM (KOREAN TRADITIONAL WRESTLING) Ssireum is a contest of physical strength and technique in which two contestants compete in direct contact
Taekwon-do (Korean martial arts)
against one another. It is a form of traditional wrestling found in Korea. There also are some sports similar to Korean ssireum in other countries, such as sumo in Japan. buh in Mongolia. sambo in Russia, and kara kuc¸ak or yag˘li guresˇ in Turkey. Ssireum involves two contestants grasping, pulling, lifting, twisting, pushing, and tumbling as each competitor attempts to throw the opponent to the ground (Fig. 22G-1). If a competitor can force any part of the opponent’s body above the knee to touch the ground, the competitor wins the bout. There are hundreds of techniques, categorized into hand techniques (throwing the opponent to the ground by using the hands), leg techniques, and trunk techniques (using the back). Studies have shown that rupture of the Achilles tendon, ankle sprains, acute dislocation of the peroneal tendon, chronic lateral ankle instability, osteoarthritis of the ankle, and osteochondral lesion of the talus are not infrequently experienced during ssireum. Acute ankle sprains and chronic lateral ankle instability are the most commonly experienced injuries in ssireum because of the repeated turnings and the difficulty in maintaining balance against force in the sand. Two frequent mechanisms occur when the opponent pushes the trunk while the foot is stuck in the sand, causing ankle twisting injury, and when the opponent lets the player down on the sand, abruptly causing ankle imbalance and ligament injury. Osteochondral lesions of the talus are also experienced because of the weight of the players and the frequency of injuries of the ankle. Similarly the high body
Taekwon-do is a well-known Korean martial art that is established as an international sport and is also being accepted for the Olympic Games. It is the martial art that mainly uses the lower extremities for hitting the opponent in the match. The various dazzling kicking techniques such as front kick, side kick, and roundhouse kick (the most commonly used kick in sparring) are the key weapons in winning the game. These maneuvers (Fig. 22G-2) subject the participants to injuries around the foot and ankle. The most common injury occurs on the dorsal lateral aspect of the midfoot when the player hits the opponent with this part of the foot with the ankle at maximum plantarflexion. Typically, the foot strikes the opponent’s elbow, dorsal foot, or even pelvis, leading to Lisfranc joint trauma or metatarsal fractures. Likewise, the anterior aspect of the ankle and shin often are bruised under the same circumstances as they strike against the guarding elbow. Fortunately these impacts rarely require surgical treatments.
Figure 22G-1 The ankle often is injured when the two ssireum contestants forcefully try to tumble the opponent down on the uneven ground.
Figure 22G-2 A taekwon-do expert attacks the opponent in the head with roundhouse kick; the forefoot or midfoot often gets injured during these kicks.
weight, poor balancing, and repetitive lifting of the large opponents on the sand are factors that contribute to the rupture of the Achilles tendon. In addition, fracture of the base of the fifth metatarsal, ankle fractures, and big toe fracture or sprain have been observed and are due partly to the uneven ground surface made of sands.
TAEKWON-DO (KOREAN MARTIAL ARTS)
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Big toes at the metatarsophalangeal (MTP) and interphalangeal (IP) joints are the second most common sites of foot and ankle injuries, often because of incorrect kicking and unbalanced landing on the floor. These are mainly ligamentous traumas that sometimes result in MTP or IP dislocations and rarely involve fractures. Front kick injuries can cause toe sprains, dislocations, or fractures, as well as acute and chronic posterior ankle impingement. Sever’s disease, calcaneal apophysitis, also can occur in children who engage in the sport. Ankle sprains often occur while kicking the opponent or while landing on the mattress or floor after the kick. Chronic lateral ankle instability is quite common because of repeated inversion injuries. Approximately 40% of a college taekwon-do team experienced at least three ankle sprains in a year, and 60% experienced ankle pain during the match.
BASKETBALL, SOCCER, RUGBY, AND BASEBALL Survey of the foot and ankle injuries in Korean college basketball, soccer, rugby, and baseball teams was performed. Ankle sprains (100%) and chronic lateral instability (50%) were very common among basketball players because of frequent jumping and landing in the limited space. This also led to second and fifth metatarsal and navicular stress fractures. Soccer players often experienced ankle sprains (100%, 23/23) on the artificial lawn after jumps and tackles. Ankle and toe fractures, as well as tibial and metatarsal stress fractures, also were noted. Approximately 26%
(6/23) of the players also experienced posterior impingement of the ankle. Rugby players often experienced ankle sprains (97%) during stumbling, feint motions, or tackles. Thirty-five percent (11/31) experienced Achilles tendinitis, and 55% (17/31) experienced tibial stress fractures. Most of the baseball players sustained ankle sprains (95%, 19/20), which often happened while catching side-passing balls during defense plays.
ACCESSORY NAVICULAR SYNDROME Although the overall incidence of accessory navicular syndrome (ANS) in Korea is similar to that in other countries (4%-12%), type-2 symptomatic ANS seems to show relatively high incidence in Korean athletes. One foot and ankle institution in Korea experienced more than 200 cases of type 2 ANS, most of them symptomatic. They were treated with bony ossicle excision and posterior tibialis tendon (PTT) reattachment. Rehabilitation started at 4 weeks after operation and players returned to sports at about 3 months postoperatively. In a retrospective review of 84 operated ANS patients, 70% were professional or amateur athletes involved in activities such as football, basketball, or marathons. The follow-up period averaged 17 months. Ninety-four percent (79/84) of the patients showed excellent or good results postoperatively and returned to previous sports activity within 3 months after operation. Poor results came from one heavyweight volleyball player and other patients who had associated PTT insufficiency greater than grade 2.
H. Australian foot and ankle conditions in sport Terence S. Saxby and Jonathan C. Dick
Australia is a very isolated country. The population is approximately 20 million people and the landmass of the country is approximately the size of the United States of America. Sport is extremely important to the Australian way of life. Almost every sport would be played to some extent in Australia.
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Games originating in North America, including baseball, basketball, and even American football are played in Australia. However, because of its historical links with Great Britain and Europe, sports played in these countries predominate. Rugby union, netball, hockey, and soccer are extremely popular sports in this country. Foot and ankle injuries sustained by
Foot/ankle injuries in surf lifesaving
FOOT/ANKLE INJURIES IN SURF LIFESAVING Surf lifesaving is an intrinsic part of Australian culture. Australians love to participate in activities based around the surf beach. Australian beaches can be extremely dangerous for swimmers. Therefore the volunteer Surf Life Saving Association was developed to reduce the risk of participation in this activity. Inflatable rescue boats (IRBs) are used to a large extent by the Surf Lifesaving Association (Fig. 22H-1). These inflatable vessels are now the primary rescue aid used by surf lifesavers in Australia. The use of IRBs has resulted in a number of serious foot and ankle injuries to the boat crew, as demonstrated by recent studies.1,2 IRBs have been designed essentially for inshore search and rescue but also are used in training and competitions.2 They are powered by a 25-horsepower outboard motor and structurally are composed of two rigid, nylon mesh pontoons with a removable lightweight laminate floor to prevent craft deformation. They are manned by a driver and a crewman. The driver sits at the rear left side of the boat and the crewman at the forward right side. The crew requires foot straps, one for the driver and two for the crewman, to give them some anchor to the boat in the often-trying conditions (Fig. 22H-2). These foot straps are not adjustable to foot size or stance position and do not allow any rotation. As a result, these foot straps have been blamed
Figure 22H-1
Inflatable rescue boat.
recently for some of the unique injuries sustained by Australian lifesavers.3 Bigby2 reported on the workers compensation claims made by Surf Lifesaving members in Queensland (northeastern state) for a 12-month period from July 1997 to assess the incidence of serious injuries sustained from IRBs and to describe their nature.2 In Queensland alone there are 2819 rescues per year, and in 731(26%)
Figure 22H-2
Inflatable rescue boat showing foot straps.
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participants in such sports are much the same the world over. Because of its isolation and historical independence, Australia has produced its own novel sports including Australian football, which is a combination of Gaelic football, soccer, and rugby. This is an extremely popular sport with a large following in certain states of Australia. It is a fast-flowing game played on a large field requiring athleticism rather than brawn. A profile of Australian Football League (AFL) injuries presenting to sports medicine clinics found that foot and ankle injuries accounted for 14.2% of all injuries.1 These are most often sprains of the lateral ligament complex of the ankle and therefore not unique to Australian sport. Australia is an island continent; therefore water sports, including surf lifesaving and other water-based recreational activities, are extremely popular. Because of the large variety of sports and recreational activities carried out in Australia by a large number of individuals, sporting injuries are quite common. Injury profiles for the majority of these activities reflect patterns of injuries seen overseas. However, there is one particular injury to the foot/ankle complex that is unique to Australian sport.
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an IRB was used. For the year there were 37 insurance claims to the workers compensation board specifically from IRB injuries. Incidence of claim for injury annually is 1.2% in IRB crewmen. Sixty-eight percent of claims involved injury to the lower limbs. Fifty percent were associated with fracture or fracture dislocations. The crewman (81%) rather than the driver was injured more often. The right side (79%) was more commonly injured. Bigby concluded that the crewman was more likely to be injured because the crewman is unable to brace himself or herself, with two foot straps being the only fixed support. Ashton reviewed 12 significant foot and ankle injuries sustained while riding in an IRB that were admitted to his regional hospital emergency department.3 Ten of these injuries required operative surgery as the initial form of treatment. They consisted of six Lisfranc injuries (dislocation of the midfoot), four ankle fractures, one tibia and fibula fracture, and one traumatic dislocation of peroneal tendons. These injuries were sustained on three occasions when the IRB overturned, four on landing after going over a wave, and four from hitting a broken wave. One occurred when a crewman alighted from the boat as it approached the beach at speed. Eleven of the 12 injuries were to the crewman. The crewman takes the initial impact of the wave and has no control of the boat’s direction. This contributes to his or her being less stable than the driver and therefore at more risk of injury3 (Fig. 22H-3).
Anatomy The tarsometatarsal joints are inherently stable because of their joint congruency and ligamentous supporting structures. There is little range of motion (ROM) at these joints, the first and fifth being most mobile. The bony configuration, with the base of the second metatarsal being recessed and the bone being shaped trapezoidally, provides economical load-bearing characteristics. The Lisfranc ligament is a large, strong, short ligament connecting the base of the second metatarsal to the medial cuneiform. No ligament connecting the base of the first and second metatarsals has yet been described. This leaves a relative weakness inherent at this level. The dorsalis pedis artery crosses over this area, and a branch dives down between the bases of the first and second metatarsal to join the plantar supply. Also the deep sensory branch of the common peroneal nerve is medial to the artery at this level. These structures may be damaged when open reduction and internal fixation are performed. Lisfranc injuries The mechanism of Lisfranc injuries sustained by IRB crew is thought to be due to abduction injuries because the feet are constrained by hard foot straps. This generally causes a homolateral type of injury. Lisfranc dislocations have since been classified by several authors, but none of the classification systems provide a helpful system that aids in treatment methods. The simplest classification, by Quenu and Kuss (1909)4, divided these injuries into three groups (Fig. 22H-4): 1. Homolateral 2. Unilateral 3. Divergent This by no means is a comprehensive classification system but is useful when describing this injury. Investigation Investigation of these injuries initially is by plain x-ray. To assess normal anatomy, the continuous line along the medial border of the second metatarsal and medial cuneiform and medial border of the fourth metatarsal and medial cuboid should be present on both anteriorposterior (AP) and oblique views. If there is any doubt about the diagnosis or further investigation is warranted, a computed tomography (CT) scan is helpful and often aids in making decisions and determining options for treatment.
Figure 22H-3
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Inflatable rescue boats at work.
Treatment Treatment of displaced Lisfranc injuries usually requires open reduction and internal fixation with either small fragment/cannulated screws and K-wires. Outcome
Further reading
Figure 22H-4
Lisfranc classification.
from these injuries is variable with a guarded prognosis, although there is an abundance of literature that supports the practice of anatomic reduction’s leading to optimal conditions for a reasonable outcome.
3. Ashton A, Grujic L: Foot and ankle injuries occurring in inflatable rescue boats (IRB) during surf life saving, J Orthop Surg 9:39, 2001. 4. Quenu E, Kuss G: E´tude sur les luxations du metatarse, Rev Chir 39:1, 1909.
FURTHER READING REFERENCES 1. Gabbe B, Finch C: A profile of Australian football injuries presenting to sports medicine clinics, J Sci Med Sport 4:386, 2001. 2. Bigby J, McClure R, Green A: The incidence of inflatable rescue boat injuries in Queensland surf lifesaver, Med J Aust 172:485, 2000.
Hardcastle P, et al: Injuries to the tarsometatarsal joint incidence, classification and treatment, J Bone Joint Surg 64-B:349, 1982. Arntz CT, Veith RG, Hansen ST: Fractures and dislocations of the tarsometatarsal joint, J Bone Joint Surg 70-A:173, 1988. Adelaar R: The treatment of tarsometatarsal fracture-dislocation, Instruct Course Lect 39:141, 1990.
I. Soccer: hallux osteochondral lesion and rupture of the Achilles tendon Veroˆnica Vianna, Sergio Vianna, and Abra˜o Altman
beaches, backyards, and public squares), and on diverse terrain (grass, dirt, and sand). Therefore Brazilian sports specialists see a great number of foot and ankle lesions that affect all levels of athletes, not only professional players. Among these are two lesions that we feel are of particular interest regarding diagnosis and treatment. 519
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Soccer is one of the most popular sports in the world, played by more than 60 million people in more than 150 countries, according to the Fe´de´ration Internationale de Football Association (FIFA).1 In Brazil soccer represents a true passion among all ages and social levels. It is practiced all over (schools, streets, soccer fields,
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An international perspective on the foot and ankle in sports
HALLUX OSTEOCHONDRAL LESION IN BEACH SOCCER PLAYERS Beach soccer is a popular soccer modality practiced barefoot along the Brazilian coast. During the game, the hallux is subjected to trauma—direct trauma against the ball, the ground, or another player and indirect trauma because of the forces from running over the sand.2 Furthermore, the hallux metatarsophalangeal (MTP) and interphalangeal (IP) joints are stressed in a repetitive mode, particularly in dorsiflexion with pivoting and running. Unlike the aforementioned stresses, kicking will induce lesions that tend to be on the dominant side, the side used to kick the ball. Milani et al.3 described 19 patients with hallux osteochondral lesions. All were males between the ages of 14 and 67 who practice beach soccer for a mean of 12.8 years. The lesions were located at the IP joint with the distribution shown in Fig. 22I-1. In all cases the lesion involved the dominant foot (the one used to kick the ball). Typically the pain and swelling during the acute phase does not stop the patient from practicing soccer. By the time the orthopaedic surgeon sees the athlete, the symptoms are more dramatic and there often is a ‘‘tumor’’ noted at the dorsomedial aspect of the IP joint of the hallux. Many will develop a callus over the lesion that can be particularly symptomatic in shoes during daily activity. The radiographic study shows an osteolytic, punched lesion with a sclerotic border (Fig. 22I-2). Altman classified these lesions as types I to V, according to the anatomic location (Fig. 22I-3). Type I, lesion at the lateral border of the distal phalanx articular facet, is responsible for 40% of the lesions.
Figure 22I-2 Radiographic aspect of a typical hallux osteochondral lesion.
Figure 22I-3 Altman’s classification for the hallux osteochondral lesions.
Conservative treatment may be successful when performed during the acute phase. It consists of antiinflammatory medication and immobilization of the hallux with taping for pain relief. In general, if the patient stops playing soccer, the pain is not a big issue.
Figure 22I-1
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Distribution of the hallux osteochondral lesion.
Technique Surgical treatment consists of resection of the osteochondral fragment and articular debridement. The results are uniformly good and the patients are able to resume playing soccer approximately 1 month after surgery. A gauze-and-tape compression dressing is applied at the conclusion of surgery and is changed the following day, when passive motion starts. Two weeks after surgery, the patient resumes walking barefoot on the sand at the beach. The athlete can start running and kicking barefoot 1 month after surgery.
Neglected rupture of the achilles tendon
NEGLECTED RUPTURE OF THE ACHILLES TENDON
Figure 22I-4 Identification of the flexor hallucis longus in the medial aspect of the foot.
Technique We position the patient prone on the surgical table and drape out the affected side. The FHL is harvested in the medial aspect of the foot while the knee is flexed to 90 degrees during identification of the tendon8 (Fig. 22I-4). A longitudinal incision is made along the medial border of the midfoot just above the level of the abductor muscle, from the navicular to the neck of the first metatarsal. The abductor muscle is reflected dorsalward, and the FHL and the flexor digitorum longus are identified within the substance of the midfoot. The FHL is divided as far distally as possible, and the distal stump is retained to be sutured to the flexor digitorum longus. The tendons must be dissected from
Figure 22I-5
Tendon transfer through the calcaneus.
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‘‘Weekend athletes’’ typically are older soccer enthusiasts who used to play soccer routinely but now participate only on weekends. They are particularly vulnerable to injury and will not uncommonly sustain a rupture of the Achilles tendon. Unfortunately the diagnosis often is missed in the acute phase, probably because of inadequate initial care. It is a problem not only in our practice but throughout Brazil both in private and public practice. Therefore it is not uncommon that Brazilian specialists encounter these chronic lesions of the Achilles tendon. Our approach has been to use the flexor hallucis longus (FHL)4 as a substitute for the ruptured tendon. Hansen5 was the first to describe the use of the FHL for chronic Achilles rupture. This is the strongest tendon after the Achilles, and it contracts in phase with the gastrocnemius-soleus complex. In addition, the force axis of the transferred FHL reproduces the one of the Achilles tendon. Its position facilitates its use during the surgical procedure without injuring the neurovascular bundle and preserves the muscle balance around the ankle joint. The role of the FHL during gait, running, and jumping is yet to be determined. Frenette and Jackson,6 studying complete tears of the FHL in athletes, concluded that its integrity is not essential for push-off and balance during gait. Motivated by a chronic laceration of the FHL in an 11-year-old runner, the authors studied nine cases of lacerations of the FHL in athletically inclined patients. All of them returned to their activities, even those patients who had no appreciable active IP joint flexion after surgery. In these cases the lack of active flexion was felt most likely to be due to adherence of the repaired tendon in the scar tissue. Perhaps the return to function despite the lack of IP flexion relates to the tendon’s role during gait, running, and jumping. MacConaill and Basmajian7 reported that the FHL shows its greatest electromyographic activity during midstance, whereas during heel-off there is negligible activity in normal subjects. In our series of FHL transfers for chronic Achilles tendon ruptures, all 37 patients had normal passive IP flexion, and despite no active IP flexion there was no limitation to daily activities or to the return to sports. Our patients have returned to the practice of sports, including soccer, modern dance, and capoeira (an Afro-Brazilian dance form that incorporates self-defense maneuvers). Preliminary studies of the gait analysis in our series have not shown discrepancies between the operated and the nonoperated side on the parameters of the gait. Perhaps if we had treated ballet dancers or sprinters, who stress their FHL more aggressively, there would have been some limitation.
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An international perspective on the foot and ankle in sports
one another, detaching any decussating tendons at the knot of Henry to allow the FHL to be withdrawn through the posterior incision. We prefer to transfer the tendon through a hole in the calcaneus tuberosity despite the level of the lesion in the Achilles tendon (Fig. 22I-5). With the foot held in approximately 10 to 15 degrees of plantarflexion, the tendon of the FHL is passed through the hole from medial to lateral and sutured to itself with absorbable suture. The FHL and the gastrocnemius-soleus complex are sutured together proximally.
Postoperative protocol Full recovery takes an average of 6 months. At this time the patient may resume all sport activities, including soccer. After surgery, compressive dressings and plaster are applied to maintain 15 degrees of ankle plantarflexion. Before discharge, the patient is placed in a short-leg, nonweight-bearing cast at 15 degrees of equinus for 2 weeks. At that time the sutures are removed and the wound inspected. Then, another short-leg, nonweightbearing cast at 15 degrees of equines is placed for 2 more weeks. Following that period, the ankle is positioned into neutral for an additional 4 weeks of a short-leg
walking cast, and weight bearing is allowed. A rehabilitation program for strengthening and range of motion is begun 8 weeks postoperatively. Running, jumping, and impact sports such as soccer and volleyball are restricted for 6 months after surgery.
REFERENCES ˜es ortope´dicas no futebol, Rev Bras Ortop 1. Cohen M, et al: Leso 32:940, 1997. 2. Nery C: Tornozelo e Pe´–Diagno´stico e Tratamento. In Cohen M, editor: Leso˜es nos Esportes, Sa˜o Paulo, 2003, Revinter. 3. Milani C, et al: Lesione osteocondrale dell’alluce in giocatori di ca´lcio sulla spiaggia. In Turra S, editor:. Ortopedia e Traumatologia delo Sport in Eta´ Evolutiva, SIOT, Pisa, 1994. 4. Wapner KL, et al: Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer, Foot Ankle 14:443, 1993. 5. Hansen ST: Trauma to the heel cord. In Jahss MH, editor: Disorders of the foot and ankle, ed 2, Philadelphia, 1991, WB Saunders. 6. Frenette JP, Jackson DW: Lacerations of the flexor hallucis longus in the young athlete, J Bone Joint Surg 59-A:673, 1977. 7. MacConaill MA, Basmajian JV: Muscles and movements. A basis for human kinesiology, Baltimore, 1969, William & Wilkins. 8. Vianna V, Vianna S: Ruptura Croˆnica do tenda˜o de Aquiles: reparo com tenda˜o flexor longo do ha´lux, Ver Bra´s Ortop 31:542, 1996.
J. Footballer’s (soccer) ankle in Venezuela Gabriel Khazen and Cesar Khazen
Football (soccer) is the most popular sport worldwide, and even though Venezuela does not have a strong reputation for its national team, football is the favorite sport among young people in our country. Although baseball has a better organization and infrastructure, particularly for teenagers and professionals, football can be played anywhere by any number of players and needs only a ball made of any material. For these reasons it is particularly popular with people of all socioeconomic means. The special characteristics of this sport make its athletes prone to acute and overuse injuries.1 Footballer’s ankle is characterized by chronic anterior ankle impinging tibial and/or talar osteophytes, resulting in painful limited range of motion, mainly in dorsiflexion. It was first described by Morris in 1943; McMurray2 in 1950 named it footballer’s ankle and suggested osteophyte excision as treatment. It has been reported that this pathology can affect 50% or 60% of the professional football players, but it has been described in many other activities, such as running and dancing.
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The exact etiology of this syndrome is still unknown, although there are many hypotheses that have attempted to explain it. The first and traditionally accepted is McMurray’s hypothesis that recurrent traction on the joint capsule during forced ankle plantarflexion when kicking the ball was the cause of these osteophytes. However, recent studies have shown that the capsule attaches on average 6 mm proximal to the anterior cartilage rim in the tibia and 3 mm distal to the cartilage border of the talus, where the osteophytes form.3 Other hypotheses suggest that direct trauma to the rim of the anterior ankle cartilage in combination with recurrent microtrauma caused by the soccer ball impact, will induce inflammation and scar tissue, which calcifies and forms the osteophytes4 (Fig. 22J-1). Massada5 described the morphologic adaptation of the talus in football players to compensate for overuse and overstress; these changes produced in the talus by the impingement of the anterior articular distal epiphysis of the tibia can be similar to the ‘‘squatting facet’’ found
Clinical evaluation
in certain societies in which this crouched position is common. In these situations, the exostoses would be without important clinical significance in the majority of cases. Ankle instability seems to be an important issue in this pathology; Cannon and Hackney6 described osteophyte formation and recurrence when lateral ankle instability was not addressed at the time of resection of the impinging lesions. Conversely, there was no osteophyte recurrence following resection when anatomic lateral ligament reconstruction was performed in the presence of lateral ankle instability. This may be the key to the high incidence of footballer’s ankle in Venezuela; most of the patients with this syndrome on whom we have had to operate needed simultaneous anatomic lateral ankle ligament reconstruction. Perhaps in our country two factors are responsible for this. First, because most of the football grounds are uneven and sandy, there is a higher incidence of ankle sprain and subsequent instability. Second, the majority of the population cannot afford appropriate footwear and equipment, leaving them more vulnerable to injury when an accident occurs (Figs. 22J-2 and 22J-3).
CLINICAL EVALUATION The main symptom of footballer’s ankle is anterior ankle pain. Patients complain of joint stiffness and pain, exacerbated by activities that force ankle dorsiflexion such as walking uphill or squatting. McMurray in 1950 pointed out that the footballer manifested stronger pain when kicking a ‘‘dead ball.’’ Physical examination should be performed carefully to establish a diagnosis and eliminate other causes of ankle pain and impingement. Palpation of the anterior distal tibia and dorsal talus causes tenderness and discomfort; and range of
Figure 22J-2 The majority of football grounds are uneven and sandy in Venezuela.
Figure 22J-3 grounds.
There is a higher risk of ankle sprain in uneven
motion is limited and painful, mostly in ankle dorsiflexion. Pain might be caused by synovial impingement between the osteophytes and the distal tibia or talar bone surface. It is important to note that 45% of football players with anterior ankle osteophytes are asymptomatic. In advanced cases, osteophytes can be palpated, and generalized synovitis may cause important swelling. Joint stability should be examined carefully. We like to perform an ankle anterior drawer test to assess anterior talofibular ligament. Subtalar forced inversion with 15-degrees ankle dorsiflexion is used to test the calcaneofibular ligament. Other causes of anterior ankle pain should be ruled out, including talar or tibial osteochondral defects; loose bodies; tendinitis; rheumatoid, posttraumatic, or crystalline arthropathies; and pigmented villonodular synovitis. 523
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Figure 22J-1 Forced ankle plantarflexion and direct trauma when kicking the ball.
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An international perspective on the foot and ankle in sports
Figure 22J-4 X-ray showing characteristic anterior tibial and talar osteophytes in footballer’s ankle.
ADDITIONAL STUDIES Ankle anterior-posterior (AP), lateral, and mortise view radiographs should be performed routinely. Anterior tibial and talar neck osteophytes can be seen in lateral views and are described as ‘‘kissing’’ osteophytes.7 Recently, an oblique anteromedial view has been suggested, with the radiographic beam tilted in a 45-degree craniocaudal direction with the leg in 30-degrees external rotation to detect medially located tibial and talar osteophytes8 (Figs. 22J-4 and 22J-5). Anterior and lateral stress radiographs under sedation or general anesthesia should be performed if lateral ankle stability is suspected. Although the efficacy of this study is hotly debated, we think it is helpful. Most of the studies that found this procedure unreliable were done in vitro; the few studies made in vivo show good correlation between lateral stress radiographs and instability. Computed tomography (CT) scan is a helpful in determining the precise size and location of osteophytes. Berberian et al.9 showed that talar spurs on average lie medial to the midline of the talus and that tibial spurs are wider and lie lateral to the midline. Thus overlapping spurs are less likely. Magnetic resonance imaging (MRI) should be ordered if the diagnosis is not clear or concomitant soft-tissue lesions must be identified.
TREATMENT The treatment of the footballer’s ankle depends on the duration and severity of symptoms as well as the ankle joint condition. Conservative treatment should be attempt
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Figure 22J-5 X-ray showing characteristic medial tibial and medial talar osteophytes in footballer’s ankle.
first, with rest, braces, nonsteroidal anti-inflammatory medication, and physical therapy. If conservative treatment fails to diminish pain and restore joint function in the absence of advanced joint osteoarthritis, osteophyte removal is the treatment of choice. This procedure can be performed arthroscopically or by small arthrotomy. Arthroscopy has the advantage of being a minimally invasive procedure and provides a magnified and extensive ankle view, with a low risk of complications.10-12 We like to place the patient supine on the operating table, with the ipsilateral hip and knee flexed 45 degrees and supported by a leg holder. A tourniquet is applied and, after draping, the ankle is placed in a noninvasive distractor and force is applied. The ankle joint, tibialis anterior tendon, and superficial peroneal nerve are delineated in the skin as landmarks to safe and correct portals placement. We create the anterolateral portal through a 1-cm longitudinal skin incision, 1 cm lateral to the superficial peroneal nerve at the ankle joint level that has been identified previously with an 18-gauge needle. Careful dissection of the joint is performed with a hemostat and a 3.5-mm arthroscope is inserted (we use this arthroscope size because it gives a larger ankle view). The anteromedial portal is identified under
Treatment
direct vision (from the anterolateral portal) and a needle inserted 0.5 cm medial to the tibialis anterior tendon, following the same steps for the anterolateral portal. First we perform a joint evaluation, examining the medial gutter and deltoid ligament and looking for the presence of tibial or talar chondral defects. The lateral gutter, anterior inferior tibiofibular ligament, anterior talofibular ligament, calcaneofibular ligament, and joint synovium are visualized. Shaving of synovitis, scar tissue, and any ligament thickening is performed first, to improve joint space and osteophyte visualization. Anterior tibial and talar osteophytes can be reached without joint distraction; extensive distal tibia and talus evaluation is performed, switching portals to identify the position and extent of the osteophytes, which are debrided aggressively with a powered 4.0 burr. Intraoperative ankle fluoroscopy or radiographs can be used to assess osteophyte resection (Figs. 22J-6, 22J-7, and 22J-8). If mechanical lateral ankle instability is present, it should be addressed in the same procedure by anatomic lateral ankle ligament reconstruction; we like to perform the Brostrom-Gould technique. As stated earlier, we believe that ankle instability and anterior ankle osteophytes are causally related, and thus combined surgery for both conditions may reduce the recurrence of exostosis as well as improve the outcome. In the presence of large or abundant osteophytes, open resection can be performed by extending the arthroscopy portals. In case lateral ligament reconstruction is necessary, the osteophytes can be removed by direct vision, slightly extending the incision.
After the procedure, we recommend that our patients avoid weight bearing on the operated ankle for 8 days and start active and passive ankle motion on the third postoperative day; a week later physiotherapy is begun to improve ankle range of motion, tendon strengthening, and proprioception. If the patient requires lateral ankle ligament reconstruction, we immobilize the ankle in a cast for 4 weeks and then put the patient in a sport Aircast (DJO, San Diego, CA) brace to be worn day and night for 4 weeks and then only
Figure 22J-6
Figure 22J-8 Anterior distal tibia after arthroscopic osteophyte debridement.
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Anterior tibial osteophyte arthroscopic image.
Figure 22J-7 Anterior tibial osteophyte arthroscopic debridement with a powered 4.0-mm burr.
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An international perspective on the foot and ankle in sports
during the night for another 2 weeks. We start passive physiotherapy at 4 weeks postoperatively in these patients and active physiotherapy at 6 weeks postoperatively. Good results have been reported widely for arthroscopic resection of anterior bony ankle impingement. Olesen reported that dorsiflexion improved in 59% of the patients, 70% had less pain, and 59% returned to sports, but 23% had given up because of the symptoms.10,11 Tol et al.13 reported a mean 6.5-year follow-up for arthroscopic excision of soft-tissue overgrowth and osteophytes. They found that patients without osteoarthritis all had excellent or good results; patients with grade I osteoarthritis had 77% good or excellent results, despite two thirds of the patients developing partial or complete recurrence of osteophytes. Fifty-three percent of the patients with grade II osteoarthritis had excellent or good results without joint narrowing progression. Between 1999 and 2002 we operated on 36 footballers with anterior ankle osteophytes who had not achieved symptomatic improvement with conservative treatment. Seventeen were high-level footballers, and the rest played for local leagues. The age of the patients ranged between 23 and 48 years. Fourteen patients needed anatomic lateral ankle ligament reconstruction because of mechanical lateral ankle instability. Using the Scranton McDermott classification, 21 patients were classified as either type I or II (type I: tibial spurs 3 mm or less; type II: tibial spurs larger than 3 mm without talar spurs); 9 patients were type III (tibial and talar osteophytes), and 6 patients were classified as type IV (tibial and talar osteophytes with ankle joint osteoarthritis signs). Seventeen of 21 patients with type I or II underwent follow-up examination. Fifteen reported less pain in the ankle after the surgery (visual analog scale [VAS]); 12 patients experience improvement in their range of the ankle dorsiflexion by 5 degrees or more; 15 patients returned to play at the same level; and only 3 patients experienced recurrence of tibial osteophyte. Eight of 9 patients with type III ankle osteophytes were available for follow-up. Because of the size of the osteophytes, 4 of these patients needed a small arthrotomy for the resection; 5 of the patients reported less ankle pain after the procedure (visual analog scale [VAS]); 4 experienced improvement in the range of ankle dorsiflexion by 5 degrees or more; 5 players returned to play at the same level and 3 experienced recurrence of ankle osteophytes. Of the four patients with type IV ankle osteophytes, three needed open resection of the osteophytes; two reported less pain after the procedure (VAS); and none experienced improvement in ankle dorsiflexion. All of
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the patients played in the veterans’ football division; one patient could return to play at the same level, and one patient needed subsequent ankle arthrodesis.
COMPLICATIONS The incidence of complications after this procedure is low. The main complication can be neurovascular damage related to the portal placement, infection, and formation of scar tissue. Osteophyte recurrence is the main chronic complication and, although the incidence has been discussed earlier in this chapter, it is clear that an aggressive and efficacious osteophyte resection and a stable ankle joint leads to a satisfactory result and the least incidence of osteophyte recurrence.
REFERENCES 1. Lees A, Nolan L: The biomechanics of soccer: a review, J Sports Sci 16:211, 1998. 2. McMurray TP: Footballer’s ankle, J Bone Joint Surg 32B:68, 1950. 3. Tol JL, van Dijk C: Etiology of the anterior ankle impingement syndrome: a descriptive anatomical study, Foot Ankle Int 25:382, 2004. 4. Tol JL, Slim E, van Dijk CN: The relationship of the kicking action in soccer and the anterior ankle impingement syndrome. A biomechanical analysis, Am J Sports Med 1:1, 2001. 5. Massada JL: Ankle overuse injuries in soccer players. Morphological adaptation of the talus in the anterior impingement, J Sports Med Phys Fitness 31:447, 1991. 6. Cannon LB, Hackney RG: Anterior tibiotalar impingement associated with chronic ankle instability, J Foot Ankle Surg 39:383, 2000. 7. Robinson P, White LM: Soft-tissue and osseous impingement syndromes of the ankle: role of imaging in diagnosis and management, Radiographics 22:1457, 2002. 8. Van Dijk CN, et al: Oblique radiograph for the detection of bone spurs in anterior ankle impingement, Skeletal Radiol 31:214, 2002. 9. Berberian W, et al: Morphology of tibiotalar osteophytes in anterior ankle impingement, Foot Ankle Int 22:313, 2001. 10. Ogilvie-Harris DJ, Mahomed N, Demaziere A: Anterior impingement of the ankle treated by arthroscopic removal of bony spurs, J Bone Joint Surg 75-B:437, 1993. 11. Olesen S, Breddam M, Nielsen AB: ‘‘Footballer’s ankle.’’ Results of arthroscopic treatment of anterior talocrural ‘‘impingement,’’ Ugeskr Laeger 163:3360, 2001. 12. Rasmussen S, Hjort Jensen C: Arthroscopic treatment of impingement of the ankle reduces pain and enhances function, Scand J Med Sci Sports 12:69, 2002. 13. Tol JL, Verheyen CP, van Dijk CN: Arthroscopic treatment of anterior impingement in the ankle, J Bone Joint Surg 83-B:9, 2001.
Biology
K. The biologic perspective of sports disorders affecting foot and ankle Mohammad Zafar, Ansar Mahmood, and Nicola Maffulli
Achilles tendinopathy is common among athletes. Its prevalence is approximately 11% in runners, 9% in dancers, and less than 2% in tennis players.
BIOLOGY Etiology The etiology of tendinopathy remains unclear, and many factors have been implicated. Tendon injuries can be acute or chronic and are caused by intrinsic or extrinsic factors, either alone or in combination. Overuse injuries generally have a multifactorial origin. Tendon vascularity, gastrocnemius-soleus dysfunction, age, gender, body weight and height, pes cavus, and lateral ankle instability are common intrinsic factors. Excessive motion of the hindfoot in the frontal plane, especially a lateral heel strike with excessive compensatory pronation, is thought to cause a‘‘whipping action’’ on the Achilles tendon and predispose it to tendinopathy. Changes in training pattern, poor technique, excessive loading, previous injuries, footwear, and environmental factors such as training on hard, slippery, or slanting surfaces are common extrinsic factors. In acute trauma, extrinsic factors predominate. Free radical damage occurring on reperfusion after ischemia, hypoxia, hyperthermia, impaired tenocyte apoptosis, cytokines, prostaglandins, and fluoroquinolones have all been linked with tendinopathy. Histopathology Histologically, tendinopathy is characterized by an absence of inflammatory cells and a failed healing response, with noninflammatory intratendinous collagen degeneration, fiber disorientation and thinning, hypercellularity, scattered vascular in-growth, and increased interfibrillar glycosaminoglycans. Frank inflammatory lesions and granulation tissue are infrequent and are associated mostly with tendon ruptures. Hence the term tendinopathy should be used as a generic descriptor of the clinical conditions in and around tendons arising from overuse, and the terms tendinosis
and tendinitis should be used only after histopathologic examination. Various types of degeneration may be seen in tendons, but in the Achilles tendon mucoid or lipoid degeneration is usually found.
Healing Tendon healing occurs in three overlapping phases. The initial inflammatory phase comprises recruitment of inflammatory cells, phagocytosis of necrotic materials, release of vasoactive factors, initiation of angiogenesis, and stimulation of tenocyte proliferation. After a few days, the proliferative phase begins. Synthesis of type III collagen peaks during this stage, which lasts for a few weeks. After approximately 6 weeks, the remodeling phase commences, with decreased cellularity and decreased collagen and glycosaminoglycan synthesis, and the repair tissue changes from cellular to fibrous. A higher proportion of type I collagen is synthesized during this stage. After 10 weeks, the maturation stage occurs, with gradual change of fibrous tissue to scar-like tendon tissue over the course of 1 year. During the latter half of this stage, tenocyte metabolism and tendon vascularity decline. Role of metalloproteases and growth factors Matrix metalloproteases (MMPs), a family of zinc and calcium-dependent endopeptidases active at a neutral pH, are important regulators of extracellular matrix remodelling via their broad proteolytic capability, and their levels are altered during tendinopathy. Twentythree human MMPs have been identified, with a wide range of extracellular substrates. MMPs can be subdivided into four main groups: collagenases, gelatinases, stromelysins, and membrane-type MMPs. Some of the studies suggest that MMP-9 and MMP-13 participate only in collagen degradation, whereas MMP-2, MMP-3 and MMP-14 participate in both collagen degradation and collagen remodelling. Wounding and inflammation also provoke release of growth factors and cytokines from platelets, polymorphonuclear leukocytes, macrophages, and other inflammatory cells. These growth factors induce neovascularization and chemotaxis of fibroblasts and tenocytes and stimulate proliferation of fibroblast and tenocytes, as well as synthesis of collagen. 527
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INTRODUCTION
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An international perspective on the foot and ankle in sports
Insulin-like growth factor (IGF) is expressed in avian flexor tendons and induces tenocyte migration, division, and matrix expression. IGF-I and II increase collagen synthesis in a dose-dependent manner in animal models and also increase proteoglycan synthesis IGF-I acts synergistically with platelet-derived growth factor BB (PDGF) to stimulate tenocyte migration. Intratendinous injection of IGF-1 has been evaluated in a rat Achilles tendon transection model. Rats in the IGF-1–treated group had higher Achilles functional index scores and accelerated recovery compared with control groups Vascular endothelial growth factor (VEGF) is an endothelial mitogen that promotes angiogenesis and increases capillary permeability. It is expressed in ruptured and fetal human Achilles tendons but not in normal adult Achilles tendons. VEGF plays a key role in tendon healing by inducing vasodilatation results partly through stimulation of nitric oxide synthase in endothelial cells. VEGF treatment at the time of surgical repair of transected rat Achilles tendons resulted in significantly improved tensile strength at 2 weeks. However, no significant difference was present by 4 weeks.1 Increased levels of transforming growth factor b2 (TGF-b2) have been reported in tendinopathic human Achilles tendons and in rabbit flexor tendons after injury. TGF-b induces increased collagen production in rabbit tenocytes, and upregulation of TGF-b receptors occurs following flexor tendon injury and in tendinopathic human Achilles tendons. Cartilage-derived morphogenetic proteins (CDMPs), the human analogs of growth and differentiation factors, are members of the TGF- superfamily and are related to bone morphogenetic proteins. Injection of CDMP-1, CDMP-2, and CDMP-3 into lacerated rat Achilles tendons results in a significant dose-related increase in strength and stiffness. Not all cytokines prove beneficial for tendon healing. The ideal cytokine or combinations of cytokines that will improve tendon healing are still to be determined. Cytokine effects often are dose dependent, and optimal dosage regimes must be established. The ideal form of administration also remains to be determined. Options include direct injection at the injury site or gene therapy. Further research will help to resolve these issues.
Tissue engineering/stem cells Mesenchymal stem cells (MSCs) prevalent in bone marrow, muscle, fat, skin, and around blood vessels are capable of undergoing differentiation into a variety of specialized mesenchymal tissues, including bone, tendon, cartilage, muscle, ligament, fat, and marrow stroma.
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MSCs can be applied directly to the site of injury or can be delivered on a suitable carrier matrix, which functions as a scaffold while tissue repair takes place. Tissue engineering also may prove useful for managing tendon ruptures. A 1-cm-long gap injury model in rabbit Achilles tendons was used to compare suture alone versus a cell-collagen gel composite contracted onto a pretensioned suture. Evaluation at 4, 8, and 12 weeks following surgery revealed that structural and material properties of the cell-treated implants typically were approximately twice the value of controls. Celltreated repairs were larger in cross section and histologically better organized than suture alone repairs. Polyglycolic acid scaffolds seeded with tenocytes were implanted into hen flexor tendon defects. Twelve weeks after surgery, tenocytes and collagen fibers became longitudinally aligned. At 14 weeks, engineered tendons displayed a typical tendon structure, with a breaking strength of 83% of normal.2 At present, tissue engineering is an emerging field, and many difficulties must be overcome before it becomes a real option in the management of tendon disorders. It is important to determine whether effective vascularization and innervation of implanted tissueengineered constructs takes place. Vascularization is important for the viability of the construct. Innervation is required for proprioception and to maintain reflexes, mediated by Golgi tendon organs, to protect tendons from excessive forces.
Gene therapy Gene therapy delivers genetic material to cells to alter protein synthesis and cell function and can be achieved via viral vectors or liposomes. Liposome constructs have been used to deliver galactosidase to rat patellar tendons. Animal studies have demonstrated that gene therapy can be used to alter the healing environment of tendons. Adenoviral transfection of focal adhesion kinase into partially lacerated chicken flexor tendons resulted in an expected increase in adhesion formation. Although this study reports an adverse outcome, it proves the feasibility of gene therapy as a management modality.3 Complementary deoxyribonucleic acid (cDNA) for PDGF–B was transfected into rat patellar tendons using liposomes, resulting in an early increase in angiogenesis, and collagen deposition and matrix synthesis were greater at 4 weeks. However, there were no differences between the treated and control groups by 8 weeks. Gene therapy can be used to manipulate the healing environment for up to 8-10 weeks. This may be long enough to be clinically significant. Many genes may prove beneficial to tendon healing, and further research is required to establish the most advantageous genes to transfer.
Principles of tendinopathy management
Conservative management Nonsteroidal anti-inflammatory drugs (NSAIDs) Although tendinopathy is a noninflammatory condition, NSAIDs are widely used in attempts at treatment. There is no biologic basis for NSAID effectiveness in treating this condition, and no evidence of any benefit particularly in athletes. NSAIDs appear to be effective, to some extent, only for pain control. This causes patients to ignore early symptoms and thus may lead to further damage of the tendon and delay definitive healing. Theoretically NSAIDs could benefit patients with tendinopathy by increasing the tensile strength of tendons via accelerated formation of cross linkages between collagen fibers. COX-2 inhibitors should be avoided in the early period following tendon injury because of their deleterious effect on tensile strength. During remodelling, on the other hand, inflammation has a negative influence, and NSAIDs such as COX-2 inhibitors might be valuable for the final outcome. Aprotinin In recent years, aprotinin has been used in the management of chronic tendinopathy. Aprotinin is a broad spectrum serine protease inhibitor derived from bovine lungs. It acts on trypsin, plasmin, and kallikrein, blocks matrix metalloproteinases, and may specifically act as a collagenase inhibitor in tendinopathy. Until recently, evidence for aprotinin use in the management of Achilles tendinopathy was based on uncontrolled studies, reporting success rates of approximately 80%. In the only randomized controlled trial to examine the role of aprotinin in Achilles tendinopathy, the authors concluded that there was no statistical significant improvement in outcome. However, this study was underpowered.4 The main reported side effect of aprotinin is that of allergic reactions. The risk of hypersensitivity/anaphylactic reaction with aprotinin is less than 0.1% on first exposure but rises to 2.7% with re-exposure. Maffulli has used aprotinin since 1988 for the management of chronic tendinopathy in more than 1200 patients. To his knowledge, only two cases of systemic allergic reactions have been reported, both in middleaged active but nonathletic women. Eccentric exercise Limited levels of evidence exist to suggest that Eccentric Exercise (EE) has a positive effect on clinical outcomes such as pain, function, and patient satisfaction/return
to work when compared with concentric exercise, stretching, splinting frictions, and ultrasound. EEs are low cost, relatively easy to perform and noninvasive. The results can be seen after 12 weeks of daily EE training.5 Laser therapy Laser therapy also has been studied in tendon healing. Using a placebo-controlled, double-blind prospective study model in 25 patients with 41 digital flexor tendon repairs, laser therapy reduced postoperative edema but provided no improvement in pain, grip strength, or functional evaluation compared with controls.6 Further well-controlled clinical studies should be performed using different laser types and dosages to delineate the role of laser phototherapy in the management of tendon injuries. Radiofrequency coblation This is a new application of bipolar radiofrequency energy used for volumetric tissue removal. Under appropriate conditions, a small vapor layer forms on the active electrode of the device. The electrical field of on the energized electrode causes electrical breakdown of the vapor, producing a highly reactive plasma that is able to break down most of the bonds found in soft-tissue molecules. Rapid pain relief has been reported in a preliminary prospective, nonrandomized, single-center, single-surgeon study of 20 patients with tendinopathy of the Achilles tendon, patellar tendon, and of the common extensor origin. Six months after the procedure, magnetic resonance imaging (MRI) showed complete or nearly complete resolution of the tendinopathy lesion in 10 of the 20 patients enrolled in the study.7 Sclerosing injections Using ultrasonography and color Doppler during eccentric calf-muscle contraction, we found that the flow in the neovessels disappeared when the ankle was dorsiflexed. These observations raised the question of whether the good clinical effects demonstrated with eccentric training could be due to action on the neovessels, and whether the neovessels and accompanying nerves were the main source of pain. In a recent study, ultrasound and color Doppler follow-up showed that most patients with good clinical results had no residual neovessels. Patients with a poor result showed residual neovascularization. These findings indicate that the area with neovessels may be important to the pain suffered during Achilles tendon loading activity.8 In a further noncontrolled pilot study, a sclerosing agent (Polidocanol) was injected into the area with neovessels on the ventral side of the tendon. The short-term (6 months) results were promising, but no real benefit 529
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PRINCIPLES OF TENDINOPATHY MANAGEMENT
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An international perspective on the foot and ankle in sports
was achieved in long term.9 For this reason we do not use sclerosing injections in our center. However, the results of a randomized controlled study comparing the effects of injections of a sclerosing substance with injections of a nonsclerosing substance are presently under evaluation. Shock wave therapy Several studies evaluated the application of electrical and magnetic fields to tendons. Pulsed magnetic fields with a frequency of 17 Hz resulted in improved collagen fiber alignment in a rat Achilles tendinopathy model.10 Extracorporeal shock wave therapy applied to rabbit Achilles tendons at a rate of 500 impulses of 14 kV in 20 minutes resulted in neovascularization and an increase in the angiogenesis-related markers endothelial nitric oxide synthase and vascular endothelial growth factor. Extracorporeal shock wave therapy also promotes healing of Achilles tendinopathy in rats. The authors proposed that improvement in healing resulted from an increase in growth factor levels, because they noted elevated levels of TGF-1 in the early stage and persistently elevated levels of IGF-1.11 However, caution should be exercised when using extracorporeal shock wave therapy because dose-dependent tendon damage, including fibrinoid necrosis, fibrosis, and inflammation, has been reported in rabbits.
and protein synthesis in human tenocytes. Even 15 minutes of cyclic biaxial mechanical strain applied to human tenocytes results in cellular proliferation. The precise mechanism by which cells respond to load remains to be elucidated. However, cells must respond to mechanical and chemical signals in a coordinated fashion. Intercellular communication to mount mitogenic and matrigenic responses is achieved via gap junctions ex vivo. Tissue-engineered tendons must allow for this intercellular communication. Mechanical loading of cells in monolayer or three-dimensional constructs can result in increased cell proliferation and collagen synthesis.
SURGICAL MANAGEMENT Indications Surgery is recommended for patients in whom nonoperative management has proved ineffective for at least 6 months. Twenty-four percent to 45.5% of the patients with Achilles tendon problem fail to respond to conservative treatment and eventually require surgical intervention. Paavola et al., in a prospective long-term follow-up study, showed that the prognosis of patients with acute to subchronic Achilles tendinopathy managed nonoperatively is favorable.12
Glyceryl trinitrate Review of literature showed that tropical Glyceryl trinitrate (GTN) is a well-tested medication with no irreversible side effects and that use of this therapy is warranted to treat chronic tendinopathies. However, further investigations are required to define the mechanism of action of GTN in tendinopathy and to delineate the most effective dosage regime to maximize effect and limit side effects. Mobilization and mechanical loading Animal experiments have demonstrated that training results in improved tensile strength, elastic stiffness, along with increase in weight, and cross-sectional area of tendons. These effects in the tendon can be explained by an increase in collagen and extracellular matrix synthesis by tenocytes. Little data exist on the effect of exercise on human tendons, although intensively trained athletes are reported to have thicker Achilles tendons than control subjects. Early resumption of activity promotes restoration of function, and motion therapy strategies aim to facilitate healing, reduce adhesion formation, and increase range of motion. Many studies have shown the benefit of early mobilization following tendon repair, and several postoperative mobilization protocols have been advocated. Repetitive motion results in increased DNA content
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Principles of surgery There are minor variations in surgical technique for tendinopathy. Nevertheless, the objective is to excise fibrotic adhesions, remove degenerated nodules, and make multiple longitudinal incisions in the tendon to detect intratendinous lesions and to restore vascularity, and possibly to stimulate the remaining viable cells to initiate cell matrix response and healing. Most authors report excellent or good result in up to 85% of cases.13,14 Management of paratendinopathy includes releasing the crural fascia on both sides of the tendon. Adhesions around the tendon are then trimmed and the hypertrophied adherent portions of the paratenon are excised. In tenolysis, classically longitudinal tenotomies are made along the longitudinal axis of the tendon in the abnormal tendon tissues, excising areas of mucinoid degeneration. Reconstruction procedure may be required if large lesions are excised. Preoperative planning Each patient should be managed on an individual basis, and appropriate workup for theatre should be instituted. Diagnosis is made on the basis of history of burning pain in the posterior aspect of the calf and ankle, often worse at the beginning of a training session and after exercise.
