Fractures of the Foot and Ankle: Diagnosis and Treatment of Injury and Disease

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Author: Jason H. Calhoun | Laugh Richard T.

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Published in 2005 by Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2005 by Taylor & Francis Group, LLC No claim to original U.S. Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number-10: 0-8247-5916-8 (Hardcover) International Standard Book Number-13: 978-0-8247-5916-2 (Hardcover) This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC) 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Catalog record is available from the Library of Congress

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Preface

There was a decrease in interest in foot and ankle orthopedic surgery in the 1960s and 1970s because of the introduction of total joint arthroplasty and arthroscopic surgery. Renewed interest in problems of the foot and ankle was sparked through the leadership of the American Orthopaedic Foot and Ankle Society in the 1980s and 1990s. Foot and ankle surgery is now one of the most rapidly growing areas of orthopedics, especially in resident subspecialty training. We have similarly seen dramatic improvements in research, medical education, and surgical technique. The present volume focuses on fractures of the foot and ankle, representing a combination of new knowledge and time-tested methodology in research and clinical practice. In Chapter 1, Stuart D. Miller and Steven A. Herbst examine fractures of the ankle and provide a review of treatment for one of the most commonly injured joints. They offer priceless advice on the value of caution over innovation. One of the most challenging types of fractures is the distal tibial articular surface: the dreaded ‘‘pilon.’’ In Chapter 2, Richard T. Laughlin discusses how the goals of treatment are to avoid complications, maintain alignments, and reconstruct the articular surface to achieve motion at the ankle, with special attention to the soft tissue envelope. Talar fractures represent an insignificant number of all foot and ankle disorders but at the same time pose a big challenge to the physician. In Chapter 3, Saul G. Trevino and Vinod K. Panchbhavi classify the different types of talar fractures and address proper modes of evaluation and treatment. Chapter 4 deals with fractures of the calcaneus, a subject of some controversy from diagnosis to treatment. The authors, Paul J. Juliano and Hoan-Vu Nguyen, painstakingly review questions of classification, surgery, salvage, and postoperative treatment and call for more research in this area. The easily overlooked injuries to the tarsometatarsal, or Lisfranc, joint complex may be the most underreported foot problems. Yet if left untreated, Lisfranc injuries can be the source of a host of injuries leading to long-term disability. In Chapter 5, Kent Heady and Saul G. Trevino offer insights on detection and treatment, with detailed descriptions of different approaches to fixation. Likewise, many patients do not realize their reliance on the hallux, or big toe, until an injury throws off their familiar weight-bearing balance. Bryan J. Hawkins reviews fractures of the metatarsals and phalanges in Chapter 6. Diabetic patients present challenges to physicians across all medical specialties. Orthopedic specialists know that diabetic patients are more susceptible to fractures in the extremities, and that they are less likely to heal satisfactorily. Michael S. Pinzur analyzes this challenge in Chapter 7. Varieties of subtalar dislocations are more common among all types of patients, and David A. Porter and Todd Arnold review them in Chapter 8. Pediatric patients and the special problems they present in the foot and ankle are discussed in Chapter 9 by Kelly D. Carmichael. Soft tissue coverage is an area of great complexity, but also one in which we have seen substantial progress. In Chapter 10, R. Michael Johnson and Steven Schmidt describe innovations in both nonoperative and operative treatment, including topical negative pressure and hyperbaric oxygen. Similarly, assessment, treatment, and aftercare of burns to the feet pose tremendous challenges to patients and caregivers, and these topics are addressed by Sidney F. Miller and Matthew R. Talarczyk in Chapter 11. In Chapter 12, Lew C. Schon and Steven A. Herbst present a variety of surgical techniques including debridement, repair, reconstruction, and transfer for the most common tendon ruptures and lacerations. In Chapter 13, Maria Guidry, Brian Hutchinson, Richard T. Laughlin, Hongbao Ma, and Jason H. Calhoun provide an overview of the evaluation and treatment of posttraumatic foot


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infections. In Chapter 14, William A. Vitello discusses the problem of complex regional pain syndrome, a poorly understood symptom complex. Improvements in emergency medicine have helped save many lives that would have been lost in the past. As a consequence, we see more high-energy foot injuries in accident survivors, and Mark D. Perry and Arthur Manoli II examine this challenge in Chapter 15. Trauma is also a major factor when amputation of the foot is necessary. In Chapter 16, Jason H. Pleimann, Robert B. Anderson, W. Hodges Davis, and Bruce E. Cohen show how partial foot amputations can provide a functional residual limb and a rapid return to daily life. Another established method of managing foot and ankle fractures is orthotic intervention. Few contemporary studies address the application of orthotics to the foot and ankle; in Chapter 17, Ge´za F. Kogler reviews clinically accepted principles for fracture management and provides a practical guide. While deformities will always pose a humbling array of challenges for the orthopedic physician, a variety of techniques, including Ilizarov fixation, offer hope for those needing foot and ankle reconstruction, as Daniel M. Thompson and Jason H. Calhoun demonstrate in the final chapter. No single volume could encompass all the knowledge and innovations that arise in the field of foot and ankle disorders. We have, however, attempted to create a broad survey of both common and rare conditions, to reinforce accepted practice as experience has demonstrated its value, and to emphasize the benefits of new knowledge as appropriate. We wish to thank all our contributors. We also thank Kristi Overgaard for her editorial contributions to this project and to many other projects in the past. But most of all, we are grateful to our patients. Their spirit and perseverance have been the inspiration for all our efforts to collect, synthesize, and apply medical knowledge.


About the Editors

JASON H. CALHOUN, M.D., F.A.C.S., is the J. Vernon Luck Distinguished Professor and Chairman of the Department of Orthopaedic Surgery at the University of Missouri, Columbia, leading the department’s clinical, educational, and research programs. He is certified by the American Board of Orthopaedic Surgery. He is the founder-member and past president of the Musculoskeletal Infection Society and the North American Association for the Study and Advancement of the Methods of Ilizarov. Dr. Calhoun is the author of numerous papers and book chapters and most recently served as coeditor of Musculoskeletal Infections. His specialty interests include foot and ankle trauma and musculoskeletal infections. RICHARD T. LAUGHLIN, M.D., F.A.C.S., is Associate Professor and Program Director of the Department of Orthopaedic Surgery at Wright State University. He is certified by the American Board of Orthopaedic Surgery. He is an active member of the Orthopaedic Trauma Association, American Orthopaedic Foot and Ankle Society, and the American College of Surgeons. His specialty interests include foot and ankle trauma and reconstruction.



Contributors

Robert B. Anderson, M.D. Miller Orthopaedic Clinic Charlotte, North Carolina Todd Arnold, M.D. Thomas A. Brady Clinic Methodist Sports Medicine Center Indianapolis, Indiana Jason H. Calhoun, M.D. Department of Orthopedic Surgery University of Missouri–Columbia Columbia, Missouri Kelly D. Carmichael, M.D. Department of Orthopaedics and Rehabilitation University of Texas Medical Branch Galveston, Texas Bruce E. Cohen, M.D. Miller Orthopaedic Clinic Charlotte, North Carolina W. Hodges Davis, M.D. Miller Orthopaedic Clinic Charlotte, North Carolina Maria Guidry, M.D. Department of Orthopaedics and Rehabilitation University of Texas Medical Branch Galveston, Texas Bryan J. Hawkins, M.D. Central States Orthopaedic Specialists Tulsa, Oklahoma Kent Heady, M.D. University of Texas Medical Branch Galveston, Texas

Steven A. Herbst, M.D. Department of Orthopaedic Surgery Union Memorial Hospital Baltimore, Maryland Brian Hutchinson, M.D. Wright State University Dayton, Ohio R. Michael Johnson, M.D. Division of Plastic Surgery Department of Surgery Miami Valley Hospital Wright State University Dayton, Ohio Paul J. Juliano, M.D. Milton S. Hershey Medical Center The Pennsylvania State University Hershey, Pennsylvania Ge´za F. Kogler, Ph.D. Department of Rehabilitation School of Health Sciences Jo¨nko¨ping University Jo¨nko¨ping, Sweden Richard T. Laughlin, M.D. Wright State University Dayton, Ohio Hongbao Ma, M.D. Department of Orthopaedics and Rehabilitation University of Texas Medical Branch Galveston, Texas Arthur Manoli II, M.D. Michigan International Foot and Ankle Center Pontiac, Michigan


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Sidney F. Miller, M.D., F.A.C.S. Department of Surgery Miami Valley Hospital Wright State University Dayton, Ohio Stuart D. Miller, M.D. Department of Orthopaedic Surgery Union Memorial Hospital Baltimore, Maryland Hoan-Vu Nguyen, M.D. Milton S. Hershey Medical Center The Pennsylvania State University Hershey, Pennsylvania Vinod K. Panchbhavi, M.D., F.R.C.S. University of Texas Medical Branch Galveston, Texas Mark D. Perry, M.D. Southwestern Medical Center Department of Orthopaedic Surgery University of Texas Dallas, Texas

Contributors

David A. Porter, M.D., Ph.D. Thomas A. Brady Clinic Methodist Sports Medicine Center Indianapolis, Indiana Steven Schmidt, M.D. Division of Plastic Surgery Department of Surgery Miami Valley Hospital Wright State University Dayton, Ohio Lew C. Schon, M.D. Department of Orthopaedic Surgery Union Memorial Hospital Baltimore, Maryland Matthew R. Talarczyk, M.D. Department of Surgery Miami Valley Hospital Wright State University Dayton, Ohio Daniel M. Thompson, M.D. Beaumont Bone and Joint Institute Beaumont, Texas

Michael S. Pinzur, M.D. Loyola University Medical School Maywood, Illinois

Saul G. Trevino, M.D. University of Texas Medical Branch Galveston, Texas

Jason H. Pleimann, M.D. Ozark Orthopaedic and Sports Medicine Clinic Fayetteville, Arkansas

William A. Vitello, M.D. Department of Surgery Wright State University Dayton, Ohio


Contents

1.

Ankle Fractures .................................................................................................................... 1 Stuart D. Miller and Steven A. Herbst

2.

Pilon Fractures.................................................................................................................... 27 Richard T. Laughlin

3.

Talar Fractures and Dislocations........................................................................................ 49 Saul G. Trevino and Vinod K. Panchbhavi

4.

Calcaneal Fractures............................................................................................................. 93 Paul J. Juliano and Hoan-Vu Nguyen

5.

Lisfranc Injuries and Midfoot Fractures............................................................................ 117 Kent Heady and Saul G. Trevino

6.

Fractures of the Metatarsals and Phalanges of the Foot ................................................... 165 Bryan J. Hawkins

7.

Foot and Ankle Fractures in Diabetic Patients.................................................................. 179 Michael S. Pinzur

8.

Dislocations of the Ankle, Subtalar, and Great Toe Metatarsal–Phalangeal Joints .......... 195 David A. Porter and Todd Arnold

9.

Pediatric Foot and Ankle Fractures................................................................................... 211 Kelly D. Carmichael

10.

Soft Tissue Coverage of the Foot and Ankle ..................................................................... 265 R. Michael Johnson and Steven Schmidt

11.

Burns to the Feet................................................................................................................ 287 Sidney F. Miller and Matthew R. Talarczyk

12.

Tendon Ruptures and Lacerations..................................................................................... 309 Lew C. Schon and Steven A. Herbst

13.

Posttraumatic Infections in the Foot and Ankle ................................................................ 345 Maria Guidry, Brian Hutchinson, Richard T. Laughlin, Hongbao Ma, and Jason H. Calhoun

14.

Complex Regional Pain Syndrome or Reflex Sympathetic Dystrophy .............................. 371 William A. Vitello

15.

Late Reconstruction........................................................................................................... 381 Mark D. Perry and Arthur Manoli II

16.

Traumatic Amputations of the Foot and Ankle ................................................................ 393 Jason H. Pleimann, Robert B. Anderson, W. Hodges Davis, and Bruce E. Cohen

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Contents

17.

Orthotic Management of Foot and Ankle Fractures ......................................................... 423 Ge´za F. Kogler

18.

Treatment of Foot and Ankle Deformities with the Ilizarov Fixator ................................ 439 Daniel M. Thompson and Jason H. Calhoun

Index........................................................................................................................................... 459

Calhoun: Fractures of the foot and ankle DK2448_c001 Final Proof page 1 15.2.2005 11:11am

1 Ankle Fractures Stuart D. Miller and Steven A. Herbst Department of Orthopaedic Surgery, Union Memorial Hospital, Baltimore, Maryland

CONTENTS I. Introduction ...................................................................................................................... 1 II. Anatomy............................................................................................................................ 2 III. Classification of Ankle Fractures ...................................................................................... 4 IV. Physical Examination ........................................................................................................ 5 V. Radiographic Examination................................................................................................ 6 VI. Outcome of Ankle Fractures ............................................................................................. 7 VII. Comparison of Operative and Nonoperative Results ........................................................ 8 VIII. Results of Operative Intervention...................................................................................... 9 IX. Historical and Research Considerations for Treatment of Ankle Fracture Subtypes: A Brief Review .................................................................................................................. 9 A. Isolated Lateral Malleolus ......................................................................................... 9 B. Posterior Malleolar Fracture ................................................................................... 10 C. Medial Malleolar Fracture....................................................................................... 11 D. Syndesmosis Involvement ........................................................................................ 11 E. Talar Shift without Fracture .................................................................................... 12 F. Osteochondral Injury ............................................................................................... 12 G. Open Fractures ........................................................................................................ 12 H. Techniques of Closed Reduction and Subsequent Care ........................................... 13 X. Surgical Techniques ......................................................................................................... 13 A. Lateral Malleolus ..................................................................................................... 13 B. Medial Malleolus ..................................................................................................... 14 C. Bimalleolar............................................................................................................... 15 D. Trimalleolar ............................................................................................................. 19 XI. Osteoporosis and Ankle Fractures .................................................................................. 19 XII. Ankle Dislocation or Ligamentous Disruption ............................................................... 21 XIII. Conclusion....................................................................................................................... 23 References ................................................................................................................................... 23

I.

INTRODUCTION

The ankle is among the most frequently injured joints. While most of these injuries are sprains and soft tissue disruption, ankle fractures are common and involve a very intricate joint. Fractures about the ankle are reported in ancient texts dating thousands of years, and a common theme is an

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appreciation for the complexity of this seemingly trivial injury. Even today, some think of these injuries as the ‘‘junior resident’s case’’ when, in fact, the decision making is complex and the results — on close inspection — are not as universally good as previously thought. The ankle suffers fools poorly, malreduction can often progress quickly to end-stage degenerative joint disease. Treatment depends on understanding the anatomy, consideration of the soft tissues, and sound surgical principles. The orthopedic guidelines are now well established: rigid internal fixation may allow early range of motion. This chapter is written to elucidate these issues and warn of pitfalls along the path of optimal fracture care.

II.

ANATOMY

Ankle anatomy holds the key to understanding fracture patterns and their appropriate treatment. Inman [1] has described ankle anatomy and motion in a classic work. The talus is not flat but rather has a dual-dome upper surface. These two shallow convex curves articulate with a matching tibia distal joint surface. The talus is asymmetric; it is wider anteriorly and has different articulating surfaces with the tibia and the fibula. The distal tibia also narrows posteriorly, and the posterior malleolus does articulate with the talus and its trigonal process. The lateral and medial malleoli provide stability, which is important for both tilt and rotation, and their articulation with the talus constitutes an important amount of joint surface area. These bones have remarkable weight-bearing capacity. The joint-reaction force across the ankle joint can exceed four times the body weight in the stance phase of gait. Any fracture malalignment will increase the contact forces across the joint. Clinical correlation of such displacement is still being decided. A cadaveric study demonstrated that a 2-mm talar shift led to a 42% reduction in the talotibial joint-contact area [2]. This led to recommendations to accept no more than 2 mm of displacement. A more recent study, rotating shortening the fibula in precise measurements, found that fibular displacement (> 2 mm shortening or lateral shift) or greater than 58 of external rotation significantly increased contact forces on the joint [3]. Some authors believe that any displacement to the ankle is unacceptable and advocate operative intervention with minimal shortening (0.5 to 1.0 mm) or displacement (1 mm) [4]. Figure 1.1 demonstrates a malreduction and subsequent return to the operating room. The clinical outcome studies are even less clear; the different patient populations and various fracture patterns do not allow broad generalizations concerning the need for operative intervention, thus these issues will be discussed later, within the context of specific injuries. The ankle ligaments form complex checkreins. Laterally, the ligamentous complex consists of three distinct thickenings of the joint capsule. The anterior talofibular ligament (ATF) travels from the anterior aspect of the fibula to the lateral aspect of the talar neck. This band restrains anterior displacement, inversion, and internal rotation of the joint [5,6]. The calcaneofibular (CF) ligament lies deep to the peroneal tendons, from the distal pole of the fibula to the calcaneus. This ligament restrains the ankle and subtalar joint to eversion stresses. The posterior talofibular ligament is a short, stout ligament connecting the posterior process of the talus to the fibula. This ligament binds so tightly that it often causes a posterior malleolus avulsion fracture with enough strain. Medially, the deltoid ligament is composed of two layers. The superficial deltoid originates on the anterior colliculus of the medial malleolus and inserts on the calcaneus, navicular, and talus and helps to resist hindfoot eversion [7]. Laboratory studies demonstrated that sectioning the superficial deltoid ligament leads to a 43% decrease in the contact area under the joint [8]. The deep deltoid is thought to be the primary medial stabilizer of the ankle. Originating on the deep surface of the posterior colliculus and inserting on the talus just posterior to the medial facet, the deep deltoid ligaments account for up to 57% of the restraint to external rotation of the talus within the mortise [9]. Recent studies further delineate the deltoid ligament complex, finding the tibiocalcaneal ligament the longest and thickest of these structures [10]. The deltoid, when it ruptures, often does so with a complex tear that often defies easy surgical reapproximation. Most sources have documented that acute repair of the deltoid is not necessary but that the ligament will heal with appropriate bony stability [11].