Surgical management
Surgical technique When an open surgical approach is necessary, we use a longitudinal curved incision, with the concave part toward the tendon and centered over the abnormal part of the tendon. Placing the incision medially avoids injury to the sural nerve and short saphenous vein, and the curvature of the incision prevents direct exposure of the tendon in case of skin breakdown. The paratenon and crural fascia are incised and dissected from the underlying tendon. If necessary, the tendon is freed from adhesions on the posterior, medial, and lateral aspects. The paratenon should be excised
obliquely because transverse excision may produce a constriction ring, which may require further surgery. Areas of thickened, fibrotic, and inflamed tendon are excised. The pathology is identified by the change in texture and color of the tendon. The lesions then are excised, and the defect can either be sutured in a sideto-side fashion or left open. Open procedures on the Achilles tendon may lead to difficulty with wound healing because of the tenuous blood supply and increased chance of wound breakdown and infection. Hemostasis is important because the reduction of postoperative bleeding speeds up recovery, diminishes the chance of wound infection, and diminishes any possible fibrotic inflammatory reaction. In patients with isolated Achilles tendinopathy with no paratendinous involvement and a well-defined nodular lesion less than 2.5 cm long, multiple percutaneous longitudinal tenotomies can be used when conservative management has failed. An ultrasound scan can be used to confirm the precise location of the area of tendinopathy.
Postoperative management On admission, patients are taught to perform isometric contractions of their triceps surae. Patients are instructed to perform the isometric strength training at three different angles, namely at maximal dorsiflexion, maximal plantarflexion, and at a point midway between the two. The foot is kept elevated on the first postoperative day, and nonsteroidal anti-inflammatory medications are given for pain control. Early active dorsiflexion and plantarflexion of the foot are encouraged. On the second postoperative day, patients are allowed to walk using elbow crutches, weight bearing as able. Full weight bearing is allowed after 2 or 3 days, when the bandage is reduced to a simple adhesive plaster over the wounds. Stationary bicycling and isometric, concentric, and eccentric strengthening of the calf muscles are started under physiotherapy guidance after 4 weeks. Swimming and water running are encouraged from the second week. Gentle running is started 4-6 weeks after the procedure, with mileage gradually increased. Hill workouts or interval training are allowed after a further 6 weeks, when return to normal training is allowed. Patients normally discontinue physiotherapy by the sixth postoperative month. For open surgery, the cast is applied for 2 weeks and the whole rehabilitation process described above is started later. Complications Subcutaneous hematoma Superficial infection Hypersensitivity of the stab wounds Hypertrophic painful scar 531
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Some patients have difficulty taking the first few steps in the morning. Pain during activities of daily living include prolonged walking and stairs. Clinically, diagnosis is made mostly on the basis of palpation and on the use of the painful arc sign. In paratendinopathy, the area of tenderness and thickening remains fixed in relation to the malleoli when the ankle is moved from full dorsiflexion into plantarflexion. If the lesion lies within the tendon, the point of tenderness and any swelling associated with it move with the tendon as the ankle is brought from full dorsiflexion into plantarflexion. In mixed lesions, both motion and fixation of the swelling and of the tenderness can be detected in relation to the malleoli. Ultrasound scan is a diagnostic aid to the surgeon. Ideally, a real time U.S. machine equipped with at least a 10-MHz sectorial transducer should be used. Commercially available soft polymer echo-free material can be used to provide adequate contact between the skin and the probe and to improve the image quality by placing the tendon in the optimal focal zone of the transducer. The variables considered in the evaluation of the tendon and of the peritendinous tissues are tendon size and borders, intratendinous and peritendinous ultrasonographic pattern, and possible surgical sequelae. An ultrasonographic diagnosis of tendinopathy can be made when the tendon presents altered intratendinous structure, at times with a well-defined focus. An ultrasonographic diagnosis of paratendinopathy is made when the peritenon is thickened or shows altered echogenicity. Any relevant comorbidity should be highlighted and managed. Although the techniques reported in this article are performed under local anesthesia, there is a small chance that general anesthesia may be necessary, and therefore baseline investigations such as blood tests, electrocardiogram and chest radiographs should be undertaken if deemed necessary. Patients should have deep vein thrombosis prophylaxis. Valid informed consent should be achieved before the operation, and the patient should be aware of risks of infection, bleeding, wound and scar problems, and operation failure, and that further surgery may be required.
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DISCUSSION The management of Achilles tendinopathy aims to return the patient to a level of activity similar to that before acquisition of tendinopathy in the shortest possible time and without significant residual pain. Physiotherapy and conservative treatment should be the first form of management. If conservative measures fail, multiple percutaneous longitudinal tenotomy is simple, requires only local anesthesia, and can be performed without a tourniquet. If postoperative mobilization is carried out early, preventing the formation of adhesions, this will allow the return to high levels of activity in the majority of patients.
Current concepts and research/the future Current management strategies, such as nonsteroidal anti-inflammatory drugs or corticosteroids, offer symptomatic relief but do not result in definitive disease resolution. Surgery may be appropriate for certain patients, but recovery may be protracted and is associated with pain and discomfort. The ideal management should accomplish its goal in a relatively short period of time with little discomfort or disability to the patient. Novel management methods should aim to stimulate a healing response to restore the normal biomechanical properties of tendon. Adhesion prevention The most important factor implicated in adhesion formation is trauma. Many attempts have been made to reduce adhesion formation using materials acting as mechanical barriers such as polyethylene or silicone, or using pharmacologic agents such as indomethacin and ibuprofen, but no simple method is widely used. Hyaluronate, a high molecular weight polysaccharide found in synovial fluid around tendon sheaths, decreased adhesion formation in rabbit flexor tendons. However, no statistically significant difference in adhesion formation was found in a rat Achilles tendon model.15 The absence of a synovial membrane around the Achilles tendon may explain this difference. 5-Fluorouracil, an antimetabolite with anti-inflammatory properties, effectively preserves tendon gliding in experimentally lacerated chicken flexor tendons.16 Physical modalities also have been used to try to limit adhesion formation. Direct current applied to rabbit tendons in vitro results in increased collagen type I production and reduced adhesion formation. However, pulsed electromagnetic field stimulation resulted in no difference in adhesion formation in rabbit flexor tendons after 4 weeks.17 Despite many efforts, adhesion formation after trauma to tendons still remains a clinical problem, and no ideal method of prevention exists. Most studies of adhesion
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formation focus on flexor tendons. Further research is required to determine whether the results also are applicable to extrasynovial tendons.
CONCLUSION Tendon injuries give rise to significant morbidity, and at present only limited scientifically proven management modalities exist. A better understanding of tendon function and healing will allow specific management strategies to be developed. Many interesting techniques are being pioneered. The optimization strategies discussed in this article are currently at an early stage of development. Although these emerging technologies may develop into substantial clinical management options, their full impact must be critically evaluated in a scientific fashion.
REFERENCES 1. Zhang F, Liu H, Stile F, et al: Effect of vascular endothelial growth factor on rat Achilles tendon healing, Plast Reconstr Surg 112(6):1613–1619, 2003. 2. Cao YL, Liu YT, Liu W, et al: Bridging tendon defects using autologous tenocyte engineered tendon in a hen model, Plast Reconstr Surg 110(5):1280–1289, 2002. 3. Lou J, Kubota H, Hotokezaka S, et al: In vivo gene transfer and overexpression of focal adhesion kinase (pp 125 FAK) mediated by recombinant adenovirus-induced tendon adhesion formation and epitenon cell change, J Orthop Res 15(6):911–918, 1997. 4. Brown R, Orchard J, Kinchington M, et al: Aprotinin in the management of Achilles tendinopathy: a randomised controlled trial, Br J Sports Med 40:275–279, 2001. 5. Silbernagel KG, Thomee R, Rhomee P, Karlsson J: Eccentric overload training for patients with chronic Achilles tendon pain–a randomized controlled study with reliable testing of the evaluating methods, Scand J Sports Med 11:197–206, 2001. 6. Ozkan N, Altan L, Bingol U, et al: Investigation of the supplementary effect of GaAs laser therapy on the rehabilitation of human digital flexor tendons, J Clin Laser Med Surg 22(2):105–110, 2004. 7. Tasto JP, Cummings J, Medlock V, et al: The tendon treatment center: new horizons in the treatment of tendinosis, Arthroscopy 19(Suppl 1):213–223, 2003. ¨ hberg L, Alfredson H: Effects on neovascularisation behind the 8. O good results with eccentric training in chronic mid-portion Achilles tendinosis? Knee Surg Sports Tramatol, Arthrosc online, 2004. ¨ hberg L, Alfredson H: Ultrasound guided sclerosing of 9. O neovessels in painful chronic Achilles tendinosis: pilot study of a new treatment, Br J Sports Med 36:173–177, 2002. 10. Lee EW, Maffulli N, Li CK, Chan KM: Pulsed magnetic and electromagnetic fields in experimental Achilles tendonitis in the rat: a prospective randomized study, Arch Phys Med Rehab 78(4):399–404, 1997. 11. Chen YJ, Wang CJ, Yang KD, et al: Extracorporeal shock waves promote healing of collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I expression, J Orthop Res 22(4):854–861, 2004.
References 16. Khan U, Occleston NL, Khaw PT, McGrouther DA: Single exposures to 5-fluorouracil: a possible mode of targeted therapy to reduce contractile scarring in the injured tendon, Plast Reconstr Surg 99(2):465–471, 1997. 17. Greenough CG: The effect of pulsed electromagnetic fields on flexor tendon healing in the rabbit, J Hand Surg Br 21 (6):808–812, 1996.
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12. Paavola M, Paakkala T, Kannus P, et al: Ultrasonography in the differential diagnosis of Achilles tendon injuries and related disorders, Acta Radiol 39:612–619, 1998. 13. Anderson DL, Taunton JE, Davidson RG: Surgical management of chronic Achilles tendonitis, Clin J Sport Med 2(1):39–42, 1992. 14. Calder JD, Saxby TS: Surgical treatment of insertional Achilles tendinosis, Foot Ankle Int 24(2):119–121, 2003. 15. Tuncay I, Ozbek H, Atik B, et al: Effects of hyaluronic acid on postoperative adhesion of tendocalcaneus surgery: an experimental study in rats, J Foot Ankle Surg 41(2):104–108, 2002.
.........................................C H A P T E R 2 3 Pediatric problems and rehabilitation geared to the young athlete Dan Kraft and Jerett Zippin CHAPTER CONTENTS ...................... Introduction
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Osteochondroses
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Congenital problems
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Nonarticular osteochondrosis
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Developmental problems in young athletes
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Conclusion
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Acute injuries
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References
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Pediatric ankle fractures
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INTRODUCTION As young athletes become more active in organized and specialized activities today, sports medicine physicians are diagnosing an increasing number of both acute and overuse injuries in this age group. Many of these injuries involve the foot and/or ankle. These injuries often involve either the apophysis or the epiphysis and require specific treatment and care that is different from that for adults. The growth plates give young athletes a unique set of problems and do not allow physicians to treat the young patients simply as smaller versions of adults. In this chapter we review some of the major foot and ankle problems that are seen clinically in young athletes. The problems are grouped into congenital problems, developmental problems, acute injuries, and problems of osteochondroses. We discuss the approach to rehabilitation under each topic and in particular that which is most applicable to treatment of younger athletes.
CONGENITAL PROBLEMS Coalitions Congenital abnormalities often become symptomatic when increased stress, such as intense activity, is applied to the area. Therefore an inactive child may not complain of pain until he or she enters organized sport and the congenital problem may appear to trigger the
symptoms. In many congenital problems, the natural history is unmasked with the longer duration and increased intensity of the activity, although the developmental and growth stage actually may be the determining factor in the onset of symptoms. Tarsal coalition is one congenital abnormality that may present in later elementary- and middle school-aged athletes as they begin increasing their participation in organized sports. Tarsal coalition is a congenital bridging of two or more tarsal bones of the foot, which can be either bony or soft tissue (cartilage or fibrous tissue). The overall incidence of tarsal coalitions has been noted in studies to range from less than 3% to as high as 12.9% of the population.1 Coalitions can be seen between any two tarsal bones, but the two most common types are calcaneonavicular (bilateral in 60%) and talocalcaneal coalitions (bilateral in 50%).2 These athletes typically present when the coalition begins to ossify. In early childhood and at elementary school age, coalition bridging is mostly nonossified, which allows some motion between the bones and keeps these patients typically asymptomatic.3 Motion becomes restricted when the bridging begins to ossify between 8 and 12 years of age for the calcaneonavicular coalition and between 12 and 16 years for the talocalcaneal coalition. This often is a prime age for middle school and early high school athletes to raise the level of their play and intensity, thus giving the appearance that the increased sports activity is causing the symptomatic foot pain. In reality, the combination of the two factors probably is the main reason for symptoms.
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Pediatric problems and rehabilitation geared to the young athlete
The young athlete may complain of insidious onset of pain or remember an acute onset of arch, ankle, or midfoot pain. The pain can be vague or localized over the coalition and be due to many factors, such as inflammation of the joints, nerve irritation or entrapment, muscle spasm, and microfractures (stress fractures) within the coalition.4,5 Any adolescent athlete with an inversion ankle injury that does not resolve after a full rehabilitation program should have tarsal coalition in the differential diagnosis. Other athletes who have not experienced an injury can present with pain located in the cuboid/navicular area that is aggravated by increased impact activities. On physical examination, the patient classically presents with a valgus heel, pronation deformity, and abduction of the forefoot. The pronation deformity is rigid, meaning that the arch does not reform when nonweight bearing and is stiff to clinical examination. Furthermore, a weight-bearing calcaneal valgus is present and fails to go into varus on toe raising. This is distinguishable from the usually asymptomatic flexible flatfoot, which re-forms its arch with nonweight bearing. Subtalar motion is diminished on examination. Passive inversion may elicit pain as the shortened peroneal tendon is stretched. Examination findings sometimes are subtle in early stages and may require further radiologic studies. Radiologic evaluation begins with plain films, which include anterior-posterior (AP), lateral, and oblique views of the foot and a tangential view of the calcaneus. The AP may demonstrate a talonavicular coalition. The oblique angle best demonstrates the calcaneonavicular coalition. The tangential view of the calcaneus (Harris axial view) best demonstrates a talocalcaneal coalition (middle facet). Bone scan typically is not used but may have a place as a screening procedure in cases that are difficult to determine. The gold standard remains computed tomography (CT). It is used to confirm diagnosis, determine surgical planning, follow up postoperatively, and evaluate degenerative changes. Magnetic resonance imaging (MRI) is becoming more useful, particularly in the young, growing population. MRI can detect soft-tissue bridging before ossification takes place.6 Treatment initially should be conservative for young athletes with tarsal coalitions. Both rehabilitation with aggressive Achilles stretching and custom orthotics can be used to improve the biomechanics of the foot and improve symptoms. Immobilization also can be used at times during a season to help the athlete calm the symptoms and possibly finish a season. Surgical intervention usually is the long-term treatment for athletes and can be done during the adolescent years or as dictated by nonresolving symptoms with sports. Athletes with no significant degenerative changes can expect to have an excellent or good surgical outcome.7 Avoiding surgery
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in the young, symptomatic athlete may increase the risk of arthritis later in life.
Flexible flat feet Flat feet, or pes planus/pes valgus, is a common problem in young athletes. Pes planus is a normal foot position up to 6 years of age.8 Most young athletes with flat feet are asymptomatic and do not require any intervention. Wenger et al.6 demonstrated that intervention with orthotics did not change the natural course of asymptomatic flat feet. The cause of this congenital problem is excess laxity of the joint capsule and ligaments, which allows the longitudinal arch to collapse during weight bearing. The arch re-forms when nonweight bearing and is accentuated with dorsiflexion of the first toe. A full examination should be performed in a young athlete with flat feet, whether symptomatic or not. Among other questions in the history, the clinician should determine the length of symptoms, the effect of these symptoms on sports activity, and any systemic symptoms. Subtalar motion is one factor that can help differentiate pes planus from tarsal coalitions. The calcaneus should move passively between 20 and 60 degrees of inversion and eversion. When Achilles tendon flexibility is measured with the knee extended and the ankle/foot held in varus, ankle dorsiflexion less than 10 degrees below neutral indicates tight heel cords and may contribute to pes planus. If the athlete has no symptoms and the examination does not suggest a secondary cause, no further workup is necessary. These young athletes should be allowed to participate in all activities without restrictions. There is no evidence to date that preventative treatment with orthotics or other shoe inserts will prevent the development of symptomatic pes planus in the future. Children with unilateral, asymptomatic pes planus require more careful monitoring, as well as evaluation for neurologic and spinal causation. If the athlete is seeking medical advice because of discomfort, then radiographs should be obtained to evaluate further for secondary causes. These may include accessory navicular, fractures, tumors, or coalitions. Painful, flexible flat feet without secondary causes often respond to conservative measures. The young athlete must understand that this may be a chronic problem, but that extra work may help to alleviate the symptoms. Orthotics, aggressive heel cord stretching, and strengthening of the intrinsic muscle of the foot and posterior tibial muscle are the mainstay of treatment. Time also should be spent examining the footwear of young athletes. Worn-out shoes should be replaced with supportive footwear, especially a shoe with good medial longitudinal arch support.
Developmental problems in young athletes
Hallux valgus Bunions in children are less common than in adults. However, some studies have reported the prevalence to be as high as 35% in the adolescent population.9 Bunions of the great toe are more common in girls than in boys. The developmental etiology of bunions is multifactorial, with an association of ligamentous laxity, hypermobile forefoot, pronation deformity, and metatarsus primus varus with hallux valgus.10,11 Shoes that place excessive stress on the first ray, such as narrow fitting and high heeled shoes, also are associated with increased irritation of bunions. Heredity is thought by some to play a role.12 A young athlete with a congenital angle between the first and second metatarsals greater than 10 degrees is more prone to developing hallux valgus in the future.11 Parents and young athletes alike need to be aware of proper-fitting shoes. Children with rapidly growing feet may need several shoe changes during a single year. Prevention of this condition is the best treatment. If symptoms begin, the child may need to weigh the benefits of flat, wide shoes outside of sports versus the looks of more trendy narrow, heeled shoes. As with adults, weight-bearing x-rays and a physical examination usually are warranted when a young athlete complains of pain over the first ray. Because the natural history of this condition occurs over many years, initial workup may find the exostosis and thickened bursa at the medial head of the first toe to be less impressive than findings in an adult. Adolescent bunions also differ from late findings in adults in the lack of arthritic changes and spurs.13 Treatment is similar to that for the adult with regard to conservative measures. These include proper footwear, avoidance of aggravating activity, nonsteroidal anti-inflammatory drugs (NSAIDs), heel-cord stretching, orthotics, and education. Surgery should be postponed until after maturation of growth because recurrence of the deformity after osteotomies and capsulorrhaphies is common in young athletes.14 Joint stiffness and discomfort at extremes of motion also is a problem for young athletes after surgery, and the athlete may never be able to return to his or her previous level. Accessory navicular Most accessory bones about the foot and ankle are normal variants and often represent secondary centers of ossification. These variants often are asymptomatic and without clinical significance. However, some young
athletes may develop symptoms that relate directly to the variant, such as the accessory navicular, or naviculare secundarium. The accessory navicular is one of several supernumerary ossicles first identified in 1605 by Bauhin (see Ref. 15). There are two types of accessory navicular. The first type is found within the posterior tibial tendon. The accessory navicular is present in about 10% of children; however, only 2% do not fuse by maturity. Anatomic studies have revealed that this accessory navicular ossicle is independent of the navicular bad break and can be thought of as a sesamoid bone. The second type is an accessory ossification center medial to the navicular. During early development, this ossification center is surrounded by cartilage that is congruent with the cartilage of the navicular. The secondary ossification center typically fuses with the navicular near maturity, usually between 9 and 11 years. This type may be associated with symptomatic medial foot pain, especially in the adolescent athlete. This ossicle accounts for approximately 70% of all accessory naviculars. The symptomatic accessory navicular should be thought of as an overuse injury. Increased stress on the overlying soft tissue causes inflammatory irritation and pain, especially if tenosynovitis has developed. It typically presents with pain and tenderness over the medial aspect of the foot, particularly the medial navicular. The athlete complains of pain with weightbearing activity that is aggravated by tight-fitting shoes. The medial arch may be flattened secondary to posterior tibialis muscle fatigue or congenital foot pronation. Often the symptoms begin at the beginning of a new season. There is a higher predominance in girls than in boys, and the majority of patients first complain of symptoms during their adolescent years. Prominence is noted on the medial navicular on clinical examination. Radiographically, the two types of accessory navicular should be distinguished because the first type does not commonly have symptoms. An oval or circular sesamoid on plain film is associated with the first type. Type II, or the commonly symptomatic ossicle, has a triangular and more irregular appearance.16 Bone scan of a symptomatic navicular will demonstrate an area of increased uptake over the medial navicular ossicle. Treatment initially should be aimed at conservative measures. These include a period of avoiding aggravating activities and using orthotics to eliminate pressure over the prominence. If pain is intolerable, immobilization in a short walking boot with or without an orthotic may be helpful to eliminate the muscle spasm and discomfort. Surgery is reserved for the persistent symptomatic ossicle that does not respond to several months of conservative treatment. 537
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DEVELOPMENTAL PROBLEMS IN YOUNG ATHLETES
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Pediatric problems and rehabilitation geared to the young athlete
ACUTE INJURIES Avulsion fracture of fifth metatarsal As in adults, young athletes often have inversion and supination injuries to their feet and ankles. In young athletes these inversion injuries often can lead to an avulsion fracture at the base of the fifth metatarsal. The middle school- or early high school-aged athlete will present with lateral foot pain and swelling. He or she typically notes a history of a significant inversion injury and the inability to continue participation. On examination the athlete will have palpable pain at the base of the fifth metatarsal that is more significant than pain at the lateral ligaments. Plain films of the foot, including AP, lateral, and oblique views, will easily detect the usually transversely oriented fracture. If concern exists regarding whether the plain films show a fracture or an unfused metatarsal physis, comparison films of the nonaffected foot may help to differentiate. Because this injury occurs with the injury mechanism commonly seen with lateral ankle sprains, the avulsion fracture may be missed if ankle films alone are obtained. The most common fracture of the fifth metatarsal seen in young athletes is a transversely oriented avulsion fracture at the base of the fifth metatarsal and through the metaphysis. As noted previously, the injury commonly arises from an acute forceful inversion and supination injury of the foot/ankle. The mechanism is similar to twisting that produces lateral ligament injury of a sprained ankle. Recent cadaveric studies indicate that the lateral band of the plantar fascia is the structure responsible for the tuberosity avulsion, and not the peroneus brevis, as once thought.17 It generally does not involve the articular surface but occasionally may extend into the cuboid-metatarsal articulation.18 As mentioned, on roentgenographs this injury sometimes is confused with an unfused apophysis in a growing athlete. If there is minimal displacement, conservative treatment is indicated using symptomatic immobilization. Our preference is to use a below-knee walking boot. However, a hard-soled shoe or a cast also is acceptable. The walking boot allows the athlete to almost immediately begin nonimpact conditioning with a stationary bike, stair-stepper machine, or elliptical trainer during the recovery time. After 3 to 4 weeks in the boot, the athlete can be weaned out of the boot into a steel-shank shoe insert. Limited impact sports activities can be started at 4 to 6 weeks while the steelshank insert is worn, and progression is allowed using pain as a guide. Both plain films and symptoms are followed to assess healing. Radiographic healing may not
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be seen for several months and generally lags behind clinical symptoms. A small percentage of avulsion fractures in young athletes will progress into nonunions. These athletes will have a history of a significant inversion injury that typically was treated with some type of immobilization. The athlete will present to the office over the next 6 to 24 months with the complaint of continued injuries and pain involving the base of the fifth metatarsal with sports activities. Plain films that include a comparison of the unaffected foot typically will be diagnostic. Surgical intervention then is typically required to allow the athlete to effectively return to sports.
Fifth metatarsal apophyseal avulsion The tendon of the peroneus brevis inserts into the apophysis. The apophysis can be distracted and avulsed with an acute inversion injury. Chronic repetitive stress results in Iselin’s disease, as discussed later in the chapter. Patients present with pain over the base of the fifth metatarsal, and there may be widening of the apophysis on plain films. The normal apophysis is parallel to the long axis of the metatarsal. The apophysis develops between the ages of 9 and 11 in females and 11 and 14 in males. It typically fuses several years later.5 If there is minimal displacement, then nonoperative treatment consists of boot immobilization for 3 to 6 weeks followed by progression to running and then to sports (2-3 months). If there is more than 2 to 3 mm of displacement, surgery should be considered. Os vesalianum sesamoid This normal variant must be distinguished from an avulsion injury in the skeletally immature athlete. Jones fracture As first described in 1902, the Jones fracture has a similar appearance to the avulsion fracture but is more distal in position.19 It is located about 1.5 to 2.0 cm from the proximal end, involving the metaphyseal-diaphyseal junction. This fracture also has a transverse orientation that is intra-articular. Although it commonly is described as occurring from an acute traumatic event, it can be secondary to chronic repetitive stress, such as from running. This fracture is not commonly seen in the same age group as the fifth metatarsal avulsion fracture. It usually occurs in the older adolescent (15 to 20 years). Risk factors for this type of fracture include intense level of repetitive running and jumping, as seen in basketball and volleyball players. Another physical risk factor is the athlete who has hindfoot varus because of the
Pediatric ankle fractures
PEDIATRIC ANKLE FRACTURES In young athletes with open growth plates, acute injuries to bone around the foot and ankle most commonly are fractures (bone or physeal). In adults, rotational forces and low-velocity sporting injuries generally cause ligamentous injuries, whereas in young athletes these same forces often result in physeal injuries. The growing bone in the young athlete differs from the adult in terms of the mechanical properties. Although the long bones in children are more compliant than in the adult, the physeal plate is vulnerable because it is the weakest link in the ligament-bonetendon complex. There are several pediatric fractures around the foot and ankle that are common yet can easily be overlooked. These fractures may have subtle clinical and radiographic findings. At the other extreme, a physician may treat an accessory ossification center noted on radiographs as an acute fracture. Recognition of the common fracture patterns and awareness of the pediatric bony variants are extremely helpful for the physician who cares for this population. Approximately 5% of all pediatric fractures are around the ankle. They most commonly occur in the growing athlete involved in organized sports. The age range most commonly involved is 10 to 15 years.20,21 The annual incidence in this population is one physeal injury per thousand.22 Radiographically, the distal tibial ossific nucleus appears between the second and third years, and physeal closure begins about age 15 in girls and 17 in boys. The distal fibula ossific nucleus is apparent during the second year and fuses with the shaft by 20 years.23 In most cases, conventional radiographs with comparison views allow adequate visualization of growthplate injuries, and evaluation and treatment can be based solely on these findings. However, the role of additional imaging is being used more often with the knowledge that better visualization of soft tissue and bone is apparent with CT and MRI. Although the role of additional studies is still controversial, and there are no set
guidelines to determine when additional studies should be used, several investigations have provided guidelines. CT or MRI may be beneficial in the patient with persistent unexplained symptoms and normal radiographs. MRI and spiral CT have been shown to detail fractures that were not visible on plain films. MRI or CT also may be helpful when surgery is contemplated and more detail of the injury, particularly nonossified areas, is required.24,25 There are several systems of classifying ankle fractures in the literature. In the pediatric population, the SalterHarris classification has been used since 1963 for planning treatment and predicting the long- term outcome of the injury.25 Dias and Tachdjian (see Ref. 23) applied these principles and combined the mechanism of injury to assist with treatment. However, this system is difficult to discuss and beyond the scope of the chapter. In general, prognosis is determined by the grade of the fracture and the effectiveness of the reduction. As in adults, fractures that involve chondral surfaces have a better long-term prognosis the more anatomic the chondral surfaces are approximated.26 Skeletal maturity at the time of injury also is important to consider because patients who are near skeletal maturity will have less risk of leg-length discrepancies in the long term. Salter-Harris I distal fibula fractures, which are the most common ankle fracture in pediatric sports, typically occur from supination/inversion injuries.27 This injury typically has the same injury mechanism as the adult lateral ankle sprain. Athletes will present with the history of an acute injury with pain and swelling over the lateral ankle. These athletes present similar to typical lateral ankle sprains, and the fractured growth plate can be missed easily. Careful palpation during the physical examination will elicit maximal tenderness at the distal fibula physis rather than the lateral ligaments. The distal fibula physis is palpated approximately 2 to 3 cm proximal to the tip of the fibula. Plain films most often are normal but rarely show widening of the physeal plate with evidence of surrounding soft-tissue swelling.28 Because plain films typically are normal, physical examination findings and an appropriate history are required to make the diagnosis. Once the clinical diagnosis is made, then the patient should be treated empirically with immobilization for 2 to 4 weeks. Immobilization can be accomplished with a walking boot, cast, or crutches and nonweight bearing. The walking boot allows the athlete to be more active in conditioning activities during the recovery phase. The athlete then can be weaned into a stirrup or lace-up–type brace, which will be used when returning to play at the 4- to 6-week mark. Although rare, Salter I fractures of the distal fibula can develop into nonunions. These athletes complain of continued lateral ankle pain with sports 539
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increased stress of the lateral aspect of the foot. A high rate of delayed union or nonunion is due to the tenuous blood supply to this area. Treatment for this fracture is somewhat controversial and is beyond the scope of this chapter. In general, we prefer to use intramedullary screw fixation if the growth plate is closed because it allows a quicker return to competitive sports as compared with bone grafting without screw fixation. This fracture and its treatment options are discussed in Chapter 4.
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activity and often need surgical intervention to resume pain-free sports activity. Salter-Harris I distal tibia fractures are less common than distal fibula fractures. Careful palpation of the distal tibia will help to differentiate this injury, as with the distal fibula injury. Immobilization with a boot or cast for 4 to 6 weeks generally will result in a good outcome. Patients should be followed with standing radiographs and comparison films for at least 1 year to ensure normal growth continues after the injury. Salter-Harris II distal tibia fractures involve a fracture through the physis and metaphysis. Diagnosis often can be made with routine radiographs, but further imaging with a CT scan or MRI may be needed if the diagnosis is in question. This type also has a low risk of physeal arrest. Most displaced Salter-Harris II distal tibia fractures can be treated with closed reduction with sedation. If soft tissue blocks closed reduction attempts, then an open reduction is indicated. Immobilization with a long-leg cast for approximately 3 weeks is followed by below-knee immobilization for approximately 3 more weeks. As with Salter-Harris I fractures, patients should be followed with routine radiographs for at least 1 year to ensure normal growth. Salter-Harris III fractures involve the fracture line proceeding from the articular surface dorsally to the physis and then laterally along the physis (Fig. 23-1). These injuries have more potential long-term consequences. There often is intra-articular damage that cannot be seen on plain films. Closed reduction of the
Figure 23-1 Anterior-posterior radiograph of young athlete with a Salter Harris III fracture of the distal tibial physis.
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fracture can be attempted; however, if there is greater than 2 mm of displacement, then an open reduction with smooth pinning is advised.29 Long-term followup is important to recognize early signs of growth arrest and deformities. Tillaux are a special form of Salter-Harris III fractures of the distal tibia. Tillaux fractures were described in 1848 and involve the distal anterolateral quadrant of the tibial physis.30 The mechanism of injury is thought to be supination/external rotation with the foot planted. As a result of the pattern of fusion, central to medial and then lateral, the lateral corner is avulsed off with the attachment of the anterior inferior tibiofibular ligament.22 These fractures occur in adolescents (12-14 years in girls and 14-18 years in boys) during the 18 months when the growth plate begins to fuse.31 They account for approximately 5% of all pediatric ankle fractures.25 This injury is complex, and additional studies usually are required to reveal the degree of displacement and extent of injury. Treatment of a nondisplaced fracture consists of closed reduction with internal rotation and axial distraction. If 2 mm or more of displacement remains, then open reduction and anatomic reduction are indicated.32 Poor anatomic reduction may result in growth deformities and long-term arthrosis. In general, Salter-Harris IV fractures account for approximately 25% of all distal tibial fractures.21 If a posterior metaphyseal fragment accompanies the type III Tillaux fracture, then it is classified as a Salter-Harris IV fracture, called a triplane fracture. Although there is a distinction between Salter-Harris III and IV distal tibia fractures by classification, similar treatment probably should be followed to avoid complications in the future. The fracture begins at the articular surface, extends through the epiphysis along the physis and into the posterior tibial metaphysis in three planes: sagittal, transverse, and then most proximally in the coronal plane. It can contain several fragments.33 Two to four fragments are seen, depending on the maturity of the growth plate. Because of the complexity, CT or MRI is helpful in defining the fracture pattern, the amount of displacement, and the adequacy of postreduction alignment. Significant shorting after this injury is uncommon because the athlete usually is close to maturity. Salter-Harris V fractures account for approximately 1% of distal tibial physeal injuries. The mechanism involves a compressive force across the physis. The plain films underestimate the damage to the physes. Unfortunately, the injury is discovered months to years after the event, when the patient has noticeable leg-length discrepancy or angular deformity. The treatment then is aimed at addressing these late complications. A high index of suspicion is required to detect these often-missed severe injuries. One clue to the diagnosis radiographically is the presence of multiple, small bone fragments at
Osteochondroses
Complications of physeal ankle fractures Complications have been well documented after treatment of ankle fractures involving the growth plate. Obviously, the initial injury and the damage that occurred during the event are unpreventable. However, the treatment following the inciting event can have a dramatic impact on long-term results. Further damage can be minimized by limiting the attempts at reduction. Early recognition and immobilization have an impact on healing and long-term outcome. The importance of the physical examination is that it may prevent ongoing injury from being missed. Compartment syndrome of the anterior compartment has been described in the literature, and sign and symptoms should not be overlooked on the initial examination.34 Although growing athletes have an incredible ability to heal quickly and often without complications, fractures involving the epiphyseal plate can result in permanent disability and deformity. The degree of angular deformity and leg-length discrepancy resulting from premature closure of the plate depends on the age and bone maturity of the athlete when the injury occurs as well as the amount of displacement of the physis and fracture. The distal tibial physis contributes approximately 4 mm of growth per year.22 An injury to this area at the end of growth most likely will not have a dramatic affect on leg length. Bony fusion generally is completed by 14 years in females and 16 years in males. Age and family history will help guide the physician in determining the predicted remaining growth of the tibia. Less than 1 cm of discrepancy is considered acceptable and does not have reproducible long-term deleterious effects on the foot and ankle. Follow-up radiographs should be obtained to evaluate for growth disturbance. Inaccurate physeal reduction leading to an asymmetrical growth arrest is a potential problem in the young athlete. If accurate reduction of the articular surface cannot be maintained with closed means, then open reduction must be undertaken. In a study by Kling et al.,20 patients with Salter-Harris III and IV ankle fractures had less growth arrest when open reduction/ internal fixation was the treatment of choice versus closed reduction. When considerable angle deformity exists after initial treatment of an unrecognized fracture, then an osteotomy can be the best solution to correct the alignment and prevent further long-term stress and complications on the joint. As with adult fractures, osteoarthritis may result from the inciting injury, particularly when the chondral surface is involved. A study by Caterini et al.35 looked at the long-term follow-up after physeal injuries of the ankle. They concluded that Salter-Harris injuries that
involved the articular surface had an increased rate of osteoarthritis as compared with those without involvement of the chondral surface. Several other studies have concluded that anatomic reduction decreases the rate of osteoarthritis. All injuries involving any joint may result in stiffness, muscle atrophy, and, rarely, complex regional pain syndrome. Careful follow-up and physical therapy addressing early range of motion and strengthening the supporting muscles may have a role in preventing these long-term complications.
OSTEOCHONDROSES The osteochondroses comprise a group of clinical syndromes that occur during years of growth and affect the primary and secondary growth centers. Typically young athletes present with symptoms of pain during sports activities. Although there have been a number of studies looking at the cause of these growth-plate problems, the etiology is still unknown. Physical activity appears to play an important role, but it is not clear whether this is the major contributing factor.36 Osteochondroses of the foot and ankle typically do not cause long-term problems and can be treated conservatively. Understanding the presentation and treatment of these overuse problems can help get young athletes back to sports activity more quickly and safely.
Kohler’s disease Kohler’s disease is a foot disorder in children characterized by sclerosis and collapse of the developing tarsal navicular. The problem is seen most typically in active children between 4 and 7 years of age and seems to affect boys more commonly than girls.37 The navicular typically is fully ossified by adolescence, and thus Kohler’s disease presents at this younger age.38 Patients often present with a noticeable limp and complain of medial foot pain that is associated directly with physical activity or immediately following activity. The pain can range from vague discomfort to disabling pain with ambulation. The physical examination may reveal an area of erythema and swelling over the navicular. On examination the area overlying the navicular may appear erythematous and swollen. Palpation over the medial aspect of the navicular produces pain. Routine radiographs are an important first step in diagnosing Kohler’s disease. Plain films also will help to rule out other possible diagnoses such as tumor, infection, and stress fractures. Most cases are unilateral, so comparison films of the uninvolved foot are helpful. The diagnosis is confirmed by the typical appearance of a narrowed or flattened navicular and/or increased 541
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the level of the physis. Long-term complications are common despite early detection and appropriate management.
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Figure 23-2 Lateral radiograph of the foot demonstrating Kohler’s disease. Note the sclerosis of the navicular.
density (Fig. 23-2).39 Occasionally there is a fragmented and patchy appearance. The joint spaces of the surrounding bones are well preserved to help rule out other systemic illnesses. A bone scan will be positive for increased uptake in the navicular with Kohler’s disease. CT scan also can be used to confirm the diagnosis but may not be needed if the clinical examination and radiographics are diagnostic. Treatment consists of a conservative approach at first. NSAIDs have been shown to help alleviate the pain initially. Several studies have looked at different treatment options from orthotics to casting for several months. It has been found that immobilization has affected the duration of symptoms. Immobilization in a walking cast or boot decreases time of symptoms by an average of 7 months. Long-term studies have not shown a difference with respect to the type of treatment used. The prognosis is excellent, with few athletes having long-term disability. Young patients can be allowed to return to play when the symptoms subside. Immobilization should be for 6 to 12 weeks. An orthotic often is used to help alleviate stress over the involved joint. When poor results do occur with conservative management, arthrodesis of the talonavicular joint sometimes is required.
Freiberg’s disease Osteochondrosis of the metatarsal head, or Freiberg’s disease, involves an evolutionary process of deterioration and collapse of the articular surface and underlying subchondral bone. It occurs more commonly in adolescents when the epiphysis is still present, and 75% of the cases are female.40 The second metatarsal is the most common site (68%) followed by the third and forth metatarsal heads being affected.41 The second metatarsal head is involved more commonly when it is longer than the first. It has been proposed that this results in increased pressure over the head and possibly disruption of the vascular supply with repeated microtrauma (i.e., running or dancing en pointe).
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The athlete typically presents with forefoot pain that is worsened with impact activities. Activities that cause extremes of motion at the metatarsal heads during weight-bearing activities such as sprinting and repetitive jumping particularly seem to exasperate symptoms. Athletes usually will complain that the pain symptoms are continuing to worsen by the time they seek medical help. The physical examination may show some mild swelling over the metatarsal head. Palpation of the midfoot and forefoot typically isolates pain to the affected metatarsal head and its metatarsophalangeal (MTP) joint. Motion at the affected MTP joint will be decreased and painful. Radiographs of the foot should be obtained when a young athlete presents with these symptoms and physical examination findings to evaluate for Freiberg’s disease and to rule out other causes, such as infection or stress fractures. Initial plain film findings, such as widening of the affected MTP joint space, may be subtle. Osteosclerosis of the metatarsal head may be seen within
Figure 23-3 Anterior-posterior radiograph of the foot demonstrating sclerosis of the second metatarsal head and early evidence for collapse consistent with Freiberg’s infraction.
Nonarticular osteochondrosis
Osteochondral talar dome lesions Osteochondral lesions of the talar dome, also called osteochondritis dissecans, may be a cause of ankle pain in children, as well as in young adult athletes. Lesions of the talar dome are well documented in the adult population (see Chapter 14); however, with advances of MRI and the growing awareness of this condition in young athletes, it is more common among adolescents than once thought. An article published by Canale and Belding43 in 1980 found the majority of the subjects to have symptoms dating back to adolescence. This disorder should be suspected in an adolescent with a history of an ankle sprain that does not improve as expected. The etiology of the lesion is controversial. Canale and Belding43 found the lesions to be caused by trauma in 31 reported lateral talar dome lesions. Medial lesions were not as conclusive, with only 64% of the cases related to a traumatic event. Like many other types of osteochondral lesions, vascular insufficiency may play a role in the development and progression of the lesion. Central lesions are rare. The male-to-female ratio ranges from 3:1 to 2:1.44 Athletes usually present with a history of an inversion injury. Acutely, there often is a large effusion and diffuse pain. Range of motion often is limited. Palpation over the anterior joint line is tender. Absence of tenderness over the lateral ligamentous complex should further raise suspicion of a talar dome lesion. Although locking and a catching sensation are classically described for loose body formation, this is an uncommon presentation. Berndt and Hardy in 1959 (see Ref. 43) published a classification system based on standard radiographs. Grade I is a depressed chondral fracture with the overlying
articular cartilage intact. Grade II is a fragment that is incompletely separated. Grade IIa has formation of a subchondral cyst seen on MRI. Grade III is a detached fragment that may have some articular cartilage still attached. The fragment is not displaced. Grade IV is a displaced fragment. Routine three-view radiographs of the ankle should be obtained before MRI, because grade IV lesions may not be readily apparent on MRI. Stage I lesions do not show up on plain film. If suspicious for this type of lesion, a mortise view with the foot in full plantarflexion will help the clinician to view posterior medial lesions, and dorsiflexing the ankle with AP radiographs will help in visualizing the lateral dome lesions. MRI will show a well-demarcated area of abnormal signal. The bone scan will show a focal increase of tracer uptake. Grade II to IV lesions may be visible on plain films. Treatment depends on the grade of the lesion. There have been higher failure rates in nonoperative treatment for adults as compared with young athletes.44 It is acceptable to immobilize a low-grade lesion to see whether symptoms resolve. If conservative measures fail, then surgical treatment is recommended. This may be an evolutionary process with grade I lesions progressing to grade IV lesions. Grade IIa and above may require immediate excision to avoid long-term arthosis.45
NONARTICULAR OSTEOCHONDROSIS Sever’s disease The differential diagnosis for heel pain in young athletes is similar to that for adults, with few additional considerations. Overuse injuries in children were relatively rare until the advent of organized sport. With rapid bone growth and increased activity levels during youth, increase stresses are placed on developing apophyseal bone. Sever’s disease, or calcaneal apophysitis, was first described in 1912 as a cause of posterior heal pain and thought to occur in physically active, overweight children.46 It now is known to occur in nonobese children as well. Sever’s disease is a traction apophysitis that causes pain along the secondary calcaneal ossification center. The insertion of the Achilles tendon over the longitudinally oriented surface subjects the epiphysis to strong traction forces. The apophysis typically is irregular looking with multiple fragments and increase density; however, it is radiographically similar to the opposite asymptomatic heel. For this reason, x-rays are not diagnostic but can be helpful in ruling out stress fractures or bone tumors.47 The epiphysis begins to fuse between 12 and 15 years of age. This area therefore is most vulnerable before this age, and the incidence of Sever’s disease is highest between 6 and 8 years of age.48 543
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several weeks on plain films (Fig. 23-3). As the disease progresses, there is increased resorption of necrotic bone with resulting fragmentation and collapse of the metatarsal head.42 Bone scan may be helpful when the clinical examination and history are suspicious but radiographs are negative. The bone scan will show increased uptake in the proximal metatarsal head and decreased uptake over the necrotic area. Treatment consists of taking anti-inflammatories and decreasing the load to the area for a period of time. Initial immobilization in a walking boot will help to calm symptoms. The athlete then may be transitioned into an orthotic and started back to nonimpact activities initially. It is not always possible to stabilize the joint and prevent pain and progressive deformity. In severe cases with persistent pain, surgery may be required to alleviate symptoms and remove impingement. In later stages, it is believed that the discomfort is associated with loose bodies. There are several procedures, depending on the extent of the disease and whether loose bodies are present. All have reported very good results.
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There appear to be several predisposing factors that contribute to Sever’s disease. Biomechanical abnormalities, overuse during activity, and increased stresses all play a role.49 Hallux valgus, pes planus, and pes cavus all may have an association with Sever’s disease. Forefoot pronation is most commonly associated. These structural abnormalities alter the biomechanics and forces applied to the heel, decreasing shock absorption and exposing the heel to abnormal stresses. Most sports such as running require repetitive heel-cord loading and expose this area to microtrauma. Athletes may ignore the discomfort initially and continue with long, intense workouts before seeking medical advice. One should be aware of the sports most commonly associated with this syndrome. Basketball, soccer, track, and gymnastics have been found to have the highest association.50 Sports played on hard surfaces also may contribute to the increased stress and microtrauma. The final predisposing factor probably is the most significant in terms of treatment. Abnormal stresses may be secondary to inflexibility. The heel-cord complex, as a result, has diminished dorsiflexion and may contribute to abnormal stresses on the apophysis during activity.51 The child may present with heel pain, particularly with running. Often the young athlete is starting a new season. The pain is absent in the morning, begins with exercise, and lessens during nonweight-bearing activity. The pain may begin insidiously, or the athlete may remember an inciting history of direct trauma to the heel.52 The pain may become debilitating and prevent the athlete from participating in his or her sport. On examination, one should look for the previously mentioned biomechanical abnormalities. Dorsiflexion of the ankle is important to document. If the dorsiflexion is less than 10 degrees, then a severe Achilles contracture is present. The patient may limp or complain of reproducible pain when he or she rises up on the toes. This is known as a positive Sever’s sign. Pain to palpation over the posterior mediolateral heel and a positive squeeze test are suggestive of Sever’s disease. Although radiographs may not help to distinguish Sever’s disease from a normal-appearing asymptomatic heel, they may rule out other mimicking conditions such as a fracture, coalition, or tumor. Treatment varies depending on the severity of the pain and the reliability of the patient. There have been no studies to date that have shown long-term sequelae after treatment for Sever’s disease. Initial management is conservative, and aggravating activities should be avoided until symptoms improve. Icing, heel lifts, antiinflammatories, and physical therapy also are helpful. In our practice, a home program of aggressive heel-cord
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stretching usually is curative. If the pain returns after treatment, one should consider orthotics if biomechanical abnormalities exist. If there is persistent heel-cord inflexibility, then nighttime splints may be helpful. Rarely is pain debilitating enough to require a walking boot. Often the pain subsides in several weeks to 2 months, and the athlete can return to sport with a functional progression program.
Iselin’s disease Iselin’s disease, or traction apophysitis at the base of the fifth metatarsal, was first described in 1912 as occurring in adolescents.53 The confusing pathology of this metatarsal can make fractures or os vesalianum difficult to distinguish from Iselin’s disease on roentgenographs. The apophysis develops between the ages of 9 and 11 years in girls and 11 and 14 years in boys. It begins to fuse 2 to 3 years later. The apophyseal growth cartilage is the weakest site for ligament and tendon attachment in growing children.26 With intense training, this area can develop microavulsion fractures or traction apophysitis. The proximal fifth metatarsal is the site of three ligament attachments: the plantar fascia and the fourth and fifth metatarsal ligaments. The peroneus brevis and peroneus tertius also insert into this area. During growth, the secondary growth center of ossification is located on the lateral plantar aspect of the tuberosity. This bone is within the cartilaginous flare onto which the peroneus brevis tendon inserts.54 With continued longitudinal stress, this bone may become irritated and painful. Young athletes, more often male, present with tenderness over the proximal fifth metatarsal. Similar to Sever’s disease, Iselin’s disease often occurs at the beginning of a season. The onset may be insidious or acute with a history of an inversion injury. The pain usually is worse during activity. Any activity that fires the peroneal muscle will elicit pain. Maneuvers such as running, especially lateral and cutting movement, will produce discomfort. On examination the area will be tender to touch. Resisted eversion or passive, extreme plantarflexion with inversion may elicit pain. Occasionally the area may appear erythematous and swollen. Weakness on resisted eversion may be evident because of protective pain. Radiographically, AP and lateral views may not show the secondary ossification center. A third medial oblique view should be taken when examination findings are suspicious. This may show a small piece of bone oblique to the fifth metatarsal shaft on the lateral plantar aspect of the tuberosity. Bone scan will show increased uptake over the proximal fifth metatarsal. Plain films will be helpful in ruling out similar conditions such as Jones fractures. Therefore history, physical examination, and
References
CONCLUSION Pediatric foot and ankle problems are common. They are similar to adult conditions but with the complicating factor of injuries to the growing bone and physis. It is important to understand and be familiar with the developing skeleton to distinguish among normal growing bone, osteochondroses, accessory bones, ligament injuries, and bone fractures. The additional confounding factor of residual growth with physeal injuries presents even more potential for complications and a greater need to be accurate with diagnosis and treatment. One should obtain comparison radiographs when subtle finding are confusing. Routine use of comparison views will result in unnecessary exposure and expense.
REFERENCES 1. Ruhli FJ, Solomon LB: High prevalence of tarsal coalitions and tarsal joint variants in a recent cadaver sample, Clin Anat 16:411, 2003. 2. Loney BW, Asher MA: Excision of symptomatic coalition of the middle facet of the talocalcaneal joint, J Bone Joint Surg Am 69:539, 1987. 3. Kulik MS, Clanton TO: Foot fellow’s review, Am Orth Foot Ankle Soc 17:286, 1996. 4. Kumai Y, Takakura Y: Histopathological study of nonosseous tarsal coalition, Foot Ankle 19:525, 1998. 5. Manusov EG, Lillegard WA: Evaluation of pediatric foot problems, Am Fam Phys 54:1012, 1996. 6. Wenger DR, et al: Corrective shoes and inserts as treatment for flexible flatfoot in infants and children, J Bone Joint Surg 71:800, 1989. 7. O’Neill DB, Micheli LJ: Tarsal coalition, Am J Sports Med 17:544, 1989. 8. Staheli LT, Chew DE: The longitudinal arch: a survey of eight hundred and eighty-two feet in normal children and adults, J Bone Joint Surg 69:426, 1987. 9. Geissele AE, Stanton RP: Surgical treatment of adolescent hallux valgus, J Pediatr Orthop 10:642, 1990.