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Figure 1.1 Inadequate fibular reduction and fixation in a young man who sustained a trimalleolar fracture dislocation. (A and B) The AP and lateral injury films demonstrate the typical posterior subluxation. (C) AP of the initial fixation with a cerclage wire left the fibula short and unstable; note the wide medial clear space. (D and E) Mortise and lateral films after return to the operating room with a long fibular plate and posterior malleolar fixation. The patient had a good result.

Superior to the ankle joint, but intimately involved with many ankle injuries, the syndesmotic ligament complex holds the fibula in close proximity to the tibia. The syndesmosis consists of four parts: the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the tibiofibular interosseous ligament, and the inferior transverse tibiofibular ligament. The fibula will externally rotate approximately 128 and displace posterolaterally with


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ankle dorsiflexion [1,12]. The mortise width does not change during such motion. The AITFL helps resist external rotation of the talus (in the face of division of the fibula) [13].

III.

CLASSIFICATION OF ANKLE FRACTURES

Three classification systems deserve mention: (1) Lauge-Hansen, (2) Danis–Weber, and (3) Arbeitsgemeinschaft fu¨r Osteosynthesefragen–Orthopaedic Trauma Association (AO–OTA) classification (Figure 1.2). For any classification system to be useful it must be reproducible and either guide treatment or effect prognosis or both. Unfortunately, the current ankle fracture classification systems fail to adequately fulfill these criteria. However, they can be helpful in understanding the mechanism of injury, methods to obtain reduction, and some aspects of treatment. The Lauge-Hansen system arose from the clinical, experimental, and radiographic observations of the author [14–18]. This system is based on the position of the foot (supination or pronation) and the deforming forces (external rotation, abduction, or adduction). The author found four primary injury mechanisms (he later added a fifth to cover axially loading injuries [17] and correlated radiographic appearance with these injury patterns. He found each of the patterns occurred in a predictable sequence based on the severity of the injury. In reality, however, all fractures do not easily conform to one of the patterns. Interobserver reliability has been found to be poor [19,20]. This system is helpful because it mechanistically explains the pattern of injuries seen and seems to help in understanding reduction maneuvers as well.

Figure 1.2

Ankle fracture classification systems.


Ankle Fractures

5

The Danis–Weber classification system is based upon the level of the fibula fracture [21]. Type ‘‘A’’ injuries occur below the level of the syndesmosis. Type ‘‘B’’ injuries occur at or near the level of the syndesmosis. Type ‘‘C’’ injuries include a fibula fracture above the level of the syndesmosis. The weaknesses of this system are poor interobserver reliability [22], lack of information regarding injury to the medial side of the ankle, and inability to reliably predict prognosis. Weber C fractures usually require operative intervention; the degree of intervention remains controversial. An exception is the clinical finding that type A fractures do well nonoperatively [23]. A third system, published by the Orthopaedic Trauma Association, is essentially a more detailed Danis–Weber system that adds degree of comminution and injury to the medial side and the posterior ankle [24]. Reliability, use in treatment, and its correlation with prognosis are yet to be determined.

IV.

PHYSICAL EXAMINATION

There is no substitute for a thorough history and physical examination. Mechanism of injury can often assist with determining the extent of injury, the likely pattern of injury, and possible associated injuries. The presence of comorbidities such as peripheral vascular disease, diabetes, autoimmune disorders, or previous injury to the ankle can all be helpful in understanding the personality of the fracture and assist the surgeon in determining the timing and type of intervention. A thorough and systematic examination is undertaken beginning with the skin. The presence of any wound should always arouse the suspicion of open fracture. Remember that any open wound can communicate with a fracture or joint. The open fracture dislocation seen in Figure 1.3 is rare. Fracture blisters should be assessed according to their location with respect to proposed surgical incisions. Two types of fracture blisters have been noted: fluid-filled and blood-filled. Both represent a cleavage between the dermis and the epidermis. Clear fluid-filled blisters have scattered area of epithelial cells remaining and may represent a lesser form of injury. Giordano and Koval [25] prospectively followed 53 patients with blisters and operated early on 19 of them with intact (nonruptured) blisters). They noted wound problems (postoperative infection) in two of these patients who had incisions through blood-filled blisters. They noted no difference in outcome of the various soft tissue treatment modalities (i.e., unroofing, aspirating, leaving intact) [25]. Varela et al. [26] also prospectively evaluated patients with fracture blisters and noted an increased

Figure 1.3 Open fracture dislocation in a young man who had transection of the posterior tibial artery along with severe bone and ligamentous damage. His wounds were cleansed, then close-reduced and fixed with a fibular plate and external fixator. He did well relying on the anterior tibial artery alone. His recovery was excellent and he underwent lateral ankle ligament reconstruction more than 1 year after his surgery.


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incidence of blister formation in those receiving surgical treatment more than 24 h after injury. (This may have reflected selection bias — i.e., the worse the injury, the more likely that surgery would have been delayed.) They noted blisters to colonize with skin pathogens shortly after rupturing. Blisters thus merit caution but are not absolute contraindications for operative intervention. Neurovascular examination begins with assessment of perfusion. The presence of diminished capillary refill, venous engorgement, pallor, or cyanosis should be noted. Pulses should be palpated. If swelling precludes palpation of pulses, the contralateral foot may give some indication of overall vascular status. Doppler examination assesses for the presence of a pulse, but does not assess for flow in the absence of a pressure cuff controlling inflow. Immediate corrective measure should be taken for any possible cause of diminished perfusion. Even a well-fixed fracture will not heal without a well-perfused environment. Sensation to light touch in all distributions should be assessed. Anatomy of the nerves of the foot and ankle is fairly straightforward. The lateral border of the foot is supplied by the sural nerve and the medial foot and ankle area by the saphenous nerve. The plantar surface is innervated by the medial and lateral plantar nerves. The first web space is maintained by the deep peroneal nerve, with the remainder of the dorsum of the foot supplied by the superficial peroneal nerve. The saphenous nerve often courses over the anteromedial corner of the ankle joint and thus may be at risk with medial malleolus repair. Tendon function can be difficult to assess secondary to pain in the acute setting but should be attempted anyway. Certainly, some active motion of the toes can be elicited, while strength of the peroneals or posterior tibial tendons can be limited secondary to pain.

V.

RADIOGRAPHIC EXAMINATION

Researchers have yet to clarify which radiographic criteria are most helpful in determining longterm prognosis. Criteria from previous studies have suggested intra-articular displacement greater than 2 mm, increased tibiofibular clear space, a displaced posterior malleolar fragment greater than 25%, and increased medial clear space are poor determinants [27]. The syndesmotic space between the tibia and fibula, specifically from the tibial incisura to the medial fibular border, is measured 1 cm proximal to the plafond [28]. The criterion for a normal space is more than 1 mm of overlap between the tibia and the fibula on any view, or a clear space between the medial border of the fibula and the medial border of the incisura fibularis measuring less than 5 mm on either the anteroposterior (AP) or the mortise view (Table 1.1). The medial clear space is often used to determine the presence of deltoid ligament disruption. When less than 1 mm or more than 4 mm of medial clear space is seen either initially or on a stress AP radiograph, or when an asymmetry of the tibial and talar crescents is detected on the lateral view, a talar shift is present [29–31]. Rather than thinking of this space as a shift, the extra width really represents external rotation of the talus [32]. The overlap of the tibia on the fibula should be symmetric. The medial clear space can be widened 2 to 3 mm with syndesmotic injury despite an intact deltoid ligament [33]. A difference of between 2 and 58 in the talocrural angle compared with the contralateral side is considered clinically significant fibular shortening [34]. Figure 1.4 reveals fibular shortening and rotation. However, when this angle was measured on plain radiographs and with the use of three-

Table 1.1 Radiographic criteria Parameter

Criteria (abnormal)

Medial clear space Talocrural angle Talar tilt Tibiofibular clear space Tibiofibular overlap

< 1 mm or > 4 mm, similar to distance between talar dome and tibia More than 2 to 58 difference from contralateral side > 2 mm, > 58 > 5 mm < 10 mm on AP view, < 1 mm on mortise


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Figure 1.4 Poor fixation. (A) Immediate postoperative film shows less than optimal fixation of the distal fibula. This construct seems doomed to failure. (B) The failure mortise view shows shortening and rotation of the distal fibula as well as widening of the medial clear space. A fairly simple ankle fracture has now become a difficult salvage situation.

dimensional computed tomography (CT), the angle could not be used to distinguish between fractures that necessitated operative treatment because of the position of the fibula and those that did not need such treatment. Talar tilt, the angle between the top of the talus and the perpendicular to a line down the tibial shaft, should be within 58 of the normal ankle on the AP view [27,29,35]. The mortise view, using a line across the tibial plafond and another across the top of the talus, should not differ by more than 2 mm [36].

VI.