10. Crawford AH, Gabriel KR: Foot and ankle problems, Orthop Clin North Am 18:649, 1987. 11. Lovell W, Price C, Meehan P: The foot. In Pediatrics orthopaedics, ed 2, Philadelphia, 1986, JB Lippincott. 12. Magee D: Orthopedic physical assessment, Philadelphia, 1987, WB Saunders. 13. Roy S, Irvin R: Sports medicine, Englewood Cliffs, NJ, 1983, Prentice Hall. 14. Mann RA, Coughlin MJ: Surgery of the foot and ankle, ed 6, St Louis, 1993, Mosby. 15. Geist ES: Supernumerary bones of the foot: a roentgen study of the feet of 100 normal individuals, Am J Orthop Surg 12:403, 1914. 16. Lawson JP, Ogden JA, Sella E: The painful accessory navicular, Skeletal Radiol 12:250, 1984. 17. Richli WR, Rosentnal DI: Avulsion fracture of the fifth metatarsal: experimental study of pathomechanics, Am J Roentgenol 66:209, 1984. 18. Quill GE Jr: Fractures of the proximal fifth metatarsal, Orthop Clin North Am 26:353, 1995. 19. Jones R: Fracture of the base of the fifth metatarsal by indirect violence, Ann Surg 35:687, 1902. 20. Kling TF Jr, Bright AW, Hensinger RN: Distal tibial physeal fractures in children that may require open reduction, J Bone Joint Surg 66A:647, 1984. 21. Mizuta T, Benson WM: Statistical analysis of the incidence of physeal injuries, J Pediatr Orthop 7:518, 1987. 22. Kay RM, Matthys GA: Pediatric ankle fractures: evaluation and treatment, J Am Acad Orthop Surg 9:268, 2001. 23. Kling TF: Operative treatment of ankle fractures in children, Orthop Clin North Am 21:2-381, 1990. 24. Carey J, Spence L: MRI of Pediatric growth plate injury: correlation with plain film radiographs and clinical outcome, Skeletal Radiol 27:250, 1998. 25. Murray K, Nixon GW: Epiphyseal growth plate: evaluation with modified coronal CT, Radiology 166:263, 1988. 26. Salter RB, Harris RW: Injuries involving the epiphyseal plate, J Bone Joint Surg 45:587, 1963. 27. Spiegel PG, Cooperman DR: Epiphyseal fractures of the distal end of the tibia and fibula, J Bone Joint Surg Am 60:1096, 1978. 28. Chambers HG: Ankle and foot disorders in skeletally immature athletes, Orthop Clin North Am 34:445, 2003. 29. Hunter-Griffin L: Injuries to the leg, ankle, and foot, In Sullivan J, Grana W, editors: The pediatric athlete, Park Ridge, IL, 1990, American Academy of Orthopaedic Surgeons. 30. Tillaux P: Trait de chirurgie clinique, vol 2, Pais, 1848, Asselin and Houzeau. 31. Koury SI, Stone CK: Recognition and management of Tillaux fractures in adolescents, Pediatr Emerg Care 15:37, 1999. 32. Simon WH, Floros R: Juvenile fracture of Tillaux, J Am Podiatr Med Assoc 15:299, 1989. 33. Dias LS, Giegerich CR: Fractures of the distal tibial epiphysis in adolescents, J Bone Joint Surg 65A:438, 1983. 34. Mubarak SJ: Extensor retinaculum syndrome of the ankle after injury to the distal tibial physis, J Bone Joint Surg Br 84:11, 2002. 35. Caterini R, Farsetti P, Ippolito E: Long term followup of physeal injury to the ankle, Foot Ankle 11:372, 1991. 36. Orava S: Exertion injuries due to sports and physical exercise, Thesis, Oulu University, Kokkola, 1980. 37. Williams GA, Cowell HR: Kohler’s disease of the tarsal navicular, Clin Orthop 158:53, 1981. 38. Ippolito PT, Pollini R, Falez R: Kohler’s disease of the tarsal navicular: long term follow-up of 12 cases, J Pediatric Orthop 4:416, 1984.
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radiographic finding of the secondary ossification center will aid in making the diagnosis. The treatment for Iselin’s disease depends on the degree of the athlete’s pain and his or her willingness to comply with the treatment program. Initially, conservative management is all that may be required.55 Avoidance of the causative stresses, ice, NSAIDs, and stretches may be helpful. In more stubborn cases, in which pain does not improve and returns, immobilization in a walking boot often relieves the symptoms. There have been several reported cases of Iselin’s disease developing into a nonunion. If this occurs, surgical intervention is warranted. This entails either fixation of the bony fragment or excision of the proximal bony fragment.
CHAPTER 23
Pediatric problems and rehabilitation geared to the young athlete
39. Pizzutillo P: Osteochondroses. In Sullivan J, Grana W, editors: The pediatric athlete, Park Ridge, IL, 1990, American Academy of Orthopaedic Surgeons. 40. Chung SM: Handbook of pediatric orthopedics, New York, 1986, Van Nostrand Reinhold. 41. Binek R, et al: Freiberg disease complicating unrelated trauma, Orthopedics 11:753, 1988. 42. Anderson J: Atlas of imaging in sports medicine, Sydney, 1998, McGraw-Hill. 43. Canale ST, Belding RH: Osteochondral lesions of the talus, J Bone Joint Surg Am 62:97, 1980. 44. Flick AB, Gould N: Osteochondritis dissecans of the talus, Foot Ankle 5:165, 1985. 45. Anderson IF, et al: Osteochondral fractures of the dome of the talus, J Bone Joint Surg Am 71:1143, 1989. 46. Sever JW: Apophysitis of the os calcis, N Y Med J17:111, 1912. 47. Shopfner CE, Coim CC: Effect of weight bearing on the appearance and development of the secondary calcaneal epiphysis, Radiology 86:201, 1966.
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48. Stanitski CL: Combating overuse injuries: a focus on children and adolescents, Physician Sports Med 21:87, 1993. 49. Micheli LJ, Ireland ML: Prevention and management of calcaneal apophysitis in children, J Pediatr Orthop 7:34, 1987. 50. Micheli LJ: Overuse injuries in children’s sports, the growth factor, Orthop Clin North Am 14:337, 1980. 51. Crosby LA, McMullen ST: Heel pain in an active adolescent, Physician Sportsmed 21:89, 1993. 52. Szames SE, Forman WM: Sever’s disease and its relationship to equines, Clin Podiatr Med Surg 7:377, 1990. 53. Iselin H: Wachtumsbeschwerden zur Zeit der Knochernen Entwicklung der Tuberositas metatarsi quint, Ttsch Z Chir 117:529, 1912. 54. Dameron TB: Fractures and anatomical variations of the proximal portion of the fifth metatarsal, J Bone Joint Surg Am 57:788, 1975. 55. Lehman R, Gregg J, Torg E: Iselin’s disease, Am J Sports Med 14:494, 1986.
.........................................C H A P T E R 2 4 Unique considerations for foot and ankle injuries in the female athlete Melanie Sanders CHAPTER CONTENTS ...................... Introduction
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Conclusion
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Sport-specific disorders
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References
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Gender-specific disorders
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INTRODUCTION The passage of Title IX* is arguably the most important event in the timeline of women’s participation in U.S. athletic endeavors. By almost any measure, the numbers of female athletes have exploded in multiple sports in the decades since 1972. Before Title IX, approximately 1 in 27 girls participated in sports; that number is now nearly 1 in 3.1 The National Collegiate Athletic Association (NCAA) tracks women’s sports participation in its member institutions; the data are self-reported and are useful for evaluating general trends. In 1981, total athletes numbered 74,239. By 1993, the total had risen to 105,532 and then in 2001 to 155,513 (Fig. 24-1). In general, the increase in participation reflects the addition of women’s teams to institutions. The increase also reflects the elevation of previously emerging sports such as ice hockey and water polo to normal status and championship competition. Additional emerging sports, such as synchronized swimming, archery, badminton, equestrian events, squash, and team handball also have increased the numbers of athletes reported. The increase in the number of women participating in sports and the increase in their level of competition has provided a new opportunity to study the effects of different sports on the athlete. Some sports provide the opportunity to directly compare injury rates for both *‘‘No person in the United States shall, on the basis of sex, be excluded from participation in, or denied the benefits of, or be subjected to discrimination under any educational program or activity receiving federal assistance.’’—Title IX of the Education Amendments of 1972 to the Civil Rights Act of 1964.
genders. Other sports are the exclusive domain of the female athlete. There is great interest in identifying preventable injuries, whether they are sport specific or gender specific. The sports identified as causing the highest number of injuries in the female athlete are basketball, volleyball, field hockey, and gymnastics. Sports engendering the fewest injuries are golf, swimming, squash, and archery.2-7 Additional information also has been garnered by the study of female military recruits and their physical performance compared with male peers. Military studies are intriguing because the male and female populations are subjected to the same conditions of training and physical standards. Their data reveal significant and more rapid improvement in performance over sequential years for women compared with men. The higher injury rates initially reported in women have gradually begun to decline as women have adapted to the rigorous schedule.8 Physiologic differences, particularly in upper body strength in women, may be permanently limiting, although women appear to have comparable or better aerobic capacity.9 Other preliminary studies seemed to indicate a significantly higher rate of injury in the female athlete; however, follow-up studies demonstrated the injury rate to be sport specific. In these studies, proper conditioning resulted in injury rates equivalent to male athletes. Anthropometric studies provide interesting data concerning anatomic differences between women and men.10 In women, lower extremities constitute 51% of their total height, compared with 56% in men. This difference improves the mechanical advantage for men in activities requiring striking, hitting, or kicking because of the greater force than can be generated by their legs as longer
CHAPTER 24
Unique considerations for foot and ankle injuries in the female athlete
Female Participation in NCAA sports 180000 Number of Female Athletes
160000 140000 120000 100000 80000 60000 40000 20000 0
Year '82 through '02
Figure 24-1
levers. The female has a wider pelvis, greater varus of the hips, and greater genu valgus than the male. As a result, females have a lower center of gravity, and in sports requiring excellent balance, such as gymnastics, females have a distinct advantage. As a result, the balance beam is a required element in competition for female gymnasts and is not included in the competition for male gymnasts. Female gymnasts typically also have better joint mobility, improving their flexibility—another trait valued in gymnastics. The alignment differences at the hip and knee may be one factor, along with the level of conditioning, contributing to higher percentages of overuse syndromes in the lower extremity in female athletes. The musculoskeletal system in women contains less muscle mass and more fat for the same body weight than in men. In males and females with equal training, female muscle mass is approximately 23% of body weight, compared with 40% in males. This limitation of muscle mass handicaps females in their attempts to increase their power and speed. The larger percentage of fat, however, is an advantage in distance swimming events because of the improvement in insulation and buoyancy for the female swimmer. For instance, the speed record for swimming the English Channel is held by Penny Dean. Her one-way time in 1978 was 7 hours, 40 minutes. It is important to preface any remarks on the female athlete with the gender-specific clinical diagnosis of the female athlete triad. The diagnosis refers to the interrelated problems of disordered eating, amenorrhea, and osteoporosis. Specific to the foot, these athletes are more at risk for stress fractures in the foot; and, in this instance, consideration of the diagnosis should be entertained and appropriate history sought. Any impression of osteopenia on plain x-ray, coupled with a history
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of amenorrhea and evasiveness about eating habits, should prompt further investigation. Failure to make the appropriate diagnosis can allow repetitive injuries to occur, possibly with significant changes in the normal bony architecture of the foot. The incidence of the disorder in young girls has been reported to be as low as 15% and as high as 65%. The prevalence may be higher in sports that select for a slim body habitus, but it has been reported in all sports. When approaching the study of foot and ankle problems in female athletes, disorders can be divided into gender-specific disorders and sport-specific disorders.
SPORT-SPECIFIC DISORDERS Ballet (also see Chapter 21) The female classical ballet dancer is unique in her requirements for the lower extremities.11,12 The dancer uses either a thin-soled slipper or toe shoe. The dancer typically will participate in several classes, rehearsal for performances, and then the performance or performances. The lower extremities are called on to absorb all the force of landings on the wooden dance floor. The consequence of the schedule of training and performance and the type of shoe for the foot leads to chronic injuries such as tendinitis, tendinosis, and impingement syndromes. The most common acute injury is the inversion sprain, usually occurring on landing a jump. Fatigue, improper technique, and anatomic variation from optimal body type all can be factors in acute and chronic injuries. The lower leg, foot, and ankle make up approximately 40% of dance injuries in a sport in which the lifetime incidence of injury is 90%.13
Sport-specific disorders
Acute injuries Nearly half of reported dance injuries are categorized as acute. The most common injuries occur as the dancer lands with a loss of balance. If the dancer lands in en pointe position, the ankle is more stable, causing a midfoot injury rather than the typical anterior talofibular ligament injury. Radiographs should be obtained in the dancer who cannot walk more than three steps (limping is acceptable) and in whom there is tenderness over important anatomic landmarks. Foot x-rays should be obtained if there is tenderness over the navicular bone or the base of the fifth metatarsal. If there is tenderness over either the fibula or the medial malleolus from the tip to 6 cm proximal to the tip, ankle films should be obtained.15,16 The most commonly overlooked fractures include the talar dome (see Chapter 14), the lateral process of the talus (see Chapter 14), the os trigonum (see Chapter 14), the anterior process of the calcaneus, and the proximal fifth metatarsal. Younger dancers can be more difficult to evaluate, often requiring repetitive x-rays. A high index of suspicion should be maintained, especially in the face of soft-tissue swelling over the physes of ankle or foot bones. As in other athletes, inversion injuries can cause damage to structures other than the anterior talofibular ligament. Syndesmosis tears, osteochondral lesions of the talus, and subluxation or longitudinal tears of the peroneal tendons all may occur. Dancers also are
at risk for subluxation of the cuboid, either associated with an inversion injury to the ankle or from repetitive plantarflexion and dorsiflexion. In this clinical entity, the base of the fourth metatarsal becomes dorsally displaced and the fourth metatarsal head displaces in a plantar direction. Additionally, cuboid dysfunction can interfere with normal function of the peroneal tendons and must be considered in dancers with peroneal tendinitis. Treatment of this unusual condition requires reduction of the cuboid with a squeeze technique after the hindfoot is mobilized and the forefoot is adducted.17 Midfoot injuries in the dancer present a significant treatment dilemma because of the prolonged healing time required for stability of the foot and the difficulty of restoring the mobility required for dancing. Midfoot injuries occur when the dancer lands in full pointe, with the posterior lip of the tibia resting and locked on the calcaneus. In this position the subtalar joint also is locked, and the heel and forefoot both are in varus. Because the ankle joint is relatively stable in full pointe, the forces at landing are transferred to the midfoot. Treatment of these acute injuries requires evaluation of both stability of the involved tarsometatarsal joints and amount of collapse of the longitudinal arch (see Chapter 5). Some diastasis may be acceptable if weightbearing views do not demonstrate collapse of the longitudinal arch. Workup should include weight-bearing views, comparison weight-bearing views, and computed tomography (CT) scan if necessary. The fifth metatarsal is a common area of injury for dancers. The most innocuous fracture is that of avulsion of the base of the fifth metatarsal. Open reduction internal fixation (ORIF) is recommended only if the fracture fragment involves greater than 30% of the articular surface and is significantly displaced. The most typical fracture involves only the most proximal 1 cm of the bone and usually is associated with an ankle sprain. It can be treated with appropriate immobilization and progressive activity as healing permits. The Jones fracture (see Chapter 4) occurs by the mechanism of adduction of the fifth metatarsal, usually while the foot is plantarflexed. Because of the negative effects of prolonged immobilization, early operative management for these fractures at the metaphyseal-diaphyseal junction is preferred. Repetitive adduction forces that occur with cutting or pivoting movements can result in diaphyseal stress fractures. There usually are prodromal symptoms preceding an acute event. The history is critical, as is review of radiographs, which typically will demonstrate periosteal reaction, cortical thickening, intramedullary sclerosis, and widening of the fracture line. Because this is a vascular watershed zone, these stress fractures should be treated with intramedullary screw fixation, bone graft, or both. 549
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Posterior ankle pain (also see Chapter 2) Ballet requires extreme plantarflexion of the foot for en pointe work. In this extreme position, soft tissues posterior to the ankle can be compressed and irritated. Any one of the following structures posterior to the ankle can cause symptoms: an os trigonum, a large posterior process of the talus, or a large dorsal process of the calcaneus. Symptomatic flexor hallucis longus (FHL) tendinitis can be caused by these impingement scenarios. Diagnosis of this suspected condition can be supported by local tenderness proximal to the sustentaculum tali and pain with resisted plantarflexion of the great toe. Magnetic resonance imaging (MRI) typically will demonstrate fluid within the sheath of the tendon and sometimes marked tenosynovitis.14 Preservation of the function of the FHL tendon is paramount in dancers. Treatment should be aimed toward minimizing the inflammatory condition, with surgical intervention timed to allow appropriate recovery. In some instances, simple release of the FHL is adequate; in other cases, excision of the os trigonum or posterior process of the talus may be required. FHL tendon symptoms are most commonly associated with ballet; however, participants in other sports such as soccer increasingly are demonstrating the same entity.
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Unique considerations for foot and ankle injuries in the female athlete
When dancers perform the demi-pointe position, the foot is twisted and inverted and can incur an oblique or spiral fracture of the mid- to distal portion of the fifth metatarsal. This ‘‘dancer’s fracture’’ now has been shown to heal well with conservative and symptomatic treatment rather than ORIF.18
women participating in this sport increase, the data will clarify further the risk of injury to female athletes.21-23
Gymnastics The female gymnast has been reported to be at higher risk for ankle injury than the male athlete. This is presumably because of the difference in alignment of the female lower extremity, with accentuated varus position of the heel. Landings on this varus position increase the probability of ankle sprain. Areas of complaint in the foot in female gymnasts include the bottom of the heel, the plantar fascia origin, and the medial longitudinal arch. Direct blows during landings or striking the heel on the floor while swinging under the lower uneven parallel bar cause pain under the heel. Tumbling is the typical cause of pain at the origin of the plantar fascia, whereas landings cause pain in the medial longitudinal arch or the forefoot. Interestingly, analysis of flexibility parameters in gymnasts compared with controls does not demonstrate a correlation to injury patterns or frequency.19 Ankle impingement syndrome (see Chapter 2) occurs in the female gymnast, with impingement occurring anteriorly when she lands short on her dismount, forcing her ankle into hyperflexion. If acute pain occurs with an instance of injury, the ankle should be rested and iced. Physical therapy modalities and anti-inflammatory drugs are also useful adjuncts. With return to the inciting activity, a large protective pad can be taped as a mechanical block along the anterior aspect of the ankle to help prevent reinjury.20
Posterior tibial tendinitis (see also Chapter 8) Hyperpronation of the foot in the female can cause either chronic posterior tibial tendinitis or insertional posterior tibial tendinitis. The previously discussed genu valgum in the female requires relatively more pronation in the foot to maintain the plantigrade position. Initial treatment for excessive pronation should include medial heel and forefoot wedge or posting within the athletic shoe, although benefit can be obtained with full-time use of mechanical correction in all shoes. Custom foot orthoses can be beneficial early in treatment. The insertional form of posterior tibial tendinitis can be more recalcitrant and difficult to treat. This disorder may be associated with the presence of an accessory navicular bone. In addition to foot orthotics, other treatments should include rest, ice massage, anti-inflammatory medications, stretching of the Achilles-gastrocnemius complex, and brace treatment with a short, articulated, ankle-foot orthosis or Arizona brace. In the very rare case, excision of the accessory navicular bone with repair or advancement of the posterior tibial tendon may be indicated. In some instances, this also will require supplementary tendon transfer.
Recreational ice hockey There has been a phenomenal increase in the numbers of women participating in organized ice hockey within the last several decades. Estimated numbers in the United States and Canada increased by 250% in the latter 1990s; and because women’s ice hockey was included in the 1998 Winter Olympic Games, participation is expected to continue to rise. Interest in injuries generated by the contact and collisions in ice hockey has led to many studies on male hockey players. The play rules are modified for women; intentional body checking is not allowed and the players are required to wear full-face protection (men wear one half). As a result, women suffer no dental or facial injuries, in sharp contrast to the high rate in men. When six male and six female collegiate teams were compared in a cohort study, the risk of severe injury (14 or more missed sessions) was 5.33 times higher for women than for men. The most common injuries in women were concussion, adductor strain, and ankle sprain. As the numbers of
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GENDER-SPECIFIC DISORDERS
Bunions (see also Chapter 19) The incidence of bunions always has been reported as significantly higher in women versus men, with the implication that women’s shoes have a slow deforming effect on the forefoot. The female athlete typically is well motivated to consider aggressive conservative treatment for bunions to remain active in her sport. Several aspects of bunions should be considered when evaluating potential causes of pain or dysfunction in the woman athlete with bunions. First, direct pressure from the shoe and especially from stitching lines on the shoe may cause soft-tissue irritation over the bunion. The structures most at risk for this type of irritation include the dorsal digital nerve and the capsular structures of the metatarsophalangeal joint. Second, the athlete may have suffered a capsular injury to the joint that will respond to rest or the use of a bunion night splint, combined with topical anti-inflammatory products. Women athletes with significant deformity may have first-metatarsocuneiform instability, which will respond well to treatment with an appropriately posted, custom, trilaminar foot orthosis. Because the risk of a significant change in the mechanical function of the foot can occur after bunionectomy, surgery
References
Stress fractures (see also Chapters 3 and 4) Stress fractures occur as a result of repetitive, low-level stresses on bone and have multifactorial causes. In many athletic settings, women appear to be at higher risk for stress fracture than men.25-28 In particular, a woman exhibiting the female athlete triad, previously mentioned, may be predisposed to stress fracture. If women with irregular menses are compared with women with regular menses, the frequency of stress fractures is increased by a factor of four. If all fractures are evaluated, the increase is three times the rate for athletes with regular menses.29 Some of the factors that have been identified as causative for stress fracture include dietary imbalance, foot structure, training surface, footwear, training variations, and temporary cessation of activity.30 Lower bone density and potentially lower calcium intake compared with male athletes also may make the female athlete more susceptible to stress fracture. Menstrual irregularities such as exercise-induced amenorrhea may result in lower bone density. In particular, females who begin their running career before menarche may delay menarche because of excessive weight loss, low body fat, and subsequent loss of normal hormonal stimulation. High-level female runners demonstrate an incidence of menstrual irregularity of 50%.31 The use of oral contraceptives as an estrogen therapy can provide some protection by helping to maintain bone density.32 Clinical symptoms of stress fracture can be insidious in onset, often interfering with the athlete’s participation in the sport but not necessarily causing complete cessation of the inciting activity. Swelling may or may not be apparent, but there generally is point tenderness over the fracture. History of change in the training schedule or other causative factors may be difficult to obtain. Careful physical examination is paramount because any bone in the foot or the tibia and fibula can be fractured. Radiographs may be required sequentially because they are not always positive for the first 3 to 6 weeks. Bone scan is extremely valuable in making an earlier diagnosis in the athlete.
CONCLUSION All medical support personnel involved in the care of the female athlete must keep several salient facts in mind.
First, the number of females involved in all sports has increased dramatically and will continue to increase. Second, like their male peers, female athletes will continue to push their limits, likely incurring injury in the process. Third, injuries in the female athlete will fall into either sport-specific or gender-specific categories, the latter of which require a higher index of suspicion and perhaps greater depth of knowledge for diagnosis and treatment. This is a pivotal time for women’s sports medicine, with great opportunity to gather data, to refine optimal treatment recommendations, and to develop strategies to prevent injury. This chapter delineates many of the injuries that the medical personnel will encounter and, we hope, has given the reader a better understanding of salient features of diagnosing and treating these injuries.
4 PEARL The female athlete triad consists of disordered eating,
amenorrhea, and osteoporosis and places the female athlete at an increased risk of stress fractures in the foot and ankle. Any impression of osteopenia on plain x-ray, coupled with a history of amenorrhea and evasiveness about eating habits, should prompt further investigation. Women with irregular menses have a fourfold increase in stress fracture risk compared with women with regular menses. The lower leg, foot, and ankle make up approximately 40% of dance injuries, and the lifetime incidence of injury is 90% in the dancer. Because the risk of a significant change in the mechanical function of the foot can occur after surgery, bunionectomy should be avoided if possible in the competitive female athlete.
REFERENCES 1. Callahan LR: The evolution of the female athlete: progress and problems, Pediatr Ann 29:3, 2000. 2. Dahm DL: Understanding ankle sprains and other foot problems in female athletes, Womens Health Orthop Ed 5:60, 2002. 3. Delee JC, et al: Incidence of injury in Texas girls’ high school basketball, Am J Sports Med 24:684, 1996. 4. Gillette JV, Haycock CE: Susceptibility of women athletes to injury, Depart Surg 236:163, 1976. 5. Haycock CE, Hillette JV: Susceptibility of women athletes to injury, JAMA 236:163, 1976. 6. Murtaugh K: Injury patterns among female field hockey players, Am Coll Sports Med 1:201, 2001. 7. Noble BH, et al: A comparison of men’s and women’s professional basketball injuries, Am J Sports Med 10:297, 1982. 8. Cox JS, Lenz HW: Women midshipmen in sports, Am J Sports Med 12:241, 1984. 9. Protzman RR: Physiological performance of women compared to men, Am J Sports Med 7:191, 1979.
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should be avoided if possible.24 Postoperative changes in the foot can include residual stiffness in the metatarsophalangeal joint and imbalance in the forefoot load, potentially causing transfer metatarsalgia or stress fracture. Stress fractures of the base of the proximal phalanx of the great toe have been reported in athletes with hallux valgus.
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Unique considerations for foot and ankle injuries in the female athlete
10. Griffin LY: The female athlete: In Hunter-Griffen L, editor: Athletic training and sports medicine, ed 2, Park Ridge, IL, 1991, American Academy of Orthopaedic Surgeons. 11. Hardaker WT Jr: Foot and ankle injuries in classical ballet dancers, Orthop Clin North Am 20:621, 1989. 12. Wiesler ER, et al: Ankle flexibility and injury patterns in dancers, Am J Sports Med 24:754, 1996. 13. Macintyre J, Joy E: Foot and ankle injuries in dance, Clin Sports Med 19:351, 2000. 14. Sammarco GJ, Miller EH: Partial rupture of the flexor hallucis longus tendon in classical ballet and modern dance, J Bone Joint Surg 61A:149, 1979. 15. Pigman EC, et al: Evaluation of the Ottawa clinical decision rules for the use of radiography in acute ankle and midfoot injuries in the emergency department: An independent site assessment, Ann Emerg Med 24:41, 1994. 16. Stiehll IG, et al: Decision rules for the use of radiography in acute ankle injuries, JAMA 269:1127, 1993. 17. Marshall P, Hamilton WG: Cubiod subluxation in ballet dancers, Am J Sports Med 20:169, 1992. 18. O’Malley MJ, Hamilton WG, Munyak J: Fractures of the distal shaft of the fifth metatarsal, Am J Sports Med 24:240, 1996. 19. Kirby RL, et al: Flexibility and musculoskeletal symptomatology in female gymnasts and age-matched controls, Am J Sports Med 9:160, 1981. 20. Hunter LY: Women’s athletics: the orthopedic surgeon’s viewpoint, Clin Sports Med 3:809, 1984.
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21. Dryden DM, et al: Epidemiology of women’s recreational ice hockey injuries, Am Coll Sports Med 2:1378, 1999. 22. Dryden DM, et al: Personal risk factors associated with injury among female recreational ice hockey players, J Sci Med Sport 3:140, 2000. 23. Schick DM, Meeuwisse WH: Injury rates and profiles in female ice hockey players, Am J Sports Med 31:47, 2003. 24. Baxter DE, Lillich JS: Bunionectomies and related surgery in the female middle-distance and marathon runner, Am J Sports Med 14:491, 1986. 25. Bennel KL, et al: Risk factors for stress fractures in track and field athletes, Am J Sports Med 24:810, 1996. 26. Benson JE, et al: Relationship between nutrient intake, body mass index, menstrual function and ballet injury, J Am Diet Assoc 89:58, 1989. 27. Dempsey RL, et al: Stress injury to the bone among women athletes, Tough Top Sports Med 11:929, 2000. 28. Eisele SA, Sammarco GJ: Fatigue fractures of the foot and ankle in the athlete, J Bone Joint Surg 75:290, 1993. 29. Baker ER, et al: Women athletes with menstrual irregularity have increased musculoskeletal injuries, Med Sci Sports Exerc 18:374, 1986. 30. Zeni AI, et al: Stress injury to the bone among women athletes, Phys Med Rehabil Clin North Am 11:929, 2000. 31. Barrow GW, Saha S: Menstrual irregularity and stress fractures in collegiate female distance runners, Am J Orthop Med 16:209, 1988. 32. Carbon R, et al: Bone density of elite female athletes with stress fractures, Med J Aust 153:373, 1990.
.........................................C H A P T E R 2 5 New advances in the foot and ankle Gregory C. Berlet, Peter B. Maurus, Terrence Philbin, and Thomas H. Lee CHAPTER CONTENTS ...................... Introduction
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Chronic ankle instability
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Osteochondral lesions of the talus
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Foot and ankle arthroscopy
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On the horizon
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References
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INTRODUCTION Orthopaedic surgery is a dynamic field of medicine with ever-changing advances in knowledge and techniques. As our patient populations continue to grow younger and more active, we search for more anatomic and less invasive methods of addressing pathology. The subspecialty of surgery of the foot and ankle likewise is participating in this exciting evolution of understanding and approaches to common acute and chronic conditions of the foot and ankle. In this chapter we discuss newer techniques and treatment options for foot and ankle disorders.
OSTEOCHONDRAL LESIONS OF THE TALUS Osteochondral lesions of the talus (OLT) are rare, representing just 4% of all such lesions in the body.1 The term OLT evolved from an 1888 report that described ‘‘osteochondritis dissecans’’ as a loose body associated with articular cartilage and subchondral bone fracture.2 Because inflammation is not an important factor in the etiology of OLT, many authors do not use the term ‘‘osteochondritis dissecans.’’ The two locations most often seen in which OLTs are involved are posteromedial and anterolateral. Trauma is cited as the etiology in more that 85% of patients.3-7 Although the etiology of nontraumatic OLT is unknown, some reports have cited a primary ischemic event or genetic predisposition (e.g., identical medial talar lesions in identical twins, multiple lesions occurring in the same patient) as a cause.8
Acute traumatic events are typically the cause of lateral lesions. Lesions on the anterolateral aspect of the talar dome are caused by inversion and dorsiflexion, resulting in the anterolateral aspect of the talar dome’s impacting the fibula. These lesions usually more shallow and ‘‘wafer shaped’’ than medial lesions.9 Medial lesions usually are caused by repetitive overuse syndromes; ; only a small number of medial lesions can be attributed to trauma. Posteromedial lesions result from inversion, plantarflexion, and external rotational forces. The posteromedial talar dome impacts the tibial articular surface, leading to a deep, cup-shaped lesion in the talus. The classic presentation for the OLT is characterized by chronic ankle pain with swelling. The pain usually is localized to the side of the ankle where the lesion is located. Other symptoms include weakness, stiffness, catching, and giving way with repeated inversion injuries. Initial physical examination signs include tenderness on palpation behind the medial malleolus with the ankle dorsiflexed (posteromedial lesions) and over the anterolateral ankle joint when in maximal plantarflexion (anterolateral lesions). A joint effusion is a clear sign of intra-articular involvement. Weight-bearing plain radiographs should be used to evaluate the ankle (anterior-posterior, lateral, and mortise views). Posteromedial lesions are evaluated best by imaging the ankle in various degrees of plantarflexion. Anterolateral lesions are evaluated best by imaging the ankle in various degrees of dorsiflexion. In our experience, magnetic resonance imaging (MRI) is the most appropriate imaging modality to evaluate for OLT. Areas of low signal intensity on T1-weighted images indicate a chronic lesion resulting from sclerosis of the
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New advances in the foot and ankle
Table 25-1 Classification system for staging osteochondral lesions of the talus using magnetic resonance imaging Stage I
Articular cartilage damage only
Stage IIa
Articular cartilage injury with underlying fracture and edema
Stage IIb
Stage II without edema
Stage III
Detached fragment (rim signal) but nondisplaced
Stage IV
Displaced fragment
Stage V
Subchondral cyst formation
bed of the talus.10 High signal rims on T2-weighted images indicate an unstable osteochondral fragment.11,12 Intra-articular, gadolinium-enhanced MRI can provide images of articular cartilage, assess stability, and detect intra-articular bodies.13 Significant ankle effusions may provide a ‘‘physiologic arthrogram,’’ negating the need for gadolinium. The OLT should be staged before treatment is determined. In 1959, Berndt and Harty14 devised a system for staging OLT. Since that time, various researchers have revised and refined their original classification systems as newer technologies, such as arthroscopy, computed tomography (CT), and MRI became available. Table 25-1 is a staging classification developed by Hepple et al.15 and is based on MRI imaging.
Treatment ............................................................. Nonoperative Generally, conservative treatment should be attempted first. Two studies reviewed the long-term outcomes of patients with OLT and the possible development of osteoarthrosis. Conservative treatment consists of protected ambulation for pain relief and an appropriate sports brace during activity. Conservative treatment should be attempted for at least 6 months. McCullough and Venugopal16 followed 10 patients for 15 years and found that although conservative treatment often does not lead to radiographic union, osteoarthrosis was uncommon unless the fragment was detached. They stated that patients with nondisplaced fragments could be treated conservatively but that acute displaced fractures should undergo immediate reduction and internal fixation. Bauer et al.17 concurred that osteoarthrosis of the ankle is a rare occurrence and found that skeletally
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immature ankles have the best prognosis for healing with conservative treatment. In summary, asymptomatic and nondisplaced OLT should undergo conservative treatment, whereas displaced or continued symptomatic lesions should be treated surgically.
Operative There are three surgical options for the displaced OLT. These are acute open reduction and internal fixation (ORIF), open or arthroscopic debridement and/or excision with drilling, and cartilage restoration procedures. Internal fixation ORIF is most appropriate for acute lesions with a significant osseous piece remaining attached to the chondral flap. Internal fixation historically has been accomplished with hardware (Kirschner wires, screws), although recent trends move toward biologic fixation. Biologic fixation can be accomplished using antegrade or retrograde bioabsorbable screws and/or antegrade biologic pins (SmartNail, Bionx Implants, Finland). An interesting recent advantage is the use of osteochondral plug transfer to internally fix an unstable osteochondritis dissecans (OCD) lesion. In two separate articles, Berlet and Yoshizumi reported on their technique for fixation and grafting of an OCD lesion about the knee.18,19 This technique (COR, Mitek Worldwide, Westwood, MA), which uses smaller diameter plugs, can function both to stabilize the lesion and graft across the lesion into healthy bone. It is the authors’ experience that most acute lesions may be reduced and secured using antegrade biologic pins. Fibrin sealant may be an appropriate adjuvant to the internally stabilized OLT and has been shown to be effective in clinical studies.20 Debridement, microfracture, and drilling If a lesion is detached or sufficiently fragmented such that it is not amenable to internal fixation, excision of the fragments, debridement, and drilling are warranted. The cartilage edges are trimmed and smoothed, and the bony base is debrided down to bleeding bone. Subchondral drilling provides vascular access channels. Mesenchymal stem cells released from the underlying bone proliferate and undergo chondrocyte differentiation to provide a fibrocartilage cap for the chondral defect. Studies have shown this method to be more effective than simple excision and curettage or simple excision alone.21-23 Retrograde drilling is ideal for cystic subchondral lesions with intact articular cartilage. Using specialized systems, accurate drilling of the lesion is possible. This drill path provides revascularization, and the bone graft serves as osteoconductive and osteoinductive material. This technique has advantages over antegrade drilling in that it does not alter the actual articular surface integrity. Retrograde drilling of a talar OCD was first
Osteochondral lesions of the talus
Cartilage restoration procedures Although microfracture and drilling techniques produce a fibrocartilage tissue in the affected area, it does not produce normal hyaline cartilage. In efforts to restore a joint surface with more anatomic and favorable biomechanical properties, newer procedures have been developed to restore a hyaline cartilage surface. Lesions greater than 10 mm in diameter may be best managed primarily with cartilage restoration procedures instead of excision and drilling. 25 Autologous osteochondral grafting (osteoarticular transfer system, mosaicplasty) The osteoarticular transfer system (OATS) and mosaicplasty transplant viable plugs of cartilage and subchondral bone from various donor sites into the talar dome. Single-plug systems, such as OATS, harvest a single, large plug to match the size of the lesion. This method is postulated to reduce the fibrocartilage ingrowth seen in multiple-plug system. Donor site morbidity, however, is a bigger concern because of the size of the graft. Arthrex OATS procedures were used in nine patients in a study by Assenmacher et al.26 At an average of 9.3 months, MRI revealed stable graft osteointegration by DeSmet criteria in all patients. Patients reported significant clinical improvement on the basis of visual analog pain scales and the AOFAS Ankle/Hindfoot scores (average 80.2).4 Al-Shaikh et al.27 reviewed the results of 19 patients who underwent the Arthrex OATS technique for lesions averaging 12 10 mm in 19 patients. Sixty-eight percent of these patients had failed prior attempts at excision, curettage, and/or drilling. At an average of 16 months, patients reported improvement in AOFAS Ankle/Hindfoot scores (88 average) and reported no significant donor site morbidity. Eighty-nine percent of these patients stated that they would have this procedure done again. Al-Shaikh et al.27 concluded that the OATS procedure is a viable salvage technique for patients who failed prior debridement procedures. In multiple-plug systems (mosaicplasty), a number of osteochondral plugs are harvested to fill the defect. These plugs can recontour the surface of the talar dome,
but critics have found that up to 20% to 40% of the defect is replaced by fibrocartilage.27 Gautier et al.28 showed good to excellent results in 11 patients at an average of 24 months, using Sulzermedica’s SDS ‘‘Soft Delivery System.’’ The lesions in this study averaged 18 10 mm, and the authors made no recommendations for absolute size limits. Previous studies, however, recommended a lower size limit of 10 mm. Hangody et al.25 looked at 36 patients treated with mosaicplasty at 2- to 7-year follow-up. All of these lesions were greater than 10 mm in diameter. Ninety-four percent of these patients reported good to excellent results using the Hannover scoring system, with no long-term knee donor site morbidity. Osteochondral plugs can also be harvested from the ipsilateral talus. Sammarco and Makwana29 harvested osteochondral plugs form the medial and lateral talar facets in 12 patients. The authors reported significant improvement in the AOFAS Ankle/Hindfoot scores and found no structural failures in the donor site or graft site. Autogenous chondrocyte implantation If the osteochondral lesion is large (greater than 2 1 cm), it is not amenable to OATS or mosaicplasty because of the expected size of the donor defect. Autogenous chondrocyte implantation (ACI) is a new technique that is showing promise for these larger lesions in the knee and ankle. In 1994, Swedish investigators first reported on this novel technique for large osteochondral lesions in the knee.30 They looked at 23 patients over a 2- to 7-year follow-up period with lesions measuring from 1.5 to 6.5 cm in diameter and in whom all prior treatments had failed. Eighty-eight percent of their patients had good or excellent results. Studies in the United States and further extensive studies in Sweden have validated these results at up to 10 years.31-34 ACI is indicated in younger patient15-59 with focal osteochondral defects without diffuse arthritis. A ‘‘kissing lesion’’ on the tibial plafond is a contraindication to this procedure because results are very poor when this is present. Other patients who could benefit from this procedure are those with failed prior surgeries and those who have large lesions with extensive subchondral cystic changes. Multifocal lesions could be treated with ACI in some cases. Patients who should not undergo ACI are those who have not had an attempt at other forms of surgical treatment, those with early degenerative changes or osteoarthritis, or those with uncorrected malalignment or instability. The basic principle is to harvest viable chondrocytes from the patient, culture the chondrocytes, and reimplant them into the patient. This technique requires a two-stage procedure. First, an arthroscopic evaluation of the lesion is undertaken. Arthroscopy allows a thorough evaluation of the size and shape of the lesion, as well as the overall integrity of the adjacent and opposite cartilage surfaces. A biopsy of healthy articular cartilage 555
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described in 1981 as an isolated case.24 More recently, a modification of this technique with arthroscopic assistance was described. Clinical research has shown good clinical results with this technique.23 A study by Taranow et al.23 looked at 16 patients after retrograde drilling and grafting of OLTs. There were no complications and a significant increase in the American Orthopaedic Foot and Ankle Society (AOFAS) Ankle/Hindfoot score. This technique is recommended for the subchondral cyst on the basis of its early surgical success and the absence of complications associated with transmalleolar osteotomies, transmalleolar drilling, and chondrolytic debridement.
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New advances in the foot and ankle
(approximately 200-300 mg) then is taken from a nonweight-bearing area of articular cartilage (typically the intercondylar notch of the knee in a separate arthroscopic procedure). This biopsy is sent for laboratory culture and growth of additional chondrocytes. The process involves enzymatic digestion of the tissue and cultivation, which leads to a tenfold increase in chondrocytes. After 2 to 3 weeks in culture under the presence of antibiotics to ensure sterility, approximately 10 to 12 million cells will be available for transplantation. The second stage of this procedure is the implantation of the cultured cells. Postoperative care is essential in ensuring a good result. Giannini et al.35 reported excellent results at up to 26 months in eight patients who underwent ACI for OLT. They not only showed improved clinical scores (AOFAS Ankle/Hindfoot scores improving from 32 to 91/100) but also showed regenerated areas of cartilage on follow-up arthroscopy and normal type II hyaline cartilage by histology. Minas and Peterson published a study of 14 patients with ACI at an average follow-up of 28 months.36 They reported an 11/14 good to excellent outcome, with two poor results and one lost to followup. In a recent study on the economics and quality of life profile of this procedure, Minas37 showed significant improvement in quality of life at 2 years, and the technique was found to be cost effective in comparison with other treatment modalities.
Other new techniques There is a new interest in bulk fresh osteochondral allografts for the replacement of large areas of focal cartilage damage. Candidates are matched to donors on the basis of joint size, and the surgery is performed within 5 days of tissue recovery to optimize the survival of the donor cartilage. Tontz et al. report on 12 patients at an average of 21-month follow-up who had bulk tibiotalar allografts.38 They reported intraoperative fracture in one patient and graft collapse in another, but overall satisfaction and relief of pain in the other 10 patients. They concluded that this technique shows promise for the treatment of articular cartilage defects in young, active patients. Gross et al.39 performed fresh osteochondral graft transplantation in nine patients for OLT (one case was for acute open fracture of the talus). Six of the nine grafts remained viable at an average of 11 years. Three cases went on to arthrodesis because of graft resorption. In a literature review on the treatment of OLT, Caylor and Pearsall40 conclude that bulk fresh allografts can provide excellent results. The concern with these fresh bulk allografts is the host immune reaction to viable cells within the graft and the possibility of major infections. Also, graft collapse has been shown to occur in some cases.41 More research in this area is needed to ensure the safety and efficacy of this procedure.
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ON THE HORIZON Tissue engineering and gene therapy currently are being studied as a way to provide a growth mechanism for normal hyaline cartilage. This current technique already has shown early success in animal models but still remains in the early experimental stages.40-45 Filling cartilage defects with scaffolds of collagen or synthetic carbons promotes cell migration provides a template for matrix formation. The chondrocyte response may be amplified by embedding growth factors into the scaffold.46 These newer modalities possibly will revolutionize our approach to cartilage lesions.
4 PEARL The time relationship between pain and instability is important. That is, pain followed by instability often is due to intra-articular pathology. Pain inhibition of normal neuromuscular pathways can mimic ligamentous instability. Therefore ankle instability episodes can originate from an OLT with ligamentous laxity. A persistent ankle joint effusion points to an intra-articular pathology, and an articular cartilage lesion should be suspected. ACI and OATS are salvage procedures to be used after debridement, microfracture, or drilling have failed. Literature supports debridement, microfracture, or drilling as the first-line treatment when an OCD fragment cannot be stabilized. Internal fixation of OLT provides the best prognosis because you are saving the patient’s own cartilage.
C A S E S T U D I E S 1 A N D 2
A 40-year-old, male physician presents to the office with severe pain and swelling in his right ankle after an eversion injury while playing basketball. He complains of pain along the anterolateral aspect of his ankle. He also has a great deal of crepitus, catching, and locking with any motion. On examination, the ankle is grossly swollen with lateral ecchymosis. Range-of-motion testing elicits severe pain and crepitus along the lateral aspect of the ankle. Ankle stability is grossly normal on examination. Plain radiographs of the ankle illustrate a lateral talar defect (Fig. 25-1, A). The ankle mortise is intact. MRI examination shows a 0.5- to 1.0-cm osteochondral defect with fluid surrounding the lesion (Fig. 25-1, B). This represents a detached osteochondral lesion of the talus. An ankle arthroscopy was performed that allowed the visualization of a large osteochondral
On the horizon
Figure 25-1 (C) Intraoperative arthroscopic image of a large displaced OLT. (D) Intraoperative image of the OLT from C after open reduction and internal fixation with bioabsorbable pins. (Photographs courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.)
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Figure 25-1 (A) Plain radiography of an ankle illustrating an anterolateral osteochondral lesion of the talus (OLT). (B) Magnetic resonance imaging (MRI) of the ankle from A illustrating a displaced OLT.
fragment (Fig. 25-1, C). The talus then was approached through a lateral incision (Fig. 25-1, D). The fragment was reduced and fixed with bioabsorbable pins (SmartNail, Bionx Implants, Finland). The patient tolerated the procedure well and has returned to normal activities without pain at 8 months.
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New advances in the foot and ankle
A 30-year-old woman presents with complaints of continued right ankle pain after an inversion injury 3 months prior. She has suffered from pain, swelling, locking, and catching since that time. She has no history of prior ankle injuries. On examination, she has an antalgic gait on the right. The foot and ankle are neurovascularly intact. There are no obvious deformities, and the ankle is stable on drawer testing. There is, however, an ankle effusion. Plain radiographs of the ankle do not show any abnormalities. An MRI showed an obvious osteochondral lesion off the posteromedial aspect of the talus. The lesion measured approximately 1 cm2, with clear fluid seen within the cavity. This represents a displaced osteochondral lesion (Fig. 25-2, A). For a lesion that cannot be fixed, first-line treatment is ankle arthroscopy with debridement and drilling. Only if this technique were to fail would we consider cartilage restoration procedures. She underwent the arthroscopy and followed a conservative rehabilitation protocol. After 8 months, she has continued pain and swelling in her right ankle. A repeat MRI shows edema and incongruity of the talus in the area of the OCD. Because of her continued symptoms, we decided to perform osteochondral autograft reconstruction of the defect (mosaicplasty) (Fig. 25-2, B). She is now 1 year out from surgery and has no pain or swelling and has returned to her normal activities.
CHRONIC ANKLE INSTABILITY
Figure 25-2 (A) Magnetic resonance imaging of an ankle illustrating a large, displaced posteromedial osteochondral lesion of the talus (OLT). (B) Intraoperative image of the OLT from A after mosaicplasty reconstruction of the defect. (Photographs courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.)
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Lateral ankle sprains are one of the most common sports-related injuries, representing as many as 40% of presenting complaints.47 Chronic lateral ankle instability has been estimated to occur in up to 42% of patients who sustain acute injuries.48,49 Functional lateral instability, as introduced by Freeman50 describes a subjective complaint of giving way in the ankle joint. Work by Tropp et al.51 further described this condition as motion beyond voluntary control but not exceeding the physiologic range of motion. Mechanical instability is motion beyond the normal physiologic limits of the ankle joint. This is manifested as excessive anterolateral ankle laxity. The lateral ankle ligaments (anterior talofibular ligament and calcaneofibular ligament) work to prevent inversion of the talus in the ankle mortise. Conservative treatment for chronic lateral ankle instability consists of rest, antiinflammatories, and physical therapy. Persistent failure (repeated giving way) of this lateral ligament complex, however, is an indication for surgical stabilization of the ankle.
Surgical options There are multiple surgical options for surgical stabilization of the chronically unstable ankle, both anatomic and nonanatomic. One should refer to Chapter 13 for
Foot and ankle arthroscopy
Thermal capsular modification Thermal capsular modification has been shown to be a new and effective treatment of lateral ankle laxity. A thermal probe applied to the anterior talofibular ligament and lateral capsule causes denaturing and ‘‘shrinkage’’ of the tissue by breaking the intramolecular bonds within the type I collagen. Thermal energy applied through a feedback-controlled probe at 65 to 70 C results in a 30% contracture of the tissue.52 Through stabilization and immobilization, these ligaments can assume a new, shortened position on healing. Postoperative immobilization is mandatory for a 9-week period to prevent stretching of the treated tissue. This procedure is indicated for patients with moderate builds, nonavulsed ligaments, no prior stabilization procedures, and a commitment to the strict postoperative protocol. Moreover, with this technique, other intra-articular pathology can be identified and treated arthroscopically. Clinical results with thermal capsular modification have been encouraging.53 Berlet et al. presented the largest series in the literature, reporting on 42 patients who underwent thermal capsular shrinkage for chronic lateral ankle instability.54 At an average followup of 12 months, there was a significant increase in the AOFAS Ankle/Hindfoot scores and the SF-12 (SF-12 Health Survey, The Health Institute, New England
4 PEARL An anatomically based physical examination will guide the physician to the appropriate diagnosis in chronic ankle pain in the athlete. Thermal capsular modification can be considered for patients with functional ankle instability and grade I/II ankle instability. Grade III and revision situations are addressed best with open techniques.
Medical Center, Boston, MA) physical and mental components. Patients’ SF-12 scores returned to normal when compared with age and sex matched controls with no history of ankle pain.54
C A S E S T U D Y 3
A 20-year-old, college cheerleader presents to the office with recurrent ankle sprains. An aggressive rehabilitation program with physical therapy has been performed for each significant injury (once a year for the last 3 years). Her recovery from the sprains is becoming more prolonged. Her last sprain resulted in the loss of a 3-month period of cheering. She has never felt that she has returned to her full strength. On physical examination, she has normal hindfoot alignment (no varus) and poor proprioception (could single balance for only 10 seconds). An anterior drawer examination showed redundancy compared with the contralateral uninjured side (translation of 3-mm side-to-side difference) and normal peroneal strength. X-rays were normal. MRI showed the anterior talofibular ligament to be in continuity but with evidence of previous injury. A thermal capsular modification was performed. Postoperative immobilization was 3 weeks nonweight bearing in a cast, 3 weeks in a weight-bearing cast, and 3 weeks in a boot walker. Physician-supervised physical therapy was initiated at 9 weeks and emphasized proprioception retraining and peroneal strengthening. This patient returned to competition at 16 weeks with no recurrent instability at 2-year follow-up.
FOOT AND ANKLE ARTHROSCOPY The introduction of arthroscopy to the armamentarium of orthopaedic surgeons has revolutionized the treatment of many commonly seen injuries. In 1918, Dr. Takagi of Tokyo University first applied an endoscopic technique to the knee joint.1-4 Since that time, arthroscopy has grown to be a safe and successful treatment modality that has gained widespread acceptance in diagnosing and treating disorders of the foot and ankle.55-71 The advantages of arthroscopy are the ability to closely inspect the articular and synovial surfaces without the need for extensile surgical approaches. The typical arthroscopic portals used in the ankle are the anteromedial, anterolateral, and anterocentral portals. Chapter 16 addresses 559
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a more exhaustive review of the traditional surgical approaches for ankle instability. Nonanatomic lateral ligament stabilizations are characterized by extra-articular tendon weave techniques. These techniques risk overconstraining the ankle joint and are not isometric in their kinematic effect on the ankle joint. Thus they should be reserved for revisions or unique clinical situations. Anatomic lateral ligament stabilizations accept the patient’s natural ligament insertion points but adjust the tension on that ligament. Isometry is not disturbed, and overconstraint is rare. Anatomic reconstructions include the modified Brostrom lateral ligament reconstruction and thermal capsular modification. The Brostrom reconstruction is described in Chapter 13.
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New advances in the foot and ankle
ankle arthroscopy more extensively. In this chapter, we describe a newer approach to posterior ankle arthroscopy.
Posterior ankle arthroscopy In certain circumstances, posterior portals are necessary. On the basis of studies in which patients were placed in the standard supine position, most investigators have commented that the anterior portals and the posterolateral portal are safe and so have recommended the use of those portals. The most common posterior portals are the posterolateral, the trans-Achilles, and the posteromedial portals.72 Posterior access is beneficial in visualizing posteromedial and posterolateral talar lesions (OLT) and mandatory to address flexor hallucis longus (FHL) stenosing tenosynovitis, posterior ankle impingement, displaced fractures of the os trigonum, insertional Achilles tendinitis, and retrocalcaneal bursitis. Of the three posterior portals, the posterolateral portal has been subjected to the most clinical research. With the patient in the prone position, this portal is made at the level or just slightly above the level of the tip of the lateral malleolus just lateral to the Achilles tendon. Typical scope placement technique is used, and a 30-degree, 4.5-mm arthroscope is used. A coaxial portal placed directly posterior to the peroneal tendons also can be used. Care must be taken not to injure the sural nerve or the small saphenous vein, which run within 3.2 mm and 4.8 mm of the portal, respectively.73 Ferkel et al.74 reports a neurologic complication of rate of 4.4% using both anterior and posterior portals. A review by Drez et al.75 of 56 ankle arthroscopies performed with a combination of anterior and posterior portals found that the posterolateral portal allowed for excellent access to the posterior recess and that the posteromedial portal was rarely needed. Ferkel et al.74 confirmed this finding in their study and recommended posterolateral ankle arthroscopy to ensure a thorough visualization of the ankle joint. The posteromedial portal is made in a para-Achilles location or in a truly posteromedial location, between the posterior tibial tendon and flexor digitorum tendons.76-78 The Achilles tendon posteromedial portal is made just medial to the Achilles tendon in the horizontal plane at the same level as the posterolateral portal. Typical scope placement technique is used, and a 30-degree, 4.5-mm arthroscope is used. Before placing the portal, position can be checked through the use of a needle and visualization through the posterolateral portal. Developing the interval between the posterior tibial tendon and the flexor digitorum longus behind the medial malleolus makes the alternative posteromedial
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portal. Structures at risk with the posteromedial portal include the FHL, tibial nerve, and tibial artery, which average 2.7 mm, 6.4 mm, and 9.6 mm away from the portal, respectively.73 Using a posteromedial portal directly behind the medial malleolus adjacent to the posterior tibial tendon, the average distance from the cannula to the posterior tibial nerve was 5.7 mm and 6.4 mm to the tibial artery. The para-Achilles posteromedial portal is best used with the patient in the prone position, whereas the posteromedial portal may be used with the patient in the standard supine position. Ankle arthroscopy with the patient in the prone position has been discussed infrequently. Zimmer and Ferkel79 discussed the use of posterior portals with the patient in the prone position but for endoscopy of the retrocalcaneal bursa only. In a cadaveric study Sitler et al.73 demonstrated that, during posterior ankle arthroscopy with the limb in the prone position, the posteromedial and posterolateral portals could be used with a relatively small risk to the neurovascular structures. The prone posterior ankle arthroscopy approach allows for visualization and accessibility to the posterior half of the tibiotalar joint, subtalar joints, and the FHL tendon and its sheath. It is the authors’ experience that 50% of the posterior ankle can be visualized from the posterior portals, although only 30% can be manipulated directly because of the curvature of the talus and tibia. Prone positioning for posterior ankle arthroscopy is most helpful for resection of pathologic os trigonum and retrocalcaneal bursitis, where the pathology is all in the posterior recesses of the ankle.
Arthroscopy of the great toe Wantanabe80 described the first arthroscopy of the first metatarsophalangeal (MTP) joint in 1972. This procedure is indicated for osteophytes, hallux rigidus, chondromalacia, osteochondral dissecans, loose bodies, arthrofibrosis, and synovitis. Dorsal osteophytes, hallux rigidus, and osteochondral lesions are common indications among athletes. Diagnostic first MTP arthroscopy may be indicated for patients who fail conservative treatment of recurrent edema, locking pain, and diminished range of motion.81 The dorsal medial, dorsal lateral, and straight medial portals are used most commonly for arthroscopic evaluation and treatment of the first MTP joint. van Dijk et al.82 reported that two portals are needed to visualize and treat disorders of the lateral sesamoid— one in the first webspace and another 4 cm proximal to the joint line between the short abductor and the flexor hallucis brevis muscle. When making portals, care must be taken to avoid injuring the branches of the deep peroneal nerve laterally, branches of the
Foot and ankle arthroscopy
Figure 25-3 Illustration of metatarsophalangeal joint scope placement. (Illustrated by Peter Maurus, MD.)
Davies and Saxby84 performed first MTP arthroscopy on 11 patients ranging from 15 to 58 years of age (mean, 30 years) with a mean follow-up of 19.3 months. At the final follow-up, all the patients exhibited minimal or no pain, decreased edema, and increased range of motion. One patient had a minor wound complication. Three patients required an arthrotomy during the surgery. In summary, first MTP arthroscopy is an evolving technique. The best indications are osteochondral lesions. Debridement of marked degenerative joint disease should be discouraged.
Endoscopic calcaneal prominence resection In 1928, Haglund85 described a clinical condition in which the retrocalcaneal bursa and Achilles tendon are compressed and irritated by a posterior-superior calcaneal prominence. When nonoperative treatment fails, the condition can be treated by open calcaneal resection, retrocalcaneal bursectomy, and Achilles debridement with repair, when necessary. Recently, endoscopic calcaneoplasty has been described. The procedure is performed with the patient in a prone position, and posteromedial and posterolateral portals are used. The portals are placed just medial and lateral to the Achilles tendon and just proximal to the superior aspect of the calcaneus. A 2.7-mm arthroscope and small joint equipment are recommended. Extra-articular endoscopic decompression of the retrocalcaneal space can be useful for treating retrocalcaneal bursitis, Haglund’s spur, and impingement. The arthroscopic approach may decrease postoperative recovery time and incisional complications. Using lateral and accessory medial portals, Leitze et al. showed at an average of 22 months postoperatively a comparable result to open retrocalcaneal decompression as measured by the AOFAS Ankle/Hindfoot scoring system. We believe that this technique is useful in minimizing wound complications and decreasing the postoperative recovery time. Leitze et al. studied this procedure in a prospective study in 2003. They performed endoscopic decompressions on 33 heels (30 patients) in which nonoperative treatments had failed. This group was compared with 17 heels (14 patients) treated with a traditional open technique. Postoperatively, the clinical scores were not significantly different on the basis of AOFAS Ankle/Hindfoot scales, but operative time was shorter, there were fewer complications, and cosmetic results were better.86 It is our experience that endoscopic resection of the Haglund’s process is rewarding when the pathology involves bursitis with a prominent Haglund’s process. Intratendinous calcifications of the Achilles insertion are handled best with conventional open techniques. 561
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superficial nerve medially, and branches of the saphenous around the medial aspect of the first MTP joint (Fig. 25-3). There is a paucity of literature on the clinical results of first MTP arthroscopy. Ferkel and Van Buecken83 reported the results of 22 patients whose ages ranged from 18 to 70 years (mean age, 40), with a mean followup of 54 months. They reported a good outcome in 73% of the cases, fair in 13.5%, and poor in 13.5%. All patients in the fair and poor categories had degenerative joint disease and required a fusion later. van Dijk et al.82 reported on 23 patients who underwent first MTP arthroscopy. The patients averaged 33 years of age (range, 16-61 years), and the follow-up period averaged 2 years. They reported excellent or good results for 14 patients and fair or poor results for nine patients. One patient experienced transient loss of medial hallux sensation and another experienced loss of lateral hallux sensation. The authors advocate sesamoid removal laterally with the scope but state that removing the medial sesamoid arthroscopically has not proven promising.
CHAPTER 25
4
New advances in the foot and ankle
PEARL
The dorsal cutaneous branches of the superficial peroneal nerve are at the greatest risk with anterior ankle portal placement. Endoscopic Haglund resection is best reserved for patients with a mild Haglund’s deformity but marked retrocalcaneal bursitis (Fig. 25-4). This may be a technique to help athletes return to play earlier.
Figure 25-4 Magnetic resonance imaging (MRI) of an ankle illustrating a mild Haglund’s deformity and marked retrocalcaneal bursitis. (Courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.)
REFERENCES 1. Alexander AH, Lichtman DM: Surgical treatment of transchondral talar-dome fractures (osteochondritis dissecans): long-term follow-up, J Bone Joint Surg 62A:646, 1980. 2. Konig F: Uber freie korper in den gelenken, Dtsch Z Chir 27:90, 1888. 3. Parisien JS: Arthroscopic treatment of osteochondral lesions of the talus, Am J Sports Med 14:211, 1986. 4. Baker CL, Andrews JR, Ryan JB: Arthroscopic treatment of transchondral talar dome fractures, Arthroscopy 2:82, 1986. 5. Pettine KA, Morrey BF: Osteochondral fractures of the talus: a long-term follow-up, J Bone Joint Surg 69B:89, 1987. 6. Van Buecken K, et al: Arthroscopic treatment of transchondral talar dome fractures, Am J Sports Med 17:350, 1989. 7. Anderson IF, et al: Osteochondral fractures of the dome of the talus, J Bone Joint Surg 71A:1143, 1989. 8. Woods K, Harris I: Osteochondritis dissecans of the talus in identical twins, J Bone Joint Surg 77B:331, 1995. 9. Bruns J, Rosenbach B, Kahrs J: Etiopathogenetic aspects of medial osteochondrosis dissecans tali, Sportverletz Sportschaden 6:43, 1992. 10. Mesgarzadeh M, et al: Osteochondritis dissecans: analysis of mechanical stability with radiography, scintigraphy, and MR imaging, Radiology 165:775, 1987. 11. Higashiyama I, et al: Follow-up study of MRI for osteochondral lesion of the talus, Foot Ankle Int 21:127, 2000.
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12. DeSmet AA, et al: Value of MI imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): results in 14 patients, AJR Am J Roentgenol 154:555, 1990. 13. Loredo R, Sanders TG: Imaging of osteochondral injuries, Clin Sports Med 20:249, 2001. 14. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus, J Bone Joint Surg 41A:988, 1959. 15. Hepple S, Winson IG, Glew D: Osteochondral lesions of the talus: a revised classification, Foot Ankle Int 20:789, 1999. 16. McCullough CJ, Venugopal V: Osteochondritis dissecans of the talus: the natural history, Clin Orthop 144:264, 1979. 17. Bauer M, Jonsson K, Linde´n B: Osteochondritis dissecans of the ankle. A 20-year follow-up study, J Bone Joint Surg 69B:93, 1967. 18. Berlet GC, Mascia A, Miniaci A: Treatment of unstable osteochondritis dissecans lesions of the knee using autogenous osteochondral grafts (mosaicplasty), Arthroscopy 15:312, 1999. 19. Yoshizumi Y, et al: Cylindrical osteochondral graft for osteochondritis dissecans of the knee: a report of three cases, Am J Sports Med 30:441, 2002. 20. Angermann P, Riegels-Nielsen P: Fibrin fixation of osteochondral talar fracture, Acta Orthop Scand 61:551, 1990. 21. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review, Foot Ankle Int 21:119, 2000. 22. Kumai T, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus, J Bone Joint Surg 81A:1229, 1999. 23. Taranow WS, et al: Retrograde drilling of osteochondral lesions of the medial talar dome, Foot Ankle Int 20:474, 1999. 24. Lee CK, Mercurio C: Operative treatment of osteochondritis dissecans in situ by retrograde drilling and cancellous bone graft, Clin Orthop 158:129, 1981. 25. Hangody L, Fules P: Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience, J Bone Joint Surg Am 85A(suppl 2):25, 2003. 26. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S: Arthroscopically assisted autologous osteochondral transplantation for osteochondral lesions of the talar dome: an MRI and clinical followup study, Foot Ankle Int 22(7):544-551, 2001. 27. Al-Shaikh RA, et al: Autologous osteochondral grafting for talar cartilage defects, Foot Ankle Int 23:381, 2002. 28. Gautier E, Kolker D, Jakob RP: Treatment of cartilage defects of the talus by autologous osteochondral grafts, J Bone Joint Surg 84B:237, 2002. 29. Sammarco GJ, Makwana NK: Treatment of talar osteochondral lesions using local osteochondral graft, Foot Ankle Int 22:693, 2002. 30. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation, N Engl J Med 331:889, 1994. 31. Gillogly SD, Voight M, Blackburn T: Treatment of articular cartilage defects of the knee with autologous chondrocyte implantation, J Orthop Sports Phys Ther 28:241, 1998. 32. Farnworth L: Osteochondral defects of the knee, Orthopedics 23:146, 2000. 33. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation, Clin Sports Med 18:13v, 1999. 34. Minas T: The role of cartilage repair techniques, including chondrocyte transplantation, in focal chondral knee damage, Instr Course Lect 48:629, 1999. 35. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint, Foot Ankle Int 22:513, 2001. 36. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation, Clin Sports Med 18(1):13-44, 1999. 37. Minas T: Implantation in the repair of chondral lesions of the knee: economics and quality of life, Am J Orthop 27:739, 1998.
References 62. Ferkel RD, Scranton PE Jr: Current concepts review: arthroscopy of the ankle and foot, J Bone Joint Surg 75A:1233, 1993. 63. Gollehon DL, Drez D: Ankle arthroscopy: approaches and technique, Orthopedics 6:1150, 1983. 64. Gollehon DL, Drez D: Arthroscopy of the ankle. In McGinty J, editor: Arthroscopic surgery update, Rockville, MD, 1985, Aspen. 65. Harrington KD: Degenerative arthritis of the ankle secondary to long-standing lateral ligament instability, J Bone Joint Surg 61A:354, 1979. 66. Johnson LL: Diagnostic and surgical arthroscopy, ed 2, St Louis, 1981, Mosby. 67. Parisien JS: Arthroscopy of the posterior subtalar joint: a preliminary report, Foot Ankle 6:219, 1986. 68. Parisien JS: Arthroscopy of the ankle: state of the art, Contemp Orthop 5:21, 1982. 69. Parisien JS, Shereff MJ: The role of arthroscopy in the diagnosis and treatment of disorders of the ankle, Foot Ankle 2:144, 1981. 70. Parisien JS, Vangsness T: Operative arthroscopy of the ankle: three years’ experience, Clin Orthop 199:46, 1985. 71. Stetson WB, Ferkel RD: Ankle arthroscopy. I. Technique and complications. II. Indications and results, J Am Acad Orthop Surg 4:17, 1996. 72. Voto SJ, et al: Ankle arthroscopy: neurovascular and arthroscopic anatomy of standard and trans-Achilles tendon portal placement, Arthroscopy 5:41, 1989. 73. Sitler DF, et al: Posterior ankle arthroscopy. An anatomic study, J Bone Joint Surg 84A:763, 2002. 74. Ferkel RD, Heath DD, Guhl JF: Neurological complications of ankle arthroscopy, Arthroscopy 12:200, 1996. 75. Drez D, Jr, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications, Foot Ankle 2:138, 1981. 76. van Dijk CN, Scholten PE, Krips R: A 2-portal endoscopic approach for diagnosis and treatment of posterior ankle pathology, Arthroscopy 16:871, 2000. 77. Berlet GC, Lee TH, Puri DR: The posteromedial portal for ankle arthroscopy, Presented at the Pan-American Congress on Medicine and Surgery of the Leg and the Foot. Sept 22–24, Buenos Aires, 2000, Argentina. 78. Acevedo JI, et al: Coaxial portals for posterior ankle arthroscopy: an anatomic study with clinical correlation on 29 patients, Arthroscopy 16:836, 2000. 79. Zimmer T, Ferkel RD: Future developments. B. Endoscopic procedures for the retrocalcaneal bursa, plantar fascia, and Achilles tendon. In Ferkel RD, Whipple TL, , editors: Arthroscopic surgery: the foot and ankle, Philadelphia, 1996, Lippincott-Raven. 80. Watanabe M: Selfox-Arthroscope (Wantantabe No. 24 arthroscope), Tokyo, Japan, 1972, Teishin Hospital. 81. Frey C, van Dijk CN: Arthroscopy of the great toe, AAOS Instruct Course Lect 48:343, 1999. 82. van Dijk CN, Veenstra KR, Neusch BC: Arthroscopic surgery of the metatarsophalangeal first joint, Arthroscopy 14:851, 1998. 83. Ferkel RD, Van Buecken K: Great toe arthroscopy: indications, technique and results, Presented at the Arthroscopy Association of North America, San Diego, April 1991. 84. Davies MS, Saxby TS: Arthroscopy of the first metatarsophalangeal joint, J Bone Joint Surg 81B:203, 1999. 85. Haglund P: Contribution to the diseased conditions of the tendoAchilles, Acta Chir Scand 63:292, 1928. 86. Leitze Z, Sella E, Aversa JM: Endoscopic decompression of the retrocalcaneal space, J Bone Joint Surg 85A:1488, 2003.
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38. Tontz WL, Jr, Bugbee WD, Brage ME: Use of allografts in the management of ankle arthritis, Foot Ankle Clin 8(2):361-373, 2003. 39. Gross AE, Agnidis Z, Hutchison CR: Osteochondral defects of the talus treated with fresh osteochondral allograft transplantation, Foot Ankle Int 22:385, 2001. 40. Caylor MT, Pearsall AW 4th, et al: Fresh osteochondral grafting in the treatment of osteochondritis dissecans of the talus, J South Orthop Assoc 11:33, 2002. 41. Hsieh PC, et al: Repair of full-thickness cartilage defects in rabbit knees with free periosteal graft preincubated with transforming growth factor, Orthopedics 26:393, 2003. 42. Guo X, et al: Expression of transforming growth factor—beta 1 in mesenchymal stem cells: potential utility in molecular tissue engineering for osteochondral repair, J Huazhong Univ Sci Technolog Med Sci 22:112, 2002. 43. Siebert CH, et al: Healing of osteochondral grafts in an ovine model under the influence of bFGF, Arthroscopy 19:182, 2003. 44. Mierisch CM, et al: Transforming growth factor—beta in calcium alginate beads for the treatment of articular cartilage defects in the rabbit, Arthroscopy 18:892, 2002. 45. Martinek V, et al: Treatment of osteochondral injuries. Genetic engineering, Clin Sports Med 20:403, viii, 2001. 46. Lohmann CH, et al: Pretreatment with platelet derived growth factor-BB modulates the ability of costochondral resting zone chondrocytes incorporated into PLA/PGA scaffolds to form new cartilage in vivo, Biomaterials 21:49, 2000. 47. Holmer P, et al: Epidemiology of sprains in the lateral ankle and foot, Foot Ankle Int 15:72, 1994. 48. Gerber JP, et al: Persistent disability associated with ankle sprains: a prospective examination of an athletic population, Foot Ankle Int 19:653, 1998. 49. Balduini FC, et al: Management and rehabilitation of ligamentous injuries to the ankle, Sports Med 4:364, 1987. 50. Freeman MAR: Instability of the foot after injuries to the lateral ligament of the ankle, J Bone Joint Surg 47B:669, 1965. 51. Tropp H, Ekstrand J, Gillquist J: Stabilometry in functional instability of the ankle and its value in predicting injury, Med Sci Sports Exerc 16:64, 1984. 52. Hyashi T, Curran-Patel S, Prockop DJ: Thermal stability of the triple helix of type I procollagen and collagen. Precautions for minimizing ultraviolet damage to proteins during circular dichroism studies, Biochemistry 18:4182, 1979. 53. Cline S, Wolin P: The use of thermal energy in ankle instability, Clin Sports Med 21:713, 2002. 54. Berlet GC, Raissi A, Lee TH: Thermal capsular modification for chronic lateral ankle instability, AOFAS Annual Summer Metting, Traverse City, MI, July 2002. 55. Andrews FR, Previte WJ, Carson WG: Arthroscopy of the ankle: technique and normal anatomy, Foot Ankle 6:29, 1985. 56. Chen YC: Clinical and cadaver studies on the ankle joint arthroscopy, J Jpn Orthop Assoc 50:631, 1976. 57. Drez D, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications, Clin Sports Med 1:35, 1982. 58. Drez D, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications, Foot Ankle 2:138, 1981. 59. Ewing JW: Ankle arthroscopy. In Arthroscopy surgery update, Ariz, 1989, Scottsdale. 60. Ferkel RD: Arthroscopy of the foot and ankle, New York, 1996, Lippincott-Raven. 61. Ferkel RD, Fischer SP: Progress in ankle arthroscopy, Clin Orthop 240:210, 1989.
.........................................C H A P T E R 2 6 The shoe in sports Carol Frey CHAPTER CONTENTS ...................... General considerations
567
Shoe fit
572
Materials
567
Sports-specific shoes
574
Lasting techniques
569
Court sport shoes
577
Upper designs and cuts
569
Field sport shoes
578
Bottoming process
569
Winter sports
579
The outer sole
570
Other sports
581
Midsoles and wedges
571
Injuries related to athletic footwear
581
Other component parts
571
Conclusions
583
New components and designs
572
References
583
The relationship of the athlete and the shoe is extremely important to athletic performance. The desire for improved performance affects all athletes and influences not only training but also equipment research and design. Athletic shoe manufacturers rely on scientific research and prior experience in the development of their products. This chapter covers important aspects of design, technology, sports-specific needs, and medical and orthopaedic considerations in the development of athletic shoewear.
GENERAL CONSIDERATIONS Construction Although product development and marketing methods are different, manufacturers use most of the major methods of shoe construction in the production of sport shoes (Fig. 26-1). The last The last, a three-dimensional (Fig. 26-2) form on which the shoe is made, is considered by many to be the foundation for shoe production and development. Foot shape may vary with sports activities, and this is a major area of concern in the development of the last. The shape of
the shoe toe box, instep, girth, and foot curvature are determined by the last. The biggest last variations occur in girth (or widest part of the forefoot) and in heel width. Straight and curved lasts Most feet have a slight inward curve. Most sport shoe companies use a last that is curved inward approximately 7 degrees. The greater the curve, the more foot mobility is allowed, a benefit for the underpronator. The straighter the shoe, the more medial support it will provide; this can help to control overpronation. Combination lasts The term ‘‘combination lasts’’ refers to any last that varies from a standard proportional last to lasts that accommodate a combination of fitting or movement requirements.
MATERIALS Upper materials ............................................................. Leather, rubber, plastic injection molding, soft nylon, mesh nylon, polyvinyl chloride (PVC)-coated fabrics,
CHAPTER 26
The shoe in sports
Figure 26-1 Generic athletic shoe. (From Reyatt T: The first step: know your feet. SHAPE Magazine, Nov 1992.)
Sole materials ............................................................. Rubber is the most widely used sole material because of its versatility, durability, and performance. The most commonly used forms of rubber are a highly compressed molded form or a blown microcellular form. Carbon rubber and styrene-butadiene rubber are the two most common rubber compounds used in athletic shoes. Often used in running-shoe soles, black carbon rubber is the hardest wearing. Styrene-butadiene rubber also is hard and is used in tennis and basketball shoes.
Figure 26-2 Different lasts used in athletic shoes. (From Reyatt T: The first step: know your feet. SHAPE Magazine, Nov 1992.)
polyurethane-coated fabrics, and canvas have been used in the manufacture of uppers. Most uppers used in sports shoes are made of soft nylon, mesh nylon, leather, canvas, suede, and synthetic materials such as Kangoran.
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568
Microcellular rubber Microcellular rubber (MCR) is a compound composed of natural rubber plus additives. MCR contains a blowing agent in powder form that decomposes during vulcanization, forming a cellular structure. MCR is used mainly for midsoles and wedges, but in some shoes it can be used as an outsole material. Ethyl vinyl acetate Ethyl vinyl acetate (EVA) contains ethylene and vinyl acetate and a powdered blowing agent that decomposes during vulcanization to form a cellular structure. Because of its lightness, flexibility, density, elongation, and impact resistance, EVA is a common material used
Bottoming process
in good-quality running shoes. EVA is available in prefabricated sheet or compression-molded forms.
Polyurethane Polyurethane (PU) is a liquid polyester that can be formed into a blown cellular structure. PU is versatile and can be used as a midsole and heel wedge material, and its lightness and durability make it a satisfactory outsole material. PU can be injected directly or used as a unit sole. PU can be used in the blown cellular state and as a hardened elastomer form in multistudded soles such as golf shoes. Hytrel Hytrel is a thermoplastic polyester elastomere developed by DuPont (E.I. duPont de Nemours and Company, Wilmington, DE). Nylon Nylon is a polyester resin with a high melting point that forms a hard outsole when injected. It is used for spike plates and as a base for screw-in studs. The hardness grade of nylon refers to the number of carbon atoms in the nylon molecule and is graded as nylon 6, 11, and 12 (nylon 6 being the hardest). Leather Split-leather and coarse full hides are used in the construction of some athletic shoes.
Figure 26-3 Methods of lasting.
UPPER DESIGNS AND CUTS
The most common methods of lasting used in shoemaking are slip lasting, board lasting, and combination lasting (Fig. 26-3). 1. Slip lasting—A slip-lasted shoe is constructed by sewing together the upper like a moccasin and then gluing it to the sole. The last usually is forced into the upper, which then takes the shape of the last. A sock liner usually takes the place of an insole. This lasting method makes a lightweight and flexible shoe with no torsional rigidity. 2. Board lasting—The upper is placed over the last and fastened to the insole with cement, tacks, or staples. This construction promotes stability and torsional rigidity but decreases flexibility. 3. Combination lasting—More than one lasting technique can be used on the same shoe. Usually the shoe is board lasted in the rear foot for stability but slip lasted in the forefoot for flexibility. Combination lasting can offer customized features necessary for some athletes.
1. U-throat—The U-throat offers a U-shaped full lacing system that extends down to the toes. 2. Vamp or blucher pattern—This upper has no seam construction across the dorsum of the midfoot, and the tongue piece continues with the uppers. Lace stays are not fixed to the throat. 3. Balmoral or brogue pattern—This design is a lowcut, laced shoe, usually with a long wingtip trimmed with pinking and perforations. The tongue, throat, and lace stays are seamed as one unit. This type of upper construction allows less space for the dorsal aspect of the midfoot and often is used in golf shoes. 4. Lace-to-toe pattern—This pattern offers lacing similar to the U-throat pattern, but in addition both quarters are pulled together across the foot for maximal support.
BOTTOMING PROCESS Bottoming is the process in which the sole components are attached to the upper. The upper determines the 569
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LASTING TECHNIQUES
CHAPTER 26
The shoe in sports
shoe fit and provides support, and the sole provides traction and cushioning.
THE OUTER SOLE The outsole is the most plantar surface of the shoe that makes contact with the ground and usually is attached to a midsole to form a complete sole. Most athletic shoes have outer soles of hard carbon rubber or blown rubber compounds. Blown rubber is the lightest outsole material but is not as durable as carbon rubber. Many outsoles are composed of both blown and carbon rubber, with blown rubber in the forefoot and midfoot and carbon rubber used in the high-wear area of the heel. Gum rubbers are hard wearing and grip well on most surfaces. PU is less versatile but also suitable for outsole material and seems to possess good durability. Nylon, leather, and PVC have specific outsole applications for certain sports.
Outer sole designs Patterns can enhance stability and traction. They also can improve shoe lightness by exposing the middle part of the midsole, thereby eliminating part of the outsole and the associated weight. The design of the outsole (Fig. 26-4) can provide cushioning, traction, pivot points, flexpaths, and wear plugs. Outsoles are specific for surface, weather condition, and sport. Outsole options include: Wear-area reinforcement (running shoes). Cantilevered designs for shock absorption (running shoes). Pivot points (court shoes). Herringbone (court shoes). Suction-cup designs (court shoes). Multiclaw or stud designs (field shoes). Radial edges (court shoes). Asymmetric studs (field shoes). Traction and wear lugs (hiking and climbing boots). Traction provided by the outsole is an important consideration in the design of a sport shoe and is directly related to the ability of the shoe to develop frictional forces with the playing surface. Traction needs depend on the specific sports needs. Too little traction may have a negative effect on athletic performance, and too much traction may put the athlete at risk for injury.1 A running shoe should create a grip firm enough with the ground so that propulsion forces created by the runner will not be lost with push-off. Push-off has the highest traction needs; therefore the forepart of the outsole should provide the most traction. The outsole
...........
570
Figure 26-4 Outsole patterns. (From Reyatt T: The first step: know your feet. SHAPE Magazine, Nov 1992.)
rubber used in running shoes usually is blown rubber (air injected to lighten it) or hard carbon rubber. Cleated shoes must address a compromise between performance and protection of the athlete. Rotational traction, which is expressed by the torque about a normal axis that is developed to resist rotation of a shoe on a playing surface, must be reduced to decrease the incidence of injury while providing sufficient traction. Both cleat length and outsole material affect friction. Torg and Quendenfeld1 concluded that the increased rotational traction characteristics of some football shoes are related to an increase in number of significant knee injuries. The necessity for lateral movement with court sports makes the traction characteristics of court shoes important. A flat outsole pattern develops the greatest frictional forces, whereas a herringbone pattern develops less.2 With sprinting, initial ground contact is made with the front of the shoe. At foot strike a large horizontal velocity is created, resulting in a high braking force that can cause a backward slide. Anterior spikes help to prevent slipping. With jumping events, an athlete converts the large horizontal momentum of run-up to a vertical momentum at foot plant. The spikes prevent foot slip and allow the development of large propulsive forces necessary for long jump and triple jump. With golf shoes, motion is primarily stationary with little horizontal velocity. Golf shoes provide a base of support that allows the performance of coordinated body movements needed in hitting the ball. A nonvertical alignment of the spikes prevents slipping in this sport, which mainly requires anterior and lateral forces. Boating shoes require a large amount of natural rubber to prevent slippage on wet surfaces.
Other component parts
Most of the recent advances in the athletic shoe industry have been made in midsole design and materials. The midsole and heel wedge are sandwiched between the upper and the outsole, attaching to both. These components provide cushioning, shock absorption, lift, and control.
Unit soles Unit soles usually contain the outsole, midsole, and heel wedge as one unit. This design is used for roller-skate boots and for other sports in which the sole does not contact the ground. This design usually is heavy and provides little flexibility but excellent torsional rigidity. Combination or prefabricated soles Midsoles are manufactured from a combination of two basic materials: EVA and polyurethane. EVA is light, has excellent cushioning properties, and can be manufactured in various densities. The firmest densities in a multidensity midsole usually are designated by a darker color. These can be placed at critical points in the midsole to aid in motion control. PU is a denser, heavier, and more durable material than EVA. New forms of lighter PU are being developed. Both EVA and PU are used to encapsulate other cushioning materials such as air bags (Nike and Etonic), gel (Ascics), silicone (Brooks), honeycomb pads (Reebok and Puma), and EVA (New Balance). Some midsoles can be contoured to the foot and are referred to as more stable, anatomic midsoles. The effect of shoe midsole composition on the amount of tibial strain produced with walking has been studied by Milgrom et al.3 Their study was designed to test the hypothesis that shoe sole composition can affect the level of bone strain and strain rates that can lead to a stress fracture. The sole materials tested were various polyurethane midsoles and one of polyurethane with embedded air cells. The sole composed of polyurethane with embedded air cells had significantly lower compression and shear strains and shear strain rates. They concluded that the polyurethane sole with the embedded air cells potentially could protect against stress fractures in a walking shoe.
OTHER COMPONENT PARTS Heel counters The heel counter is a firm cup built into the rear of the shoe that holds the heel in position and helps to control excessive foot motion. Most heel counters today
are made of a durable plastic, thermoplastic, stytherm, or polyvinyl. The medial side of the heel counter may be extended or reinforced for additional pronation control. Contoured or notched counters also reduce irritation of the Achilles tendon, especially in plantarflexion.
Toe box The toe box provides a stiff material inserted between the lining and upper in the toe area to prevent collapse and protect the toes. Foxing Foxing is a stripping material that gives medial and lateral support to the outside of the shoe and usually is made of suede or rubber. In running shoes, the most important foxing is at the toe, where it is called the toe cap. In court shoes, the foxing runs completely around the sole for lateral support. Cantilevered or angled radial outsole A cantilevered outsole provides a concave outsole design in which the outer edges flare out on impact to dissipate shock. This design is used extensively by AVIA. Shank The shank is the bridge between the heel and the ball area of the shoe. It is a reinforcing material that is arched and somewhat narrowed to conform roughly to the narrow underpart arch area of the midfoot. Shanks are not common in wedge-soled shoes but are important for torsional rigidity in shoes with heels to support the metatarsal arch. Tongues Tongues are designed primarily to protect the dorsum of the foot from dirt, moisture, and lace pressure. Lacing loops or tongue slits help to prevent the tongue from slipping. Sock linings, arch supports, and inserts Sock linings cover the insole and improve comfort and appearance. A prime function of the sock lining is to serve as a buffer zone between the shoe and the foot. Sock linings are molded, soft support systems that can function in aeration, moisture absorption, hygiene, shock absorption, and motion control. Arch supports, heel cups, and other types of padding can be added to provide support, cushioning, and motion control. Custom-molded ‘‘foothotics’’ have been made popular by the ski industry. These semirigid insole devices are custom molded to the foot and may help increase comfort, shock absorption, and performance. Custom insoles can be used in any sport shoe, provided there is enough room to accommodate the insert. 571
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MIDSOLES AND WEDGES
CHAPTER 26
The shoe in sports
NEW COMPONENTS AND DESIGNS Air soles First introduced in 1979 by Nike, this concept used encapsulated air units in the midsole to enhance cushioning. Ambient air (Etonic) or Freon (Nike) also can be used. Depending on the model, the air units may be in the heel, forefoot, or both. Initial reports noted that, although air systems had superior shock absorption and potential energy rebound, stability was poor.4 Stability in the context of sports refers to the ability of the shoe to resist excessive or unwanted motions of the foot and ankle. Shoes with soft, well-cushioned midsoles allow significantly more motion than firmer shoes, and a poor design can encourage instability. Newer designs have addressed the stability problem with success. Air systems are not as susceptible to compaction as EVA, PU, and other midsole materials and therefore are thought to be more durable. Energy return Compression of a viscoelastic midsole material allows a small amount of strain energy to be stored in the compressed elastic components of the midsole. Theoretically, when weight is released the elastic components spring back and stored energy is returned to the athlete. It has been suggested that by increasing the energy return of a shoe, the oxygen cost of an activity can be reduced and performance enhanced. There is little evidence to support these claims. The arch of the human foot is also a viscoelastic system and therefore can return energy.5,6 The ‘‘pumps’’ The pumps are actually inflatable linings in the tongue and other parts of the shoe that are pumped up by a device built into the top of the shoe. This provides a tight, secure fit. Both Nike and Reebok have used this fit feature. Replaceable plug systems A heel plug is found in multidensity outsoles, where the most durable rubber is placed in the high-wear area of the heel. Adidas designed a rear-foot plug system that allows three different hardnesses of replaceable plug to be inserted into the heel wedge to improve shock absorption. Brooks marketed a pronation control system that allows pronation to be controlled by inserting medial heel plugs of varying hardness. Pronation control devices Control over pronation in runners and other athletes is a major concern of the sport shoe industry. Most of
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the motion-control features fall into two categories: (1) a harder density material built into the medial aspect of the midsole and/or heel to counteract pronation and (2) an added medial component to the inside or outside of the shoe that limits pronation. In the past, most of the pronation-control devices have focused on the rear foot. More attention now is placed on controlling the entire foot.
Women’s shoes There has been a lot of recent interest in manufacturing women’s athletic shoes, but only a few companies have tried to market shoes for women. In the past, most women’s models were simply men’s models with cosmetic changes. It has been hard to change the common perception that men’s shoes are better than women’s.
SHOE FIT A last is a three-dimensional facsimile of a foot and the form over which the upper is fashioned. The fit of all shoes depends largely on the shape of the last. In fitting a shoe correctly, the shape of the athlete’s foot is important in that the shape of the shoe should match the shape of the foot. Curved lasts are better suited for athletes with high arches who do not overpronate. These shoes offer less medial support but greater foot mobility. Furthermore, a curve-lasted shoe is desirable for a faster runner who wants a more responsive shoe. Straight lasts provide more support to the medial side of the foot and are better suited for athletes with low arches or those who overpronate. Shoes should feel comfortable and fit well the first time they are put on. Runners and athletes should shop for shoes after a run or after a training session, when their feet are at their largest. The shoe should be fit to the largest foot. There should be a finger’s breadth from the end of the toe box to the end of the longest toe, and the athlete should be able to fully extend all toes. One should keep in mind that although the most common regular shoe width is C for men and B for women, the average athletic shoe width is a D for men and C for women. This reflects additional allowances for foot expansion and movement during sport. Width fittings are not commonly available in athletic footwear. Athletic shoes generally are built on ‘‘universal’’ lasts, and width adjustments are incorporated into lacing patterns. When fitting new shoes, the athlete should wear the socks normally used while training. If the athlete normally wears orthotics, these should replace the sock liner of the shoe during fitting.
Shoe fit
Laces ............................................................. Beginning at the bottom, laces should be pulled one set of eyelets at a time to tighten. This provides a more comfortable shoe fit and distributes stress evenly across the eyelets and the dorsum of the foot. The majority of athletes can use the conventional crisscross to the top of the shoe technique, aiming for a snug but comfortable fit. However, there are many lacing techniques (Fig. 26-5), and shoe manufacturers have added extra eyelets so that athletes can lace them for a custom fit.
Independent lacing (Fig. 26-5, C) One lace is provided near the throat of the shoe and one for the forefoot, which can be tied at different tensions for a custom fit.
Lacing techniques.
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Figure 26-5
Variable lace patterns (Fig. 26-5, A and B) Many sport shoes incorporate a lacing system that provides a variable or wavy eyelet pattern allowing lacing to be adjusted for wider or narrower feet. The eyelets placed more widely allow the lacing to pull the quarters in more tightly and are more suitable for narrow feet. The more narrowly placed eyelets allow for more girth and thus are more suitable for a wider foot.
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The shoe in sports
For pain and/or prominences on the dorsum of the foot (Fig. 26-5, D) This lace pattern can relieve pressure over prominences and painful areas on the dorsum of the foot. The athlete starts with a conventional lacing system until just distal to the problem area. The lace is then moved vertically to the next eyelet so that it does not cross over the dorsum of the foot. A conventional lacing is used to complete the shoe closure. Many soccer players prefer this lacing pattern. Square-box lacing (Fig. 26-5, E) In this method, the laces never cross over the dorsum of the foot but rather pass under the eyelet. This helps to distribute lace pressure more evenly over the dorsum of the foot than the crisscross lacing system. Square-box lacing is useful for an athlete with a high arch, rigid feet, or a dorsal prominence or for an athlete with a deep peroneal nerve entrapment. Single-lace cross (Fig. 26-5, F) The single-lace cross may help the athlete who is having problems with black or sore toenails. One lace runs from the inside most proximal eyelet to the opposite most distal eyelet. The other end of the lace goes side to side through every remaining eyelet. This pattern pulls up the toe box of the shoe, relieving pressure on the toes. For heel spillage (Fig. 26-5, G) This is a conventional pattern of lacing until the last eyelet. By looping the end of each lace and using the loop as an eyelet, one can obtain a more secure fit around the heel. This method is helpful to prevent heel slippage.
1. Running, training, and walking shoes—includes most shoes used for running and walking. 2. Court sport shoes—-includes all shoes used for major and minor court sports. 3. Field sport shoes—cleated, studded, and spiked shoes used in most field sports. 4. Winter sport shoes—shoes for all winter sports activities, including skating and skiing. 5. Outdoor sport shoes—shoes for recreational sports, such as hunting, fishing, and boating. 6. Track and field shoes—diverse area of sports that has its own category of shoes. 7. Specialty sport shoes—shoes for all minor specialized sports and some major ones not covered under other groups, such as golf and aerobic dancing.
Running, training, and walking ............................................................. Hiking, race walking, and exercise walking are included in this category.
Hiking boots These are used on rugged terrain. The upper of a hiking boot should be water resistant. There should be few seams for both comfort and water resistance. The soles, which are heavily lugged for traction and durability, are made of rubber, PU, or PVC compounds. There should be some flexibility in the forepart of the shoe at the metatarsophalangeal joints. Other features of a good hiking boot include a firm heel counter, a padded area around the ankle area, a smooth or seam-free lining, and a high, wide toe box. A wedge or a heel with a shank is required. Climbing boots are different from hiking boots in that they have inflexible soles and a thicker upper (Fig. 26-6).
Show lacing Show lacing is not practical for wearing purposes. Retailers and manufacturers use this method to show their shoes. Elastic lacing Elastic laces can be beneficial to athletes with wide or expanding feet. However, with the use of elastic laces, shoes will lose some stability because, as the foot rolls in, the laces will give. The elastic lace eliminates the need for lacelocks used by many triathletes because the extra stretch allows shoes to be pulled on easily.
SPORTS-SPECIFIC SHOES Manufacturers group athletic shoes into the following sales categories:
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Figure 26-6 Hiking boots.
Sports-specific shoes
Race-walking shoes The construction of a race-walking shoe is similar to that of a track shoe. A firm, light midsole is important. Outsoles are made from carbon rubber or gum rubber. A firm heel counter is desirable.
Running ............................................................. Spikes Little body weight is placed on the heel in sprinting. For most track runners, even those who run the longer distances, landing and propulsion are carried out on the ball and middle part of the foot. For this reason, track shoes used in the faster and shorter races have just enough padding at the heel to prevent a contusion (Fig. 26-8).
Figure 26-7
Exercise walking shoes.
Figure 26-8
Spikes.
A slight wedge in the shoes for longer races gives more torsional rigidity and support. Torsional rigidity often is omitted in track shoes for lightness. Track shoe lasts are designed to hug the foot at the heel, waist, and girth. The toe box is semipointed to prevent the toes from splaying under the pressure of landing and take-off. Certain specifications for track spikes may vary for different events. A maximum of six sole and two heel spikes is permitted; spikes must not project more than 25 mm or exceed 4 mm in diameter. Added spike receptacles may be present for optimal adjustment and may be filled with flat screws when not in use. Grooves, ridges, and appendages are permitted on the sole and heel. With the use of synthetic and rubber tracks, track spikes have shortened to approximately 9 mm and reverted to six spikes for better traction. With the use of shorter spikes, shoe manufacturers invented removable plastic ‘‘claws.’’ When used in conjunction with replaceable variable length spikes, track shoes have more versatility for different track surfaces. Nylon sole plates receive the spike receptacles. These often are covered with textured rubber for added traction. For curve running (200- to 400-m races) adequate torsional stability is recommended. Lightweight MCR, PU, or EVA foams are used to provide some padding, particularly in the heel area. A spikeless track shoe, usually made with a thin rubber outsole covering a midsole with a maximum heel height of 13 mm, may be preferred if the track surface is hard. Following the same pattern as sprint shoes, middledistance shoes vary only in the midsole area. A thin wedge or shank may help to control overpronation and torque during bend running. Participants in the short and long hurdles require sprint shoes with lasts that are wider in the toe and shorter front spikes to avoid clipping the hurdle with the lead foot. A more heavily padded heel is desirable to cushion the landing. 575
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Exercise walking shoes The design of this shoe is similar to a training running shoe that has many of the features needed in walking such as lightness; flexible forefoot; comfortable, soft upper; and good shock absorption (Fig. 26-7). For the urban walker, weight is not as important a consideration, and leather often is used for the upper material. An ample toe box and soft sock liner are added for comfort. The sole is also different, with a wedge incorporated into the design. The tread has a smooth, low profile with a herringbone pattern. Many outsoles have a rocker profile to encourage the natural roll of the foot during the walking motion. This feature also helps to reduce excessive flex at the metatarsophalangeal joints and will reduce stress on the midfoot. A walking shoe should have a firmer landing area on the heel than most running shoes. The bias-out or upswept heel of many running shoes does not offer the landing platform needed by walkers. Most walkers also benefit from the use of a more resilient compound in the rear part of the shoe. A heel height of 10 to 15 mm is recommended for exercise walking to support the correct walking motion and reduce overstretching of the Achilles tendon.
CHAPTER 26
The shoe in sports
Flats More research and design has been done in this area than in all other areas of athletic footwear. The features most required in a running shoe used for training on hard road surfaces are shock absorption, flexibility, control and stability in the heel counter area, torsional rigidity in the waist or shank, lightness, traction, comfort, motion control, and good fit. Because of the specific needs of individual runners, athletic shoewear companies now produce models for specific foot types, gait patterns, and training styles. There are designs for light runners, heavy runners, heel strikers, motion control, stability, lightweight trainers, and rugged terrain. This segmentation of the market is crossing over into other major segments of the athletic shoe market such as tennis and basketball. Uppers usually are made of lightweight soft or mesh nylon. A rigid heel counter is a requirement because, like walkers, most runners land heel first. The midsoles of training shoes should be lightweight and offer good shock-absorbing properties. PU and EVA are the most commonly used materials, but ambient air, Freon, and silicone also can be used. All these materials have good to excellent shock absorbency and are built into heel wedge and midsole combinations. The shape of the sole is wedged from heel to toe, with approximately a double thickness at the heel to the metatarsophalangeal joint flexion points. A flared heel increases stability in the heel area (Fig. 26-9). Traction is obtained by rubber outsole materials and a good tread design. To obtain the best traction on loose or open terrain surfaces, a deeper sole tread is desired. On smoother, harder surfaces such as pavement, a lowerprofile sole offers better stability and adequate traction. Flexpath designs on the outsole increase flexibility.
Throwing events ............................................................. Shoes for throwing events, in which athletes tend to be larger, are primarily made of leather or suede for
Figure 26-9
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Flats.
maximal durability and support. Because of tremendous stresses applied to the medial and lateral portion of the shoe, the uppers are made with extra support around the girth. A shot-put shoe should have reinforced leather uppers, a sturdy heel counter, firm toe box, and reinforcement in the quarter for lateral support. A good grip from a rubber sole and adequate shank provides some control for anterior and lateral movements across the circle. Discus shoes are similar to shot-put shoes but have more flexibility in the forefoot and a wrap-up sole for improved turning motion in the circle. Javelin boots are the only throwing shoes made with spikes for run-up and planting. Soles have a heavy-duty forefoot and heel spike plates containing six front and two back spikes, which may be as long as 25 mm for competition on grass runways. A buckle or strap may be used across the girth to provide additional support.
Jumping events ............................................................. For jumping events, the spike placement changes from the asymmetric pattern, with two spikes in front for stability (the International Association of Athletics Federations [IAAF] rules that there may be a maximum of six forepart spikes and two heel spikes). Most long jumpers do not use heel spikes. The forepart spike plate is sturdy for extra support. Heel cushioning is used for shock absorption. Similar to long-jump shoes, triple-jump shoes vary only in the midsole, where a sturdy wedge gives better support for landing during the midstance and toe-off stress during this event. Most triple jumpers use heel spikes. Regardless of their style, high jumpers use a one-foot take-off. Because foot plant and take-off are critical for a successful jump, the ‘‘jump foot’’ shoe is emphasized by designers. The take-off shoe is made in right and left foot versions. Forward and backward ascent styles (‘‘Fosbury Flop’’) have different spike placements and gradient on the sole for take-off. The jump shoe can
Court sport shoes
be built with a maximal elevation of 10 mm in the forepart to aid lift-off. Six forepart spikes and two heel spikes may be used. Most shoe companies now produce counterpart trailing shoes that are lighter, with fewer spikes and more flexibility to assist the run-up.