OUTCOME OF ANKLE FRACTURES

Numerous studies have compared operative and nonoperative results [37–40]. The results of these studies have varied considerably. The difficulties outlined above in classification as well as in the assessment of severity of injury, reduction, presence and degree of arthrosis, and the lack of sensitive and reproducible outcome instruments have hampered all of these studies. As the general trend in orthopedics shifted toward operative intervention and AO technique became widely accepted and practiced, greater than 90% ‘‘good and excellent’’ results were published [41]. During the 1990s when standardized outcome instruments began to be routinely used in orthopedics these measures were applied to ankle fractures. The results have shown residual functional deficits at greater than 2 years even after relatively trivial injuries. A recent Swedish study using standardized outcome instruments has shown that only one third of patients with operatively treated Weber B ankle fractures report a complete recovery [42]. Forty-four percent of the subjects in this study had work-related problems, and 61% had some problems with sport activities. The SF-36 subscores for physical functioning, physical and emotional role function,


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vitality, and mental health were lower compared with an average Swedish population (p < .05). Another study showed similar results using Olerud and Molander ankle score and the University of California, Los Angeles, (UCLA) activity score 8 to 24 months after operatively treated malleolar fracture compared with healthy controls [43]. Similarly, a study using SF-36 data demonstrated significant deficits compared with the normal population in almost all domains at 4 months after operative treatment; later results improved to near-normal values at 2 years in all domains except physical functioning, which remained depressed [44].

VII.

COMPARISON OF OPERATIVE AND NONOPERATIVE RESULTS

Support of nonoperative treatment results at 20 years of follow-up for bi- and trimalleolar fractures were reported with an average American Orthopaedic Foot and Ankle Society (AOFAS) score of 98 points [45]. Additionally, some studies have noted equal or increased arthrosis in operative fractures despite better reduction than in nonoperative patients [38]. These studies demonstrate a poor relationship of arthrosis to initial injury and accuracy of reduction. While operative treatment does not invariably lead to arthritis, these results do illustrate the difficulty in evaluating the literature. Studies have demonstrated no difference in operative and nonoperative treatment of ankle fractures [46]. A well-designed randomized study requiring near-anatomic closed reduction (2 of 22 patients failed the closed reduction criteria) compared closed vs. open reduction and noted no difference in gait analysis and range of motion between the two groups [46]. The poor results of suboptimal operative fixation, as shown in Figure 1.5, may limit some outcome studies. A general consensus in the literature is that patients seem to have improved outcomes if anatomic reduction is attained and maintained whether that is operatively or nonoperatively.

Figure 1.5 Poor fixation. (A and B) AP and lateral views of bimalleolar fracture fixation demonstrate a number of errors. First, the distal tibia screw is much too long and may impinge upon the soft tissues. Second, and more important, the fractures are not anatomically reduced. The medial malleolus is displaced and the distal fibula is shortened and rotated.


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9

Operative or closed manipulative anatomic reduction is but one key to a successful outcome. Other likely influences are soft tissue damage, osteochondral injury, tendon or ligament injury, age of patient, etc. Variability also exists because of the different patient populations, different selection criteria for treatment, and nonstandardized outcome measures.

VIII.

RESULTS OF OPERATIVE INTERVENTION

Lindsjo [47] reported in a series of 321 consecutive operative cases that the most decisive factors influencing the clinical result were the type of fracture, the accuracy of the reduction, and the sex of the patient. The clinical results were ‘‘excellent’’ to ‘‘good’’ for 81% of the dislocation fractures, 38% of the impact fractures, and two of the six combined shaft and ankle fractures. In 14% of the dislocation fractures and 50% of the impact fractures posttraumatic arthritis developed. There was a significantly higher degree of arthritis among the patients with a posterior articular surfacebearing fragment. There was also a strong correlation between the degree of arthritis and poor clinical results. The clinical and radiographic results from use of the AO Association for the Study of Internal Fixation (ASIF) method were better than those of conservative treatment or other operative methods. Other studies have shown that age, open injury, involvement of lateral malleolus, reduction obtained of medial and lateral malleoli, and the syndesmosis related to an overall outcome score combining subjective, objective, and radiologic results [40]. Weber classification in unimalleolar fracture, presence of a multimalleolar fracture, age, initial displacement, and operative reduction were related to outcome in a study by Kennedy et al. [48]. Significant correlations have also been found between: (1) the adequacy of the reduction of the syndesmosis and late arthritis, (2) the adequacy of the initial reduction of the syndesmosis and the late stability of the syndesmosis, (3) the late stability of the syndesmosis and the final outcome, and (4) the adequacy of the reduction of the lateral malleolus and that of the syndesmosis [49]. This study along with a literature review led to the conclusion that in supination–external rotation (SER) and pronation–external rotation (PER) injuries, reduction of the syndesmosis is key to optimizing results and that lateral malleolus must be reduced for this to be achieved. Chissell and Jones [50] supported this conclusion stating that syndesmosis widening greater that 1.5 mm lead to poorer results. Pettrone et al. [40] in a study attempting to identify predictive factors noted age, reduction, and completeness of the syndesmosis and deltoid reconstruction to be predictive in 81% of patients.

IX.

HISTORICAL AND RESEARCH CONSIDERATIONS FOR TREATMENT OF ANKLE FRACTURE SUBTYPES: A BRIEF REVIEW

A.

Isolated Lateral Malleolus

Historically, the treatment of the isolated lateral malleolus fracture has ranged from nonoperative to operative. In the absence of medial-sided fracture or deltoid disruption, an isolated lateral fracture can include the Lauge-Hansen SER II–III and Supination Adduction I (SAD) variant. With deltoid disruption it can include the SER IV and the Pronation Abduction III (PAB), or the PER III or IV (Figure 1.1). The low SAD type fibula fracture (Weber type A) is usually a tension failure of the lateral malleolus in adduction. Treatment can usually be accomplished nonoperatively. The diagnosis of PAB III with deltoid disruption is usually not subtle. Both the AITFL and the PITFL are damaged, the syndesmosis is widened, and the talus shifted. The fibula is typically comminuted. This fracture requires meticulous attention to recreating fibular length and rotation. The PER IV injury characteristically involves a Weber B or most often a Weber C type fibula fracture. Despite the biomechanical evidence that the syndesmosis should be stable when the rigidly fixed fibular fracture is within 4.5 cm of the joint (see ‘‘Syndesmosis Involvement’’ section below), Parfenchuck et al. [51] reported three of seven PER IV fractures with deltoid injury that displaced either early or late. This may be due to the variability of the ligamentous complex of the syndesmosis [52]. Stabilization of the syndesmosis when in doubt is recommended.


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SER type fractures are most common but very controversial. SER IV can sometimes be difficult to diagnose over SER II, but the fractures seem to fare better with operative treatment. The SER II injury is not only a common fracture but also one that has generated a significant amount of controversy. The controversy surrounds the decision to operate. There are multiple reports in the literature detailing good results of isolated lateral (SER II injuries) malleolus fractures treated nonoperatively [53]. Conversely, others indicate the necessity to fix fractures with displacement. The definition of displacement, and in what direction, is varied and controversial. Some suggest 0- to 5-mm posterior or lateral displacement, or any fibular shortening [27,54]. Others base their assessment of fibular shortening on the presence of a decreased talocrural angle (2 to 58) compared with the normal side. Michelson, however, has shown with CT that the fibular external rotation that is apparent on plain films is actually a relative displacement to an internally rotated proximal fibula and that the talocrural angle consistently overestimates fibular shortening in this setting (see ‘‘Radiographic Examination’’ section). Yablon et al.’s [55] cadaveric and clinical study concluding that the lateral malleolus is the key to reduction of the talus in bimalleolar fractures should be applied with caution in the face of an intact medial side. The data from Thordarson et al.’s [3] cadaveric fibular malunion model suggesting increased joint-contact pressures with shortening or malrotation of the fibula are not applicable in the SER II injury as the deltoid is theoretically intact. Cadaveric and clinical data are inconclusive when it comes to surgical decision making in the minimally displaced SER II injury. The criteria utilized are variable and adjusted for each patient’s injury, activity level, and age. The presence of medial-sided tenderness is unreliable for deep deltoid injury, but does play a role in our decision making. A young athlete with a fracture at the level of the syndesmosis or higher (Weber B or C) with any of the following would warrant fixation: 1. 2. 3. 4.

Displacement (lateral or posterior > 2 or 3 mm) in any direction or a talocrural angle > 58 than that of the opposite side Significant medial-sided tenderness and swelling Any appreciable talar shift (medial clear space > 4 mm) Positive stress radiograph

Injuries that have these criteria are more likely to be unstable and may be more reliably treated with surgical intervention. Conversely, the presence of some or even all of these variables in an elderly diabetic might not be a definite indication for surgery.

B.

Posterior Malleolar Fracture

A posterior malleolus fracture can occur with any of the rotational ankle fractures with the exception of the supination-adduction injury. It is an avulsion type fracture that is the result of the pull of the posterior tibiofibular ligamentous attachment. An unusual variant is a pilon type fracture due to axial load (Figure 1.6). These are reduced and fixed if displaced more than 2 mm. The main issues to consider in the treatment of these injuries are (1) what size fragment constitutes a fracture that makes the ankle ‘‘unstable,’’ (2) is the stability affected by the stability of other parts of the ankle injury (medial or lateral malleoli fracture or deltoid injury), (3) does fixing the fragment improve those parameters, (4) is contact stress significantly affected by a fracture of the posterior malleolus and at what percentage is this critical. Unfortunately, the available literature limits absolute conclusions as to optimal treatment. Harper [56] noted no instability when a fracture up to 50% of the joint surface was created in a model with an intact fibula. Raasch et al. [57] showed that in the absence of an unstable fibula (section of ATFL and fibula) the talus was stable after up to 40% of the posterior malleolus had been resected. After sectioning of the ATFL and fibula the talus was unstable with as little as 30% of the posterior malleolus removed. Clinically, these results were supported in a review of ankle fractures with greater than 25% posterior malleolar fragments. Another study demonstrated no difference in operative and nonoperative treatment of the posterior malleolus after open reduction and internal fixation (ORIF) of the medial and lateral malleoli [58]. Somewhat contradictory results were reported by Scheidt et al. [59] who showed residual rotational and translational instability in a cadaveric study with 25% posterior malleolar fragments


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Figure 1.6 Posterior malleolus fracture with minimal displacement.

with or without internal fixation. Hartford et al. [60] evaluated contact pressures in a cadaveric study and noted pressures to increase when greater than 33% of the lateral malleolus was involved with or without sectioning of the deltoid ligament. Heim [61] believed that the late poor results in trimalleolar fractures were related to technical errors in fixation and that the degree of arthrosis was less in those fractures that were well reduced. In conclusion, it appears that the contact stresses are shifted in a large unfixed posterior malleolar fracture. It is still unclear what effect this type of fracture has on ankle stability, but likely the effect is minimal especially in the face of intact or rigidly fixed medial and lateral malleoli.

C.

Medial Malleolar Fracture

Nondisplaced fractures have shown good results with nonoperative treatment [62]. Historically, the suggested treatment for displaced isolated medial malleolar injury had been operative. Often the periosteal sleeve folds into the fracture, causing displacement and potentially leading to nonunion, which can be a difficult problem to treat. Residual displacement has been thought to contribute to instability, nonunion, and arthrosis. Displaced medial malleolar fractures or those associated with a fibular fracture should be treated operatively. However, recent evidence in the case of the isolated medial malleolar fracture suggests that nonoperative treatment may have a role. High rates of union (43/45) were noted with an average displacement of 2.3 mm (range 1 to 5 mm) and satisfactory results [63]. Occasionally, medial-sided fixation and reduction of the talus can assist in judging fibular length and rotation [64].

D.

Syndesmosis Involvement

The syndesmotic ligaments hold the fibula to the tibia. They allow for rotation (128) of the fibula and some widening of the mortise during dorsiflexion, and help transfer weight (15%) to the fibula. The accuracy of reduction of the syndesmosis has been correlated with outcome in several studies [50]. Criteria for reduction are found in previous sections. One must realize that subtle widening however is difficult to detect. Ebraheim et al. [65] evaluated the radiographic and CT assessment of subtle syndesmosis injury in a cadaveric study and found radiographs to be much less sensitive than CT. Some believe that the stress lateral radiograph is more accurate than the stress mortise radiograph. Magnetic resonance imaging (MRI) has also been shown to be accurate in establishing injury to the syndesmosis. Much has been written about when the syndesmosis should be stable based on the radiographic level of the fibula fracture and the presence or absence of medial-sided injury [66]. Previously it was


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thought that the medial side was the key to the stability and reduction of the talus beneath the tibia. Later with the work of Yablon et al. [55] it became obvious that accurate lateral fixation was indeed critical. Boden et al. [67] studied the effect of a deltoid injury in PER-simulated fractures. They concluded that in the presence of deltoid ligament injury the critical zone of fibula injury, that is the level of the fibular fracture which when stabilized would lead to a stable syndesmosis, was less than 3 to 4.5 cm above the ankle. When above this level, in the presence of a deltoid injury, the syndesmosis remained unstable. In the presence of a rigidly stabilized medial bone injury they did not note the need for syndesmotic stabilization. Solari et al. [9] concluded that Weber C fractures with medial malleolar fracture might not need syndesmotic stabilization as significant rotational stability was achieved with fracture fixation alone. However, additional rotational stability was noted with the addition of a syndesmosis screw in the presence of bimalleolar fixation. The premise for many of these biomechanical and clinical studies lies in the assumption that the deltoid is not injured if there is a medial-sided bone injury. This has recently been questioned by Tornetta [68] who has demonstrated deltoid incompetence after medial malleolar fixation, indicating a bony and ligamentous component to the injury in some instances. Countless authors have noted occurrences of syndesmosis widening in fractures that, based on the biomechanical studies, should have been stable. We test all cases and view Weber C fractures with even higher suspicion. Intraoperatively, we perform both a lateral translation stress test under fluoroscopy and an external rotation stress mortise view. When any doubt exists, fixation of the syndesmosis seems a small price to pay when contrasted with damage done from ankle subluxation with an incompetent ligament.

E.

Talar Shift without Fracture

Ankle diastasis can occasionally be seen without fracture. Injury mechanism has been postulated to be an external rotation injury with deltoid rupture and syndesmosis widening. The shift is usually evident on plain films but occasionally requires stress views. MRI can be helpful in diagnosing injury of the syndesmosis as well. Treatment is by casting a close observation if no displacement is evident on the standard radiographs. Any displacement should be treated with one or two syndesmosis screws [69].

F.

Osteochondral Injury

Osteochondral injury may accompany ankle fracture. More violent lesions in younger patients tend to show higher-grade lesions. One study documented a 38% incidence of lateral talar dome lesion after SER IV ankle fracture [70]. Arthroscopy can be interesting for seeing the damage to the chondral surface as well as for discerning fracture alignment [71,72]. The role of arthroscopy for treatment of trauma involving ankle fracture is not yet delineated. Certainly, ankle arthroscopy can be helpful in diagnosing and treating problems after ankle fracture [73].

G.

Open Fractures

Historical control group was treated with irrigation and debridement and delayed fixation or closed reduction than with a protocol of intravenous antibiotics, initial open reduction, and internal fixation with delayed wound closure. Results were comparable between the two groups. There was one infection in each group [74]. Another series of 38 open fractures followed a similar protocol. Three patients required subsequent arthrodesis and nine had poor results. They noted one possible deep infection and five superficial infections [75]. Wiss et al. [76] reported similar results in a series of 62 consecutive patients. They noted 5% deep infection rate, 20% poor results, and an 8% late arthrodesis rate. Certainly, standard orthopedic principles seem applicable in these circumstances. A dirty comminuted fracture might be best treated with pins and an external fixator while a simple medial puncture hole might do well with standard ORIF.


Ankle Fractures

H.

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Techniques of Closed Reduction and Subsequent Care

Most ankle fractures can be treated in a closed fashion. The essential component to closed treatment is stability of the fracture. The ankle joint may be conceptualized in one plane as a ring [77]. Like pelvic fractures, one break in the ring is stable, while two disruptions will be inherently unstable. The medial malleolus or the deltoid ligament constitute the medial side and the fibula is the lateral side; the syndesmosis actually affects the medial component — with a syndesmotic rupture, the talus will rotate and shift, thus gradually increasing the medial clear space. A syndesmotic sprain without fracture may be treated carefully in a closed fashion with a short leg cast. The foot is placed in a neutral position and the patient transferred to a walking boot in 4 weeks to begin careful weight-bearing. Care must be taken, with frequent follow-ups to look for any residual widening, evidence of which usually mandates operative intervention for debridement and repair of the syndesmosis and stabilization. An isolated medial malleolus fracture, which is minimally displaced, may be treated in a closed fashion. Risks of displacement, posterior tibial tendon irritation, and nonunion should be reviewed. The difference between a medial malleolus fracture and a distal tibial pilon fracture may be somewhat subjective — a CT scan will help to define the fracture pattern and displacement when doubts arise. A non-weight-bearing short leg cast for 4 weeks may be changed to a walker boot, with careful progression to walking. The lateral malleolus fracture still challenges the surgeon, as decision making can be complex. With the ‘‘bimalleolar equivalent’’ fracture, the distal fibula fracture is accompanied by a deltoid ligament rupture. This fracture should be fixed in all patients without a contraindication for surgery. The art of reducing these fractures is being lost by the current generation of surgeons, since so many go on to internal fixation. The older patient, or the very infirm, may sometimes be better treated with closed reduction and casting. The reduction is accomplished by a combination of internal rotation of the foot and lateral to medial pressure on the lateral malleolus [78]. The cast is molded carefully and the reduction should be checked once the plaster is dry. The reduction should then be checked weekly; two to three cast changes are common. The only way to suitably hold rotation at the ankle is via a long leg cast. After 1 month, a patellar-tendon-bearing cast may be applied. The patient may advance to a walker boot or ankle stirrup brace at 8 weeks depending on radiographic signs of healing. While the risk of displacement, with proven increase in the incidence of posttraumatic arthrosis, is significant, a number of patients have done very well under close supervision. Much easier for the surgeon is the isolated distal fibular fracture. A small avulsion fracture from the ATF ligament may be treated as a severe sprain, with a walker boot or a stirrup brace for 4 weeks. The Weber A isolated distal fibula fracture below the mortise does well with closed treatment. Most patients prefer a short leg walking cast for comfort but little is lost with a functional walker boot. The common SER distal fibula fracture does well with nonoperative treatment [79]. While some Scandinavian studies have shown equivalent results with walker boot vs. stirrup splint vs. short leg cast [80], most patients are best served with a short leg cast. The issue of weight-bearing remains controversial. The conservative approach is to maintain non-weightbearing status in a cast for 4 weeks, then begin walker boot ambulation and mobilization. Patients should be briefly counseled on the controversy regarding fibula fracture (as discussed above); some advocate aggressive surgical intervention while other surgeons do not recommend surgery unless displacement of the fragments exceeds 2 mm. The good results with most minimally displaced fractures are discussed — our offices would be overwhelmed with posttraumatic arthrosis if many of these fractures led to significant ankle degenerative changes. Some patients will want ‘‘perfect’’ reapproximation of their fracture and opt for operative intervention. An informed discussion helps to alleviate confusion and align expectations.