COURT SPORT SHOES
Tennis Tennis requires body control with quick side-to-side movement, sprinting, jumping, and stretching. The sport is played on lawn, clay, asphalt, and synthetic and rubberized courts. The selection of an appropriate sole must be made for each surface. On clay courts, soles with too deep a tread pattern may be prohibited because of excessive court maintenance, even though most players would prefer the traction. On artificial or synthetic surfaces, harder soles with high rubber content or dual-density PU are preferred for durability. A tennis shoe should provide good lateral support; light to medium weight; a flat sole with a good heel wedge; a firm heel counter; a well-cushioned insole and midsole; ample toe box; good ventilation; nonslip traction; a pivot point; and reinforcement for toe drag. The upper should provide a sufficiently high quarter pattern to provide good ankle and lateral foot support. Over-the-ankle-line midcut models are available for those players who prefer more ankle support. Manufacturers of tennis shoes recommend more cushioning in the ball of the foot for the serve-andvolley player. For the baseline player, a solid heel counter, strong reinforcement in the heel and midfoot area, and good rear-foot stability are recommended (Fig. 26-10). Basketball Basketball requires backward, forward, and vertical accelerations; quick stops; and side-to-side movements. The playing surface usually is wood but may be synthetic or rubberized material. The shoe should provide good lateral and medial support; light to medium weight; a flat sole; a slight heel wedge; good cushioning; a large, firm heel counter; toe drag reinforcement; ventilation, a pivot point; and good traction. High rubber content in the sole is recommended. Soles with multiple-edge patterns, such as circles, squares, or diamonds offer better traction than herringbone patterns (which are
Figure 26-10 Tennis shoes.
excellent for forward stops but not for good lateral stops). High-cut designs are available for full ankle support. In addition to offering added ankle support, highcut uppers must not restrict ankle flexion. Proprioceptor straps are popular. Some players prefer low-cut uppers for better ankle flexibility, but the incidence of ankle injuries may increase with use of these shoes7 (Fig. 26-11). The emphasis of recent design research in basketball shoes has been the reduction of inversion injuries to the ankle. Shoes with increasing amounts of ankle restriction in the upper significantly reduce ankle joint inversion.8 However, with increasing amounts of ankle restriction, movements not only are restricted in the sagittal plane but also in the frontal plane, leading to reduced agility. Therefore a design compromise must be met between performance and protection of the athlete from injury. Barrett et al.9 studied 622 college basketball players to see whether shoe type and height had an effect on the incidence of ankle sprains. In a prospective, randomized study, the player was given a pair of high-top, high-top with inflatable air chambers, or low-top basketball shoes to wear during all games during the season. There was no significant difference noted among the three groups
Figure 26-11
Basketball shoes.
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Racquet sports These sports require forward, backward, and side-to-side movements. The body must be moved with control in all directions. Wear patterns produced in even a short time show that court shoes used in racquet sports are subjected to heavy abuse.
CHAPTER 26
The shoe in sports
in this study, and there was no significant relationship between shoe type and incidence of ankle sprains.
Volleyball Volleyball requires quick movements, sudden stops, jumping, and side-to-side motion. The indoor sport usually is played on wood surfaces. The shoe should provide lateral support, be lightweight, provide a flat-herringbone or deep-ripple rubber sole, good cushioning, ventilation, firm heel counter, and toe-drag protection.
FIELD SPORT SHOES Field sports combine many types of movement and a variable degree of body contact. Running is basic to all these sports. Spike and stud formations vary from sport to sport but almost all have replaceable or detachable cleats, studs, or spikes affixed into nylon soles. Generally, smaller studs in a denser formation help to prevent ankle and knee injuries secondary to less penetration of the cleat into the playing field. In addition, weight distribution is better in multistudded designs.
Soccer Soccer involves mainly running, kicking, jumping, sliding, stretching, and multidirectional movements. The playing surfaces are natural grass and artificial turf. Soccer is played almost entirely by the feet, with the ball being kicked off the medial, lateral, and dorsal aspects of the foot. Soccer shoe lasts tend to be snug fitting, often using European lasts, which are somewhat narrower than American lasts. Thinner soft leathers are preferred for the upper because players like to feel the ball, but the tongue should be well padded to reduce lace pressure and to cushion the dorsal kicking area of the foot. Some players use the tongue and lace area to produce spin and control the ball (Fig. 26-12). Soles should be flexible at the metatarsophalangeal joints for running and have torsional stability.
Figure 26-12
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Soccer shoes.
Football Running is the primary motion in football, along with quick lateral movements and the production of great forces secondary to blocking and hitting. Studies have shown that injuries may be caused from wearing fewer, longer cleats, which produce excessive pressure beneath the cleats from increased foot fixation.1 More specifically, the excessive resistance to rotation causes knee injuries during the twisting motions of football. The maximal diameter of a cleat tip should be seven sixteenths of an inch, and the maximal overall length is one-half inch. A seven-stud pattern is preferred on natural grass. Nylon soles are preferred because they shed dirt easily and prevent caking of mud between the studs. Multistudded rubber soles are common on natural grass. Shoewear exists for linemen, backs, and kickers. Uppers for linemen must provide support and protection. High-cut or semi-high-cut boot designs are preferred. A sturdy toe box and firm heel counter are recommended. Astroturf linesmen’s shoes are multistudded for grass and have shorter, more numerous studs for traction and stability. The uppers used for backs are similar as for linemen. For added mobility, a low-cut design usually is preferred. Lightweight Astroturf shoes with nylon or cotton mesh uppers reinforced with suede are popular. These shoes usually have a rubber outsole with a waffle design that wraps up at the toe and front quarter for better lateral support. For placekickers, a shoe with a square toe box usually is hand made for the kicking foot and conventional for the nonkicking foot. The shoe usually is custom made for the individual kicker at the professional level. A soccer shoe usually is preferred for kickers who kick from the side of the foot. For punting, either a soccer or a back’s shoe is used. Some players kick in a traditional football back’s shoe (Fig. 26-13). Heidt et al.10 evaluated the shoe-surface interaction in anterior translation and rotation of 15 football shoes produced by three manufacturers. The shoes evaluated in this study included traditional cleated football shoes, court shoes, molded-cleat shoes, and turf shoes. No overall differences among shoes on grass versus Astroturf were reported. There were significant differences noted for cleated and turf shoes. Shoes tested in conditions for which they were not designed were found to have excessive or extreme minimal friction characteristics that could be unsafe. Torg et al.11 found that an increase in ambient temperature could affect shoe-surface interface friction and potentially place the knee and ankle at increased risk of injury. They tested artificial turf football shoes, a natural grass soccer-style shoe, and a basketball-style turf shoe.
Winter sports
Football shoes.
Only the basketball-style shoe could be called ‘‘safe’’ or ‘‘probably safe’’ at all five temperatures studied. Lambston et al.12 reported on a study of football cleat design. The four major football shoe styles in the study included edge (longer irregular cleats placed at the periphery of the sole and smaller pointed cleats placed at the interior), flat (cleats in the forefoot area are the same height, shape, and diameter, similar to a soccer shoe), screw-in (seven screw-in cleats 0.5 inches in height and diameter), and pivot disk (10-cm circular edge on the sole of the forefoot with one 0.5-inch cleat in the center) type shoes. The edge design was found to produce a higher torsional resistance than the other three designs combined. This higher torsional resistance was associated with a significantly higher rate of anterior cruciate ligament injuries.12
Baseball The sport of baseball requires sprinting, throwing, and complex batting movements. The playing surface usually is natural but may be artificial turf with dirt or clay on infield base paths. A traditional baseball shoe has a U-throat, and a conventional lacing system is the ultimate design. Lasts are similar to those used for a football shoe. On natural turf, steel cleats with a design of three
in the front and two in the heel are used extensively. Removable cleats are available in steel, PU, and nylon. For pitchers, a pitching toe often is added for toe-drag reinforcement.
Rugby The movements in rugby are similar to those of a football lineman or back. A drop kick is used, but the ball must touch the ground before it is kicked. The surface is natural grass. The rugby boot is similar in design to a soccer shoe with four front cleats and two heel cleats. A semicut or three-quarter cut style commonly is used for ankle protection. For linemen and some wing quarterbacks, a hard, square toe box is used. Multistudded versions of rugby boot models also are made for firm playing surfaces.
WINTER SPORTS Skating ............................................................. Skating mechanics are similar for all skating events, although footwear and blades are specialized. Ankle movement and support are essential to skating 579
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Figure 26-13
CHAPTER 26
The shoe in sports
performance. However, the subtalar joint must be free to allow positioning of the blade on the ice. The traditional leather boot and the injectionmolded model are the two main types of boots available. A leather boot should have good ankle support and a firm heel counter with elongation of the medial side. Uppers are made from thick-grade leather or split leather, with a leather or textile lining that gives the foot and ankle stability but allows some flexibility. Metal eyelets are used in the lower portion of the throat, and metal hooks above the ankle. Ice hockey skates were the first to use injectionmolded models. A viscous plastic is injected under pressure into molds to form the lower and upper parts of the boot. The two parts are placed together, completing a hinged outer shell. A soft foam liner then is added. The hinged, two-piece design gives the boot some of the lateral flexibility needed in ice skating. Leather boots tend to become more flexible with age.
Figure skating Figure skating requires the athlete to jump, skate, balance, spin, dance, and lift. The performing surface is the ice on artificial or natural rinks. The upper is either full- or top-grain cowhides. Good-quality boots are lined with lightweight, top-grain leather or suede. A firm heel counter, usually elongated on the medial side for added arch support, is important. Soles are PVC or PU molded units with a shank for added support. Screw-in blades often are used so that the position of the blades may be changed. The lasts used in figure skating are semipointed, with a narrow shank and heel to contain the foot and maintain position. The quality of the blades helps to determine the quality of the skate. Blades commonly are made of tubular steel or plastic frame with high-tempered steel that is hollow ground to give two skating edges to the blade. The blades can be nickel- or chrome plated. Figure skating and free-style blades have a front to back curvature called a radius or rocker. The placement of the blades usually is slightly medial to the midline of the sole. For jumps or spins, a toe rake or pick is used. With forward motion, the picks also can help to prevent the blade from sliding sideways. For figures, a pair of skates without a pick and with less sharply ground blades often is preferred. Ice hockey Ice hockey requires skating, quick stops, quick turns, and balance on the ice of artificial and natural rinks. A high-cut model of leather or ballistic nylon with leather reinforcement is available. A good skating boot requires a firm, protective, leather toe box of polyethylene or firm fiber and comfortable ankle padding, with a high cut
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over the Achilles tendon for protection. A molded boot with a hinged upper can provide additional protection and durability. High-grade boots have a leather lining. The goalie wears a specially designed molded or leather boot with a protective casing. The boots have a low-cut design at the ankle, which allows increased flexibility and also accommodates goalie pads. The blades are thick and reinforced, with increased surface area in contact with the ice to block shots at the goal.
Speed skating Speed skating requires balanced skating with a low center of gravity in the lunge position. Skaters often compete with bare feet in skates. The skating surface is ice on artificial or natural ice tracks. The uppers have a deep-cut U-throat with a full lacing pattern to the toes. A three-quarter ankle boot is the preferred design, with a firm heel counter elongated on the medial side. Thin (one-sixteenth inch), straight blades of either tubular steel or plastic frames are used. The blade is long (30 to 45 cm) and is placed distal to the skating boot via a high-profile frame to allow a lean of low angle between the skate and the track. Higher-quality blades are chrome plated.
Alpine skiing ............................................................. Alpine skiing requires ankle and knee flexion, forward lean, and balance on snow-covered surfaces. Ski boots provide a high-cut upper of a hinged or one-piece, injection-molded plastic, outer shell to support the lower leg. The boot should provide rigid support for the foot and ankle and allow forward ankle flexion. Adjustable buckles, dial closure devices, or straps are used for instep support and a comfortable, snug fit. More recently, rearentry and midentry boots have eliminated buckles and overlaps on the vamp, instep, and ankle regions to reduce pressure. Inner liners can contain a foot bed, a variety of wedges, or adjustable canting devices. To relieve pressure, conforming foam or pressure-flow bags can be used (Fig. 26-14). Ski boots are one of the last categories of athletic footwear to accommodate the female athlete. Important design differences include an elevated heel for a shorter female Achilles tendon, easier forward flexion, and a more flared ankle cuff.
Cross-country skiing ............................................................. Cross-country skiing requires fast walking movements, running, jogging, downhill skiing, and balance on snow-covered terrain. Boot and bindings act together as a hinge between the foot and the ski and must be compatible. Boots are made of leather, Gore-Tex, nylon,
Injuries related to athletic footwear
of smooth calf or kid leather with perforations for ventilation. Racing shoes usually are unlined and tend to stretch. Rigid soles are made of reinforced steel, nylon, or PU and can protect the foot from pedal pressure. Depending on the system, shoes are affixed to pedals by cleats, which improve cycling efficiency by locking the foot to the pedal for upward and downward thrust. Most shoes have adjustable cleats, permitting angular and fore and aft adjustments (Fig. 26-15). Clips hold the foot to the pedal, but clipless systems are available.
INJURIES RELATED TO ATHLETIC FOOTWEAR Ski boots.
or poromeric materials that allow air to circulate and transpire. Boots should be waterproof, as seam free as possible, with rigid heel counters. Good forefoot flexion is essential. Rubber soles are preferred for use on snow and ice.
OTHER SPORTS Aerobic dancing Aerobic dancing requires stationary running, skipping, jumping, stretching, dancing, and stair climbing. The dance surface is on carpet or covered surfaces. The shoe requirements are a combination of a lightweight, shockabsorbing running shoe and a modified indoor court shoe. Medial and lateral support is needed, as well as a wrap-up toe and heel protection. The forefoot requires stabilization and good shock absorption. EVA and PU combinations, air systems, and gel are used in shockabsorbing forefoot pads. Flexibility in the forepart is important. Bicycling Bicycling involves use of the gluteus, quadriceps, hamstrings, and calf muscles to generate the power necessary to perform upward and downward thrusts through the forefoot. The foot often is placed into a valgus or varus position on the pedal, causing pressure to develop on the lateral or medial sides of the foot. Cleat and pedal placement can be changed to prevent this canting. A cycle racing shoe has a last similar to that used for a sprinting shoe, with a wide girth, semipointed toe, narrow waist, and narrow heel. A high toe box is required for toe movement. Uppers usually are made
A properly designed and constructed athletic shoe can help to protect athletes from both external and internal forces that may lead to injury.
Toes ............................................................. Ingrown and black toenails (subungual hematoma) are common problems seen in athletes and usually are the result of tight-fitting shoes or shear forces that cause the toes to abut the end of the toe box. An adequate high and wide toe box and proper shoe fit should reduce the incidence of this injury. Corns result from pressure on the toes from the toe box. If the athlete has hammertoes, then the proximal interphalangeal joint is more prominent, and a corn can result in this location. A high toe box and proper shoe fit usually eliminate this problem. The use of various pads, splints, and lambs wool can be helpful.
Forefoot ............................................................. Blisters Blisters are caused by friction of the skin’s rubbing against a shoe, sock, or other material. Applying a piece of moleskin or paper tape can be helpful. A cushioned
Figure 26-15
Cycle racing shoes.
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Figure 26-14
CHAPTER 26
The shoe in sports
liner such as Spenco (Spenco Medical Products, Waco, TX) may help to cut down on shearing and sliding inside the shoe.
Calluses Similar to corns, calluses are hyperkeratoses caused by friction and pressure that may or may not be painful. Calluses may occur over the ball of the foot at sites of pressure on the skin from underlying bone. A cushioned shock liner can help to equalize the weight load. Calluses may be pared, and pads made from adhesive felt or foam rubber may be placed proximal to the callus. A Spenco insole, contoured anatomic foot bed, or other shock-absorbing and friction-reducing materials are used in many athletic shoes to prevent calluses. Following proper lacing techniques will help to improve foot stability and reduce shear forces between the foot and the shoe. Metatarsalgia Metatarsalgia is a nonspecific diagnosis that describes pain in and about the head of the metatarsal, metatarsophalangeal joint, and adjacent soft-tissue structures. Metatarsalgia can result from atrophic fat pad, basic anatomy of the metatarsals, increased pressure on the metatarsal heads, neurologic dysfunction, postsurgical changes, metabolic disorders, and inflammation. A wellcushioned liner and midsole material in addition to a rocker sole, which allows the athlete to roll off the painful forefoot, can be useful. Sesamoiditis The sesamoid bones are prone to injury because of their location under each big toe joint. Cavus feet, equinus of the first metatarsal, or rigid foot can cause excessive pressure to be placed on the sesamoids. A shoe with a good, shock-absorbing, midsole material extending out into the forefoot must be worn to protect the area. A rocker sole can be helpful. Orthotics that incorporate a sesamoid pad placed just proximal to the injured sesamoid to float the painful area is a useful way to treat this problem. Interdigital neuroma The most common location for an interdigital neuroma is in the third webspace. Excessive pressure on the ball of the foot or a shoe that does not fit well in the girth may contribute to this problem. A shoe with excellent shockabsorbing properties that extend out into the forefoot must be worn to protect the area. A rocker sole can be helpful. Orthotics incorporating a metatarsal pad placed just proximal to the involved webspace to help spread
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the metatarsal heads can take pressure off of the inflamed nerve.
Nerve entrapment Cutaneous nerves, including the sural, saphenous, deep peroneal, and superficial peroneal nerves, can lie under pressure areas of an athletic shoe and result in a painful nerve irritation. Their location makes them vulnerable to compression. Nerve compression is a direct result of wearing irritating or tight-fitting shoes. Ski boots and ice skates are the two major types of athletic footwear that produce this problem. To avoid this problem, shoes should be padded, lacing techniques modified, and careful shoe fit followed.
Heel ............................................................. Plantar fasciitis To prevent this common injury, a shoe must have excellent shock-absorbing abilities in the heel. A varus heel pad or wedge also can be indicated to decrease forces on the medial aspect of the heel. Once the problem develops, heel cups, foam pads with a cutout, or orthotics with a well-cushioned heel and a well to float the painful area can be indicated. A shoe with a firm medial heel counter can decrease pronation and stress on the plantar fascia. Bursitis The retrocalcaneal and pre-Achilles bursa can be irritated during sports. This disorder can result from poor shoe fit, an ill-padded heel counter, or excessive heel motion. The athlete should be advised to buy a shoe with well-padded heel counter, an Achilles notch that accommodates the Achilles tendon in plantarflexion, and an adequate heel height of at least 15 mm. Achilles tendon Low heel elevation in an athletic shoe often is a factor in the development of Achilles tendinitis. To prevent irritation of the tendon, a shoe with a well-padded Achilles tendon pad or notch should be worn. Heel lifts can be worn to elevate the foot in the shoe and reduce tension on the tendon. A firm heel counter can reduce the sideto-side motion of the heel and the Achilles tendon, thus reducing irritation of the tendon.
Ankle ............................................................. Sports involving walking, running, or jumping often can result in inversion injuries to the ankle. If an athlete has a tendency to inversion injuries of the ankle, a shoe should be worn that has a firm heel counter, a
References
CONCLUSIONS Each year athletic shoes tend to get better. In the last 10 years, motion control has improved, shock absorption has followed a pendulum and found its middle ground, and the trend is toward lighter materials. Although maximal foot speed may increase slightly in a lighter shoe, protection of the foot must not be compromised. Footwear should be designed to enhance athletic performance and prevent overuse.
REFERENCES 1. Torg JS, Quendenfeld T: Effect of shoe type and cleat length on incidence of severity of knee injuries among high school football players, Res Q 42:203, 1971.
2. Valiant GA: The effect of outsole pattern on basketball shoe traction, In Terauds J, Gowitzke BA, Hole LE, editors: Biomechanics in sports III & IV, Del Mar, CA, 1986, Academic Publishers. 3. Milgrom C, et al: The effect of shoe sole composition on in vivo tibial strains during walking, Foot Ankle Int 22:598, 2001. 4. Clarke TE, et al: The effects of shoe design parameters on rear foot control in running, Med Sci Sports Exerc 15:376, 1983. 5. Alexander RM: How elastic is a running shoe? New Sci 123:45, 1989. 6. Kerr RF, et al: The spring in the arch of the human foot, Nature 325:147, 1987. 7. Garrick JG, Requ RK: Role of external support in the prevention of ankle sprain, Med Sci Sports Exerc 5:200, 1973. 8. Robinson JR, Frederick EC, Cooper LB: Systematic ankle stabilization and the effect on performance, Med Sci Sports Exerc 18:625, 1986. 9. Barrett JR, et al: High versus low-top shoes for the prevention of ankle sprains in basketball players. A prospective randomized study, Am J Sports Med 21:582, 1993. 10. Heidt RS, et al: Differences in friction and torsional resistance in athletic shoe-turf surface interfaces, Am J Sports Med 24:834, 1996. 11. Torg JS, Stilwell G, Rogers K: The effect of ambient temperature on the shoe-surface interface release coefficient, Am J Sports Med 24:79, 1996. 12. Lambston RB, Barnhill BS, Higgins RW: Football cleat design and its effect on anterior cruciate ligament injuries. A three-year prospective study, Am J Sports Med 24:155, 1996.
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moderately flared heel for a runner, and the stability of a high-cut model rather than a low-cut model for field or court sports. Hockey skates and alpine ski boots should provide good ankle support. Taping, various shoe wedges, braces, and orthoses all are used in the treatment and prevention of ankle sprains.
.........................................C H A P T E R 2 7 Orthoses and insert management of common foot and ankle problems John S. Gould and David Ford CHAPTER CONTENTS ...................... Introduction
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Ankle
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Forefoot
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Knee pathology
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Midfoot
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Conclusions
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Hindfoot
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Suggested reading
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INTRODUCTION The proper use of shoe inserts (orthotic devices/orthoses), shoe modifications, and, on occasion, braces, provides an armamentarium of nonoperative solutions to a wide range of foot problems. These approaches may be curative or palliative, permanent or temporizing, and may avoid the need for surgery or be an adjunct to it. It is essential that the pedorthist has the knowledge of materials, their durability and wear characteristics, fabrication skills, fitting capabilities, and imagination to carry out his or her part of the equation. To assist in the details of the prescription, he or she should also know enough biomechanics to understand the effect that the device or modification will have on the foot. If the physician—whether an orthopaedist, a rheumatologist, a physiatrist, or even an endocrinologist managing a diabetic—is personally to prescribe, he or she must know something about these devices or refer to someone who does. We do not feel that the pedorthist should be the prescriber any more than a pharmacist should prescribe drugs. Consequently, the physician should know what effects he or she wishes to achieve with the device and shoe modification and generally how the device should be made. He or she does not need to know about specific materials or fabrication or fitting. The ideal arrangement for patient care is for the pedorthist actually to attend the clinic with the physician so that there is a complete understanding of these issues when the patient is seen and a disposition provided. Many orthopaedic foot and ankle specialists have
this arrangement and have such persons in their own foot and ankle clinics. Sports medicine specialists usually have ready access to pedorthists and always to physical therapists, who can act as an intermediary between the physician and the pedorthist. It is totally outdated for a physician to mix his or her own medications or make his or her own orthoses in the office, although this comment does not exclude the use of some over-the-counter devices that may be available in such circumstances. In this chapter, we present information anatomically, starting with the forefoot and progressing proximally, as the physician may encounter in a patient. Problems in the athlete are highlighted. A variety of diagnoses that present in these areas are covered. It is fully accepted that there are various alternative methods to achieve the same effect. We do not attempt to be comprehensive in suggesting solutions but discuss the options we use that have proved to be effective in our practice.
FOREFOOT Intractable plantar keratosis (IPK) IPKs are calluses under bony prominences on the plantar aspect of the foot. They may be caused by a plantarflexed metatarsal head because of a hammertoe or a fracture, the elevation of an adjacent lesser toe metatarsal head that causes a transfer of pressure, or developmental problems of a similar nature (second metatarsal head callus adjacent to a bunion; a rotated fifth
CHAPTER 27
Orthoses and insert management of common foot and ankle problems
metatarsal head in a bunionette, a prominent sesamoid, and so forth). The solution is relatively simple: material is placed proximal to or around the prominent area (‘‘posting’’) to ‘‘offload’’ the prominent area and softer material is placed under the callus and prominence to cushion it. Using a material such as cork built into the insert material, we make a full-length, total-contact insert (TCI) with posting proximal to the lesion and create a well under the lesion. We then fill this well with a viscoelastic polymer, which adds excellent cushion, does not flow out of the well, and compresses more slowly than most other materials (Figs. 27-1 and 27-2). A similar solution is used for apical calluses (on the tips of hammer, claw, or mallet toes).
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Morton’s neuroma or intermetatarsal neuritis Irritation of the intermetatarsal nerve, which leads to neuritis or intraneural fibrosis (the Morton’s neuroma), is anatomically caused by the distal edge of the intermetatarsal ligament between the adjacent plantar plates of the metatarsophalangeal (MTP) joint. A metatarsal pad made of felt or other less compressible materials can be placed under the adjacent metatarsals proximal to the condylar heads of the adjacent metatarsals, thereby elevating them to decrease the contact of the edge of the plate when the patient is standing and walking. Some doctors place the pad on the patient’s foot with some adhesive or attach it to the sock liner in the shoe. We prefer to incorporate the pad into a total-contact insert, professionally placing the pad in the right place
for the patient (Figs. 27-3 and 27-4). We also may add other features to the insert, such as longitudinal arch support when a symptomatic, flexible flatfoot accompanies the problem.
Figure 27-1 Total-contact insert (TCI) under construction (before adding topping), with posting pad proximal to intractable plantar keratosis (IPK) site.
Figure 27-3 Total-contact insert (TCI) under construction, with posting pad proximal to the 3/4 intermetatarsal space (for intermetatarsal neuritis or Morton’s neuroma).
Figure 27-2 Plantar surface of total-contact insert (TCI), with cork posting around the area of intractable plantar keratosis (IPK). The relief well within the posted area is filled with a viscoelastic polymer.
Forefoot
metatarsal bar was placed in this location of the outer sole, but the rocker sole allows much easier walking than the bar. Before this stage of care, some surgeons may use total-contact casting, various commercially available boots that unweight the sole of the foot, and heelweight-bearing–only postsurgical shoes. All of these measures may, at one stage or another, be adjunctive during the care of these problems. The orthoses and modified shoe may be used after the acute care to prevent later recurrence.
Ulcers under the metatarsal heads Ulcers or deep blisters may occur under the metatarsal heads. This is a particularly common and challenging condition with the insensate foot but can occur in athletes as well. Although it is critical to analyze why the ulcer or blister occurred and to recognize the presence of structural problems, the pedorthic approach is an important adjunct to care. The insert should be full length, with posting around a relief well under the ulcer. Again, we fill this well with the viscoelastic polymer. In addition, a relief well also is created in the insole of the shoe by use of a burring tool. Finally, a mild rocker sole is placed on the outside of the shoe with the apex proximal to the ulcer site (Fig. 27-5). In the past, a
Figure 27-5
Rocker sole on a running shoe.
Figure 27-6 Full-length, spring-steel shank, which may be placed under a total-contact insert (TCI), incorporated within it, or placed in the sole of the shoe.
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Figure 27-4 Plantar surface of total-contact insert (TCI) with metatarsal pad in place proximal to 2/3 and 3/4 interspaces.
Metatarsopharangeal joint synovitis, ‘‘turf-toe,’’ arthritis, hallux rigidus, and rheumatoid arthritis The treatment of an inflammatory condition of these joints should be immobilization while still allowing the patient to ambulate. This can be accomplished by using a stiff-sole shoe or insert. This effect can be obtained by placing a thin, spring-steel shank between the cushioned, total-contact insert and the insole on the shoe, or by incorporating the stiff material within the insert, or adding it to the sole of the shoe between the outer sole and midsole, or using a shoe that is made with a stiff shoe from the factory (Figs. 27-6 and 27-7). It is essential, however, to also use a rocker sole on the shoe (see Fig. 27-5) so that the patient can walk without the foot lifting up within the shoe; this would not only make the walking difficult but also increase the symptomatology. In a patient with hallux rigidus, there are two problems: pain in the joint from impingement, arthritis, and synovitis, and lack of motion. The previous prescription deals with these problems well, but some physicians will use the more rigid insert ‘‘Morton’s extension,’’ which lies from the heel to the end of the great toe but not all the way across the foot (Fig. 27-8). In the rare athlete with rheumatoid arthritis foot, not only is there arthritis of the joints but also there may be dislocations at the MTP joints with hammertoes, plantar prominences, and nodules. Again, the stiff rocker sole is essential, but one must add the proximal posting, relief wells filled with viscoelastic material, and
CHAPTER 27
Orthoses and insert management of common foot and ankle problems
Figure 27-7 Plantar surface of a total-contact insert (TCI) with a steel shank before incorporation.
over the counter and are lighter in weight than the calfskin (although perhaps less durable for scuffing and wear). We seldom prescribe custom shoes (made specifically for the individual patient) rather than these ‘‘prescription shoes,’’ which are more readily available, less costly, and better in appearance. Finally, we use a multi-ply insert for rheumatoid patients to provide increased cushioning. Other joint conditions can affect the forefoot locally. Freiberg’s infraction is treated as an inflammatory arthritis of the MTP joint with a stiff rocker sole and a relief well under the metatarsal head if it is tender. The turftoe is a general term for a hyperextension injury to the plantar plate of the MTP joint of the great toe. The injury can be as simple as a minor tear of the plate, with or without intra-articular synovitis, or as complex as complete avulsion of the plate, with retraction of the sesamoids and with or without subluxation of the joint. Various articular surface injuries can occur, from a chondral abrasion to an osteochondral fracture. Severe injuries should be treated surgically, for example when retraction of the sesamoids is noted or when an injury and symptoms become chronic. The rocker sole is essential, and a stiffening device is added to the insert or sole of the shoe, as noted. For many running athletes, the rocker sole is a routine modification to their shoes, and a stiff insert or sole is compatible with their sporting function. A professional tour golfer can wear an insert but cannot modify his or her shoe. A rocker sole can be tolerated in football and lacrosse, but less so in basketball and tennis.
Sesamoid pathology For sesamoiditis, the stiff-sole approach with a rocker is appropriate, but we also add a relief well with the viscoelastic polymer (Fig. 27-9). When there is an IPK under a prominent sesamoid, the relief well alone is sufficient, with proximal or surrounding posting. For avascular necrosis and fracture care, the stiff rocker sole may be a satisfactory temporizing approach until definitive surgical measures can be taken.
MIDFOOT Figure 27-8 Plantar surface of a total-contact insert (TCI) with a steel-shank Morton’s extension before incorporation.
one additional orthotic plus two other shoe modifications. The first is increased depth of the toe box to accommodate the toe deformities. The second is softer materials for this hypersensitive foot, such as deerskin or an elastic synthetic material (e.g., Spandex). Both the elastic-material shoe and the deerskin are available
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Plantar fibromatosis Thickening of the plantar fascia because of plantar fibromatosis, a benign but aggressive tumor, can cause pain resulting from tenderness of the lesion in its early stages or because of pressure on the underlying tissues, including the plantar nerves. Good total-contact inserts with an appropriately placed relief well filled with the viscoelastic polymer can be adequate treatment. If the lesion is particularly large, the insole also can be burred out;
Midfoot
Figure 27-9 Plantar surface of a total-contact insert (TCI) with a relief well filled with viscoelastic polymer under first metatarsal head and sesamoids.
Figure 27-10 Double rocker sole for midfoot plantar lesions.
and finally, the sole of the shoe can be modified by use of what is called a ‘‘double rocker’’ sole. In this situation, the sole of the shoe becomes concave under the lesion and convex on either side of it (Fig. 27-10).
Figure 27-11 (A) Full-length University of California Biomechanical Laboratories (UCBL) insert with deep heel cup and high sides to control subtalar and transverse tarsal motion (forefoot component of the insert has not been trimmed to final contour). (B) Close-up view of deep heel cup and sides in UCBL insert.
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Midfoot arthritis Tarsometatarsal (TMT), naviculocuneiform, and transverse tarsal arthritis all are treated with a stiff rocker sole shoe and total-contact inserts. The two more proximal levels and, to a slight degree, the TMT, also have some degree of varus/valgus and abduction/adduction and pronation/supination movement. This is controlled by use of an insert, which cups the heel more and is higher distally, medially, and laterally; this is the University of California Biomechanical Laboratories (UCBL) type (Fig. 27-11, A and B).
CHAPTER 27
Orthoses and insert management of common foot and ankle problems
HINDFOOT Plantar fasciitis Plantar fasciitis, an enthesopathy of the origin of the plantar fascia on the medial tubercular process of the calcaneus, usually is a self-limited disease. Stretching exercises and a device to cushion the heel are the fundamental approaches to treatment. Over-the-counter heel cups and various heel cup and longitudinal arch supportive devices have been prescribed (Fig. 27-12). The pedorthic concept is to support the plantar fascia to decrease the strain on this structure and to provide a heel cup to gather the fat pad and decrease the pressure on the sensitive point on the medial aspect of the heel. In chronic cases, we prescribe a custom-made insert, either full length or three-quarter length (with Velcro on the underside to prevent the device from slipping out of place). A shallow cup is created with posting of the longitudinal arch, thus satisfying the pedorthic concept. It also is important to flatten out the outside of the heel component so that the insert will not rock in the shoe. In the athlete, it also is important to use
Figure 27-12
Silicone heel cups.
a ‘‘topping’’ on the insert that is both nonskid and washable.
Tarsal tunnel syndrome with or without chronic plantar fasciitis Patients with plantar fasciitis may become chronic with attenuation of the fascia and, at times, neuritic symptoms. In these patients, the insert with its posted arch increases their pain. In these patients, we use a fulllength, total-contact insert, post the arch, and add a ‘‘nerve- relief channel,’’ filled with the viscoelastic material. The channel starts at the medial wall of the insert under the posterior tibial nerve and its lateral plantar nerve branch over the soft spot on the medial aspect of the heel pad where the nerve enters the foot. It continues onto the plantar aspect of the heel, following the nerve course (Fig. 27-13, A and B). In cases of central heel-pad syndrome, which includes the first branch of the lateral plantar nerve, the channel is widened posteriorly and on the plantar pad to include this nerve area. This also is done when the patient complains of pain around the peripheral margin of the heel or on the lateral border, all symptoms of involvement of this nerve branch. Flexible flatfoot with or without an accessory navicular Flexible flatfoot is treated with a full-length or threequarter–length total-contact insert, usually of the UCBL variety. The three-quarter length does not add material under the forefoot and therefore is easier to wear in a variety of shoes, including loafers (Fig. 27-14, A and B). When the insertion of the posterior tibial tendon is tender, particularly with a prominent accessory navicular, a relief channel with the viscoelastic filler is used. In early adolescence, when this condition is most prevalent and the foot is still growing, the inserts may need adjustment at frequent intervals, and many pedorthists will adjust their fees to make this approach
Figure 27-13 (A) Total-contact insert (TCI) with posteromedial nerve-relief channel filled with viscoelastic polymer for tarsal tunnel syndrome. (B) Plantar aspect of TCI with nerve-relief channel filled with viscoelastic polymer carried onto plantar surface for tarsal tunnel syndrome (channel is extended more posteriorly and more centrally on the heel for central heel pad syndrome—note the proximal and distal cork posting on this insert).
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Hindfoot
The insert is a well-stabilized UCBL (the outer surface is flattened to prevent rocking) with a relief channel under the high contact area (Fig. 27-16).
Figure 27-14 (A) Full-length, total-contact insert (TCI). (B) Three-fourths length TCI.
more acceptable to parents. If the patient has a juvenile bunion associated, the shoewear also must be forgiving, and shoes made of flexible material and with available wider widths are needed. Because this flatfoot is flexible, it is essential that the fitting of the insert be done in a nonweight-bearing mode to properly position the foot in a neutral position of the talonavicular and naviculocuneiform joints (no sag in the talometatarsal angle or abduction or uncovering of the talus at the talonavicular joint on the anterior-posterior view) (Fig. 27-15).
Cavus or cavovarus foot The patient with the cavus foot has numerous symptoms at various times. First, there is tripod weight bearing with high contact and often with callusing under the first and fifth metatarsal heads and the heel. The high arch causes dorsal pressure on the foot, possibly irritating the superficial peroneal nerve. Dorsal arch pain also may occur, with or without plantar fasciitis. The lack of flexibility also contributes to higher impact on the heel. Finally, the varus position of the heel places lateral stress on the ankle ligaments. A total-contact insert, which fills the arch, helps to distribute the weight bearing better, and posting behind the first and fifth metatarsal heads, with relief under them and the heel, is added. A wedge of solid ankle cushion heel (SACH) material, which has more flexibility than the usual heel leather, is added to the shoe heel, along with a lateral heel flare to decrease the tendency for the heel to roll, an action that puts stress on the ankle (Fig. 27-17). A crepe sole is more flexible than leather and also is desirable, along with a rocker design, to compensate for the lack of flexibility. The middle-aged patient’s now-symptomatic cavus foot can be relieved with this combination of insert and shoe modification. Insertional tendinitis of the tendo achilles and Sever’s disease Although the insertional tendinitis of the tendo Achilles occurs in middle age and Sever’s disease occurs in adolescence, both are treated similarly. A lift of 3=8 to 5=8 inch is added inside or outside the shoe to decrease
Fixed flatfoot deformity in the adolescent Fixed flatfoot often is a condition that requires surgery for various tarsal coalitions. When an insert is indicated, it must be accommodative and must cushion the foot properly, particularly under the prominent talar head.
Figure 27-16 Before (L) and after (R) views of the heel portion of an insert in the fabrication process. The plantar aspect of the insert’s heel component is squared off with grinding and sanding to stabilize the insert in the shoe and has the desired effect of properly supporting the foot.
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Figure 27-15 Plaster mold of the plantar aspect of the foot made from an impression taken of a patient’s foot with a foam box or casting. The total-contact insert (TCI) is vacuum formed from the mold.
CHAPTER 27
Orthoses and insert management of common foot and ankle problems
Figure 27-17 A lateral heel flare has been added to the heel of this running shoe to prevent a varus roll and increased stress on the lateral ankle. The flare can be increased when heel varus is more pronounced.
stress on the tendon, and the heel counter is padded with a cushioning material, or a backless shoe is used. Alternatively, there are over-the-counter devices in which a silicone pad is attached to a little sock, which can be worn with the heel lift. In addition, an overthe-counter device also has been fabricated that pads around the sensitive heel area and includes a lift under the heel (Fig. 27-18).
Posterior tibial tendon dysfunction Although posterior tibial tendon dysfunction is common in middle age, tenosynovitis, stage one and early stage two of the posterior tibial tendon dysfunction syndrome occur in the younger patient. Support of the longitudinal arch is essential, along with control of the hindfoot to prevent valgus. We tend to use the UCBL insert with posting of the longitudinal arch to control this foot. The standard total-contact insert with the posted arch can be sufficient, along with various similar over-the-counter devices. In addition, it is essential to use a firm medial counter. This can be provided over the counter in many brand-name running shoes. It also can be added by various means, ranging from simple
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Figure 27-18 An over-the-counter anklet to protect the tendo Achilles for insertional tendinitis. Padding is provided on either side of the tendon to help cushion the structure. A heel cup/ extension or lift also is shown and is used with the anklet. Some brands also incorporate the heel lift into the lining of the anklet.
fiberglassing of the counter (which does not seem to hold up) to adding material to the outside, such as a synthetic foam material (to avoid adding significant weight to the shoe) covered by leather (Fig. 27-19).
Figure 27-19 A medial stabilizer is added to the medial counter of the shoe for posterior tibial tendinitis or posterior tibial tendon dysfunction.
Suggested reading
ANKLE Subtalar arthritis, sinus tarsi syndrome For subtalar arthritis, the UCBL insert can support and control the motion in the subtalar joint and is the device of choice. Sinus tarsi syndrome, apparently synovitis of the subtalar joint secondary to intra-articular ligament injury, is treated primarily by splinting with an orthotic device and prescribing medications, with arthroscopic debridement as a subsequent alternative. Peroneal subluxation, peroneal tenosynovitis, peroneal tears Orthotic treatment of peroneal subluxation, peroneal tenosynovitis, and peroneal tears constitutes, in our opinion, a minor adjunct to what often are surgical conditions. In synovitis, in particular, a lateral heel wedge with an insert to create a valgus heel position to help splint these tendons may be used. Ankle ligament sprains Taping, bandaging, and over-the-counter ankle supports constitute part of the treatment of ankle ligament sprains. We may use elastic sheath supports, which provide medial/lateral support and compression, or laceup devices with Velcro-strap support in the early stages of management, along with physical therapy. Many athletes who wear cleated shoes have their ankles taped for practice and games. Few tolerate braces for prophylaxis of sprains.
KNEE PATHOLOGY Some sports medicine and knee specialists will prescribe orthotic devices with medial or lateral heel wedges to load or unload the medial or lateral knee compartments, and after sprains, strains, and suspected menisci injuries. Such wedges also may be helpful in early unicompartmental arthritis.
CONCLUSIONS Orthotic devices and modification of standard and prescription shoes are an essential part of the armamentarium of the orthopaedic surgeon specializing in foot and ankle and sports medicine. Some over-the-counter devices are appropriate, and, in other instances, custom devices should be fabricated. Many of these approaches may return an athlete to participation rapidly. When surgery is indicated, the devices may also be a valuable adjunct to care.
SUGGESTED READING Baxter DE, editor: The foot and ankle in sport, St Louis, 1995, Mosby. Janisse DJ, editor: Introduction to pedorthics, Columbia, MD, 1998, Pedorthic Footwear Association. Pedorthic Footwear Association desk reference and directory, 1994/95 ed, Columbia, MD, 1994, Pedorthic Footwear Association.
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When a sufficient course of a good, nonoperative regimen is not successful, surgery may be indicated.
.........................................C H A P T E R 2 8 Principles of rehabilitation for the foot and ankle Erin Richard Barill and David A. Porter CHAPTER CONTENTS ...................... Introduction
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Cryotherapy/rest, ice, compression, and elevation (RICE)
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Range of motion/mobilization
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Protected weight bearing
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Gait evaluation
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Strengthening
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Proprioception
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Cardiovascular activities
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INTRODUCTION The foot and ankle often are injured during sporting events, recreational activities, and occupational accidents. Injuries to the foot and ankle may be acute or chronic in nature and often cause considerable disability in athletes. Garrick and Requa1 reported that foot and ankle injuries represented more than 25% of the 1600 athletic injuries in their series.2,3 It has been suggested that the sprained ankle is the single most common injury in sports.2,4-7 The foot and ankle serve as the junction of the body to the weight-bearing surface. This elegant collection of tissues, each with a variety of specialized functions, allows efficient, upright stance and locomotion.8 Athletic populations have unique and strenuous demands. Even with minor injuries, improper or incomplete rehabilitation can lead to significant impairment. A detailed, focused approach to rehabilitation of the foot and ankle is crucial to the athlete. Fortunately, most competitive athletes have access to daily evaluation and monitoring of progress, as well as skilled assistance to help them comply with rehabilitation protocols. Recent technologic and procedural advances contribute greatly to the treatment of the competitive athlete. Principles of
Functional progression
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Phases of rehabilitation
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Rehabilitation of Achilles tendon repair
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Rehabilitation after lateral ankle reconstruction
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Rehabilitation of ankle fractures
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Conclusion
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References
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Further reading
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rehabilitation must continue to advance and keep up to date with technologic and procedural advances. A proper and advanced approach to rehabilitation can provide an environment conducive to a complete, full, and functional recovery.
CRYOTHERAPY/REST, ICE, COMPRESSION, AND ELEVATION (RICE) Initial treatment of acute foot and ankle injuries and postoperative ankles still follows the RICE principle. There are several cold agents to choose from, including the cold pack, ice bags, cold whirlpool, ice immersion, and the Aircast Cryocuff. The primary objective of ice is to reduce swelling and help manage pain. It has been found that pain is inhibited by cold through a decrease in nerve conduction velocity. As the temperature decreases, there is a corresponding decrease in sensory and motor nerve velocity, eventually causing synaptic transmission to be blocked.9 In our experience, we have found the ankle and foot Cryocuffs to be effective because they combine compression and cold. In addition, elevation can help to reduce hydrostatic pressure and diminish edema. Physiologically, the application of
CHAPTER 28
Principles of rehabilitation for the foot and ankle
cold agents also results in arteriolar vasoconstriction, a decrease in local metabolism, and an elevation in pain threshold. The application of cold is most effective immediately after injury or within the first 72 hours. Hocutt et al.10 found that patients with grade III ankle sprains that were treated with ice in the first day returned to functional activities such as running and jumping after 6 days, whereas those treated on the second day went 11 days before they could run or jump. In contrast, those who received heat in the first day had a recovery time of 14.8 days. A contraindication to cryotherapy is individuals with hypersensitivity to cold. Cold should be avoided in patients with Raynaud’s syndrome or peripheral vascular disease (see Chapter 10). Cold therapy also must be monitored closely in postoperative patients who have wet dressings because the combination of wet dressings with cold application can decrease the skin temperature to a dangerous level.
RANGE OF MOTION/MOBILIZATION There always has been an interesting rehabilitation dilemma between the need for early range of motion and the need to immobilize tissues to decrease swelling, protect injuries, and protect against pathologic motion. This section discusses the advantages of early motion. Galileo first recognized the relationship between applied load and bone morphology. In 1892, Julius Wolff, a German anatomist, was the first to link these two vital concepts in his landmark thesis, ‘‘The Law of Bone Transformation.’’ Wolff explained that every change in the function of a bone is followed by certain definite changes in internal architecture and external confirmation in accordance with mathematical laws. Stated simply, ‘‘form follows function.’’ Application of early motion on ligament healing demonstrates that the ligament hypertrophies to compensate for decreased tensile strength of the individual fibers. Obviously the amount of tension and stress must not overcome the ultimate load to failure of the tissue and must not lead to fatigue or plastic deformation. Wolff’s law also may apply to these soft tissues, and physiologic stress may allow more functional and stronger healing of soft tissues. Experimental studies of ligaments after injury indicate that exercise and joint motion stimulate healing and influence the strength of ligaments after injury.11-16 Some of the early research on restoration of early range of motion was performed in the hand and the knee. These historical papers revealed insight on how early range of motion decreases complications and
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actually enhances the healing process. Early mobilization may result in an earlier return to work and daily activity, less muscle atrophy, and better mobility compared with immobilization by casting.14,17,18 The value and benefit of early motion was investigated in the area of rehabilitation after flexor tendon repairs of the hand. The obvious need for full motion in the hand prompted investigation into safe rehabilitation practices, which would eliminate postoperative adhesions and stiffness but allow reliable healing of the tendon. Gelberman et al.19,20 noted an improved healing response, improved strength, and a more normal pattern of vascularity to the healing tendon with protective early mobilization. Several other studies also noted that early range of motion decreased adhesions around the repaired tendon and had a positive influence to the healing tissue.21,22 Early motion after flexor tendon repair has become standard today. Over the past 2 decades, there have been significant studies in the area of rehabilitation after knee injury and surgery. The focus of knee rehabilitation has centered on obtaining full symmetrical range of motion following a knee injury or surgery. Obtaining full knee extension was one of the most important criteria in allowing the anterior cruciate ligament to heal anatomically and yet still avoid a knee flexion contracture. Close observation of patients who were doing well demonstrated that early range of motion was not detrimental to the ligament (and in fact could be advantageous to proper ligament healing/strengthening) while allowing an earlier and safe return to function.23 Early motion and weight bearing led to a significant decrease in muscle atrophy and decreased complications from arthrofibrosis with an earlier return to function. Robert Salter and associates24 investigated the effect of joint motion on cartilage nutrition. Early continuous passive motion in synovial joints allows and promotes cartilage nutrition and health. Salter et al.24 demonstrated that small cartilage defects actually could heal with continuous motion, further supporting the benefit of motion on articular cartilage nutrition and healing. These advances in hand and knee rehabilitation gave us reason to approach the foot and ankle with a similar approach. Thus early mobilization of the foot and ankle following injury is our currently favored treatment method when applicable. This method specifically avoids or reduces immobilization. We have followed the principle that unnecessarily protracted immobilization can prolong the recovery period. Early mobilization can expedite the return to work and resumption of athletic activity while potentially decreasing the risk of complications. Eiff et al.17 used a prospective randomized study to determine which treatment for first-time ankle sprains, early mobilization or immobilization, is more effective. They reported that, in first-time lateral ankle sprains,
Protected weight bearing
although both immobilization and early mobilization prevent late residual symptoms and ankle instability, early mobilization allows earlier return to work and may be more comfortable for patients. Active and passive range of motion is useful to regain motion in cardinal and diagonal planes. Passive range of motion allows the muscles to relax while working the mobility of the joint. Active range of motion requires independent muscle action and incorporates muscle re-education. It is important to work range of motion in the direction opposite of the mechanism of injury (i.e., we allow dorsiflexion and eversion and avoid plantarflexion and inversion initially after a grade II or III lateral ankle sprain). Once the injury has healed, range of motion should include all directions. In addition to active and passive range of motion, joint mobilization should be incorporated in the rehabilitation program. Accessory movements, termed joint play, are not volitional but accompany voluntary movements or occur passively in response to the ground or other forces. The amount of joint play is a function of ligament and soft-tissue compliance as well as bony configuration.25 Mobilization techniques involve oscillation, distraction, and gliding movements of the joints in the planes of accessory motions. The range of mobilization is always advanced in a graded manner but always stays within the physiologic limits of the joint.25 There is much discussion with regard to immediate, short-term protection of ankle injuries. Some of the more common methods consist of elastic wrapping, taping/ strapping, semirigid pneumatic ankle brace, nonrigid functional ankle brace, and a removable walking boot. A device we like is the Aircast walking boot with built-in Aircast Cryocuff (Fig. 28-1). The device allows
Early weight bearing has been shown to increase the stability of the lateral ankle ligaments after injury while decreasing the amount of muscle atrophy. Protected weight bearing provides a safe and earlier return to activity when appropriate by decreasing joint stiffness, muscular strength deficits, and proprioception dysfunction (Fig. 28-2). We favor a postoperative protocol that allows for early weight bearing whenever possible. We recognize there are times when this is not possible such as in hindfoot fusions. However, in the sports population, early weight bearing can have such a positive impact that we try to tailor our surgical and nonoperative approach to allow early protected weight bearing. An intriguing area of research that is revealing to us is the investigation of weightlessness. Costill et al.26 examined the effect of a 17-day space flight (essentially, total weightlessness) on muscle. They reported that there was an 11% decrease in peak muscle power, a decrease in muscle fiber diameter, and a 21% decrease in force when the muscle was contracted at peak power velocity.
Figure 28-1
Figure 28-2
PROTECTED WEIGHT BEARING
Patient wearing Aircast walking boot.
597
...........
Aircast Cryocuff and walking boot.
patients to weight bear immediately, work on range of motion by removing the boot, and use a continuous cold/compression device. Once the ankle has healed, a more functional brace is used for return to activity (2-4 weeks after injury). We particularly stress the use of the boot at night for the first 3 to 4 weeks to keep the foot and ankle complex in a 90-degree dorsiflexed position during sleep, when the relaxation of muscular control and the forces on the heel passively place the complex in a plantarflexed and inverted position. The rigid boot counteracts this position.