X.

SURGICAL TECHNIQUES

A.

Lateral Malleolus

The surgical approach to the lateral malleolus is relatively simple, adhering to extensile approach principles. The relative paucity of soft tissue coverage and difficulty of local wound flaps in the


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distal leg add complexity to these injuries and plans for surgical repair. Soft tissue handling must be done with care. Because of the limited success of ankle joint arthroplasty procedures and of the known morbidity of ankle arthrodesis, all efforts to reestablish anatomic alignment must be taken. The patient should be positioned in a lateral or semi-lateral position. While the approach works with the patient in a supine position, the need for constant retraction of soft tissues against gravity may require more assistance for the surgeon. An incision just posterior to the fibula, leaving a scar over soft tissue rather than over bone, is preferred. This line also usually falls posterior to the superficial peroneal nerve, easing exposure. Care must be taken to avoid injury to both the sural and the superficial peroneal nerves, which may have a variable course in this portion of the leg [81,82]. The dissection is made with a full-thickness subcutaneous tissue layer to the fibular periosteum, which is then incised leaving enough tissue to close the periosteum and not involve the fascia of the peroneal musculature. The fracture site is easily identified and a small curette used gently helps to clean out hematoma in the bony gap. Copious irrigation also helps to clear interposing soft tissue that may hinder anatomic reduction. Once the bone ends are cleared, the fracture can be reduced and held with a bone clamp. The fact that most fractures at this level are in supination and external rotation, and that gentle manipulation of the distal fragment and sometimes the foot will facilitate anatomic reduction, should be kept in mind. Care should be taken for a gentle reduction; vigorous manipulation often breaks fragile bone spikes, which offer clues to appropriate length and rotation. A lag screw placed perpendicularly to the fracture will usually hold the bones together. Then, a one-third tubular plate may usually be applied using AO principles [83]. The plate acts to control rotation and to further stabilize the fracture. The location of the plate can vary according to fracture orientation and surgical preference. A posterior position of the plate is usually more stable [84], but may be more prone to cause irritation to the peroneal musculature and thus require later removal. A plate too anterior can cause subcutaneous irritation and require later removal as well. Most times, a compromise position of the plate laterally on the fibula, just anterior to the peroneal muscle, works well. The plate is often twisted 108 for best approximation to the bone; little bending is needed. The distal tip may be bent and flattened in distal fractures to minimize protrusion in the subcutaneous tissue. Care must be taken not to make the distal screws too long; a painful screw tip in the lateral gutter impinging on the talus makes for an unhappy recovery. A higher Weber C type fibula fracture or a very large patient will often require a more substantial plate such as the low contact dynamic compression plate (LC-DCP) plate (Synthes, Paoli, PA). In these instances, the thinner 1/3 tubular plate might bend and allow deformity. Some people have avoided a plate altogether, but simple interfragmentary screws are not justified for early weight-bearing unless the fracture is 21⁄2 times longer in length than in width [85]. The soft tissue envelope should be closed over the plate when possible. A layer of fascia between the plate and the subcutaneous tissue may help avoid difficulty with any wound dehiscence. The technique of a slightly longer incision and lifting the subcutaneous flap anteriorly may also help with minor skin problems, allowing communication to the bone [37]. Numerous studies have demonstrated that a drain has no benefit. The skin is closed according to preference and the leg is placed in a well-padded splint, with posterior L-shaped slab and medial to lateral U-shaped plaster slab. This splint is left in place for 2 weeks to avoid irritation to the soft tissues, bringing the patient back to the office then for splint removal, stitch removal, radiographs, and placement of a short leg cast.

B.

Medial Malleolus

The medial malleolus is usually best approached from an anterior joint line incision. This approach allows visualization of the anteromedial corner of the ankle joint and thus alignment of the joint surface. A previously popular approach, directly medial, does not easily allow such a view of the joint surface and can fool the surgeon with medial bone approximation but joint misalignment. The saphenous nerve and lesser saphenous vein are the major neurovascular structures to respect and can usually be retracted. The periosteum at the fracture should be lifted for 2 to 3 mm and the bone surfaces cleared of hematoma and debris. The simple fracture can usually be easily reduced and held with a small bone clamp, the reduction can be held with two guidewires from a 4-mm cannulated screw set. The guidewire is


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15

inserted at a right angle to the fracture line from the tip of the malleolus into the distal tibia. A 35- to 45-mm screw length seems optimal for purchase in the thicker cancellous bone. A longitudinal cut in the deltoid ligament insertion into the medial malleolus is made along each of the guidewires to facilitate screw placement down to bone. While a solid screw can be used with the standard drilland-screw technique, the cannulated screw is much easier as the guidewire holds reduction nicely. Also, should the screw need to be removed later, a cannulated screw is more easily approached with less dissection of the deltoid. The old ‘‘malleolar’’ screws were 4-mm partially threaded solid screws with a large head — these are now out of vogue due to the need to remove the screw due to prominence of the head as well as the fact that they would often break due to the thin shaft and large screw surface area. Bioresorbable screws have worked well for medial fixation [86]. The extension of the medial malleolar fracture to a variant of the distal tibial pilon is somewhat subjective. Medial malleolar fractures can be confusing and may have pilon type extensions into the tibial metaphysis; comminution of the distal fibula suggests such an impaction type of injury [87,88]. More vertical fracture lines may require screws placed at more of a right angle to the shaft of the tibia (Figure 1.7). The anterior corner incision is easily extended in an extensile fashion to allow access to the distal tibia. A CT scan can help determine complex fracture orientations. The posterior extension toward the posterior tibial tendon and tarsal tunnel demands careful reduction — irritation on the tendon can cause a great deal of pain later. Comminution of the medial malleolus fracture may require more extensive fixation — we frequently use Kirschner wires to augment one or two screws to hold smaller fragments. Figure 1.8 demonstrates comminution of the medial malleolus with a high fibular fracture. Sometimes only one screw will fit and a second starts to cause fragmentation; this situation calls for Kirschner wires to hold the rotational component of the fracture. A simple bend on the distal aspect of the wire and tamp against the bone will usually suffice to limit irritation of subcutaneous tissues and also prevent migration of the pins. A tension band construct may work well, particularly in osteoporotic bone [89,90]. Despite the difficulty of comminution, the medial malleolar fractures often heal very nicely. The attention to joint line apposition should help limit posttraumatic arthrosis. Rehabilitation may be very slow in these injuries and some patients have taken 1 year to progress to painless heavy activity. Medial malleolar nonunion is a difficult problem and these fractures should initially be treated aggressively with stable fixation and bone grafting.

C.

Bimalleolar

The bimalleolar fracture requires careful anatomic reduction. Fixing the fibular fracture first in standard fashion and then the medial malleolus is advocated. Such a progression is done by starting with the patient in a lateral position and then removing the bump and rolling the patient supine to finish the medial side. An intraoperative fluoroscopy machine makes visualization of screw length and fracture reduction easy; less advanced sites still use radiographs. The finer resolution of a radiograph is less helpful than the ability to visualize the ankle in various degrees of rotation, thus the preference for the smaller fluoroscopy machines. The bimalleolar equivalent fracture, encompassing the distal fibula with a deltoid ligament rupture, is common and should be fixed. The deltoid ligament does not require open repair but will heal with anatomic bone reduction [91,92]. These injuries really have potential for crippling arthrosis of the joint, and an exacting attempt for anatomic reconstruction of the fibula must be made. While a medial arthrotomy can easily be done to clean out the gutter in late cases, most acute fractures will reduce with proper rotation of the talus under the tibia. These fractures must be radiographically or fluoroscopically examined, preferably intraoperatively, to confirm anatomic reduction. Rehabilitation after surgery depends upon the patient’s health, demands, and configuration of the fracture. Comminuted fractures in older patients deserve more conservative mobilization than a simple fracture in a young adult. Care must be taken to avoid cast disease — the damaging effects of prolonged immobilization. The surgeon must remember the desired results of painless full-range of motion and balance worries of fracture collapse with the understanding that immobilization longer than 4 to 6 weeks in a cast may lead to severe stiffness and weakness [93]. In other words, the desire for good-looking radiographs must be tempered by the understanding of the soft tissue restrictions.


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Figure 1.7 Comminuted medial malleolar fracture. (A and B) AP and lateral leg films reveal the medial malleolus fractures and the high fibula break. (C) This AP postoperative film reveals the comminution of the medial malleolus and the extensive screw fixation needed. A single syndesmotic screw held stability.

The issue of syndesmosis fixation remains controversial, as discussed previously. We prefer to fix the syndesmosis when in doubt, the morbidity from the extra fixation pales in light of the difficulties with a wide syndesmosis and premature arthrosis. Figure 1.9 demonstrates the variable nature of these injuries and the value of checking position radiographically in the operating room. The syndesmotic screws are stronger if placed through the plate but often the plate is too anterior to allow such design. Syndesmosis is reduced by internal rotation and placement of large pointed reduction forceps on the medial malleolus (usually via a small stab wound) and on the lateral


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Figure 1.8 Complex ankle fracture in a middle-aged male who had a high fibular fracture with a seemingly simple medial malleolar break. His accident was in a rural situation and he had to walk several miles on the fracture. (A and B) AP and lateral views demonstrate the injury. (C and D) Postoperative mortise and lateral radiographs demonstrate Kirschner wire augmentation of comminuted medial malleolar fixation. Bioresorbable syndesmotic screws were used.


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malleolus (usually on one of the screws in the plate). The ankle should be brought into full dorsiflexion, although Tornetta et al. [94] have questioned whether the syndesmosis can ever be too tight. A bioresorbable alternative is available, and good results have been reported with polylactic acid screws [95] and with polylactic acid or polyglycolic acid mix component screws [96], as seen in Figure 1.8. A popular screw choice is to stabilize the syndesmosis with a 4.5-mm

Figure 1.9 Demonstration of syndesmotic instability. (A and B) AP and lateral view of injury demonstrate distal fibula fracture with medial clear space widening. (C) AP film in splint looks nicely reduced and might fool the surgeon into not fixing the syndesmosis. (D) Intraoperative fluoroscopy view without stress shows nice reduction of the fracture.


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Figure 1.9 Continued (E) Intraoperative fluoroscopy view with external rotation stress demonstrates medial widening. (F) Intraoperative fluoroscopy view after syndesmotic fixation shows no widening with stress.

cannulated screw, since it affords excellent bone purchase and can be percutaneously removed in 3 to 4 months. The screw should be fully threaded, acting as a position screw, not a lag screw.

D.

Trimalleolar

The trimalleolar ankle fracture pattern represents a worse disruption of the ankle joint complex. The fracture of the posterior malleolus may be minor, a small avulsion of the tibia from the posterior tibiofibular ligament. Alternatively, the posterior malleolus fragment may constitute an important part of the joint and need anatomic reduction. Current guidelines call for reduction if 25% of the joint surface is involved [97]. This 25% number evolved through better understanding of the size of the posterior malleolus needed to prevent posterior subluxation of the joint [97–100]. These fractures can be very difficult to reduce as the talus subluxes posteriorly; manual reduction without adequate anesthesia can damage the cartilage surface. Thus, caution should be exercised, and general anesthesia is indicated for patients who do not reduce easily. Fixation of the posterior fragment can be tricky. Getting to the piece to reduce it involves dissection around the fibula or percutaneous manipulation. A large reduction clamp anterior and posterior on the tibia, observing reduction with the fluoroscopy unit, is preferred. The posterolateral dissection around the fibula and the peroneal tendons can be trying and difficult to visualize. One study describes a fibular osteotomy to see the fracture site better [101]. Once reduced, a cannulated screw guidewire holds the fracture in place, and an anterior-to-posterior 4.5 cannulated screw works well to hold position. The posterior tibiofibular ligament often causes the avulsion of the posterior malleolus, and thus anatomic reduction of the fibula fracture will aid in posterior malleolus reduction [55,102]. These fractures can lead to poor results if not reduced, as demonstrated in Figure 1.10.

XI.

OSTEOPOROSIS AND ANKLE FRACTURES

The depletion in bone mineral content and osteoporosis, which is becoming endemic in the older population of the U.S., makes the treatment of ankle fractures more challenging. The fracture itself may be the first sign of a weak bone that should be treated pharmacologically. A routine bone density scan for all women as they approach menopause and then careful monitoring afterward according to guidelines is recommended. The challenge of ORIF can be difficult with a weak bone. Screws cannot be expected to maintain compression of position in soft weak bone. Newer techniques have been developed to


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Figure 1.10 A high fibula fracture along with the medial and posterior malleoli in a middle-aged woman. (A and B) Mortise ankle and lateral leg views demonstrate the syndesmotic instability and the fractures. (C) Postoperative mortise view shows a lack of attention to the fibula and syndesmosis; this fracture is doomed to failure due to the wide medial clear space. (D) Mortise view after return to the operating room for late syndesmotic fixation. While the situation is improved, the medial clear space remains abnormal.


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Figure 1.10 Continued (E) After removal of syndesmotic screws, the patient went on to end-stage arthritis as seen in this AP view. (F) AP view of ankle after total ankle arthroplasty salvage for arthritis.

aid with such fixation. Among the best of these are axial wires to augment fibular fixation [103] and transsyndesmosis fixation of the fibula to utilize the tibia for stability. Our experience leads to bit of an ‘‘overkill’’ in metal application: later removal of hardware is far better than early return for loss of fixation. Another presentation, of multiple syndesmotic fixation for a neuropathic fracture, helps to demonstrate the value of inserting screws into the tibia through the fibular plate as a way of maintaining reduction [104]. Figure 1.11 demonstrates a classic example; a 70-year-old woman, overweight and underactive, had a fairly routine-looking fracture. The soft quality of the bone and the comminution led to the decision for syndesmotic screws to stabilize the construct. For some reason (probably their inactivity levels), such patients rarely have any symptoms from the long screws, and hardware removal is unusual.

XII.

ANKLE DISLOCATION OR LIGAMENTOUS DISRUPTION

While this chapter deals primarily with fracture, ankle ligaments play a crucial role in support of the joint. Disruption of the deltoid ligament in the common Weber B fracture pattern is usually cause for surgical intervention and ORIF. Here, the ligament plays the same role as the medial malleolus — if either is ruptured along with the distal fibula fracture, the ankle becomes unstable. There is no reason to repair the deltoid ligament acutely, and late reconstructions are thankfully very rarely necessary. The ankle syndesmosis connects the tibia to the fibula in an essential manner — widening of the mortise due to ligament injury will tend to lead to terrible arthritic degeneration unless corrected. Appreciation of the fine articular anatomy lends to understanding of the need for anatomic restoration of fractures as well as joint alignment. Simple ATF inversion sprain may be difficult to clinically separate from a distal fibular fracture. These sprains almost always warrant radiographs to rule out fracture of the distal fibula or of the talus.


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Figure 1.11 Osteoporosis and ankle fractures in a woman who had already started treatment for osteoporosis when she fell on the steps. (A and B) Mortise and lateral films reveal a bimalleolar fracture. (C and D) Postoperative mortise and lateral views reveal the difficulties of surgery. The bone was very soft and comminuted; longer screws into the tibia help to support the fibula fixation. In older patients, they do not seem to need removal. A bone graft was used to enhance healing in the fibula. The medial malleolus began to further comminute with a screw and thus Kirschner wires were used to hold alignment. The woman had a slow, guarded, but uneventful recovery.


Ankle Fractures

XIII.

23

CONCLUSION

Ankle fractures tolerate fools poorly. Rigid adherence to reduction criteria will help to diminish the chance of posttraumatic arthritis. Some of these ankles seem doomed to arthritis despite excellent reduction, and the limitation of articular cartilage to severe trauma should be respected. The literature clearly demonstrates that improvement in articular restoration has predictive value. On the other hand, the common isolated distal fibula fracture should not be overtreated, as most orthopedic surgeons have seen many slightly shortened and rotated fibula fractures present asymptomatically years after the injury. Regardless of the method, an anatomic reduction of the mortise is the key to getting a good result. Fixation that allows early motion leads to the best results. While innovation can be helpful in developing new ideas in orthopedics, ankle fractures that seem particularly prone to seemingly good ideas in the operating room later fail. We very strongly warn against internal fixation constructs that deviate from common methods. One particular problem seems to be the idea that a cerclage wire around the fibula can hold the bone securely, let the mistakes of those surgeons help prevent repeat errors. The other problem that had been seen was the concept that fixation of one side of the ankle joint could make the bimalleolar fracture act as a simple malleolar fracture. Obviously, the forces causing the different fracture patterns disrupt the ligaments and cause different varieties of instability — which must be respected in terms of postoperative immobilization. When in doubt, a conservative approach is usually best.