CHAPTER 28
Principles of rehabilitation for the foot and ankle
More specifically, Costill et al.26 examined single muscle fiber changes after weightlessness. The single fiber diameter decreases were 20% after 17 days suspended leg weightlessness (for example crutch-assisted nonweight bearing) and demonstrated similar profound muscular atrophy. Research suggests that early loading of damaged soft tissue can enhance collagen fiber realignment and healing.13,14,16,27,28 Using a removable Aircast walking boot allows the patient to progress to weight bear immediately after injury. Being in a walking boot instead of an ankle cast allows the patient to take the boot off to begin rehabilitation activities. The walking boot provides more support than elastic wrapping, taping, and other semirigid bracing systems, and it also allows the patient the ability to apply cold compression simultaneously.
GAIT EVALUATION The evaluation of a patient’s gait immediately after injury and before return to activity can provide a clinician with valuable information on how abnormalities in ambulation contribute to the rehabilitation and prevention of injuries. Often abnormal gait mechanics can predispose the other joints of the lower extremity and back to overload and pain. Restoring normal gait after acute injuries can help to prevent these abnormal mechanics and significantly reduce the amount of time required for return to normal function. It is important that a clinician evaluates the entire lower extremity and its function during gait. Normal gait is composed of two phases, a stance phase (60%) and a swing phase (40%). The stance phase is composed of five categories, including initial contact (heel strike), loading response (foot flat), midstance (single leg support), terminal stance (heel off), and pre-swing (toe-off). The swing phase consists of initial swing (acceleration), midswing, and terminal swing (deceleration).29-31 In acute injuries, a clinician will notice gait abnormalities because of pain, decreased range of motion, strength deficits, and lack of proprioception. The majority of the time, a patient will present antalgic with a decreased stance phase. If a patient is unable to walk without antalgia, a clinician should educate the patient on normal gait mechanics using assistive devices; for example, crutches. A patient may discontinue assistive devices when he or she can walk normally. It is extremely important that as clinicians we correct gait immediately to prevent abnormal gait habits from becoming permanent. It is likely that some failure to return to full strength return after a lower-extremity injury is related
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598
to adaptive gait changes that become permanent in unloading the injured extremity. In chronic injuries or before return to activity, a clinician should take a closer look at lower-extremity biomechanics and gait abnormalities to facilitate return to function while preventing future problems. Observation of gait should include lateral, anterior, and posterior view. It is important to observe and evaluate the foot, ankle, knee, and hip/pelvis position and biomechanics during the gait cycle. Treatment of gait deviations includes flexibility, strengthening, and proprioception. An orthotic can be an excellent adjunct to rehabilitation if the gait deviation is a result of abnormal biomechanics and structural problems within the foot.
STRENGTHENING Muscle strengthening should be initiated once the patient has recovered 95% to 100% of the range of motion of that joint. Initiating strengthening too early can cause an increase in joint stiffness, therefore decreasing the function of the joint. Working isometrically, isotonically, or isokinetically can achieve strengthening. Isotonic strengthening, which is most commonly performed, uses concentric and eccentric contractions. Concentric contraction causes muscle shortening, whereas in an eccentric contraction the muscle lengthens while maintaining a load. Both phases are extremely important and should be included in a comprehensive rehabilitation program. There are several methods of strengthening, including weights, Thera-Band, and water resistance. TheraBand is a useful tool to provide resistance in all directions of the foot and ankle. It has different levels of resistance to allow the athlete to progress. Once the athlete can complete 3 sets of 15 repetitions through a full range of movement, the next level of resistance should be started. This same concept can be used with ankle weights.
PROPRIOCEPTION Many rehabilitation programs often fail to pay attention to proprioception deficits. Proprioception is the ability of the body to vary the forces of muscles in response to outside forces. Muscles, tendons, and joint receptors provide this information, which affects posture, muscle tone, kinesthetic awareness, and coordination.29,30 When an individual is injured, the proprioceptive input to that joint is altered and diminished. Diminished proprioception can lead to a recurrence of injury because of the joint’s decreased ability to respond to outside forces.
Functional progression
Table 28-1 Increase exercise capacity program (with boot/postoperative shoe/brace on) Exercise 10 minutes on a stationary bike 3 days a week. Exercise 20 minutes on a stationary bike 4 days a week. Exercise 30 minutes on a stationary bike 4 days a week. Once you are able to ride the bike 30 minutes a day for
Proprioception can be improved with a number of treatment techniques. Early weight bearing can help to decrease the amount of proprioception loss. A patient can practice standing with equal weight on both feet, progressing to single leg stance. A biomechanical ankle proprioception system (BAPS) board or kinesthetic awareness trainer (KAT) can be used as a patient advances through rehabilitation (Fig. 28-3).
CARDIOVASCULAR ACTIVITIES During the rehabilitation program it is extremely important to keep the patient active. If the patient becomes sedentary, the cellular metabolism levels will decrease and the individual will lack energy, and may experience both diminished desire and blunted motivation because of a form of depression seen after injury in athletes. This consequently can then present a challenge for recovery and rehabilitation. Early in the rehabilitation, we feel that it is vital to start a sensible regimen of lowresistance exercise bike or pool therapy training 3 to 4 days a week for 10 to 15 minutes with a progression by 5 to 10 minutes of training per session per week. If the bike is used, then a walking boot or protective brace is used. Pool therapy is not initiated until the sutures are removed and the wound is fully healed. By initiating early activity during the rehabilitation program, the cellular metabolism will be maintained. The early exercise also provides psychological benefits for the athlete. Physically it allows an active blood flow to the involved extremity, and psychologically it helps to keep the patient motivated and counteracts the potential for depression. Our experience with and observation of clinical healing and postoperative wound healing have proven that it
is important to progress the patient’s activity gradually. Increasing the time increments of 10 minutes a week on a bike will allow the patient to be working approximately 30 minutes per session in a 3-week span (Table 28-1). Typically, low-impact, weight-bearing exercise will be introduced when the athlete is able to walk normally in a protective device and regular shoe. The rehabilitation program will begin replacing one day of bike with a StairMaster/elliptical machine (Fig. 28-4, A and B). We allow an additional day of StairMaster or elliptical each successive week until the athlete has been converted to StairMaster or elliptical 4 to 6 days per week. The athlete will continue to increase low-impact, weight-bearing exercise as tolerated. We have found that when an athlete can work out on the StairMaster or elliptical machine 4 to 5 days a week for 30-plus minutes, it is safe to initiate running. Running should gradually replace StairMaster/elliptical each week. It is important to give the athlete a set of running guidelines that allows for a gradual progression of activity (Table 28-2).
FUNCTIONAL PROGRESSION A functional progression is a series of sport-specific skills that increase in the level of difficulty that an athlete must complete before he or she can safely return to competition. Yamamoto and Fragi described a functional progression in the rehabilitation of injured West Point cadets.32,33 The emphasis in this program was placed on restoring agility through dynamic exercise after knee injury. Kegerreis et al.34 added specific movement patterns and skills to the program and introduced the importance of addressing the psychological needs of 599
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Figure 28-3 Biomechanical ankle proprioception system (BAPS) board for balance and range of motion.
4 days a week, then you may start replacing one of your days of biking per week with 1 day of StairMaster or elliptical trainer. You will do the StairMaster or elliptical for the same amount of time you normally would ride the bike.
CHAPTER 28
Principles of rehabilitation for the foot and ankle
Figure 28-4 (A) Patient performing StairMaster with Aircast walking boot. (B) Patient performing StairMaster with ankle stabilizing orthosis (ASO) brace. Table 28-2
Running progression
Day Week no.
1
2
3
1
10
0
10
2
0
16
3
25
4
30
4
5
6
7
Total minutes
0
12
0
14
36
0
18
0
20
0
54
20
0
25
25
0
30
125
0
30
35
0
35
40
170
Previously running 30-45 minutes per day. Subtract times from time spent on low-impact aerobic training.
the injured athlete. They also addressed the scientific principles that play an important role in the functional progression and the need to break down sport-specific functions to be addressed in the order of difficulty. The functional progression is vital to a complete sportspecific rehabilitation program. It serves as the key element in advancing the athlete from clinical rehabilitation to athletics. Each sport has certain demands and skills that stress the foot and ankle differently. It is extremely important that the athlete advance one step at a time without pain or apprehension. Once the athlete has completed the list of activities in order without pain or apprehension, he or she may return to full sport activity. There are several physical and psychological benefits that the functional progression will address. The
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600
functional progression promotes healing through the application of Davis’ law and Wolfe’s law, which were discussed earlier. It is important that the healing tissue be stressed in the way required of it before injury so that the tissue will be ready to fully accept preinjury activity requirements. As described in Davis’ law and Wolfe’s law, injured tissue and bone stressed in this controlled manner will lead to further tissue and bone healing and strength. In addition, the functional progression breaks up the monotony of traditional rehabilitation and allows the athlete to begin performing activities related to function. Psychologically it allows the athlete to increase self-confidence and mentally prepares him or her to return to sport. As the athlete completes each step, confidence will increase and apprehension will
Rehabilitation of Achilles tendon repair
Table 28-3
Functional progression—court sports
Begin with step one. If you can do this exercise without pain or limping, you may proceed to the next step. It is very important that you perform each exercise correctly, without apprehension. When you have successfully completed each step of the functional progression, you may then attempt to return to your sport. You should wear the Aircast, Swedo, knee brace, or tape as instructed. Heel raises injured leg—10 times Walk at fast pace—full court
Phase I Phase one emphasizes pain modulation and inflammatory control of the soft tissues. Controlling pain and inflammation will allow patients to be better able to perform their rehabilitation exercises. Restoration of normal range of motion and joint accessory motions, including glide, roll, and spin, are stressed in this phase. Early return of pain-free range of motion will enhance the rehabilitative process and allow the patient to begin isolated and functional rehabilitation exercises in phase II with greater effectiveness. Once a patient has minimal pain and has normal to near normal range of motion, he or she may be advanced to phase II.
Jumping on both legs—10 times Jumping on the injured leg—10 times Jog straight—full court Jog straight and curves—2 laps Spring: 12, 34, full speed—baseline to court Run figure eights: 12, 34, full speed-baseline to
1 4
court
Triangle drills: sprint baseline to 12 court, backward run to 12 court, defensive slides along baseline, both directions Cariocas (cross-over drill) 12, 34, full speed—12 court Cutting 12, 34, full speed—full court
decrease, allowing the athlete to enter the competitive environment at the level of function needed for playing standards (Table 28-3).
Phase II Once inflammation is decreased, pain has subsided, and range of motion is near normal, phase II may begin. Foot and ankle flexibility with functional strengthening are initiated and are the focus of this phase. In addition, cardiovascular conditioning and proprioceptive training also are started at this time. The goals of this particular phase are to improve flexibility, restore strength, and begin light, sport-specific functional training. A patient may be progressed to phase III when he or she is ready for a gradual return to activity and participation in sports. Phase III Emphasis in phase III is on functional return to activities of daily living (ADLs) and previous activity/sport participation. Advanced activity-specific exercise should be implemented with special attention to mechanics of the activity. Proper mechanics, as well as maintenance of flexibility and strength, can prevent further chance of reinjury. To ensure safe return to sport, athletes should perform a functional progression. External supports such as braces, straps, taping, and orthotics may be used at this time to allow the patient to participate in his or her activity pain free.
PHASES OF REHABILITATION REHABILITATION OF ACHILLES TENDON REPAIR The rehabilitation after an Achilles repair is an example of progression toward a more functional recovery. Recently, rehabilitation after an Achilles repair has progressed from long-leg casting to short-leg casting to the use of intermittent immobilization and early weight bearing. Mandelbaum et al.35 have established an accelerated rehabilitation protocol for the Achilles repair. Their protocol involves early range of motion at 72 hours and early weight bearing at 2 weeks postrepair. This functional approach allows the competitive athlete 601
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The cornerstone to appropriate rehabilitation is an accurate diagnosis, so that an appropriate rehabilitation program can be established efficiently and safely. For any injury or condition, the rehabilitation can be divided into three general phases. Each phase has specific goals, and, although there is a time frame assigned to each phase, advancement from one phase to another should be based on the patient’s achieving the prescribed goals rather than on time. A clinician must be willing to adapt and modify the exercise program for each patient. There are a variety of rehabilitative techniques to choose from; each can have benefit to the patient. As a clinician, it is important to stay up to date with current rehabilitative trends.
CHAPTER 28
Principles of rehabilitation for the foot and ankle
to return to sports more quickly without a reported increase in complications. At Methodist Sports Medicine, more than 75 acute Achilles repairs have been performed over the past 8 years using an ankle-block anesthetic, no casting, intermittent immobilization with a removable boot, and cryotherapy. Patients have been full weight bearing by 2 weeks, and range of motion is started at the first postoperative visit, along with a bike program and sitting toe raises. We use the concept that early-protected range of motion and weight bearing encourage strong tendon healing and protect against disuse atrophy. The re-rupture rate has been consistent with that of less accelerated protocols (<2%). This is an example of our rehabilitation program. Immediately postoperatively the patient is placed in an Aircast walking boot with a built-in Cryocuff. The walking boot also has one 9 16 -inch felt heel lifts placed inside to put the foot/ankle in a slight equines position for healing. (We will use two heel lifts if the repair is 3-8 weeks after the tear.) The patient is instructed to be nonweight bearing for the first 5 to 7 days and is appropriately trained in axillary crutch use for walking and negotiating stairs. This decreases the risk of early postoperative swelling and allows appropriate initial wound healing. The immediate postoperative protocol consists of rest, elevation, and continuous daytime Cryocuff use. The patient also is instructed to wiggle toes and perform leg lifts every 3 to 4 hours in the first postoperative week. Dressing changes and rehabilitation will begin 1-week postoperatively. Physical therapy will consist of a home exercise program, gradual progression of weight bearing, and a light bike program to maintain cellular metabolism. Biking is performed with the ankle immobilized in the boot. The home exercise program includes toe curls (Fig. 28-5 A), active plantarflexion, resistiveband plantarflexion (Fig. 28-5, B), and sitting calf raises (Fig. 28-5 C). We use the concept of early-protected motion and resistance training, which encourages stronger tendon healing and protects against disuse atrophy. Exercises are performed at a higher frequency with a low load (see phase I exercise prescription) to continuously stimulate the tendon to heal. It is extremely important to avoid ankle dorsiflexion activity or a heel cord stretch to protect the tendon from overstretching. Partial weight bearing is started at 1 week with a gradual progression to full weight bearing at 2 to 3 weeks postoperatively. The first week of rehabilitation allows partial weight bearing in the walking boot with axillary crutches and the amount of weight bearing is increased as tolerated by pain and swelling. After the first week, the patient may begin using one crutch under the opposite arm and then progress to full weight bearing when the athlete is able to walk normally.
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Figure 28-5 (A) Towel toe curls. (B) Resisted plantarflexion using Thera tubing. (C) Single-leg balance for proprioception.
Rehabilitation of Achilles tendon repair
A bike program is initiated in the first week using the walking boot. The program consists of 10 minutes three times the first week and increases by 10 minutes per week and to 4 days over the first month. We progress this slowly to give the incision/wound time to heal without increasing the moisture or swelling to the ankle. Once clinical wound healing has occurred, a patient can be more aggressive with cardiovascular activity. The second phase of rehabilitation begins approximately 6 weeks after repair. At this time, an increase in weight-bearing exercise is allowed, and proprioception retraining with an emphasis on normal gait is initiated. Athletes at this time are instructed in a program to wean out of the boot into an athletic shoe with one 9 16 -inch felt heel lift. Our goal is to wean the patient out of the boot over 2 weeks with normal pain-free gait (Table 28-4). Exercises in the second phase consist of balance, standing calf raises, and elliptical/StairMaster progression. Single-leg balance (Fig. 28-6) is first initiated barefoot on a hard surface with a goal of approximately 60 seconds. Once that is achieved, balance is progressed to a soft surface with other possible variations (i.e., ball toss). Patients will begin bilateral calf raises (Fig. 28-7) with a progression to single calf raises. Thera-Band exercise is performed in all directions to incorporate the entire ankle. However, dorsiflexion past neutral is not allowed. Once completely out of the boot, 1 day of elliptical/StairMaster may be substituted for the bike each week, so that over a 4-week period the athlete transitions into full cardiovascular workouts with a StairMaster/elliptical 4 to 5 days a week. It is important to avoid passive dorsiflexion or
Table 28-4
Achilles tendon stretching to protect the Achilles repair from stretching out. We have found that normal dorsiflexion will return naturally without being aggressive with dorsiflexion motion. The final phase of rehabilitation starts approximately at the 3-month mark. Patients will continue to work on balance, ankle strength, and unilateral calf raises. At this time, full lower-extremity strengthening will be initiated. Exercise will include stepdowns (Fig. 28-8, A) leg press (Fig. 28-8, B), knee extensions (Fig. 28-8, C),
Figure 28-6
Single-leg balance for proprioception.
Figure 28-7
Bilateral calf raise.
Wean out of boot/postoperative shoe
Week 1: Wear your boot/postoperative shoe from 8 4 PM. Wear the brace/shoe insert/steel shank after 4
AM
to
PM.
Week 2: Wear your boot/postoperative shoe every Monday, Wednesday, and Friday from 8 AM to 4 PM. After 4 PM, wear the brace/shoe insert or steel shank. Wear your brace/shoe insert/steel shank all day Tuesday, Thursday, Saturday, and Sunday. Week 3 and beyond: Wear your brace/shoe insert/steel shank every day of the week. You should wear the boot if you are doing excessive walking.
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CHAPTER 28
Principles of rehabilitation for the foot and ankle
Figure 28-8 (A) Stepdown for balance and strengthening. (B) Leg press using single leg. (C) Knee extension machine for quadriceps strengthening.
and hamstring curls that can be advanced per patient tolerance. Weighted calf raises typically are initiated around 4 months. Once an athlete is capable of using a StairMaster/ elliptical machine for 30 minutes 5 days a week, he or she may begin light jogging (usually at 3-4 months after the repair). It also is important to begin sportspecific skills, such as shooting a basketball or hitting a tennis ball. Agility drills should be advanced gradually per patient tolerance. Before return to sport, the patient should successfully complete a functional progression to ensure a safe return to competition. Return to sports normally occurs at 5 to 8 months after surgery.
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REHABILITATION AFTER LATERAL ANKLE RECONSTRUCTION The treatment and rehabilitation after acute ankle sprains begins by positioning the ankle in a position that reapproximates the torn ligament ends (neutral dorsiflexion with weight bearing). The application of a removable walking boot with an Aircast Cryocuff and immediate weight bearing place the ankle mortise in its most stable position. Early range of motion, Achilles stretching, and peroneal strengthening is started immediately after injury. However, plantarflexion and inversion will result in separation and possible elongation of
Rehabilitation after lateral ankle reconstruction
(A) Resisted eversion using Thera tubing. (B) Resisted dorsiflexion using Thera tubing.
the injured ligaments and therefore should be avoided. Once the ligaments have healed, then advancing the rehabilitation is safe. A similar approach can be used following a lateral ankle reconstruction. For the reliable athlete with close medical monitoring and sturdy tissue at the time of reconstruction, there may be a place for intermittent immobilization with early weight bearing and specific range-of-motion exercise. Overall the objective is to obtain as ‘‘normal’’ an ankle as possible. This is an example of our rehabilitation program. Immediately after surgical reconstruction, the athlete is placed in an Aircast walking boot with a Cryocuff placed inside the boot. Dressing changes and rehabilitation will begin 3 days postoperatively. The clinical goals in the first phase of rehabilitation (4 weeks) consist of restoring full eversion and dorsiflexion, normalizing gait, increasing calf flexibility, and beginning light strengthening. Physical therapy will consist of a home exercise program, progression to full weight bearing, a light bike program, Cryocuff, and desensitization massage. Competitive athletes with training room availability use on-site athletic trainers’ and physical therapists’ expertise. The home exercise program consists of range of motion exercises and strengthening with Thera-tubing (Fig. 28-9, A and B) in the directions of eversion and dorsiflexion. Over the first 4 weeks, the patient is instructed to avoid inversion and plantarflexion to protect the integrity of the newly reconstructed ligaments. It also is important to begin Achilles tendon stretching using a towel (Fig. 28-10) with progression to a stair stretch. Exercises are performed at a high frequency with a low load to stimulate the ligament to heal without creating swelling or reinjury. The Cryocuff will be used to help control swelling and inflammation and is most helpful in the first week after surgery. Partial weight bearing is started immediately after surgery with progression to full weight bearing in the
Figure 28-10 Achilles/calf stretch with towel.
next 7 to 10 days in the walking boot. A bike program is initiated the first week postreconstruction with the walking boot. The program will advance each week as the incision/wound has had time to heal. Once clinical wound healing has occurred, a patient can be more aggressive with cardiovascular activity. Desensitization massage is an important part of the early rehabilitation program. Because of the highly innervated foot and ankle, the patient often will experience some surface hypersensitivity after surgery. It is important to stimulate this nerve tissue with light massage and tactile stimulation to reeducate and desensitize the tissue to normal pressure and touch. This can be accomplished with a light massage 3 to 5 minutes several times a day. The second phase of rehabilitation begins 1-month postoperatively. At this time patients are instructed to wean out of the boot into a stirrup ankle brace (Fig. 28-11). Our goal is to wean the athlete out of the boot within 2 weeks and obtain a normal, pain-free gait (see Table 28-4). 605
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Figure 28-9
CHAPTER 28
Principles of rehabilitation for the foot and ankle
the toes pointed to isolate the peroneal tendons. The athlete then everts the foot and ankle to strengthen the tendons. We have found this to be a very effective means of maximizing peroneal strength. Bilateral calf raises are initiated with progression to single calf raise. We like to have the patient work on eccentric phase of calf raise by going up on both and lowering slowly on the injured side. Once the patient has no difficulty with the eccentric phase of the exercise, he or she may add the concentric phase of the exercise. Proprioception exercise (Fig. 28-14) should begin with one-foot balance, with progression of balance with opposite hip/ leg exercise. Cardiovascular exercise should be advanced from the bike to StairMaster/elliptical machine (4-6 weeks after surgery) and eventually to light jogging (6-10 weeks after surgery).
Figure 28-11
Patient using active ankle brace.
Exercises in the second phase include range of motion/strengthening in all four directions, aggressive heel-cord stretching (Fig. 28-12), calf raises, and proprioception exercise. Dorsiflexion and inversion strengthening still are performed with Thera-tubing. Aggressive peroneal strength (Fig. 28-13) is accomplished by having the athlete lie in a lateral position with ankle weights hung over the end of the foot and
Figure 28-13 weight.
Figure 28-12
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606
Aggressive Achilles/calf stretch on step.
Aggressive peroneal strengthening with cuff
Figure 28-14 Single-leg balance for proprioception using opposite hip strengthening with Thera tubing.
Rehabilitation of ankle fractures
Figure 28-15 Cybex isokinetic strengthening for inversion/ eversion.
There are several other ways to strengthen the ankle postoperatively, including Cybex/Biodex (Fig. 28-15) and the multiaxial machine. As long as the emphasis is on pain-free strengthening involving dorsiflexion, eversion and plantarflexion these exercise follow the same clinical guideline set in this phase. The final phase of rehabilitation (2 months) should focus on advance strengthening of the entire lower extremity and sportspecific agility drills. The final goal of this phase is return to sport after finishing a sport-specific functional progression. Exercises in the final phase will continue to focus on ankle strengthening, flexibility, and proprioception activity. Advanced lower-extremity exercise can include leg press, knee extension, and hamstring curls as tolerated. Sport-specific skills, such as kicking a soccer ball, ball handling drills, or catching a football should be implemented at this time. The intensity of these activities can be increased as tolerated. Before return to sport, the patient should successfully complete a sport-specific functional progression program to ensure safe return to competition. Return to sports participation is 10 to 12 weeks.
and protected weight bearing. The goal of rigid, stable, internal fixation is to allow a more functional recovery. This is an example of our rehabilitation program. Immediately after surgery, the patient is placed in an Aircast walking boot with a Cryocuff for cold and compression. Early immobilization consists of rest, elevation, and continuous daytime Cryocuff use. Patients are instructed to stay down as much as possible to help decrease swelling. Nonweight bearing with axillary crutches is initiated initially after surgery to reduce the risk of immediate postoperative swelling. The patient should also wiggle the toes and perform leg lifts every 3 to 4 hours while awake. Dressing changes and rehabilitation will begin 1 week postoperatively. If stable bone alignment is demonstrated on radiographs, range-of-motion exercises are started. Range of motion should be initiated in a manner that does not put tension on an injured or repaired ligament. For an isolated lateral fibula or stable bimalleolar fracture, range of motion can include all directions. If the patient has a medial ligament injury, dorsiflexion with eversion should be avoided until the ligament is healed. Range of motion and light tubing exercises are guided by pain and should be performed several times a day in high repetitions (15-20); towel stretch for the Achilles and manual plantarflexion stretch can be started (20 seconds, 5 repetitions) if there is no contraindicating ligament injury. The home exercise program will consist of toe curls (see Fig. 28-5, A), range of motion in appropriate directions, resistive band in appropriate directions, desensitization massage, and a light bike program wearing the boot (Fig. 28-16). Partial weight bearing is started at 1 week, with progression to full weight bearing in the walking boot in 2 weeks (if the fracture is stable and does not involve a weight-bearing surface). Patients are instructed to use
REHABILITATION OF ANKLE FRACTURES
Figure 28-16
Stationary bike using Aircast walking boot.
607
...........
The treatment and rehabilitation after acute displaced ankle fractures in the athlete can be particularly exciting with the ability to anatomically and rigidly fix bony fractures and anatomically repair torn ligaments. Displaced fractures should be treated with anatomic open reduction and internal fixation. We have progressed from short-leg casting and nonweight bearing to the use of intermittent immobilization, early range of motion,
CHAPTER 28
Principles of rehabilitation for the foot and ankle
be substituted for the bike with use of the brace and athletic shoes (see Fig. 28-4, B). Patients typically are given a home exercise program to be performed two to three times a day. Athletes who have athletic training resources should work under the guidance of the athletic training staff. The final phase of rehabilitation (2 months) should focus on advance strengthening of the entire lower extremity and sport-specific agility drills. The final goal of this phase is the return to sport after finishing a sport-specific functional progression program.
Figure 28-17 Patient using Aircast stirrup brace.
axillary crutches and increase weight bearing as tolerated. After the first week of partial weight bearing, the patient may begin using one crutch under the opposite arm and eventually progress to full weight bearing over the next week. Once a patient can walk normally with the walking book (typically within 3 weeks), we begin weaning the patient out of the boot and into a stirrup brace (Fig. 28-17) and regular shoe over the next 2 weeks. Patients with highly comminuted fractures and those with weight-bearing joint injury or significant cartilage injury do not follow this same protocol. The second phase of rehabilitation begins approximately 1 month after surgery. At this time, an increase in weight-bearing exercise, proprioception, and gait training with an athletic shoe is initiated. Exercises consist of progression of Thera-Band activities to include directions originally avoided because of ligament complications. Standing calf stretching, balancing exercises, double to single leg calf raises, and elliptical/StairMaster progression are included during this phase. Thera-Band exercise should continue to be high repetitions (15-20) in all directions. Single leg balance is first initiated in a regular shoe and then progressed to bare foot on a hard surface. Our goal is approximately 60 seconds. Balance can be advanced by use of a soft surface and balance board (Fig. 28-18). The patient should work aggressively with calf stretching using a stair or an incline board for 3 minutes three times a day. Bilateral standing calf raises should be initiated with progression to singleleg calf raises (Fig. 28-19). Once completely out of the boot, elliptical or StairMaster progression should
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608
Figure 28-18 Single-leg balance for proprioception on Thera disk.
Figure 28-19
Unilateral calf raise.
References
CONCLUSION The athlete will desire and in most instances demand 100% strength, 100% motion, and 100% function. This is a challenge for the surgeon, therapist, and trainer. The understanding of muscle function and its need for motion with controlled resistance to return to functional ability has shown us that our rehabilitation must take this into account. We have discussed our principles of rehabilitation and some specific approaches for athletes and their injuries. We also have tried to relate the basics of science understanding that underlie our principles and specific approaches. The area of rehabilitation of the foot and ankle will continue to progress as we understand more clearly the appropriate use of weight bearing, early motion, and function resistance. Also, as our understanding of proper anatomic repair and reconstruction advance, our rehabilitation must and will advance also. This is an exciting time in the treatment of athletes with foot and ankle injuries. We hope that this chapter both encourages you and challenges you in your treatment of your athletes.
4 PEARL Rehabilitation Pearls Every injury has a position that must be protected and an opposite motion that must be rehabilitated. Every week of immobilization will add 2 weeks to the rehabilitation. Once an athlete can use the StairMaster or elliptical machine 30 minutes 4 to 5 days a week without problems, he or she may start running. A good surgery that is poorly rehabilitated will equal a poor result. The athlete’s goal is always 100% full function.
REFERENCES 1. Garrick JG, Requa RK: The epidemiology of foot and ankle injuries, Clin Sports Med 7:29, 1988. 2. Backx FJG, et al: Sports injuries in school-aged children. An epidemiologic study, Am J Sports Med 17:234, 1989. 3. Kimura IF, et al: Effect of the air stirrup in controlling ankle inversion stress, J Orthop Sports Phys Ther 9:190, 1987. 4. Clanton TO, Wood RM: Etiology of injury to the foot and ankle. In DeLee JC, Drez D Jr, Miller MD, editors: Orthopaedic sports medicine principles and practice, Philadelphia, 2003, Saunders. 5. Schafle MD, et al: Injuries in the 1987 National Amateur Volleyball Tournament, Am J Sports Med 18:624, 1990. 6. Smith DK, Gilley JS: Imaging of sports injuries of the foot and ankle. In DeLee JC, Drez D Jr, Miller MD, editors: Orthopaedic sports medicine principles and practice, Philadelphia, 2003, Saunders. 7. Watson AWS: Sports injuries during one academic year in 6799 Irish school children, Am J Sports Med 12:65, 1984. 8. Casillas MM: Ligament injuries of the foot and ankle in adult athletes. In DeLee JC, Drez D Jr, Miller MD, editors: Orthopaedic sports medicine principles and practice, Philadelphia, 2003, Saunders. 9. Cooper PS: Proprioception in injury prevention and rehabilitation of ankle sprains. In Sammarco GJ, editor: Rehabilitation of the foot and ankle, St Louis, 1995, Mosby. 10. Hocutt JE, et al: Cryo-therapy in ankle sprains, Am J Sports Med 10:316, 1982. 11. Buckwalter JA: Activity vs rest in the treatment of bone, soft tissue and joint injuries, Iowa Orthop J 15:29, 1995. 12. Buckwalter JA: Effects of early motion on healing of musculoskeletal tissues, Hand Clin 12:13, 1996. 13. Burroughs P, Dahners LE: The effect of enforced exercise of the healing of ligament injuries, Am J Sports Med 18:376, 1990. 14. Glasoe WM, et al: Weight-bearing immobilization and early exercise treatment following a grade II lateral ankle sprain, J Orthop Sport Phys Ther 29:394, 1999. 15. Kellet J: Acute soft tissue injuries—a review of the literature, Med Sci Sports Exerc 18:489, 1986. 16. Vailas AC, et al: Influence of physical activity on the repair process of medial collateral ligaments in rats, Connect Tissue Res 9:25, 1981. 17. Eiff MP, Smith AT, Smith GE: Early mobilization versus immobilization in the treatment of lateral ankle sprains, Am Orthop Soc Sport Med 22:83, 1994. 18. Klein J, Hoher J, Tiling T: Comparative study of therapies for fibular ligament rupture of the lateral ankle joint in competitive basketball players, Foot Ankle 14:320, 1993. 19. Gelberman RH, et al: The effects of mobilization on the vascularization of healing flexor tendons in dogs, Clin Orthop 153:283, 1980. 20. Gelberman RH, et al: Influences of the protected passive mobilization interval on flexor tendon healing, A prospective randomized clinical study, Clin Orthop 264:189, 1991. 21. Aoki M, et al: Biomechanical and histological characteristics of canine flexor repair using early postoperative mobilization, J Hand Surg 22A:107, 1997. 22. Duran RJ, et al: Management of flexor tendon lacerations in zone 2 using controlled passive motion postoperatively. In Hunter JM, et al, editors: Rehabilitation of the hand, St Louis, 1978, Mosby. 23. Shelbourne KD, Nitz PA: Accelerated rehabilitation after ACL reconstruction, Am J Sports Med 18:292, 1990.
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Exercises in the final phase will continue to focus on ankle strengthening; flexibility; and proprioception activity; and advanced lower-extremity exercise, including leg press, knee extension, and hamstring curls as tolerated and indicated. Sport-specific skills, such as kicking a soccer ball, ball handling drills, or catching a football should be implemented at this time, increasing the intensity of these activities as tolerated. Return to sports can be as early as 4 weeks after rigid fixation of an isolated fibula fracture to 8 to 10 weeks after a bimalleolar and equivalent repair. Fractures that require fixation of the syndesmosis can take 4 to 6 months before return.
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Principles of rehabilitation for the foot and ankle
24. Salter RB, et al: The biological effect of continuous passive motion on the healing of full thickness defects in articular cartilage, J Bone Joint Surg 62A:1232, 1980. 25. Davis P, Baxter DE, Pati A: Rehabilitation strategies and protocols for the athlete. In Sammarco GJ, editor: Rehabilitation of the foot and ankle, St Louis, 1995, Mosby. 26. Costill DL, et al: Comparison of a space shuttle flight (STS-78) and bed rest on human muscle function, J Appl Physiol 91:57, 2001. 27. Linde F, et al: Early mobilizing treatment in lateral ankle sprains, Scand J Rehab Med 18:17, 1986. 28. Scheuffelen C, et al: Orthotic devices in functional treatment of ankle sprains: stabilizing effects during real movement, Int J Sports Med 14:140, 1993. 29. Campbell MK: Rehabilitation of soft tissue injuries. In Hammer WI, editor: Functional soft tissue examination and treatment by manual methods: the extremities, Gaithersburg, MD, 1991, Aspen. 30. DeCarlo M, Barill E, Oneacre K: Conservative treatment of soft tissue injuries. In Hammer WI, editor: Functional soft tissue examination and treatment by manual methods: the extremities, Gaithersburg, MD, 1991, Aspen. 31. Epler M: Gait. In Richardson JK, Iglarsh ZA, editors: Clinical orthopaedic physical therapy, Philadelphia, 1994, Saunders. 32. Tippett SR, Voight ML: Functional progression for sport rehabilitation, Champaign, IL, 1995, Human Kinetics. 33. Yamamoto SK, et al: Functional rehabilitation of the knee: a preliminary study, J Sport Med 3:288, 1975.
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34. Kegerreis S, Malone T, McCarroll J: Functional progressions: an aid to athletic rehabilitation, Phys Sport Med 12:67, 1984. 35. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation, Am J Sport Med 23:392, 1995.
FURTHER READING Clanton CO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA, editors: Surgery of the foot and ankle, St Louis, 1999, Mosby. Kern-Steiner R, Washecheck HS, Kelsey DD: Strategy of exercise prescription using an unloading technique for functional rehabilitation of an athlete with an inversion ankle sprain, J Orthop Sport Phys Ther 29:282, 1999. Pugia ML, et al: Comparison of acute swelling and function in subjects with lateral ankle injury, J Orthop Sport Phys Ther 31:348, 2001. Rozzi SL, et al: Balance training for persons with functionally unstable ankles, J Orthop Sport Phys Ther 29:478, 1999. Smith LS, et al: The effects of soft and semi-rigid orthoses upon rearfoot movement in running, J Am Podiatr Med Assoc 76:227, 1986.
.........................................C H A P T E R 2 9 Epidemiology and management tips in the professional athlete David A. Porter, Padraic Obma, and Larry L. Nguyen CHAPTER CONTENTS ...................... Introduction
611
Lateral ankle sprains
618
Epidemiology
611
High ankle sprains/syndesmotic injuries
619
Turf-toe/hallux rigidus
614
Achilles tendinitis/rupture
619
Base of fifth metatarsal fractures/Jones fractures
616
Difficult injuries
620
Midfoot sprains/Lisfranc injuries
616
Acknowledgments
621
Navicular fractures
617
Bibliography
621
Medial ankle sprains/deltoid injuries
618
INTRODUCTION Athletic competition has become normative in culture today. People enjoy competing against a worthy rival in the name of sportsmanship, the thrill of pushing the limits of the human body, for fitness, for the thrill of victory, and more recently as a full-time career. Evaluation and management of the elite athlete has been covered in Chapter 1. Foot and ankle injuries are among the most common maladies that plague the elite athlete. In professional sports, these injuries can result in the inability to participate and hinder a team’s chances for victory. For the individual, a prolonged recovery can lead to loss of playing time, a depressed sense of worth, an inability to contribute, and even a substantial loss of revenue, while jeopardizing a career. As more emphasis is placed on professional and intercollegiate athletics, awareness has heightened concerning the incidence of foot and ankle injuries in these elite athletes. The injuries in the elite athlete are similar to those seen in recreational and lower-level competitive athletes, but the demands can be greater and the ramifications more profound. This chapter is intended to provide information on the epidemiology of sport-specific foot and ankle injuries, to facilitate and guide physicians, physical therapists, athletic trainers, and students in the recognition of foot and ankle
injuries in this specific population. Our hope is that this information will help providers be more aware of the common and unique injuries encountered by professional athletes in their sport. This chapter will not delve deeply into treatment protocols because the previous chapters have attempted to cover treatment in far greater depth than merited here. This chapter, however, does comment on the epidemiology of sport-specific foot and ankle injuries and addresses some thoughts on the management of such injuries in the professional athletes. The management comments come from the senior author (D.A.P.). We are indebted to the professional trainers for their cooperation and contributions to this chapter (see later).
EPIDEMIOLOGY To ascertain the occurrence and sport-specific injuries in professional athletes a survey was delivered to the head athletic trainers of each professional team in the National Football League (NFL), the National Basketball Association (NBA), Major League Baseball (MLB), the National Hockey League (NHL), and Major League Soccer (MLS). Thirty-four of 132 surveys were returned: 2 NFL, 7 NBA, 13 MLB, 8 NHL, and 4 MLS. The following head athletic trainers responded for their respective teams.
CHAPTER 29
Epidemiology and management tips in the professional athlete
NFL Cincinnati Bengals
Paul Sparling
New Orleans Saints
Scottie Patton
NBA
Montreal Canadiens
Graham Rynbend
Phoenix Coyotes
Gord Hart
San Jose Sharks
Ray Tufts Dave Boyer
Wally Blase´
Tampa Bay Lightning
Charlotte (New Orleans) Hornets
Terry Kofler
MLS
Golden State Warriors
Tom Abdenour
Los Angeles Lakers
Gary Vitti
Milwaukee Bucks
Troy Wenzel
Orlando Magic
Ted Arzonico
Utah Jazz
Gary Briggs
Anaheim Angels
Ned Bergert
Arizona Diamondbacks
Paul Lessard
Baltimore Orioles
Richie Bancells
Chicago White Sox
Herm Schneider
Colorado Rockies
Tom Probst
Florida Marlins
Larry Starr
Houston Astros
—
Milwaukee Brewers
Roger Caplinger
Montreal Expos
Ron McClain
New York Yankees
Gene Monham
Oakland Athletics
Larry David
Texas Rangers
Danny Wheat
Toronto Blue Jays
Scott Shannon
NHL
...........
Don Fuller
Atlanta Hawks
MLB
612
Minnesota Wild
Buffalo Sabres
Jim Pizzutelli
Columbus Blue Jackets
Chris Mizer
Dallas Stars
Dave Suprenant
Chicago Fire
Rich Monis
Colorado Rapids
Theron Enns
DC United
Rich Guter
New England Revolution
Mike Fritz
The participants responded to a list of questions about foot and ankle disorders in the professional athlete. This included a survey of the most common foot and ankle injuries in the trainer’s sport and a series of questions about treatment and rehabilitation protocols for the more occult and controversial foot and ankle maladies. The specific topics about which we inquired were turf-toe, base of fifth metatarsal/Jones fractures, midfoot sprains/Lisfranc injuries, navicular fractures, medial ankle sprains/deltoid injuries, lateral ankle sprains, high ankle sprains/syndesmotic injuries, and Achilles tendinitis/rupture. Also, the head athletic trainers were asked about their anecdotal experiences with their most memorable/difficult/unusual professional athletic injury. The 34 participants were asked to list the five most common foot and ankle injuries treated among their professional athletes. Equal weight was given to all responses, whether listed first or last, and to each responder. The results are listed below. The results also were subdivided among each particular sport and are plotted in Figs. 29-1, 29-2, 29-3, 29-4, and 29-5. The five most common foot and ankle injuries (and the number of responses) were lateral ankle sprains (27), plantar fasciitis (21), corns and callosities (21), ingrown toenails (20), and Achilles tendinitis or ruptures (12). Additional injuries listed (in descending number of responses) include subungual hematomas (10), shin splints (10), medial ankle sprains (9), syndesmotic sprains (9), hallux rigidus (7), base of fifth metatarsal fractures (7), phalangeal fractures (5), leg contusions (5), metatarsal fractures (3), Lisfranc/
Epidemiology
Most Common Football Injuries
Number reported
2
Turf-toe Corns/callosities Med ankle sprain Plantar fasciitis Lat ankle sprain Achilles tendonitis High ankle sprain Midfoot sprain/Lisfranc Jones fracture Navicular fracture
1
0 Injuries
Figure 29-1 The most common injuries reported among football players were turf-toe or hallux rigidus, plantar fasciitis, and lateral ankle sprains (two responses each). Additional responses include corns and callosities, medial ankle sprains, syndesmotic injuries, and Achilles tendinitis. Most Common Basketball Injuries 8 7 Ingrown toenail Corns/callouses Plantar fasciitis Med ankle sprain Lat ankle sprain High ankle sprain Achilles tendonitis Other
Number reported
6 5 4 3 2 1 0 Injuries
Figure 29-2 Basketball injuries were noted to include lateral ankle sprains (8), plantar fasciitis (7), corns/calluses (6), ingrown toenails (4), and Achilles tendinitis (4).
must be well versed in a variety of foot and ankle injuries that can be both a real nuisance (ingrown toenail) to a career-threatening syndesmotic ankle injury. We hope that the first 28 chapters addressed these injuries and ailments to you, the reader, in a satisfactory fashion. This chapter focuses specifically on the professional athlete. 613
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midfoot sprains (3), ankle fractures (2), metatarsalgia (1), interdigital neuromas (1), medial malleolus fractures (1), and heel exostosis (1). Thus there were nearly equal numbers of injuries among the foot and the ankle. Also, one notes that the severity of the injuries can extend from a subungual hematoma or callus to a fracture dislocation of the ankle or foot. Thus the provider
CHAPTER 29
Epidemiology and management tips in the professional athlete
Most Common Baseball Injuries 14 Midfoot sprains/Lisfranc Plantar fasciitis Lateral ankle sprain High ankle sprain/syndesmosis Achilles tendonitis Shin splints Turf-toe/hallux rigidus Base of 5th/Jones fracture Ingrown toenail Corns/callouses Subungual hematoma Other Navicular fractures
12
Number reported
10
8
6
4
2
0 Injuries
Figure 29-3 Baseball injuries most commonly were plantar fasciitis (11); lateral ankle sprains (10); and ingrown toenails, corns/calluses, and shin splints (9 each).
Common Hockey Injuries 8 7
Number reported
6
Ingrown toenail Subungual hematoma Corns/calluses Toe Fx Lat ankle sprain Base of 5th/Jones fracture High ankle sprain/syndesmosis Other Navicular fractures
5 4 3 2 1 0
Injuries
Figure 29-4 Hockey players were reported to incur injures commonly related to skatewear and trauma such as ingrown toenails (6), corns/calluses (5), lateral ankle sprains (5), toe fractures (4), and high ankle/syndesmotic sprains (4).
TURF-TOE/HALLUX RIGIDUS Turf-toe involves a severe dorsiflexion injury to the great toe metatarsophalangeal (MTP) joint as described in Chapter 18. Other, less common mechanisms include varus/valgus stresses resulting in a combined turf-toe
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614
and ‘‘traumatic bunion.’’ The joint capsule is strained, the plantar plate can be stretched, and the articular cartilage can be contused and lead to long-term joint arthrosis. These injuries are commonly described in football, with hard turf and flexible shoes increasing the incidence. This can be quite debilitating, with long periods of recovery, especially if the plantar plate is
Turf-toe/hallux rigidus
Most Common Soccer Injuries
Number reported
3
Ingrown toenail Subungual hematoma Midfoot sprains/Lisfranc Plantar fasciitis Med ankle sprain Lat ankle sprain Achilles tendonitis High ankle sprain Turf-toe Base of 5th/Jones fracture Navicular fracture
2
1
0 Injuries
Figure 29-5 Soccer injuries most commonly were subungual hematomas, midfoot sprains, medial ankle sprains, lateral ankle sprains, and high ankle/syndesmotic sprains (2 each).
steroid injections, iontophoresis, and electrical stimulation. Full-length or extended shank, rigid orthotic inserts, and shoewear modifications were key elements of conservative treatment. Return to play was based on being pain free and having stable, full range of motion and the ability to perform with an orthotic insert and modified shoewear. A sports-specific functional assessment examination also was used as a criterion for return to sports. In general, the period of recovery lasted from weeks to months, depending on the degree of the turf-toe injury or the extent of arthrosis. Chronic aggravating symptoms may persist for several months, and a severe turf-toe injury can be career threatening. Hallux rigidus has rarely been career ending. We have noted some football players who were able to compete at a very high level for several years without surgical intervention yet with profound arthrosis. For the athlete who requires surgery, we prefer a combined cheilectomy and dorsal proximal-phalanx closing-wedge osteotomy (Moberg) for the athlete with dorsal spurs, early joint space narrowing and limited extension (60 degrees). We believe that the health providers should be aggressive with turf-toe injury management whether the approach is nonoperative treatment or operative. We favor anatomic repair for magnetic resonance imaging (MRI)-documented plantar plate rupture and for athletes with acute proximal migration of the sesamoids on weight-bearing radiographs. The trainers reported surgical experience in three cases of turf-toe, from two baseball trainers and one soccer athletic trainer. It was reported that these surgeries were performed after a period of conservative 615
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disrupted. One can imagine the difficulty in a football player dependent on push-off if there is significant limitation of motion and loss of power. Turf-toe (hyperextension with primary plantar soft-tissue injury) does occur in other sports but is much less frequent and typically is less severe. That being said, we have treated a Division I baseball pitcher who suffered a complete plantar plate disruption coming off the mound to field the ball, necessitating surgical repair. He is now in the minor leagues pitching without pain. Hallux rigidus is arthrosis of the first MTP joint and is characterized by a painful loss of motion (extension) with the formation of prominent dorsal osteophytes. The cause is multifactorial, but it is considered a degenerative process. Twenty-six athletic trainers from all the sports polled responded with their experiences with hallux rigidus. Baseball injuries consisted of acute hyperdorsiflexion injury to the great toe MTP joint caused by stepping on the front edge of the base or running into a wall or by an exacerbation of a chronic condition from pushoff running. Basketball players commonly were injured acutely from sudden stops or jumps causing hyperdorsiflexion of the great toes. Football trainers described the classic hyperextension injury to the great toe as a player pushes off on the playing field or another player lands on the injured player’s heel with the athlete’s great toe extended and the foot in equinus. Hockey injuries were less common; some were associated with off-theice workouts. Turf-toe and hallux rigidus commonly were treated nonoperatively with taping, ice, anti-inflammatories,
CHAPTER 29
Epidemiology and management tips in the professional athlete
treatment. Injuries involved a disruption of the plantar MTP soft tissues that required surgical reconstruction of the plantar complex. Return to play was allowed after 10 to 12 weeks of immobilization followed by aggressive physical therapy (PT) and range of motion. The trainers did not relate experiences with surgery for hallux rigidus.
BASE OF FIFTH METATARSAL FRACTURES/JONES FRACTURES Base of the fifth metatarsal fractures occur commonly with foot-twisting injuries. There are two basic fracture patterns seen. The first and most common pattern is an avulsion fracture off of the proximal tuberosity. The pull of the peroneus brevis tendon insertion and, perhaps more truly, the insertion of the lateral plantar fascia and abductor digiti minimi to the base of the fifth metatarsal can avulse a fragment of bone and can be treated nonoperatively in almost all instances, even in the professional athlete. Less common but more debilitating are the metaphyseal-diaphyseal transverse fractures or true Jones fractures that occur at the vascular watershed area of the fifth metatarsal (see Chapters 3 and 4). It can appear as an acute injury or as a chronic stress fracture. This fracture occurs in a location with less than optimal perfusion and requires a longer healing time. Fracture healing can be unreliable, especially when treated nonoperatively. Twenty-two professional athletic trainers describe their experiences with base of the fifth metatarsal fractures and Jones fractures. Five baseball injuries resulted from inversion-plantarflexion midfoot twisting injuries associated with running on inclined uneven surfaces such as running the bases. The two football injuries occurred with ankle inversion injuries and direct trauma/ supination of the foot. Seven basketball injuries are reported. Some trainers relayed the more common acute inversion sprain injuries, yet in basketball these fractures were more commonly a result of overuse jumping and running and appeared more commonly as stress fractures of the fifth metatarsal. Two soccer injuries also represent a mix of acute trauma and stress reactions associated with running the playing field. Six hockey players reportedly suffered a fifth metatarsal injury, with the majority of injuries occurring with direct blows to the foot from puck impact trauma. Treatment options depended on the type of fracture. The more common avulsion fractures were treated symptomatically with rest, ice, compression, elevation, and taping. Immobilization in a walking boot or cast was indicated for more comminuted, more painful injuries or mildly displaced fractures. Surgical treatment,
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616
including open reduction internal fixation, was reserved for intra-articular fractures displaced more than 2 to 3 mm or Jones fractures. The trainers responding had many experiences related to base of the fifth metatarsal fractures. Baseball injuries were commonly treated nonoperatively with PT and taping. Football injuries were treated more aggressively with casting or surgical intervention because of the more forceful nature of the trauma. Basketball injuries also were treated aggressively with rest, immobilization, casting, PT, and orthotics to allow return to play. One trainer described the use of a bone stimulator device to hasten fracture healing. Many basketball injuries were treated operatively to shorten the disability period and presumably because of a higher incidence of Jones fractures in these athletes. Soccer injuries were treated with a mixture of nonoperative and operative interventions. One soccer trainer describes ‘‘inosine treatment.’’ Hockey trainers described a variety on nonoperative measures that included casting, taping, elastic braces, and modified shoewear. PT modalities included ultrasound, cryotherapy, iontophoresis, whirlpools, microcurrent treatments, and bone stimulators. One can see that there will be a variety of approaches encountered even when dealing with the professional athlete and fifth metatarsal injuries. Since this survey was completed, we see the use of a bone stimulator becoming almost routine in all fifth metatarsal fractures, whether an avulsion or in conjunction with operative treatment for Jones fractures. We favor operative treatment with a 4.5 to 6.5 intramedullary screw for all Jones fractures in the professional athlete and nonoperative boot immobilization for the avulsion fracture. There should be greater than 95% healing in both cases with this treatment.
MIDFOOT SPRAINS/LISFRANC INJURIES Sixteen professional athletic trainers relayed their experiences with midfoot injuries. Four baseball injuries resulted from sudden trauma to the foot’s being caught in unusual positions, whether plantarflexion-inversion or dorsiflexion-eversion. Two football injuries resulted from a forceful heel impact to the plantarflexed foot. Four basketball injuries consisted of sudden unusual positions of the foot in a sudden sprint, landing, or stepping on another player’s foot. Three soccer injuries resulted from an opponent’s strike to the unsuspecting player with the foot planted. Two hockey injuries occurred on dry land exercises. Experiences from the responding trainers varied widely. Immobilization with a walking boot occasionally was used, depending on the severity of the injury, by
Navicular fractures
NAVICULAR FRACTURES The most common types of navicular fractures seen in athletics are dorsal chip avulsion fractures and stress fractures. The navicular stress fracture is discussed in Chapters 3 and 4. Avulsion fractures from the dorsal lip are the most common type of navicular fracture. They usually are related to excessive plantarflexion forces with eversion or inversion components. The avulsion fracture normally is easily recognized on a lateral
radiograph of the foot. Stress fractures usually present with insidious onset and pain related to activity and have become recognized more commonly in the last 10 years. The navicular stress fracture is easily missed on initial examination because the fracture often is not visible on routine foot radiographs. The posterior tibial tendon insertion onto the medial navicular tuberosity provides a traction point for midfoot twisting injuries and the medial anchoring point for dorsal stress. The bifurcate ligament attachment on the lateral navicular is the lateral anchoring point for dorsal tension stress. The dorsal tension created by these opposing forces results in the fracture’s perpetuating from the dorsal articulation with the talar head. The palpable pain is noted dorsally on the navicular just lateral to the anterior tibial tendon insertion (‘‘N’’ spot). Eleven trainers described experiences with navicular fractures. In baseball, one trainer described a plantarflexion twisting injury during a throw. Two other cases were described as an overuse phenomenon to an accessory navicular and a stress fracture from running the bases. One football injury was described as an overuse stress reaction. Basketball players incurred injuries from poor foot mechanics, pes cavus anatomy, and overuse. Hockey and soccer players suffered navicular fractures as a result of a direct blunt trauma (four cases). Conservative treatments reported consisted of orthotics and modified shoewear to accommodate the stresses of the midfoot arch for stress and overuse injuries. Direct trauma and acute fractures were treated with immobilization in a boot, cast, or ankle-foot orthosis (AFO) with a period of rest. Return to play generally was directed toward an asymptomatic ability to play. When the players were pain free with provocative testing, they were allowed return to sports. For a direct traumatic injury, this generally took 7 to 10 days of initial immobilization followed by 2 to 3 weeks of PT strengthening and proprioceptive retraining with accommodative arch supports. Navicular fractures can cause prolonged pain and an extended duration for recovery. Three athletes required 2 to 3 months for recovery and still played through enduring pain. This was seen most commonly in basketball players. Two players required surgical intervention. One baseball player had prolonged symptoms greater than 6 months and underwent surgery to return to play in 6 to 8 weeks. One basketball player underwent surgery after a computed tomography (CT) scan identified a displaced fracture and returned to play after healing and pain-free rehabilitation. Presumably these two athletes had a navicular stress fracture. Our approach to the dorsal lip chip fracture commonly is nonoperative. We see a lot of athletes with this on routine radiographs. It is important to rule out a navicular stress fracture if the pain is not associated 617
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one baseball, two football, and two soccer trainers. It seemed that hockey players were allowed sooner return to sports, possibly because of the more supportive nature of the ice skate. In general, athletes were allowed return to play with a pain-free full range of motion and the ability to perform with an orthotic insert and modified shoewear. The ability to function at a tolerable level of comfort and to run, in addition to undergoing a sport-specific functional assessment examination, were criteria used to judge return to sports by these trainers. A grading system was used by one football trainer that encompassed a grade 1 sprain requiring 4 to 6 weeks of rehabilitation, grade 2 sprain requiring 8 to 12 weeks, and a grade 3 sprain requiring 12 to 24 weeks of immobilization/rehabilitation. Depending on surgeon preference and radiographic evidence of stability or bony union, if a fracture was involved, screws were removed 12 to 16 weeks after surgery and the patient was given arch supports and a rigid-soled shoe. Surgical intervention for Lisfranc injuries was reported infrequently. One baseball trainer reported surgery for a prolonged duration of symptoms. Two football trainers and one basketball trainer related surgery for displaced injuries (presumed midfoot dislocation). The hardware commonly was removed at 3 to 6 months. Baseball players and football players did not return to play the same season. We favor an aggressive approach to this injury. We believe that complete disruption of the midfoot ligaments requires surgical anatomic stabilization with 4.0- to 4.5-mm screws to decrease the risk of a careerthreatening chronic ligament insufficiency, arch collapse, and pain. Either evidence of widening of the interval between the medial cuneiform and base of the second metatarsal on weight-bearing radiographs or MRI evidence of the tarsometatarsal ligament disruption is an indication to operative stabilization. Close reexamination with weight-bearing radiographs weekly also is required for the ‘‘stable’’ midfoot sprain to ensure maintained anatomic alignment because late diastasis (1-4 weeks post injury) can occur. Further information can be found in Chapter 5.
CHAPTER 29
Epidemiology and management tips in the professional athlete
with acute trauma. We use CT radiography to ensure that there is not an associated stress fracture. Only occasionally is there a need to remove the symptomatic dorsal chip fracture. Navicular stress fractures should be treated aggressively with either nonoperative immobilization and/or screw fixation (4.0-5.0 screws). With either approach, the athlete will have to be nonweight bearing for 6 weeks. We have taken a more aggressive surgical approach with screw fixation because we note about 90% success with operative fixation and only 70% with nonoperative treatment. We have moved away from bone grafting in most of our operative cases unless there is significant cyst formation or significant ‘‘displacement’’ (2 mm).
MEDIAL ANKLE SPRAINS/DELTOID INJURIES Twenty-nine trainers described their experience with medial ankle injuries. (See Chapter 13 for a more exhaustive discussion of this injury.) Ten baseball trainers described most commonly an ankle trauma as a result of running the bases with an eversion axial-loading injury. Football injuries occurred as a result of a plantarflexion external rotation injury (pile-up or chop block). Basketball players routinely described an eversion injury related to stepping on another player’s foot. Soccer players most commonly suffered an eversion injury as a result of an opponent player’s applying a laterally directed force to the planted foot. Hockey players experienced a plantarflexion-eversion twisting injury during play of having the skate caught in the ice or on the puck. The cornerstone of treatment was nonoperative, consisting of rest, ice, compression, taping, and elevation during the initial 2 to 3 days. Anti-inflammatory medications were prescribed along with PT early range of motion protocols. PT modalities included pulsed ultrasound, electrical stimulation, cold therapies, proprioception, and strengthening programs. Most athletes were placed in removable, prefabricated walking boots, and rarely was casting immobilization used. Orthotic shoe inserts were used commonly, especially in basketball, to help support the medial arch and counteract pronation. Criteria for return to play were based on a pain-free range of motion with no swelling or symptoms related to stress testing, such as a single-leg stance or hop. Grading systems similar to lateral ankle sprains were used. Grade 1 injures required 2 to 4 weeks of rehabilitation. Grade 2 injuries required 3 to 8 weeks. Grade 3 injuries required 8 or more weeks. The ability to return to sports was determined by a pain-free full range of motion and a functional assessment based on sportspecific task exercises.
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One football player required operative repair of the medial deltoid ligament in association with a mortise dislocation and widening. He was allowed return to sport after full range of motion and pain-free sport-specific activities. The time to return was not reported. We most commonly see medial ligament injury in association with either a syndesmosis injury or fibula fracture. Isolated medial deltoid ankle injury mechanisms are as described by these trainers. We have had to repair only two isolated deltoid ligaments in the competitive athlete. Chronic medial ligament insufficiency is a very difficult problem to treat, so we are aggressive with repair if the ligament is disrupted in a professional athlete. This is most commonly associated with operative fixation of a fibula fracture.
LATERAL ANKLE SPRAINS All the professional athletic trainers responded with their experiences involving lateral ankle sprains. The lateral ankle sprain continues to be the most common sports injury, as noted by these results, and is discussed in more detail in Chapter 12. Operative management is discussed in Chapter 13. Baseball injuries commonly were related to plantarflexion inversion injuries. This injury occurs during the course of running in the outfield to catch a ball or running around the bases. Basketball injuries notoriously resulted from stepping on another player’s foot or landing awkwardly. Football injuries occurred with the foot planted and the player twisting and rolling to the ground. Soccer-player injuries happened as a mixture of all these. Hockey injuries were caused as the skate was caught in the ice or were reported as a common plantarflexion inversion injury during on- or off-the-ice training. The treatment of lateral ankle sprains was determined by severity of injury and length of symptoms. Initial treatment of acute injury involved protection, rest, ice, compression, and elevation (PRICE) to limit the extent of injury, control edema, and minimize pain. A regimen of anti-inflammatory drugs commonly was used. After the initial treatment, strengthening exercises were initiated, concentrating on the peroneal muscles and dorsiflexors. This was followed by proprioception exercises, functional conditioning, and endurance training, then by return to play when asymptomatic. Indications for surgery in the acute phase are controversial. Responding trainers relayed that conservative treatment consisted of rest, ice, compression, taping, and elevation during the initial 2 to 3 days. Anti-inflammatory medications were prescribed, along with PT early range-of-motion protocols thereafter. PT modalities included pulsed ultrasound, electrical stimulation, edema
Achilles tendinitis/rupture
HIGH ANKLE SPRAINS/SYNDESMOTIC INJURIES Twenty-two professional athletic trainers reported their experiences with high ankle sprains. High ankle sprains are discussed in Chapter 13. Baseball injuries were a result of unusual positioning of the foot (presumably dorsiflexion and eversion) as an unexpected force was applied. This occurred often as players collided into one another as an opponent was sliding into a baseman or suddenly misstepping on uneven surfaces. Football injuries were reported with the classic plantarflexion (or dorsiflexion) external rotation injury and a pileup. Basketball injuries occurred with stepping on another player’s foot. Soccer injuries happened as an opponent slid into the player. Hockey injuries occurred as the player’s foot was suddenly plantarflexed into the ice and a rotational force applied. According to respondents, high ankle sprains were treated nonoperatively in similar fashion to lateral ankle
sprains. Conservative treatment consisted of rest, ice, compression, taping, and elevation during the initial 2 to 3 days. Anti-inflammatory medications were prescribed along with PT early range of motion protocols thereafter. PT modalities included pulsed ultrasound, electrical stimulation, and proprioceptive and strengthening programs. Most injuries commonly were placed in removable, prefabricated splints, and rarely was casting immobilization used. High ankle sprains reportedly were treated more conservatively (regarding return to play) than their lateral ankle injury counterparts, with an initial period of protective, partial weight bearing. Grading systems again were used. Grade 1 sprains were protected for 3 to 6 weeks. Grade 2 sprains were treated with variable periods of restriction for 6 to 12 weeks. Grade 3 sprains required more than 3 months for return to play. Athletes were allowed return to play after a painfree full range of motion, a painless external rotation or compression testing, and a sports-specific functional assessment examination. Two football trainers and one baseball trainer described experiences with operative repair of syndesmosis injury. The indication for operative fixation depended on the severity of the injury and the degree of joint displacement. Two compression screws commonly were used to support the syndesmosis and commonly were removed at 12 weeks after the initial surgery. We believe that operative fixation is optimal for grade 2 (occult complete disruption), grade 3 (overt dislocation of the tibia fibula interval and deltoid), and Maisonneuve injuries. Chronic and incompetent syndesmosis injuries can be career threatening, and thus stable, anatomic alignment must be obtained and maintained.
ACHILLES TENDINITIS/RUPTURE Achilles tendon injuries can plague the elite athlete. Injuries include tendinopathy, insertional problems (bursitis and tendinopathy), and complete rupture (see Chapter 7). Acute ruptures can result in a long period of rehabilitation, and have the potential for long-standing weakness. Acute and chronic Achilles tendinitis, usually the result of an overuse injury, can be a chronic nuisance injury resulting in suboptimal performance. All 26 professional athletic trainers described their experiences with Achilles tendon disorders. Baseball injuries ranged from the acute traumatic eccentric ankle dorsiflexion injury to the recurrent aggravation of preexisting chronic tendinitis associated with running the bases and overuse. Occasional injuries occurred early in the season with poor conditioning and foot mechanics from the off season. Football and basketball injuries occurred with sudden push-off explosive jumping forces 619
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control, cold therapies, and proprioceptive and strengthening programs. Most athletes commonly were placed in removable, prefabricated splints, and rarely was casting immobilizations used. Grading systems were used. Grade 1 sprains were allowed to continue play as tolerated to pain with anti-inversion taping and modified shoe inserts. Grade 2 sprains were treated with variable periods of restriction for 1 to 3 weeks. Grade 3 sprains required 3 to 5 weeks of immobilization and activity limitations. Football injuries were treated more conservatively, with a 1- to 2-week longer period of restrictions, presumably because of the greater amount of forceful contact used on the field of play. The criteria for return to play consisted of pain-free full range of motion; ability to perform a balanced, singleleg stance; and completion of a sport-specific function assessment test. No cases of surgical intervention were presented for acute lateral ankle sprains. We are aggressive with intermittent immobilization, cold compression therapy (Aircast Cryocuff, Summit, NJ), and aggressive PT. We are happy to use the expert and available training staff employed by the professional teams. The PT opportunities available enable a quicker return to play. We encourage use of the boot immobilization at night (when relaxation of the muscles and nonweight bearing lead to a position of plantarflexion [PF] and inversion) for 4 full weeks but allow daily activities in a stirrup brace as soon as the ankle is stable to talar tilt on clinical examination (1-3 weeks). We operate on acute routine lateral ankle sprains only if there is an associated osteochondral fracture requiring fixation.
CHAPTER 29
Epidemiology and management tips in the professional athlete
and overuse stress phenomenon. Soccer injuries more commonly were listed as repetitive stress injuries exacerbated by push-off drills and backpedaling. Hockey injuries were seen with sudden eccentric contraction during loading for push-off. One trainer described an acute laceration from another skate blade. Achilles tendinitis injuries were commonly treated nonoperatively with PT, stretching, proprioceptive training, and taping modalities (avoiding extremes of dorsiflexion). Orthotic inserts and heel lifts commonly were prescribed but quickly discontinued in most cases to ‘‘avoid contracture.’’ Rarely were casting and immobilization used for more acute Achilles tears. Chronic injuries may benefit from hydrotherapy, whirlpools, and electrical stimulation. Football injuries are treated more aggressively with immobilization, night splints, and anti-inflammatory medications. Athletes were allowed return to play after a pain-free examination and full range of motion. A sports-specific functional assessment test with the ability to run, jump, and weight bear with multidirectional take-off exercises defined the level of proficiency at which the player may return to the field. Occasional chronic irritation and the ability to play through mild soreness may be required of the chronic injury. Acute ruptures required several months of recovery with intense therapy before obtaining a suitable level of function for play. Surgical intervention is required with a complete rupture and occasionally chronic, debilitating tendinitis. Fourteen trainers described their experiences with operative intervention in the elite athlete. Most commonly, acute complete and high-grade partial ruptures confirmed by a positive Thompson’s test and MRI scan warranted operative intervention in the professional athlete. One baseball trainer cited an instance of nonoperative casting for an Achilles tear necessitating 9 to 12 months of rehabilitation before return to play. One baseball trainer and one basketball trainer described episodes of operative treatment of chronic Achilles tendinitis (insertional) with Hagland’s deformity. Surgical rehabilitation generally requires 12 to 16 weeks of rehabilitation before achieving a pain-free range of motion and the ability to return to sports. We believe that complete ruptures of midsubstance or insertional avulsion have a better chance of full recovery and a lower rerupture rate with operative repair. We tend to be aggressive with repair in the professional athletes but tell trainers, athletes, and management that the time to return to play can be 6 to 12 months. We have only occasionally had to operate on insertional tendinitis in the professional athlete and prefer a posterior tendon-splitting approach to disrupt as little of the tendon insertion as possible. With localized debilitating pain, this approach lets us get to problem with minimal incisions and maximal benefit. We have not had to
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operate on midsubstance tendinosis in the professional athlete despite a common experience in the nonprofessional, middle-aged athlete.
DIFFICULT INJURIES The professional athletic trainers polled were polled about the most difficult/memorable/unusual foot and ankle injury they had experienced in the past 5 years. Six trainers cited chronic plantar fasciitis and heel pain as the most recalcitrant injury poorly amenable to rehabilitation. Six trainers listed high ankle syndesmotic sprains as difficult to treat, inasmuch as two players had required surgery for prolonged symptoms and all the players required a lengthy respite from play, often frustrating the players. The high ankle sprains would reach a plateau of recovery before recurring setbacks in progress. Four trainers cited Achilles tendon rupture for their magnitude of injury and the prolonged rehabilitation period following surgical intervention. Both football trainers and one baseball trainer mentioned Lisfranc fracture/dislocations on the basis of the severity of the injury, with multiple tarsal joint involvements, necessitating surgery and prolonged periods of recovery. One soccer trainer mentioned Lisfranc fracture/dislocation for its subtle appearance and difficulty in diagnosing the occult injury, which further prolonged the return to play. Three trainers listed navicular stress fractures as their most intriguing injuries because of their gradual symptomatic onset and the moderate workup for midfoot pain before the detection of this injury. Two lateral ankle sprains developed recurring symptoms that plagued the player but were treated with taping and never underwent surgical intervention. One lateral malleolus refracture in a hockey player was under constant stresses from ice skating. One medial malleolus fracture was listed. One medial malleolar fracture developed a nonunion that required multiple surgeries and bone grafts and had an associated talar osteochondral lesion that prolonged the recovery process. Three episodes were cited of base of the fifth metatarsal fractures—one nonunion, one revision surgery, and one somewhat humorous episode of falling after being bitten by the pet dog. As professional and recreational sports become a more integral part of our society, more athletes will experience these common and uncommon injuries. The rehabilitation of the elite athletes related to our readers by the experiences of the contributing professional athletic trainers will, we hope, aid in expediting the recovery of future players. We hope that this chapter has helped you to be on guard concerning these common and difficult foot and ankle injuries in professional
Bibliography
athletes. We also hope that the management pearls aid you in making decisions and in educating the everconcerned athlete.
ACKNOWLEDGMENTS We acknowledge Sara Carpenter, MS, PT, OrthoArkansas, PA and Josh Landers, DPT, OrthoArkansas, PA.
BIBLIOGRAPHY
Nunley JA, Vertullo CJ: Classification, investigation, and management of midfoot sprains, Am J Sports Med 30:871, 2002. Nussbaum ED, et al: Prospective evaluation of syndesmotic ankle sprains without diastasis, Am J Sports Med 29:31, 2001. Paavola M, et al: Achilles tendinopathy, J Bone Joint Surg Am 84A: 2062, 2002. Porter DA: Ligamentous injuries of the foot and ankle. In: Fitzgerald R, Kaufer H, Malkani A, editors: Orthopedics, St Louis, 2002, Mosby. Vanore JV, et al: Diagnosis and treatment of first metatarsalphalangeal joint disorders. Section 2: hallux rigidus, J Foot Ankle Surg 42:124, 2003. Yoshino N, et al: Bilateral isolated tarsal navicular fracture dislocation: a case report, J Orthop Trauma 15:77, 2001.
Mizel MS, Miller RA, Scioli MW, editors: Orthopaedic knowledge update foot and ankle 2, Rosemont, IL, 1998, AAOS.
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Abductor digiti quinti muscle, 235, 235f Abductor hallucis tendon transfer, 426, 428f Accessory navicular bone, 537 in children, 537 description of, 36, 43 displaced, 304f flexible flatfoot with, 590 imaging of, 187f, 202f, 300f, 303f in Korea, 516 orthoses for, 590, 591f radiographs of, 537 signs and symptoms of, 537 treatment of, 537 Achilles tendinitis, 148 ankle-foot orthosis for, 7f chronic, 480 classification of, 148 in dancers, 480 extracorporeal shock wave therapy for, 173 insertional, 150, 377 classification of, 377 magnetic resonance imaging of, 151f, 162f, 167f nonsurgical treatment of, 153 orthoses for, 591 retrocalcaneal bursitis. see Retrocalcaneal bursitis surgical treatment of, 162, 162f, 377 symptoms of, 171b, 377 noninsertional, 148 adhesion excision, 154 classification of, 376 imaging of, 149f nonsurgical treatment of, 153, 162b surgical treatment of, 154 tenotomy, 154 nonsurgical treatment of, 151, 480 paratendinitis, 376 peritendinitis adhesion excision, 154, 154f arthroscopy for, 377 in dancers, 479 definition of, 148 refractory, 153 signs and symptoms of, 149f with tendinosis, 148–150 treatment of, 153 posterior ankle impingement caused by, 376 prevalence of, 148 in professional athletes, 619 risk factors, 148b shoes, 154f, 582
Achilles tendinitis (Continued) surgical treatment of, 153, 620 ankle neutral position, 171 partial weight bearing after, 170–171, 172f postoperative management, 169 return to sport after, 172 splinting, 169–170 success rates, 172 treatment of, 151, 153, 480, 620 Achilles tendinopathy adhesion prevention, 532 biology of, 527 etiology of, 527 gene therapy for, 528 healing of, 527 histopathology of, 527 management of, 529 aprotinin, 529 Eccentric Exercise, 529 glyceryl trinitrate, 530 laser therapy, 529 nonsteroidal anti-inflammatory drugs, 529 radiofrequency coblation, 529 resumption of activity after, 530 sclerosing injections, 529 shock wave therapy, 530 surgical, 530 prevalence of, 527 stem cells for, 528 tissue engineering for, 528 ultrasound of, 529 Achilles tendon anatomy of, 147, 479 blood supply to, 147 collagen fibrils of, 147–148 contracture of, 183–185 degeneration of, 165f length of, 147 magnetic resonance imaging of, 155f noninflammatory atrophic degeneration of, 150 reattachment of, 162–164, 162f rehabilitation of, 601 rupture of. see Achilles tendon rupture stretching of, 191 Achilles tendon rupture acute, 173 clinical findings, 174f etiology of, 173 magnetic resonance imaging of, 176f mechanism of, 173 mini-open technique for, 175 nonsurgical treatment of, 173 surgical treatment of, 174, 176f, 177f
Achilles tendon rupture (Continued) Thompson test for, 175f, 529 chronic, 178, 530 in dancers, 480 diagnosis of, 493f, 529 epidemiology of, 529 flexor hallucis longus repair of, 521, 521f gastro-soleus release, 496f, 530 incidence of, 529 in Kendo, 510, 510f neglected, 521 pain associated with, 488–489 percutaneous technique for, 495f in professional athletes, 619 proximal, 529 rehabilitation after, 530 repair of, 489, 490f, 529 reruptures, 530 signs and symptoms of, 529 in soccer players, 488–489 tendon transfers for, 531 Thompson test for, 175f, 529 treatment of, 529 surgical, 494f, 495f, 529, 530 “two flaps technique,” 496f Achillotendoscopy, 377 Adductor canal syndrome, 223, 224f Adhesions, 532 Adolescents fifth metatarsal base fractures in, 115 fixed flatfoot deformity in, 591 Tillaux fracture in, 96, 99f triplane fracture in, 96, 99f Aerobic dancing, 581 Air soles, 572 Aircast walking boot, 597, 597f, 605 Allodynia, 503 Allografts, 326, 334f, 556 Alpine skiing, 580, 581f Amitriptyline, 505 Ankle anatomy of, 33, 34f degenerative changes of, 365t hindfoot anatomy of, 294f “meniscoid” of, 35 osteophytes, 33 plantarflexion of, 311, 311f radiographs of, 186, 187f Shenton’s line of, 87f stability of, 88 subluxation of, 267f, 268f supination-inversion injury of, 98f
623
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A
Index Ankle fractures, 88 bimalleolar, 94, 94f lateral malleolus. see Lateral malleolus, fractures medial malleolar, 88, 88f. See also Medial malleolus fractures pediatric, 96 in pediatric patients. see Pediatric patients, ankle fractures in rehabilitation of, 607 Salter-Harris classification of, 96, 97f, 539–540, 540–541 trimalleolar, 94, 94f Ankle impingement, 33 anterior. see Anterior ankle impingement anterocentral, 33–34 flexor hallucis longus tendonitis vs., 37t lateral, 35 os trigonum. see Os trigonum posterior, 36, 37t, 38, 370 causes of, 370 characteristics of, 370 flexor hallucis longus tendinitis, 373 loose bodies, 372–373 os trigonum syndrome, 370, 371f osteochondral defects, 373 peroneal tendon tendinitis, 375 posterior tibial tendinitis, 374 posttraumatic calcifications, 371 posterolateral, 36 spurs, 33–34 Ankle instability, 486 after ankle sprain, 274t chronic, 267, 558 osteochondral lesions of the talus associated with, 319–320 surgical treatment of, 558 thermal capsular modification for, 559 footballer’s ankle, 523 lateral modified Bromstrom technique for. see Modified Bromstrom technique stabilization operations for, 274–275 medial, 280–281 rehabilitation for, 267–268, 269t subtalar instability and, 339 surgical repair of, 486 Ankle joint diastasis of, 17–18 lateral, pain in, 208–209 Ankle ligaments, 265 anterior talofibular ligament, 265–267, 266f calcaneofibular ligament, 265–267, 266f lateral, 265, 266f failed reconstruction of, 278 free tendon transfer for, 279–280 modified Brostrom procedure for. see Modified Brostrom procedure rehabilitation program for, 279t prevention of, 268 summary of, 270 Ankle pain anterolateral, 34 anteromedial, 33 lateral causes of, 35 description of, 35–36 medial, 42 posterior, 36, 37t differential diagnosis, 40 posterolateral, 36, 37t, 39 posteromedial, 37t, 40 Ankle reconstruction, 604
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Ankle sprain high, 17–18, 34, 619 incidence of, 318 instability after, 274t inversion, 532 lateral, 273. See also Ankle ligaments, lateral in dancers, 475 incidence of, 558 in professional athletes, 618 residual symptoms after, 476–477 treatment of, 273, 618 lateral process talar fractures vs., 97 medial, 43, 280 anatomy of, 281 arthroscopic grading of, 284t biomechanics of, 281 chronic, 284 in dancers, 475 in professional athletes, 618 nerve injury with anatomy of, 530 clinical presentation of, 531 nerve blocks for, 529 nonsurgical treatment of, 531 oral medications for, 532 pathoanatomy of, 530 surgical treatment of, 506 topical medications for, 532 treatment of, 531 nonoperative management of, 273 orthoses for, 593 osteochondral lesions of talus and, 318 pain after, 274t posterior impingement secondary to, 39 signs and symptoms of, 273 surgical treatment of, 273 arthroscopy, 274 contraindications, 273–274 goals, 274 indications for, 273–274 radiographic criteria for, 273–274 tarsal coalition and, 345–346 Ankle stirrup brace, 266f Ankle syndesmosis pathology of, 34–35 repair of, 95f space measurements, 87, 87f sprain of, 34 Ankle tunnels, 217t, 218f Ankle-foot orthosis Achilles tendinitis, 7f case study use of, 4–5, 6f Ankylosing spondylitis, 241 Anterior ankle impingement, 33, 364 arthroscopic treatment of, 366 bony impingement associated with, 365 in dancers, 477 definition of, 364 lesions associated with, 365 location of, 365–366 radiographs of, 364f rehabilitation of, 366 scoring systems for, 364–365 Anterior drawer test, 267, 267f Anterior process calcaneal fractures, 100 avulsion etiology of, 100, 101f compression etiology of, 100–102, 101f mechanism of, 100–102, 101f treatment of, 102 Anterior syndesmosis, 34 Anterior talofibular ligament, 265–267, 266f anatomy of, 286f
Anterior talofibular ligament (Continued) in modified Brostrom technique, 276, 278 sprain of, 475 tear of, 35, 476 Anterior tarsal tunnel syndrome, 10 Anterior tibia, 365 Anterior tibiofibular ligaments, 24f anatomy of, 286–287, 286f Basset’s ligament, 34, 34f insertion of, 35 Anthropometric measurements, 61 Antifungal agents onychomycosis treated with, 261–262 tinea pedis treated with, 259 Aprotinin, 529 Arch supports, 571 Arterial disease, 247 Arthritis enteropathic, 242 gouty, 243–244 midfoot, 589 psoriatic, 242 in Reiter’s syndrome, 242 rheumatoid, 243 subtalar, 593 Arthrodesis calcaneocuboid distraction, 198–199 hallux rigidus treated with, 416 metarsocuneiform joint, 443 posterior tibialis tendon dysfunction treated with, 198–199 subtalar, 199 triple, 199 Arthroscopy, 559 accessory instruments, 357 Achilles tendon peritendinitis, 377 anatomy imaged using, 361 for ankle sprain, 274 anterior and posterior, 380 anterior ankle impingement treated with, 364, 366 contraindications, 355–356 equipment for, 356 examination using anterior ankle, 362 14-point, 361, 362t posterior ankle, 362 21-point, 361, 361t grasper, 357 great toe, 560 hallux rigidus treated with, 417 history of, 355, 559–560 indications for, 355 irrigation for, 357 loose bodies, 370 operative setup for, 356 ossicles, 370 osteochondral defects of the talus, 367 patient positioning for, 356 peroneal tendons, 376f portals, 357 accessory inferior, 358 anterolateral, 358, 358f anteromedial, 357, 358, 358f function of, 357 posterolateral, 359, 359f, 560 posteromedial, 359, 360f, 361f, 560 transmalleolar, 359 transtibial, 359 posterior ankle, 560 in prone positioning, 560 subtalar joint, 343f, 378, 378f surgical technique, 356
Index
B Balance board training, 268–270 Ballet, 469, 482, 548. See also Dancers Baseball shoes, 579 Basketball shoes, 577, 577f Basset’s ligament, 34, 34f Baxter’s nerve neurapraxia, 481 Bicycling, 581, 581f Biomechanics, 62, 69 Bisphosphonates, 246 Black heel, 255, 256f Blisters, 581 Boating shoes, 570 Bone densitometry, 246, 247 Bone density, 58, 59t Bone grafts, 419 Bone remodeling, 45–46, 55 Bone resorption, 45–46 Bone scans procedure for, 64–65 stress fracture imaging using, 64, 65f tarsal navicular stress fracture imaging using, 74 Bone scintigraphy procedure for, 64–65 sesamoid pain evaluations, 79–80 stress fracture imaging using, 64, 65f Bone stimulator, 5 Bone strain definition of, 65 features of, 66, 66t history of, 65 scintigraphy of, 65–66 Borrelia burgdorferi, 244–245 Botulinum toxin injections, 230 Boxer’s fracture of fifth metatarsal, 30f Bromstrom technique, 274–275. See also Modified Bromstrom technique Brostrom-Gould reconstruction technique, 342, 342f
Bunionettes, 384 callus reduction, 385–386 clinical presentation of, 384–385 in dancers, 470, 474 fifth metatarsal head and, 385f illustration of, 385f physical examination, 385 radiographs of, 386f treatment of conservative, 385 osteotomy, 386, 387 surgical, 386, 387 Bunions. see Hallux valgus Bursectomy, 471 Bursitis calcaneal, 481 retrocalcaneal, 151, 167f, 171b, 175f, 377, 582 sesamoid, 471 shoe-related causes of, 582 C Calcaneal bursitis, 481 Calcaneal fat pad insufficiency, 226 Calcaneal fractures anterior process, 100 avulsion etiology of, 100, 101f compression etiology of, 100–102, 101f mechanism of, 100–102, 101f treatment of, 102 anterolateral process, 305 classification of, 305–306 diagnosis of, 306, 307f eversion abduction mechanism of, 305–306, 307f imaging of, 307, 308f, 309f incidence of, 305 inversion mechanism of, 305, 306f malunited, 308 mechanism of, 305, 306f nondisplaced, 308 nonunion of, 308 physical examination, 307, 307f rehabilitation of, 308 return to sports after, 308 signs and symptoms of, 306–307 treatment of, 308 peroneal tendon dislocation and, 140 Calcaneal nerve medial, 220f neuroma of, 221f Calcaneal osteotomy, 194, 197f Calcaneal tuberosity, 147 Calcaneocuboid distraction arthrodesis, 198–199 Calcaneocuboid joint compression of, 307f dorsiflexion of, 307f Calcaneocuboid ligaments, 297 Calcaneofibular ligament, 143–144, 265–267, 266f, 276–277, 295f, 475 Calcaneonavicular coalitions, 346, 347f, 348, 350f Calcaneonavicular ligament, 297, 298f Calcaneonavicular tarsal coalition, 201f Calcaneus anatomy of, 297 blood supply to, 297 Haglund’s deformity, 147, 148f ligaments of, 297f posterior tuberosity of, 169, 171f prominence, endoscopic resection of, 561 Calcifications, 371 Calcitonin, 246 Calcium deficiencies stress fractures and, 58
Calcium deficiencies (Continued) supplementation for, 58–61 Calcium deficiency, 247 Calcium pyrophosphate dihydrate crystal deposition, 244 Calf raise, 603f, 608f Callus bunionette, 385–386 definition of, 582 description of, 254–255 diffuse, 387–388 discrete, 387–388, 390f in intractable plantar keratoses, 387, 390f shoe-related, 582 Cancellous bone graft, 115 Candida onychomycosis, 261 Capsaicin, 505 Capsular interposition, 416, 417f Capsular reefing, 406, 406f Carbamazepine, 505 Cardiovascular rehabilitation, 599, 599t Cartilage-derived morphogenetic proteins, 528 Cavovarus foot, 591 Cavus foot, 591 Cellulitis, 245 Cheilectomy hallux rigidus treated with, 414–415 postoperative course after, 415 results of, 415 Chevron osteotomy bunionette treated with, 387, 388f hallux valgus treated with, 441, 441f intractable plantar keratoses treated with, 392f Chevron-Akin osteotomy, 16–17, 19f Chilblain, 248, 252 Children. see Pediatric patients Chinese habits and sports ankle injuries, 511–512 foot injuries, 511–512 herb ointment therapies, 512–513 traditional Chinese medicine for, 513 Chondrocytes, 555–556 Chronic Achilles tendon rupture, 178 Chronic exertional compartment syndrome, 452 causes of, 452 compartment pressure testing, 453, 453f diagnostic studies, 453, 463t fasciotomy for, 455f history-taking, 452 pain associated with, 452–453 pathophysiology of, 452 physical examination, 453 treatment of, 454, 455f Claudication, 248 Claw toe, 397, 402, 426–427 Cleated shoes, 570 Collateral ligaments, 411 Comminuted fractures, 99 Common peroneal nerve anatomy of, 210–213 compression of, 210–213, 213f injuries to, 212f, 213f Communication, 25 Compartment syndrome anterior, 215–217 in dancers, 482 posterior, 7–8 Complementary deoxyribonucleic acid, 528 Computed tomography footballer’s ankle, 524 ossicles, 370–371, 372f osteochondral lesions of the talus, 320–321, 373, 373f
625
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Arthroscopy (Continued) synovitis treated with, 367 two-portal posterior, 356, 357f Athletes Achilles tendon injuries in, 619 ankle injuries in, 612–613 ankle sprains in high, 619 lateral, 618 medial, 618 deltoid injuries in, 618 female. see Female athletes foot injuries in, 612–613 Lisfranc injuries in, 616 midfoot sprains in, 616 navicular fractures in, 617 stress fractures in, 46, 47t turf-toe in, 614 Athlete’s foot. see Tinea pedis Australian sports description of, 516–517 surf lifesaving, 517, 517f Autologous chondrocyte implantation, 325–326, 487, 555 matrix-induced, 326 Avascular necrosis of the sesamoid, 417, 438–439 Avulsion fractures anterior process calcaneal, 100, 101f fifth metatarsal base fracture, 114, 616 os calcis, 35f, 35
Index Computed tomography (Continued) stress fracture evaluations description of, 66 navicular bone, 66, 67f syndesmotic injuries, 288 Condylectomy hard corn treated with, 396f partial, 389, 391f Conservative treatment, 4 bunionettes, 385 case studies of, 4–5 costs of, 5 description of, 4 economic impact of, 5 fifth metatarsal base fractures, 116, 117f flexor hallucis longus tendinitis, 40 hallux valgus, 436 impingement syndromes, 29 insertional plantar fasciosis, 229 intractable plantar keratoses, 389, 390f medial tibial stress syndrome, 447 metatarsophalangeal joint instability, 31, 31f, 404, 405f plantar fasciosis, 229 sinus tarsi syndrome, 33 stress fractures, 449 turf-toe, 428 Contact dermatitis, 251, 252f Continuous passive motion, 488 Corns, 253–254, 581 Corticosteroids flexor hallucis longus rupture caused by injection of, 125 plantar fasciosis treated with, 229, 229f Cotton test, 287 Crohn’s disease, 242 Cross-country skiing, 580 Cryotherapy, 132, 595 Cuboid anatomy of, 297 compressive injuries of, 108–109, 111f “locked,” 32 subluxation of, 32, 32t, 33f, 549 Cuboid fractures, 303 “chip,” 108 diagnosis of, 303 imaging of, 303, 305f, 306f incidence of, 303 magnetic resonance imaging of, 303, 306f mechanism of, 303 occult, 306f treatment of, 303 Cuneiforms bipartite, 108, 110f configuration of, 473–474 dislocation of, 108 fracture of, 108 medial, 108, 110f Cushing’s disease, 247 Cytokines, 528 D Dancers Achilles tendon injuries in, 479 peritendinitis, 479 rupture, 480 tendinitis, 480 ankle sprains in lateral, 475 medial, 475 anterior ankle injuries in, 477 bunionettes in, 474 compartment syndrome in, 482
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Dancers (Continued) demi-pointe stance, 469–470, 470f, 550 en pointe stance, 469, 470f feet of, 470 fifth metatarsal fractures in, 474, 474f, 549 flexor hallucis longus tendinitis in, 479, 549 Freiberg’s infraction in, 472, 473f great hallux interphalangeal joint injuries, 472 heel pain in, 480 lateral ankle injuries in, 475 lateral branch of the deep peroneal nerve impingement in, 477, 477f leg pain in, 481 medial ankle injuries in, 474 medial tibial stress syndrome in, 481 metatarsal injuries in, 473 metatarsophalangeal joint injuries in, 470 bunions, 470 dislocation, 472 hallux rigidus, 470, 471f idiopathic synovitis, 473 instability, 472 lateral proper digital nerve entrapment, 472 midfoot injuries in, 549 plantar fasciitis in, 480 posterior ankle injuries in, 477 flexor hallucis longus tendinitis, 479, 549 impingement syndrome, 477 posterior ankle pain in, 549 second metatarsal base stress fracture in, 473, 474f sesamoid bone injuries in, 471 “shin splints” in, 481 stress fractures in, 481 summary of, 482 trigger toe in, 123 Dancer’s pad, 80 Dancer’s tendinitis, 40, 42, 122 Davis’ law, 600–601 Deep peroneal nerve, 215, 532 lateral branch of the, 476, 477f Delayed hypersensitivity reaction, 251 Delayed union Jones fracture, 116 medial malleolus fractures, 89f Deltoid ligament anatomy of, 281, 281f chronic insufficiency, 284–285 deep, 281, 281f injury to acute repair, 284 diagnosis of, 282 magnetic resonance imaging of, 283 mechanisms of, 282 in professional athletes, 618 radiologic evaluations, 282 reconstruction, 285–286, 285f surgical treatment of, 283–284 syndesmosis injury associated with, 282, 282f, 283–284 treatment of, 283 posterior, 296f, 308–311, 311f restraint functions of, 281 strain of, 475 Demi-pointe stance, 469–470, 470f, 550 Dermatologic disorders, 251 black heel, 255, 256f contact dermatitis, 251, 252f friction blisters, 256 frostbite, 252 hyperhidrosis, 253 hyperkeratosis, 253, 254f piezogenic pedal papules, 256
Dermatologic disorders (Continued) sunburn, 255 traumatic, 255 xerosis, 255 Dermatophyte infections, 259 Desensitization massage, 605 Diabetes mellitus, 245 Dicloxacillin, 259 Dislocations foot. see Foot fractures and dislocations metatarsophalangeal joints, 472 peroneal tendon, 140, 142f subtalar joint, 344 Distal metatarsal articular angle, 439f Distal oblique osteotomy, 387, 389f, 391f Dorsal closed wedge osteotomy, 169, 171f Dorsal osteophyte, 10f Dorsal pedis artery, 295f “Double crush” phenomenon, 221–222 Drawer sign, 404f, 384 Dropfoot, 212f Dropped metatarsal, 30–31 Dual energy x-ray absorptiometry, 58 DuVries-type arthroplasty, 31 E Eccentric Exercise, 529 Egyptian foot, 470 Ehlers-Danlos syndrome, 278–279 Elastic lacing, 574 Elavil. see Amitriptyline Elsmlie procedure, 342f En pointe, 469, 470f Endoscopy calcaneal prominence resection, 561 Haglund’s deformity resection using, 169, 170f, 561–562 plantar fascia release using, 232–233 Enteropathic arthritis, 242 Enthesopathies, 242–243 Entrapment common peroneal nerve, 210–213, 212f lateral proper digital nerve, 472 peroneus brevis, 132 Epitenon, 147–148 Ethyl vinyl acetate, 568 Excision interdigital neuroma, 393, 393f os trigonum, 39 indications for, 38–39 lateral approach, 39 medial approach, 41 talocalcaneal coalitions, 350f Exercise walking shoes, 575, 575f Exertional compartment syndrome, 43 Exostosis, 395f Extensor hallucis brevis, 412 Extensor retinaculum, 131 External rotation test, for syndesmosis injury, 282, 283f Extracorporeal shock wave therapy. See also Shock wave therapy Achilles tendinitis treated with, 173 plantar fasciosis treated with, 229–230 F Fasciotomy, 419, 490f, 528 Fat pad insufficiency, 226 Female athletes. See also Women acute injuries in, 549 bunions in, 550 dancers, 548 gymnasts, 550
Index Fifth metatarsal base fractures (Continued) percutaneous intramedullary screw fixation, 115, 118f tuberosity description of, 114 treatment of, 116 zone 1, 113, 113f, 116 zone 2, 113, 113f, 116–117, 118f zone 3, 113, 113f, 117–118 Fifth metatarsal fractures avulsion fracture, 35 base. see Fifth metatarsal base fractures in dancers, 474, 549 Jones fracture, 474, 474f spiral diaphyseal, 474 stress fracture of, 81, 82, 83, 538 Figure skating shoes, 580 First metatarsophalangeal joint anatomy of, 412f arthroscopy of, 560, 561, 561f biomechanics of, 435 dorsal impingement, 29 hallucal sesamoid fractures, 80 hallux rigidus in, 29 range of motion for, 438–439 Flatfoot, 346, 536, 590, 591 Flats, 576, 576f Flexor digitorum longus, 126 anatomy of, 126 release of, 401f tendinitis of, 126 transfer of for hammertoe repair, 401f, 402f for tendinosis, 156 Flexor hallucis brevis, 16 split tendon of, 412 Flexor hallucis longus, 16, 121 Achilles tendon repair using, 521, 521f anatomy of, 36, 38f, 39f, 121–122 functions of, 121–122 os trigonum excision, 39–40 pseudocyst, 125 release of, 361 rupture of complete, 125 partial, 123. See also Trigger toe sheath of, 42f tendinitis of, 122 chronic, 122 clinical findings of, 123 conservative treatment of, 40 in dancers, 479 differential diagnosis, 122, 236 etiology of, 122 illustration of, 479f magnetic resonance imaging of, 122f os trigonum and, 38–39, 371 osteochondral defect as cause of, 373–374 pain caused by, 374 plantar medial midfoot pain caused by, 236 posterior impingement syndrome, 37t, 373 radiographs, 122 treatment of, 122 tenolysis of, 38–39, 41 transfer of for Achilles tendon rupture, 179–180, 179f for tendinosis, 156, 157f, 158f trigger toe. see Trigger toe tumor masses, 125 Flexor retinaculum release, 374f Fluconazole, 259, 261–262 Folate deficiency, 247
Foot dorsiflexion of, 424f radiographs of, 186, 187f, 188f stress fracture risks and, 62–63 Foot arch, 62–63 Foot fractures and dislocations ankle. see Ankle fractures diagnosis of, 85 lateral process talar fracture. see Lateral process talar fracture physical examination of, 85 radiographs of, 85 treatment of, 87 Foot shuffling, 509f, 509 Football shoes, 578, 579f Footballer’s ankle ankle instability, 523 clinical evaluation of, 523 computed tomography of, 524 diagnostic studies, 524, 524f etiology of, 522 magnetic resonance imaging of, 524 morphologic adaptation, 522–523 radiographs, 524f signs and symptoms of, 523 treatment of, 524 Forced plantarflexion sign, 477–478 Forefoot pain in, 221–222 shoe-related injuries, 581 Foxing, 571 Fractures ankle. see Ankle fractures avulsion anterior process calcaneal, 100, 101f fifth metatarsal base fracture, 114, 616 os calcis, 35, 35f calcaneal. see Calcaneal fractures cuboid, 303 “chip,” 108 diagnosis of, 303 imaging of, 303, 305f, 306f incidence of, 303 magnetic resonance imaging of, 303, 306f mechanism of, 303 occult, 306f treatment of, 303 fifth metatarsal. see Fifth metatarsal fractures foot. see Foot fractures and dislocations location of, 10 medial malleolus. see Medial malleolus fractures navicular. see Navicular fractures os peroneus, 139, 139f stress. see Stress fractures talus. see Talus fractures Freiberg’s disease/infraction in children, 542, 542f in dancers, 472, 473f description of, 30, 30f orthoses for, 588 types of, 473 Friction blisters, 256 Frostbite, 252 classification of, 252 diagnosis of, 252 prevention of, 253 treatment of, 252–253 Frostnip, 252 Functional progression, 599, 601t
627
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Female athletes (Continued) ice hockey, 550 increases in, 547 male athletes vs., 547–548 menstrual disturbances in, 57 musculoskeletal system, 548 posterior tibial tendinitis in, 550 stress fractures in, 49, 551 Female athletic triad, 246–247, 469 Ferkel’s phenomenon, 34 Fibroblasts, 527 Fibro-osseous tunnel, 36–38, 39f Fibula distal, 140, 141f, 143 supination-eversion fracture of, 7f Fibular fractures bimalleolar fracture and, 94, 95f displaced, 90, 92f head, 207f nondisplaced, 90–91 Salter-Harris I, 539–540 stress fractures ankle joint diastasis caused by, 17–18 magnetic resonance imaging of, 24f Fibular hallux sesamoidectomy, 419–420 Fibular ligaments anterior talofibular, 265–267, 266f anatomy of, 286f in modified Brostrom technique, 276, 278 sprain of, 475 tear of, 35, 476 anterior tibial, 24f anterior tibiofibular, 24f anatomy of, 286–287, 286f Basset’s ligament, 34, 34f insertion of, 35 Fibular notch, 286, 286f Fibular tip fracture of, 35f, 35 impingement under, 36, 36f Fifth metatarsal apophyseal avulsion of, 538 boxer’s fracture of, 30f bunionette on, 385f Freiberg-like syndrome of, 30 proximal end of, 113–114 tendon attachments of, 113f tuberosity of, 114 vascular anatomy of, 114, 114f watershed area, 114 Fifth metatarsal base fractures, 109, 616 in adolescents, 115 avulsion, 114, 616 in basketball players, 616 classification systems, 109–110, 110–112, 112–113, 113f delayed union of, 116 diagnosis, 114, 115 etiology of, 114 historical description of, 109 nonunions, 118 patterns of, 616 physical examination, 114 in professional athletes, 616 radiographs, 115 recurrent, 118 stress fractures, 82 treatment of cancellous bone graft, 115 conservative, 116, 117f inlay bone grafting, 115 medullary curettage, 115
Index G Gabapentin, 505 Gait evaluation of, 598 phases of, 598 Gastrocnemius muscle, 210–213 Gene therapy, 528 Girdlestone-Taylor procedure, 31 Glutaraldehyde solution, 253 Glyceryl trinitrate, 530 Golf shoes, 570 Gout, 243 Great-toe disorders acute, 422 anatomy of, 411 arthroscopy of, 560 in dancers, 472 description of, 411 functional disability caused by, 411 hallux rigidus. see Hallux rigidus metatarsophalangeal joint. see Metatarsophalangeal joint sesamoid disorders. see Sesamoid disorders turf-toe. see Turf-toe Grecian foot, 469 Groin pain of neural origin, 223, 223f Gymnasts, 550 H Haglund’s deformity, 150 cavus foot with, 480, 480f clinical findings, 151 description of, 147 endoscopic resection of, 169, 170f, 561–562 history of, 150–151 illustration of, 148f, 149f insertional Achilles tendinitis and, 150 magnetic resonance imaging of, 167f, 562f nonsurgical treatment of, 153 radiographs of, 481f risk factors for, 151 surgical treatment of, 164, 166f, 167f symptoms of, 171b Hallux metatarsophalangeal joint anatomy of, 411 biomechanics of, 412 dislocations of, 423t, 429, 430f, 431t hyperflexion injuries, 431 injuries to. see Great-toe disorders range of motion, 412, 422 turf-toe injury. see Turf-toe Hallux osteochondral lesions, 520f Hallux rigidus, 413 in dancers, 470, 471f definition of, 413, 615 in first metatarsophalangeal joint, 29 grade I, 470 grade II, 470–471 grade III, 471 nonoperative treatment of, 413–414, 615 orthoses for, 413–414, 587 severity of, 413 surgical treatment of arthrodesis, 416 arthroscopy, 417 cheilectomy, 414–415 implant arthroplasty, 417 interposition arthroplasty, 416–417, 417f Moberg osteotomy. see Moberg osteotomy options for, 414 phalangeal osteotomy, 415, 415f resection arthroplasty, 416, 417f symptoms of, 413
...........
628
Hallux saltans, 40, 40f Hallux sesamoid, 419 stress fractures, 79, 80 Hallux valgus chevron procedure for, 441, 441f in children, 537 conservative management of, 436 decision making associated with, 439 distal soft-tissue procedure, 441 in female athletes, 550 orthotic device associated with, 437–438 physical examination, 438 proximal osteotomy for, 441 radiographs of, 439f second metatarsophalangeal joint dislocation and, 19f shoe considerations, 537 toe spacer for, 4f treatment of, 537 types of, 435 windlass mechanism of, 435–436 Hammertoe, 397 characteristics of, 397 surgical treatment of, 398, 399f Hard corns, 394, 394f Hawkins classification, of lateral process talar fractures, 98, 99f Healing, 527 Health Insurance Portability and Accountability Act, 25 Heel counters, 571 Heel cups, 590f Heel disorders black heel, 255, 256f piezogenic pedal papules, 256 Heel pad insufficiency, 226 Heel pain of neural origin, 218–221 plantar. see Plantar heel pain recalcitrant, 218–221 Heel spurs, 236, 480 Heel strike during running, 446, 446f during walking, 226 Helomas, 253–254 High ankle sprain, 17–18, 34, 619 Hiking boots, 574, 574f Hindfoot anatomy of, 293, 294f inversion of, in posterior tibialis tendon disease or dysfunction, 186f occult fractures of, 293 plantar fasciitis. see Plantar fasciitis tendons attaching to, 297–298, 299f “Hip pointer,” 222–223 History taking, 3 Hyaluronate, 532 Hyaluronic acid, 489f Hyperflexion injuries, of hallux metatarsophalangeal joint, 431 Hyperhidrosis, 253 Hyperkeratosis, 253, 254f Hyperparathyroidism, 247 Hyperuricemia, 243 I Ice hockey, 550, 580 Idiopathic synovitis, 31 Iliac crest graft, 380f Immobilization fifth metatarsal stress fractures managed with, 82
Immobilization (Continued) posterior tibialis tendon dysfunction managed with, 191 Impingement syndromes ankle, 33 anterior. see Anterior ankle impingement anterocentral, 33–34, 35 flexor hallucis longus tendonitis vs., 37t lateral, 35–36 os trigonum. see Os trigonum posterior. see Posterior ankle impingement posterolateral, 36 spurs, 33–34 conservative treatment of, 29 fibular tip, 36, 36f idiopathic synovitis, 31 interphalangeal joint, 29 lesser metatarsophalangeal joints, 30 midfoot lateral, 32 medial, 31 os trigonum, 38f word origin of, 29 Infectious disorders, 257 tinea pedis, 258, 258f viral warts, 257, 258f Inflammatory phase, of healing, 527 Inflatable rescue boats, 517–518, 517f Ingrown toenail. see Onychocryptosis Inlay bone grafting, 115 Insertional Achilles tendinitis, 150, 377 classification of, 377 magnetic resonance imaging of, 151f, 162f, 167f nonsurgical treatment of, 153 orthoses for, 591 retrocalcaneal bursitis. see Retrocalcaneal bursitis surgical treatment of, 162, 162f, 377 symptoms of, 171b, 377 Insertional plantar fasciosis, 227 botulinum toxin injections for, 230 conservative treatment of, 229 corticosteroid injections for, 229, 229f extracorporeal shock wave therapy for, 229–230 leg length evaluations, 229 onset of, 228 platelet-rich plasma injections for, 230 surgical treatment of, 230, 231, 232f symptoms of, 228 training modifications for, 229 Instability ankle. see Ankle instability subtalar, 339 Insulin-like growth factor, 528 Interdigital nerve entrapment, 10 Interdigital neuroma, 392, 393f, 582 Interdigital plantar nerve entrapment, 221–222, 221f, 222f Interdigital spaces dermatophyte infections of, 259 tinea pedis in, 258–259 Intermetatarsal angle, 439–440 Intermetatarsal diastasis, 107f Interphalangeal joint great toe, 472 impingement syndrome of, 29 Interposition arthroplasty, 416, 417f Intractable plantar keratoses, 387, 585 callus formation associated with, 387, 390f case studies, 389 definition of, 387, 585–586 discrete, 391f illustration of, 390f radiographs of, 388–389
Index
J Japanese martial arts Judo, 507, 508f Kendo, 509, 510f Sumo, 508, 509f Jogger’s foot, 10, 233–235 Jones fracture. See also Fifth metatarsal base fractures diagnosis of, 114 fifth metatarsal, 474, 474f historical description of, 109 in pediatric patients, 538 treatment of, 116, 117f, 539 Joplin’s neuroma, 472 Judo, 507, 508f K Kendo, 509, 510f Knee joint denervation of, 207–208, 207f innervation of, 208f pain in, 207–208 Knot of Henry, 40, 121–122 Kohler’s disease, 541 Korean sports accessory navicular incidence in, 516 basketball, 516 soccer, 516 ssireum, 514 Taekwon-do, 515, 515f L Laceration peroneal tendons, 140 tibialis anterior, 128 Laces, of shoes, 573, 573f Lachman test, 30–31, 31f, 422–423 Lapidus procedure, 11–12 Laser therapy, 529 Lateral compartment muscles, 121 Lateral exertional compartment syndrome, 9–10 Lateral femoral cutaneous nerve anatomy of, 222–223 compression of, 222–223, 223f neurolysis of, 223f Lateral gutter, 362 Lateral malleolus deformity of, 284–285 fractures of, 90 fibular displacement secondary to, 90 nonoperative management of, 92 operative management of, 90–91, 92–94 Lateral plantar nerve compression of, 219f
Lateral plantar nerve (Continued) decompression of, 236, 237f first branch of, entrapment of, 233, 233f, 234f, 235f Lateral process talar fractures, 97, 315, 315f, 316f, 317f ankle sprain vs., 97 comminuted, 99 description of, 35 etiology of, 97 Hawkins classification of, 98, 99f radiographic evaluations, 98 sequelae of, 99 sports with high rates of, 97 treatment of, 99, 100f Lateral proper digital nerve entrapment, 472 “Leather bottle sign”, 127 Leg compartments, 452f Leg-length discrepancy, 63 Lesser-toe disorders bunionettes. see Bunionettes claw toe, 397, 402, 403f hard corns, 394, 394f intractable plantar keratoses. see Intractable plantar keratoses mallet toe, 397, 398f, 400, 400f soft corns, 394, 395f Lidocaine patch, 505 Ligaments anterior talofibular, 265–267, 266f anatomy of, 286f in modified Brostrom technique, 276, 278 sprain of, 475 tear of, 35, 476 anterior tibiofibular, 24f anatomy of, 286–287, 286f Basset’s ligament, 34, 34f insertion of, 35 Basset’s, 34, 34f calcaneocuboid, 297 calcaneofibular, 143–144, 265–267, 266f, 276–277, 295f, 475 calcaneonavicular, 297, 298f collateral, 411 deltoid. see Deltoid ligament medial metatarsosesamoid, 411, 412f posterior inferior tibiofibular, 286–287 spring repair of, 15f strains of, 43 superficial posterior tibiotalar, 281 talocalcaneal interosseous, 293, 294f talofibular, 294–297 talonavicular, 294f, 297 talotibial, 294–297 tibiocalcaneal, 281 tibionavicular, 281 tibiospring, 281 tibiotalar, 281 Liposomes, 528 Lisfranc injuries, 102, 529, 616 causes of, 529 cuboid injuries presenting with, 108–109, 111f diastasis, 106, 107f, 108f, 491f, 529 frequency of, 102 injury patterns, 103 misdiagnosis of, 103 Myerson classification, 103, 105f Nunley classification, 103, 104f physical examination of, 104 radiographic evaluations, 104, 107f simple lateral, 103 sports-specific occurrence of, 102
Lisfranc injuries (Continued) “subtle” injuries, 102, 104 in surf lifesaving, 518, 519f treatment of, 106 closed, 106, 108f guidewires, 491f, 529 open reduction, 106 outcomes, 106 rehabilitation after, 106–108 screw fixation, 106, 109f Weber clamps, 106, 108f variants of, 108 “Locked” cuboid, 32 Loose bodies, 370, 372–373 Lower leg disorders chronic exertional compartment syndrome. see Chronic exertional compartment syndrome diagnostic studies, 463t nerve entrapment. see Nerve entrapment pain locations of, 462t physical examination findings, 462t popliteal artery entrapment syndrome. see Popliteal artery entrapment syndrome summary of, 462 Lower-extremity nerve injuries compression sites, 217t differential diagnosis, 206f knee joint pain, 207–208 lateral ankle joint pain, 208–209 lateral femoral cutaneous nerve, 222–223 mechanism of, 206–207 overview of, 205 pathophysiology of, 206–207 peroneal nerve, 210 anatomy, 210, 211f common, 210–213, 212f, 213f deep, 215 superficial, 213–215, 214f, 215f posterior tibial nerve. see Posterior tibial nerve saphenous nerve, 223, 224f sural nerve, 224 Luteal phase deficiency, 56–57 Lyme disease, 244 Lymph edema, 249 Lymphatic disease, 249 M Maffulli technique, 154, 155f Magnetic resonance imaging Achilles tendinitis, 149f Achilles tendon rupture, 176f cuboid fractures, 303, 306f deltoid ligament injury, 283 flexor hallucis longus tendinitis, 122f global compression injuries of the talus, 335f insertional Achilles tendinitis, 151f medial malleolus, 73, 78 osteochondral lesions of the talus, 321 posterior tibialis tendon disease or dysfunction evaluations, 187, 190f sinus tarsi syndrome, 343 stress fractures, 66, 67f, 67t, 449 syndesmosis injury, 288, 289f tarsal coalition, 10, 11f Maissoneuve’s fracture, 287 Mallet toe, 397, 398f, 400, 400f Marfan’s syndrome, 278–279 “Marsupial meniscus,” 297f, 294–297 Martial arts Judo, 507, 508f Kendo, 509, 510f Sumo, 508, 509f
629
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Intractable plantar keratoses (Continued) treatment of chevron osteotomy, 392f conservative, 389, 390f metatarsal osteotomy, 391, 391f, 392f padding, 389, 390f partial condylectomy, 389, 391f proximal closing wedge osteotomy, 392f surgical, 389, 391 warts vs., 387–388, 390f Intramedullary nailing, 92–94 Intraosseous talar cysts, 378, 379f, 380f Iselin’s disease, 544 Isolated tendinosis, 150 Isotopic bone scan stress fracture imaging using, 64, 65f technetium-99 methylene diphosphonate, 64 Itraconazole, 261–262
Index Matrix metalloproteases, 527 Matrix-induced autologous chondrocyte implantation, 326 Maturation stage of healing, 527 Medial calcaneal nerve, 220f Medial clear space, 86, 87f Medial malleolus fractures delayed union of, 89f imaging of, 88, 88f magnetic resonance imaging, 73f, 78f stress fractures, 76 anatomy of, 77 description of, 10 illustration of, 16f, 17f, 18f imaging of, 73f, 78f, 77 physical examination, 77 presentation of, 77 treatment, 77 vertical repair, 15–16 Medial malleolus osteotomy, 331f Medial metatarsosesamoid ligament, 411, 412f Medial plantar nerve decompression, 236, 237f Medial shift calcaneal osteotomy, 194, 197f, 198–199 Medial talar dome osteochondritis dissecans, 187f Medial talar osteophyte, 16f Medial tibial stress syndrome, 445 athletes with susceptibility to, 446 bone scan evaluations, 446–447, 447f case study of, 447–448 in dancers, 481 diagnostic studies, 446 history-taking, 446 pain associated with, 447 physical examination, 446 posterior, 481 sites of, 445–446 treatment of, 447 conservative, 447 operative, 447 Medullary curettage, 115 Menarche, age of, 57, 61f “Meniscoid lesion,”, 365–366 Menstrual disturbances, 55 Meralgia paresthesia, 222–223 Mesenchymal stem cells, 528 Metabolic bone disease, 245 Metabolic diseases, 245 Metatarsal bar, 80 Metatarsalgia definition of, 582 description of, 383 differential diagnosis, 384 evaluative algorithm for, 383, 384f signs and symptoms of, 30–31 Metatarsals displacement of, 111f dropped, 30–31 fifth. see Fifth metatarsal fourth “dropped,” 32f stress fractures of, 69 head of, 30 dislocation, 429 ligaments that stabilize, 411 ulcers under, 587 osteotomy of, 391, 391f, 392f second base of, 74f, 76f, 75, 473, 474f stress fractures of, 69, 74f, 76f, 75, 473 stress fracture of, 14f, 45, 69 third, 69
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630
Metatarsophalangeal joints capsulitis of, 403–404 congruent, 437f dislocation of, 472 dorsiflexion of, 436f first anatomy of, 412f arthroscopy of, 560, 561, 561f biomechanics of, 435 dorsal impingement, 29 hallucal sesamoid fractures, 80 hallux rigidus in, 29 range of motion for, 438–439 gouty arthritis of, 243–244 hallux anatomy of, 411 biomechanics of, 412 dislocations of, 423t, 429, 430f, 431t hyperflexion injuries, 431 injuries to. see Great-toe disorders range of motion, 412, 422 turf-toe injury. see Turf-toe incongruent, 437f inflammation of, 403–404 instability of, 403 axial misalignment associated with, 405f capsular reefing and flexor tendon transfer for, 406, 406f case study of, 405 conservative treatment of, 31, 31f, 404, 405f in dancers, 472 diagnosis of, 403 illustration of, 15f interdigital neuroma vs., 393 pain associated with, 403 surgical treatment of, 406, 407f, 408f surgical treatments for, 31 toe taping for, 405f Lachman test, 30–31, 31f lesser dorsal impingement of, 30 instability of, 30 plantar plate injury in, 16–17 plantar surface of, 79 second dislocation of, 19f instability of, 403, 404f subluxation of, 20f soft-tissue arthroplasty, 403 subluxated, 437f, 441 synovitis of, 473, 587 Midfoot arthritis of, 589 articulation of, 103 dorsal osteophyte on, 31 impingement syndromes of, 31, 32 injuries to classification system for, 103, 104f, 105f in dancers, 549 lateral, 32 medial, 31 pain in, 75 sprains of, 616 Moberg osteotomy complications of, 416 indications for, 415 postoperative care, 416 procedure for, 415–416 Mobilization, 596 Moccasin-type tinea pedis, 258–259 Model’s foot, 470 Modified Bromstrom technique complications of, 275
Modified Bromstrom technique (Continued) contraindications, 275–276 postoperative care, 278 results of, 275 sutures used in, 277–278, 277f technique, 276, 276f, 277f, 278f tenodesis vs., 275 Morton’s feet, 29 Morton’s neuroma, 221–222, 586 surgical resection of, 205–206 Motocross, 501f, 531 Mulder’s sign, 393 Muscle mass, 61 Muscle strengthening, 598 Musculoskeletal system evaluation, 3–4 N Nail disorders, 259 onychocryptosis, 260, 260f onychomycosis, 261, 261f subungual hematoma, 259, 259f Narcotics, 504–505 Navicular bone. See also Talonavicular avulsion injuries accessory, 537 in children, 537 description of, 36, 43 displaced, 304f flexible flatfoot with, 590 imaging of, 187f, 202f, 300f, 303f in Korea, 516 orthoses for, 590, 591f radiographs of, 537 signs and symptoms of, 537 treatment of, 537 blood supply to, 297, 298f dorsal osteophyte on, 10f tarsal, medial prominence of, 43 Navicular fractures avulsion, 298, 299 dorsal computed tomography of, 301f description of, 298 nonunion of, 300f, 301f physical examination, 300f medial description of, 299 treatment of, 301–302 in professional athletes, 617 stress computerized tomography of, 67f, 66 description of, 12f, 10, 52 Nerve blocks, 529 Nerve compression, 205–206 Nerve entrapment, 7–8 causes of, 456 diagnostic studies, 457, 463t history-taking, 456 lower extremity, 456 peroneal nerve, 456, 457–458 physical examination, 457 shoe-related, 582 signs and symptoms of, 456–457 sites of, 456f treatment of, 457 Nerve injuries with ankle sprain anatomy of, 530 clinical presentation of, 531 nerve blocks for, 529 nonsurgical treatment of, 531 oral medications for, 532 pathoanatomy of, 530 surgical treatment of, 506
Index
O Occlusive disease, 247–248 Onychocryptosis, 260, 260f Onychomycosis, 261, 261f Open reduction and internal fixation lateral malleolar fractures treated with, 92f medial malleolar fracture, 88 Oral contraceptive pills, 57–58 Orthoses accessory navicular treated with, 590, 591f ankle sprain treated with, 593 ankle-foot Achilles tendinitis, 7f case study use of, 4–5, 6f cavovarus foot treated with, 591 description of, 585 Freiberg’s infraction treated with, 588 hallux rigidus treated with, 587 insertional Achilles tendinitis treated with, 591 intermetatarsal neuritis treated with, 586 intractable plantar keratosis treated with, 585 midfoot arthritis, 589 Morton’s neuroma treated with, 586 plantar fibromatosis, 588 sesamoid disorders treated with, 418 sinus tarsi syndrome treated with, 593 subtalar arthritis treated with, 593 tarsal tunnel syndrome treated with, 590 total-contact insert, 585–586, 586f, 587f turf-toe treated with, 587 University of California Biomechanics Laboratory, 237, 589f Os calcis, 360 avulsion fracture of, 35f, 36f, 35
Os peroneum, 115 Os peroneus, 139, 139f Os subfibulare, 35 Os subtibiale, 43, 475 Os trigonum, 122, 294–297, 296f asymptomatic, 36–38 attachments, 39 definition of, 36, 370 flexor hallucis longus tendinitis associated with, 38–39, 371 magnetic resonance imaging of, 313f, 314f nonsurgical treatment of, 479 plantarflexion test for, 370–371, 372f posterior ankle impingement caused by, 38f, 370, 479 prevalence of, 370 radiographs of, 314f, 371f, 478f removal of, 360–361, 362–364, 363f signs and symptoms of, 370 surgical excision of, 39 indications for, 38–39 lateral approach, 39 medial approach, 41 talar compression syndrome associated with, 36–38 tests for, 370–371 Os vesalianum, 115, 538 Ossicles ankle impingement caused by, 370 arthroscopic removal of, 370 computed tomography of, 370–371, 372f Osteoblasts, 45–46 Osteochondral allografts, 556 Osteochondral autograft transfer system, 324, 331f, 334, 475, 555 Osteochondral lesions of the talus, 317, 527, 553 acute, 323, 327 Altman’s classification, 520f anterolateral located, 369f arthroscopy of, 326f, 367 articular cartilage intact, 323–324, 329f, 331 asymptomatic, 330–331 chronic, 323, 330 classification, 321, 323f, 324f, 325f, 327, 367–368 clinical presentation of, 553 computed tomography of, 320–321, 373, 373f “coring” of, 476f definition of, 367 description of, 317–318 diagnosis of, 318 dome, 527 in children, 543 description of, 318 radiographs of, 329f retrograde drilling and bone graft for, 329f surgical treatment of, 487 transmalleolar pinning of, 325f epidemiology of, 367 imaging, 320 incidence of, 318, 553 lateral, 553 locations of, 553 magnetic resonance imaging of, 321, 475f, 558f mechanism of, 318, 319f medial, 553 physical examination, 319 posterior ankle impingement caused by, 373–374 posteromedially located, 368f radiographs, 320–321, 321f, 553–554, 557f staging of arthroscopic, 367–368 classification system for, 554t
Osteochondral lesions of the talus (Continued) stage 1, 554t stage 2, 327–328, 331, 554t stage 3, 328–329, 331, 554t stage 4, 328–329, 331, 554t stage 5, 331–334, 554t treatment of, 323, 554 acute injuries, 323 allografts, 326, 334f author’s suggested approach, 327 autologous chondrocyte implantation, 325–326, 487, 555 chronic injuries, 323 debridement, 554 drilling, 554 excision and curettage, 323, 326f, 327f matrix-induced autologous chondrocyte implantation, 326 microfracture, 554 nonoperative, 323, 554 open reduction and internal fixation, 554 osteochondral autograft transfer system, 324, 331f, 334 tunnel technique, 487f Osteochondral plugs, 555 Osteochondritis dissecans. See also Osteochondral lesions of the talus dome in children, 543 definition of, 318 medial talar dome, 187f Osteochondroses, 541 Freiberg’s disease, 542, 542f Iselin’s disease, 544 Kohler’s disease, 541 nonarticular, 543 of the sesamoid, 417, 419 Sever’s disease, 543, 591 Osteoclasts, 45–46 Osteoid osteoma, 68 Osteopenia, 245–246 Osteophytes ankle, 33 anterior, 366 anteromedial, 366 medial talar, 16f midfoot, 31 naviculum, 10f removal of, 29 sinus tarsi syndrome caused by, 32–33, 33f tibiotalar, 477f Osteoporosis causes of, 246–247, 246t description of, 245–246 stress fractures affected by, 55 treatment of, 246 Osteotomy bunionette treated with, 386 Chevron bunionette treated with, 387, 388f hallux valgus treated with, 441, 441f intractable plantar keratoses treated with, 392f Chevron-Akin, 16–17, 19f distal oblique, 387, 389f, 391f medial malleolus, 331f metatarsal, 391, 391f, 392f, 442f Moberg complications of, 416 indications for, 415 postoperative care, 416 procedure for, 415–416 phalangeal, 415, 415f proximal, 441 proximal closing wedge, 392f
631
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Nerve injuries with ankle sprain (Continued) topical medications for, 532 treatment of, 531 Neurolysis of lateral femoral cutaneous nerve, 223f of tibial nerve, 215–217, 216f Neuroma calcaneal nerve, 221f illustration of, 206f interdigital, 392, 393f, 582 Joplin’s, 472 Morton’s, 221–222, 586 surgical resection of, 205–206 treatment of, 205–206 Neurontin. see Gabapentin Nitinol step staples, 196–197, 198f Noninsertional Achilles tendinitis, 148 adhesion excision, 154 classification of, 376 imaging of, 149f nonsurgical treatment of, 153, 162b surgical treatment of, 154 tenotomy, 154 Nonsteroidal anti-inflammatory drugs Achilles tendinopathy treated with, 529 nerve injuries treated with, 504–505 pain management using, 504–505 peroneal tendinitis treated with, 132 posterior ankle impingement syndrome treated with, 38 posterior tibialis tendon dysfunction managed with, 191 Nonunions fifth metatarsal base fractures, 118 treatment of, 82 Nutrition, 58 Nylon sole plates, 575
Index Osteotomy (Continued) proximal crescentic, 440f proximal phalanx, 416 Weil, 406, 408f, 472 Overuse injuries, 49–52 Oxycodone, 504–505 P Pain Achilles tendon rupture, 488–489 ankle. see Ankle pain nonsteroidal anti-inflammatory drugs for, 504–505 stress fracture-related, 63, 64, 68 Paratenon, 147–148 release of, 154f Partial condylectomy, 389, 391f Partial weight bearing, 170–171, 172f, 489, 607–608 Patience, 6 Peasant foot, 470 Pediatric patients accessory navicular in, 537 ankle fractures in, 96, 539 classification of, 539 osteoarthritis secondary to, 541 physeal, 541 radiographs of, 539 Salter-Harris I, 539–540 Salter-Harris III, 540 Salter-Harris IV, 540 Salter-Harris V, 540–541 site of, 539 coalitions, 535 fifth metatarsal avulsion fracture in, 538 flat feet, 536 hallux valgus in, 537 Jones fracture in, 538 os vesalianum sesamoid in, 538 osteochondroses in, 541 Freiberg’s disease, 542, 542f Iselin’s disease, 544 Kohler’s disease, 541 nonarticular, 543 Sever’s disease, 543 tarsal coalition in, 535, 536 Percutaneous intramedullary screw fixation, 115, 118f Percutaneous longitudinal tenotomy, 532 Periosteum anatomy of, 29 cambium layer of, 29 Periostitis, 65 Peripheral nerve surgery, 207 Peripheral neuropathy, 245, 393 Peritendinitis adhesion excision, 154, 154f arthroscopy for, 377 in dancers, 479 definition of, 148 refractory, 153 signs and symptoms of, 149f with tendinosis, 148–150 treatment of, 153 Pernio, 248 Peroneal nerve, 210 anatomy, 210, 211f common, 210–213, 212f, 213f deep, 215 entrapment, 456, 457–458 superficial, 213–215, 214f, 215f anatomy of, 213–215, 532 compression of, 213–215, 214f, 215f injuries to, 213–215, 214f, 215f
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632
Peroneal retinaculum in peroneal tendon dislocations, 143 repair of, 143 Peroneal subluxation, 36, 37f Peroneal tendons accessory, 134f arthroscopy of, 376f dislocation of, 140 classification, 142f surgical management of, 142 distal fibula morphology and, 143 fusiform swelling of, 136–139 laceration of, 140 subluxation of chronic, 141 orthoses for, 593 retinaculum repair, 143–144 surgical management, 142 tendinitis of, 375 tenosynovitis of, 593 zone A, 135, 136f zone B, 136–139, 136f zone C, 136–139, 136f zone D, 139–140 zones of, 122f, 135 Peroneal tubercle excision of, 138f illustration of, 136–139, 136f Peroneus brevis anatomy of, 131, 132–133, 297–298, 299f attritional tears of, 135 avulsion of, 139–140, 142–143 description of, 121 entrapment of, 132 function of, 131–132 tear of, 134 tendinitis, 132, 133f, 134, 135 Peroneus longus anatomy of, 131, 299f calcification of, 135 entrapment of, 134, 135, 136f rupture of, 37f, 135 tendinitis, 132, 133f, 134 Pes cavus in children, 536 stress fractures and, 62–63 Pes planus in children, 536 stress fractures and, 63 Phalangeal osteotomy, 415, 415f Physical examination description of, 3–4 fifth metatarsal base fractures, 114 foot fractures and dislocations, 85 Lisfranc injuries, 104 medial malleolus stress fracture, 77 stress fracture evaluations, 64 talar compression syndrome, 36 tibialis anterior tendinitis, 126–127 Piezogenic pedal papules, 256 Plantar aponeurosis, 436f Plantar fascia anatomy of, 227–228 chronic inflammation of, 233–235 endoscopic release of, 232–233 microtears in, 228, 228f release of, 230, 231, 232f rupture of, 228, 228f Plantar fasciitis, 489 botulinum toxin injections for, 230 in dancers, 480 definition of, 590 fasciotomy for, 490f, 528
Plantar fasciitis (Continued) midsubstance, 236, 237f nonoperative treatment of, 528 pain from, 218–221 risk factors, 528 shoe-related causes of, 582 silicone heel cups for, 590f surgical treatment of, 529 tarsal tunnel syndrome with, 590 Plantar fasciosis, 227 botulinum toxin injections for, 230 conservative treatment of, 229 corticosteroid injections for, 229f, 229 extracorporeal shock wave therapy for, 229–230 leg length evaluations, 229 onset of, 228 platelet-rich plasma injections for, 230 surgical treatment of, 232f, 230, 231 symptoms of, 228 training modifications for, 229 Plantar fibromatosis, 588 Plantar heel pain case studies of, 238 causes of, 226 description of, 226 differential diagnosis, 226 entrapment of first branch of lateral plantar nerve as cause of, 233, 233f, 234f, 235f fat pad insufficiency, 226 insertional plantar fasciosis. see Insertional plantar fasciosis midsubstance plantar fasciitis as cause of, 236, 237f tarsal tunnel syndrome as cause of, 236 Plantar heel spur, 236 Plantar keratoma, 253–254 Plantar keratoses. see Intractable plantar keratoses Plantar nerve interdigital, entrapment of, 221–222, 221f, 222f lateral, compression of, 219f Plantar plate description of, 435, 436f rupture of, 16–17, 18f Plantar warts, 258f causes of, 257 diagnosis of, 257 treatment of, 257–258 “Plantarflexion sign,” 36 Plantarflexion test, 370–371, 372f Platelet-derived growth factor, 528 Platelet-rich plasma injections, 230 Polyglycolic acid, 528 Popliteal artery entrapment syndrome, 458 anatomic, 458 anatomy of, 458, 459f, 461f arteriogram of, 461f diagnostic studies for, 460, 463t functional, 458 history-taking, 458 pain associated with, 458–460 physical examination, 460, 462t treatment of, 460 Posterior ankle impingement, 36, 37t, 38, 370 causes of, 370 characteristics of, 370 in dancers, 477 flexor hallucis longus tendinitis, 373 forced plantarflexion sign, 477–478 lateral ligament sprain as cause of, 479 loose bodies, 372–373 os trigonum, 38f, 370, 371f, 479
Index Proteoglycans, 488f Proximal closing wedge osteotomy, 392f Proximal crescentic osteotomy, 440f Proximal osteotomy, 441 Proximal phalanx osteotomy, 416 Pseudocyst, 125 Pseudogout, 244 Pseudomeniscus, 479 Psoriatic arthritis, 242 Publicity, 21 Q Qi, 513 R Race-walking shoes, 575 Racquet sport shoes, 577 Radiofrequency coblation, 529 Radiographs fifth metatarsal base fractures, 115 flexor hallucis longus tendinitis, 122 foot fractures and dislocations, 85 Iselin’s disease, 544–545 Kohler’s disease, 541 lateral process talar fractures, 98 Lisfranc injuries, 104, 107f osteochondral lesions of the talus, 320–321, 321f posterior tibialis tendon disease or dysfunction evaluations, 186 soft corns, 395f stress fracture imaging, 64 subtalar dislocation, 344 subtalar instability, 340, 341f trigger toe, 123 Range of motion, 596 Raynaud’s phenomenon, 248 Rehabilitation Achilles tendon repair, 530, 601 ankle fractures, 607 ankle joint instability, 267–268, 269t cardiovascular activities, 599, 599t cryotherapy, 595 functional progression, 599, 601t gait evaluation, 598 lateral ankle reconstruction, 604 mobilization, 596 muscle strengthening, 598 phases of, 601 proprioception, 598, 606f protected weight-bearing, 597 range of motion, 596 stress fractures, 68 Reiter’s syndrome, 242 Releve´ position, 469–470, 470f Remodeling phase, of healing, 527 Resection calcaneonavicular coalitions, 348 Haglund’s deformity, 169, 170f Morton’s neuroma, 205–206 talocalcaneal coalitions, 348, 350f, 351f Resection arthroplasty, 416, 417f Resisted eversion, 605f Rest, 6–7 Retrocalcaneal bursa, 147 Retrocalcaneal bursitis, 151, 167f, 171b, 175f, 377, 582 Retrocalcaneal space, 561–562 Rheumatoid arthritis, 243, 587–588 Rheumatologic disorders, 241 ankylosing spondylitis, 241 enteropathic arthritis, 242 psoriatic arthritis, 242 Reiter’s syndrome, 242
Rheumatologic disorders (Continued) Still’s disease, 241 systemic lupus erythematosus, 243 RICE, 595 Rocker sole, 587f Rugby shoes, 579 S Salter-Harris classification, 96, 97f III, 540 IV, 540 V, 540–541 Sand toe, 423t Saphenous nerve compression, 223, 224f Sarcoidosis, 245 Sclerosing injections, 529 Screw fixation fifth metatarsal base fractures treated with, 115, 118f Lisfranc injuries repaired with, 106, 109f percutaneous intramedullary, 115, 118f Second metatarsals base of, 74f, 76f, 75, 473, 474f stress fractures of, 69, 74f, 76f, 75, 473 Second metatarsophalangeal joint dislocation of, 19f instability of, 403, 404f subluxation of, 20f Selective estrogen receptor modulators, 246 Sesamoid bursitis, 471 Sesamoid disorders, 417 avascular necrosis, 417 bipartite, 426 bone grafts for, 419 diagnosis of, 418 instability, 471–472 magnetic resonance imaging of, 418 nonoperative treatment of, 418 osteochondrosis, 417, 419 plantar prominence, 417–418 radiographs of, 418 surgical treatment of, 418 tibial, 438f Sesamoid fracture, 417, 418–419 Sesamoidectomy, 413 biomechanical sequelae of, 420–421 fibular hallux, 419–420 incisions for, 420f indications for, 419 postoperative care, 420 results of, 420 tibial hallux, 419 Sesamoiditis, 417, 471, 582, 588 Sever’s disease, 543, 591 Shank, 571 Shenton’s line, 87f Shin splints, 445–446, 481. See also Medial tibial stress syndrome Shock wave therapy, 530. See also Extracorporeal shock wave therapy Shoes aerobic dancing, 581 air soles, 572 alpine skiing, 580, 581f arch supports, 571 Balmoral pattern, 569 baseball, 579 basketball, 577, 577f bicycling, 581, 581f board-lasting, 569f, 569 boating, 570 bottoming, 569 cleated, 570
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Posterior ankle impingement (Continued) osteochondral defects, 373 peroneal tendon tendinitis, 375 posterior tibial tendinitis, 374 posttraumatic calcifications, 371 Posterior compartment muscles, 121 Posterior compartment syndrome, 7–8 Posterior inferior tibiofibular ligament, 286–287 Posterior pseudomeniscus, 39 Posterior talofibular ligament, 294–297 Posterior talotibial ligament, 294–297 Posterior tibial artery, 295f Posterior tibial nerve anatomy of, 41, 42f branches of, 218–221 injuries to, 215 compression of, 217–218, 219f heel pain syndrome of neural origin, 218–221 tarsal tunnel syndrome. see Tarsal tunnel syndrome proximal, 215–217 Posterior tibial rim, 371–372 Posterior tibial tendon anatomy of, 183–185, 184f, 297–298, 299f dysfunction of, 592, 592f functions of, 183–185, 374 graft of, 285f tendinitis of, 374, 550 Posterior tibial tendoscopy, 374–375 Posterior tibialis muscle, 183, 185 Posterior tibialis tendon disease or dysfunction abduction deformity secondary to, 189f case studies, 200, 201f description of, 183 diagnosis of, 185 differential diagnosis, 189t hindfoot inversion associated with, 186f history-taking, 185 magnetic resonance imaging evaluations, 187, 190f physical examination, 185 radiographic evaluations, 186 stage I characteristics of, 190–191, 190t surgical treatment of, 191, 192t stage II characteristics of, 190–191, 190t medial shift calcaneal osteotomy for, 194, 197f surgical treatment of, 191, 192t, 193f stage III characteristics of, 190–191, 190t medial shift calcaneal osteotomy for, 198–199 percutaneous Achilles tendon lengthening for, 199 surgical treatment of, 192t, 198 staging of, 190, 190t tenderness evaluations, 185, 185f “too many toes” sign, 185, 185f treatment of, 191 conservative, 191 immobilization, 191 Posterior tibiotalar ligament, 281 Posteroanterior dancer’s view, 75 Postmenopausal women, 55–56 Posttraumatic calcifications, 371 Pre-Achilles bursa, 147 Pressure-specified sensory device, 210–213, 212f, 219f Primary lymph edema, 249 Progesterone, 56–57 Proliferative phase, of healing, 527 Proprioception, 598, 606f Protected weight-bearing, 597, 602
Index Shoes (Continued) combination-lasting, 569f, 569 construction of, 567 cross-country skiing, 580 curved lasts, 572 cuts, 569 energy return in, 572 exercise walking, 575, 575f field sport, 578 figure skating, 580 fit of, 572 flats, 576, 576f football, 578, 579f foxing, 571 golf, 570 hallux valgus, 537 heel counters, 571 hiking boots, 574, 574f ice hockey, 580 jumping events, 576 laces, 573, 573f lace-to-shoe pattern, 569 lasting techniques, 569 lasts used in, 567, 568f, 572 materials used in, 567 ethyl vinyl acetate, 568 Hytrel, 569 microcellular rubber, 568 nylon, 569 polyurethane, 569 sole, 568 upper, 567 midsoles, 571 outer sole of, 570, 570f pronation control devices, 572 “pumps,”, 572 race-walking, 575 racquet sports, 577 replaceable plug systems, 572 rugby, 579 running, 570, 575 shank, 571 skating, 579 slip-lasting, 569f, 569 soccer, 578, 578f sock linings, 571 speed skating, 580 spikes, 575 straight lasts, 572 tennis, 577, 577f throwing events, 576 toe box, 571 toe injuries caused by, 581 tongues, 571 unit soles, 571 upper designs, 569 U-throat, 569 Vamp pattern, 569 volleyball, 578 wedges, 571 winter sports, 579 Show lacing, 574 Simian foot, 470 Single-lace cross, 573f, 574 Single-leg balance, 608f Sinus tarsi anatomy of, 339 denervation of, 208–209, 210f innervation of, 208–209, 209f local anesthetic block of, 209f pain in, 208–209 Sinus tarsi syndrome, 32–33, 33f, 342, 593 Skating shoes, 579
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“Snowboarder’s ankle,” 97 “Snowboarder’s fracture,” 35 Soccer Achilles tendon injuries and disorders in lesions, 488–489 rupture, 521 beach, 520 description of, 519 hallux osteochondral lesions in, 519, 520f popularity of, 519 Soccer shoes, 578, 578f Sock linings, 571 Soft corns, 394, 395f Soft-tissue distractor, 368–369, 369f Soleus muscle, 147 accessory, 479 Soleus syndrome, 43 Speed skating, 580 Sports program rehabilitation, 21 return to, 18 Spring ligament repair of, 15f strains of, 43 Spurs ankle impingement caused by, 33–34 talus neck, 34 tibial lip, 33 Square-box lacing, 573f, 574 Squeeze test, for syndesmosis injury, 282, 282f, 287 Ssireum, 514 Stem cells, 528 Stenosing tenosynovitis causes of, 135 chronic, 136–139 description of, 131 overuse and, 135 surgical treatment of, 135 Stieda’s process, 294–297 Still’s disease, 241 Stress fractures, 448 acute fractures vs., 73 in age groups, 49 age of menarche and, 57, 61f anatomic distribution of, 52, 53t in athletes epidemiology of, 46, 47t sites, 52, 55t training factors, 62 bone scan of, 449, 449f bony tenderness associated with, 64 case studies, 451–452 cause of, 448, 551 in dancers, 481 diagnosis of, 63 computerized tomography, 66 history-taking, 63 imaging, 64 isotopic bone scan, 64, 65f magnetic resonance imaging, 66, 67f, 67t physical examination, 64 predisposing factors, 63 radiographs, 64, 481–482, 482f diagnostic studies, 449, 449f, 463t dietary behaviors and, 58 differential diagnosis, 68 epidemiology of, 46 etiology of, 45 evolving, 65 in female athletes, 49, 551 fifth metatarsal, 82f, 83f, 81 foot arch and, 62–63 gender differences, 49
Stress fractures (Continued) grading of, 66, 67, 67t hallucal sesamoids, 79, 81 history of, 45 history-taking, 448 incidence of, 46 leg-length discrepancy and, 63 location of, 10 magnetic resonance imaging of, 449 medial malleolus. see Medial malleolus in men, 49 metatarsal, 14f, 45 midtibial, 18, 25f in military epidemiology of, 46, 49 gender differences, 49 training factors, 62 multifactorial nature of, 448 muscle mass and, 61 navicular, 10, 12f oral contraceptive pills and, 57–58 osteoid osteoma vs., 68 pain associated with description of, 63, 64 treatment of, 68 pes planus and, 63 physical examination, 449, 462t racial differences, 49, 51t recurrence of, 46 relative frequency of, 49, 51t return to activity after, 450 risk factors for, 52, 448 anthropometry, 61 biomechanics, 62, 69 bone geometry, 58 calcium metabolism alterations, 58 diet, 58 low bone density, 58, 59t menstrual disturbances, 55 modification of, 68 nutritional status, 58 osteoporosis, 55 soft tissue composition, 61 training, 62 second metatarsal base, 473 sites of, 52, 55t summary of, 70 tarsal navicular, 73 tibial. see Tibial fractures, stress treatment of, 68, 449 activity resumption after, 68, 69f additional, 69 conservative, 449 fitness maintenance, 68, 69f intramedullary nailing, 450–451 operative, 450 rest, 68 types of, 45 in women, 49, 551 Subluxation cuboid, 33f, 32, 32, 32t peroneal tendon chronic, 141 retinaculum repair, 143, 143–144 surgical management, 142 Subtalar arthritis, 593 Subtalar arthrodesis, 199 Subtalar coalition, 40 Subtalar dysfunction, 32–33 Subtalar joint anatomy of, 294f, 339, 340f arthritis of, 122 arthroscopy of, 378, 378f
Index
T Taekwon-do, 515, 515f Talar compression syndrome, 36 Talar cysts, 378, 379f, 380f Talar dome, 24f, 322f anatomy of, 368, 368f, 373 osteochondral defects in, 368, 527 in children, 543 description of, 318 radiographs of, 329f retrograde drilling and bone graft for, 329f surgical treatment of, 487 transmalleolar pinning of, 325f Talar neck fracture of, 100f spurs on, 34 Talar tilt, 86–87 Talocalcaneal coalitions, 348, 350f, 351f Talocalcaneal interosseous ligament, 293, 294f Talocrural angle, 86 Talofibular ligament, 294–297
Talo-first metatarsal angle, 186, 188f Talonavicular avulsion injuries alternative shoe lacing for, 299–301, 302f corticosteroids for, 299–301 diagnosis of, 298 imaging of, 299, 301f, 302f incidence of, 298 mechanism of, 298 rehabilitation of, 302 return to sports after, 302 treatment of, 299 Talonavicular ligaments, 294f, 297 Talotibial ligament, 294–297 Talus. See also Talonavicular avulsion injuries anatomy of, 33, 34f, 293, 294f beak of, 308–311 blood supply to, 293, 295f global compression injuries of description of, 308 drilling of, 336 imaging of, 307f magnetic resonance imaging of, 335f mechanism of, 318 treatment, 335, 335f lateral process of, 293, 295f osteochondral lesions of. see Osteochondral lesions of the talus osteochondritis dissecans of, 475 posterior anatomy of, 36, 38f, 296f, 360f lateral tubercle of, 36–38 medial tubercle of, 36–38 posterior process of, 293, 296f stress fractures of, 5 vascular anatomy of, 293, 295f Talus fractures lateral process, 97, 315, 315f, 316f, 317f ankle sprain vs., 97 comminuted, 99 description of, 35 etiology of, 97 Hawkins classification of, 98, 99f radiographic evaluations, 98 sequelae of, 99 sports with high rates of, 97 treatment of, 99, 100f posterior process, 308 diagnosis of, 311 imaging of, 312, 313f incidence of, 308 internal fixation of, 312–314 mechanism of action, 308, 311f occult, 313f physical examination for, 312 “pinch test,” 312f, 312, 312f plantarflexion as cause of, 311 “posterior compression test,” 312f rehabilitation of, 314 return to sports after, 314 treatment of, 312 Tarsal coalition, 10, 345 ankle sprain and, 345–346 in children, 535, 536 clinical presentation of, 10, 345 definition of, 345 etiology of, 345 incidence of, 345 magnetic resonance imaging of, 11f, 10, 347f, 346 physical examination findings, 536 radiographic evaluation of, 347f, 346, 536 treatment of nonoperative, 346, 536
Tarsal coalition (Continued) surgical, 347 Tarsal navicular stress fracture, 73 Tarsal tunnel, 218f Tarsal tunnel syndrome anterior, 10 causes of, 236 clinical features of, 236 high, 7–8 history of, 217–218 medial heel wedge for, 236 orthoses for, 590 with plantar fasciitis, 590 plantar heel pain caused by, 236 studies of, 217–218 symptoms of, 217–218 treatment of, 217–218 Tarsometatarsal instability, 11–12, 15f Tarsometatarsal joint anatomy of, 102 dislocations of. see Lisfranc injuries osseous anatomy of, 102–103 vascular structures of, 103 Technetium-99 methylene diphosphonate isotopic bone scan, 64 Tegretol. see Carbamazepine Tendinitis. See also Peritendinitis Achilles. see Achilles tendinitis flexor digitorum longus, 126 flexor hallucis longus, 122 chronic, 122 clinical findings of, 123 conservative treatment of, 40 differential diagnosis, 122 etiology of, 122 magnetic resonance imaging of, 122f os trigonum and, 38–39 posterior impingement syndrome vs., 37t radiographs, 122 treatment of, 122 peroneus brevis, 132, 135 peroneus longus, 132, 133f, 134 tibialis anterior, 126 Tendinopathy. see Achilles tendinopathy Tendinosis peritendinitis with, 148–150 surgical treatment of, 155 debridement of tendon, 155 tendon transfer, 156 turndown procedure, 160, 160f, 161–162 V-Y advancement, 156, 159f Tendon transfers abductor hallucis, 426, 428f Achilles tendinitis treated with, 156, 157f, 158f Achilles tendon ruptures treated with, 179–180, 179f, 531 hammertoe treated with, 400, 400f, 401f lateral ankle ligament injuries reconstructed using, 279–280 posterior tibialis tendon dysfunction repaired with, 192–194 Tendoscopy peroneal, 375–376, 375f posterior tibial, 374–375 Tennis shoes, 577, 577f Tenodesis modified Bromstrom technique vs., 275 sural nerve risks, 275 Tenosynovitis, 593 Tenotomy, 154 Terbinafine, 261–262 Thermal capsular modification, 559
635
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Subtalar joint (Continued) articulating surfaces of, 339 dislocation of, 344 instability of, 339 medial, 344 Subungual hematoma, 259, 259f, 581 Sumo, 508, 509f Sunburn, 255 Superficial peroneal nerve anatomy of, 213–215, 532 compression of, 213–215, 214f, 215f injuries to, 213–215, 214f, 215f Superficial posterior tibiotalar ligament, 281 Sural nerve, 224 fascial constriction, 9 tenodesis risks for, 275 Surf lifesaving, 517, 517f Syndesmosis anatomy of, 286, 286f ankle pathology of, 34–35 repair of, 95f space measurements, 87, 87f sprain of, 34 anterior, 286f injury to chronic, 285, 290 clinical tests for, 287 computed tomography of, 288 deltoid injuries and, 282, 282f, 283–284 description of, 24f diagnosis of, 282, 282f, 283f, 287 fixation of, 619 magnetic resonance imaging of, 288, 289f mechanism of, 287 in professional athletes, 619 radiographic diagnosis of, 287, 288f, 501f squeeze test for, 282, 282f, 287 subacute, 290 surgical treatment of, 289–290 treatment of, 288 ligaments that stabilize, 286–287, 286f medial clear space, 287–288 posterior, 286–287, 286f Synovial hernias, 35 Synovitis, 367 classification of, 367 idiopathic, 31 metatarsophalangeal joint, 587 signs and symptoms of, 367 Systemic lupus erythematosus, 243
Index Thompson test, 175f, 529 Thrombophlebitis, 248 Tibial fractures Salter-Harris I, 540 stress fractures bone density and, 58 in dancers, 481, 482f description of, 18, 25f, 448 foot arch and, 62–63 grading of, 66, 67t longitudinal, 451f midanterior cortex, 449, 450, 450f pain associated with, 448 site of, 448 Tibial lip spurs, 33 Tibial physis, 99f Tibial plafond, 356 Tibial sesamoid subluxation, 438f Tibialis anterior, 126 anatomy of, 103, 126 avulsion of, 127f, 129f functions of, 126 laceration of, 126, 128 rupture of, 128 extensor retinaculum repair, 131 mechanism of, 128 spontaneous, 128 surgical treatment, 128, 129f tendinitis of, 126 Tibiocalcaneal ligament, 281 Tibiofibular shuck test, 287 Tibionavicular ligament, 281 Tibiospring ligament, 281 Tibiotalar ligament, 281 Tibiotalar osteophytes, 477f Tillaux fracture adolescent variants of, 96, 99f description of, 35 Timing, 10, 25 Tinea pedis, 258, 258f Tinea unguium. see Onychomycosis Toe box, 571 Toe curls, 602f Toe spacer, 4f Toeoff splint, 6f “Too many toes” sign, 185, 185f Total-contact insert, 586f, 587f, 590f, 591f, 585–586 Traditional Chinese medicine, 513
Training documentation of, 3 stress fractures and, 62 Training surfaces, 62 Transforming growth factor b2, 528 Treatments. See also specific disorder, treatment of review of, 12–13 timing of, 10, 25 Trichophyton rubrum, 258, 261 Trigger toe, 123 case study of, 124–125 clinical appearance of, 123f, 124f clinical findings of, 124 differential diagnosis, 123 etiology of, 123 radiographs of, 123 surgical treatment of, 123–124, 124f Triplane fracture, 96, 99f Triple arthrodesis, 199, 347–348 Turf-toe, 421 causative factors, 422 classification of, 422, 423t, 424t grade 1, 425 grade 2, 425–426 grade definition of, 614–615 history of, 421 incidence of, 421 in Judo, 508, 508f magnetic resonance imaging of, 425f mechanism of injury, 421 in professional athletes, 614 radiographs of, 423–424, 424–425, 426, 427f sequelae of, 428–429 shoe-surface interface and, 422 surgical treatment of abductor hallucis tendon transfer, 426, 428f literature regarding, 426 open synovectomy and cheilectomy, 428 postoperative management, 427–428 treatment of, 16, 615 conservative, 428 nonoperative, 425 orthoses, 587 principles, 425 short-leg cast, 425, 425f surgical. see Turf-toe, surgical treatment of valgus injuries, 421, 421f varus injuries, 421–422 Turf-toe inserts, 413–414
Turndown procedure, 160, 160f, 161–162 Tylomas, 253–254 U Ulcerative colitis, 242 United Arab Emirates bike riding, 531–532 description of, 531 falcon hunting, 498f, 500f, 531 horses, 531 motocross sports, 501f, 531 niche sports in, 531 University of California Biomechanics Laboratory orthosis, 237, 589f Upper-extremity nerve injuries, 217t V Varicose veins, 249 Variostabil boot, 494f, 531 Vascular disorders, 247 arterial disease, 247 venous disease, 248 Vascular endothelial growth factor, 528 Venous claudication, 249 Venous disease, 248 Venous thrombus, 248–249 Viral warts, 257, 258f Vitamin B12 deficiency, 247 Volleyball shoes, 578 V-Y advancement, 156 chronic Achilles tendon rupture repaired using, 178–179 patient positioning for, 160 procedure for, 159f W Warts, 257, 258f, 387–388, 390f Wedged heel shock absorbers, 5f Weight-bearing, 597, 602, 607–608 Weil osteotomy, 406, 408f, 472 Windlass mechanism, 228, 228f, 236 Wolfe’s law, 600–601 Women. See also Female athletes postmenopausal, 55–56 stress fractures in, 49 X Xerosis, 255 Z Zostrix. see Capsaicin
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