REFERENCES 1. Inman, V.T., The Joints of the Ankle, Williams & Wilkins, Baltimore, 1976. 2. Ramsey, P.L. and Hamilton, W., Changes in tibiotalar contact area caused by lateral talar shift, J. Bone Jt. Surg., 58A, 356–357, 1976. 3. Thordarson, D.B., Motamed, S., Hedman, T., Ebramzadeh, E., and Bakshian, S., The effect of fibular malreduction on contact pressures in the ankle fracture malunion model, J. Bone Jt. Surg., 79A, 1809–1815, 1997. 4. Chapman, M.W., Fractures and fracture-dislocations of the ankle, in Surgery of the Foot and Ankle, 6th ed., Mann, R.A. and Coughlin, M.J., Eds., Mosby-Year Book, St. Louis, MO, 1993, p. 1439. 5. Colville, M.R., Marder, R.A., Boyle, J.J., and Zarins, B., Strain measurement in lateral ankle ligaments, Am. J. Sports Med., 18, 196–200, 1990. 6. Bulucu, C., Thomas, K.A., Halvorson, T.L., and Cook, S.D., Biomechanical evaluation of the anterior drawer test: the contribution of the lateral ankle ligaments, Foot Ankle, 11, 389–393, 1991. 7. Rasmussen, O., Kromann-Andersen, C., and Boe, S., Deltoid ligament: functional analysis of the medial collateral ligamentous apparatus of the ankle joint, Acta Orthopaed. Scand., 54, 36–44, 1983. 8. Earll, M., Wayne, J., Brodrick, C., Vokshoor, A., and Adelaar, R., Contribution of ankle deltoid ligament to ankle joint contact characteristics: a cadaver study, Foot Ankle Int., 17, 317–329, 1996. 9. Solari, J., Benjamin, J., Wilson, J., Lee, R., and Pitt M., Ankle mortise stability in Weber C fractures: indications for syndesmotic fixation, J. Orthopaed. Trauma, 5, 190–195, 1991. 10. Boss, A.P. and Hintermann, B., Anatomical study of the medial ankle ligament complex, Foot Ankle Int., 23, 547–553, 2002. 11. Harper, M.C., The deltoid ligament. An evaluation of the need for surgical repair, Clin. Orthopaed., 226, 156–168, 1988. 12. McCullough, C.J. and Burge, P.D., Rotatory stability of the load-bearing ankle: an experimental study, J. Bone Jt. Surg., 62B, 460–464, 1980. 13. Sarsam, I.M. and Hughes, S.P.F., The role of the anterior tib-fib ligament in talar rotation: an anatomic study, Injury, 19, 62–64, 1988. 14. Lauge-Hansen, N., Ligamentous ankle fractures, diagnosis and treatment, Acta Chir. Scand., 97, 544–550, 1949. 15. Lauge-Hansen, N., Fractures of the ankle. II. Combined experimental-surgical and experimentalroentgenologic investigations, Arch. Surg., 60, 957–985, 1950. 16. Lauge-Hansen, N., Fractures of the ankle. IV. Clinical use of genetic roentgen diagnosis and genetic reduction, Arch. Surg., 64, 488–500, 1952. 17. Lauge-Hansen, N., Fractures of the ankle. V. Pronation–dorsiflexion fracture, Arch. Surg., 67, 813–820, 1953. 18. Lauge-Hansen, N., Fractures of the Ankle. III. Genetic roentgenologic diagnosis of fractures of the ankle, Am. J. Radiol., 71, 456–471, 1954.


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19. Nielsen, J.O., Dons-Jensen, H., and Sorensen, H.T., Lauge-Hansen classification of malleolar fractures: an assessment of the reproducibility in 118 cases, Acta Orthopaed. Scand., 61, 385–387, 1990. 20. Rasmussen, S., Madsen, P.V., and Bennicke, K., Observer variation in the Lauge-Hansen classification of ankle fractures: precision improved by instruction, Acta Orthopaed. Scand., 64, 693–694, 1993. 21. Muller, M.E., Allgower, M., Schneider, R. et al., Manual of Internal Fixation, Springer-Verlag, Berlin, 1970. 22. Thomsen, N.O., Overgaard, S., Olsen, L.H., Hansen, H., and Nielsen, S.T., Observer variation in the radiographic classification of ankle fractures, J. Bone Jt. Surg., 73B, 676–678, 1991. 23. Hughes, J.L., Weber, H., Willenegger, H., and Kuner, E.H., Evaluation of ankle fractures: non-operative and operative treatment, Clin. Orthopaed., 138, 111–119, 1979. 24. Orthopaedic Trauma Association Committee for Coding and Classification, Fracture and dislocation compendium, J. 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Ramsey, P.L. and Hamilton, W., Changes in tibiotalar area of contact caused by lateral talar shift, J. Bone Jt. Surg., 58A, 356–357, 1976. 32. Michelson, J.D., Fractures about the ankle, J. Bone Jt. Surg., 77A, 142–152, 1995. 33. Close, J.R., Some applications of the functional anatomy of the ankle joint, J. Bone Jt. Surg., 38A, 761, 1956. 34. Sarkisian, J.S. and Cody, G.W., Closed treatment of ankle fractures: a new criterion for evaluation—a review of 250 cases, J. Trauma, 16, 323–326, 1976. 35. Cox, J.S. and Hewes, T.F., Normal talar tilt angle, Clin. Orthopaed., 140, 37–41, 1979. 36. Stiehl, J.B., Late reconstruction of ankle fractures and dislocations, in Operative Foot Surgery, Gould, J.S., Ed., W.B. Saunders, Philadelphia, 1994, p. 356. 37. Ali, M.S., Mclaren, C.A., Rouholamin, E., and O’Connor, B.T., Ankle fractures in the elderly: nonoperative and operative treatment, J. Orthopaed. Trauma., 1, 275–280, 1987. 38. Bauer, M., Bergstrom, B., Hemborg, A., and Sandegard, J., Malleolar fractures: nonoperative versus operative treatment. A controlled study, Clin. Orthopaed., 199, 17–27, 1985. 39. Beauchamp, C.G., Clay, N.R., and Thexton, P.W., Displaced ankle fractures in patients over 50 years of age, J. Bone Jt. Surg., 65B, 329–332, 1983. 40. Pettrone, F.A., Gail, M., Pee, D., Fitzpatrick, T., and Van Herpe, L.B., Quantitative criteria for prediction of the results after displaced fracture of the ankle, J. Bone Jt. Surg., 65A, 667–677, 1983. 41. Baird, R.A. and Jackson, S.T., Fractures of the distal part of the fibula with associated disruption of the deltoid ligament. Treatment without repair of the deltoid ligament, J. Bone Jt. Surg., 69A, 1346–1352, 1987. 42. Ponzer, S., Nasell, H., Bergman, B., and Tornkvist, H., Functional outcome and quality of life in patients with type B ankle fractures: a two-year follow-up study, J. Orthopaed. Trauma, 13, 363–368, 1999. 43. Belcher, G.L., Radomisli, T.E., Abate, J.A., Stabile, L.A., and Trafton, P.G., Functional outcome analysis of operatively treated malleolar fractures, J. Orthopaed. Trauma, 11, 106–109, 1997. 44. Obremskey, W.T., Dirschl, D.R., Crowther, J.D., Craig, W.L., III, Driver, R.E., and LeCroy, C.M., Change over time of SF-36 functional outcomes for operatively treated unstable ankle fractures, J. Orthopaed. Trauma, 16, 30–33, 2002. 45. Wei, S.Y., Okereke, E., Winiarsky, R., and Lotke, P.A., Nonoperatively treated displaced bimalleolar and trimalleolar fractures: a 20-year follow-up, Foot Ankle Int., 20, 404–407, 1999. 46. Rowley, D.I., Norris, S.H., and Duckworth, T., A prospective trial comparing operative and nonoperative treatment of ankle fractures, J. Bone Jt. Surg., 68B, 610–613, 1986. 47. Lindsjo, U., Operative treatment of ankle fracture-dislocations. A follow-up study of 306/321 consecutive cases, Clin. Orthopaed., 199, 28–38, 1985. 48. Kennedy, J.G., Johnson, S.M., Collins, A.L., DalloVedova, P., McManus, W.F., Hynes, D.M., Walsh, M.G., and Stephens, M.M., An evaluation of the Weber classification of ankle fractures, Injury, 29, 577–580, 1998. 49. Leeds, H.C. and Ehrlich, M.G., Instability of the distal tibiofibular syndesmosis after bimalleolar and trimalleolar ankle fractures, J. Bone Jt. Surg., 66A, 490–503, 1984. 50. Chissell, H.R. and Jones, J., The Influence of the diastasis screw on the outcome of Weber C ankle fractures, J. Bone Jt. Surg., 77B, 435–438, 1995.


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51. Parfenchuck, T.A., Frix, J.M., Bertrand, S.L., and Corpe, R.S., Clinical use of a syndesmosis screw in stage IV pronation–external rotation ankle fractures, Orthopaed. Rev., Suppll., 23–28, Aug. 1994. 52. Snedden, M.H. and Shea, J.P., Diastasis with low distal fibula fractures: an anatomic rationale, Clin. Orthopaed., 382, 197–205, 2001. 53. Kristensen, K.D. and Hansen, T., Closed treatment of ankle fractures. Stage II supination–eversion fractures followed for 20 years, Acta Orthopaed. Scand., 56, 107–109, 1985. 54. Phillips, W.A., Schwartz, H.S., Keller, C.S., Woodward, H.R., Rudd, W.S., Spiegel, P.G., and Laros, G.S., A prospective, randomized study of the management of severe ankle fractures, J. Bone Jt. Surg., 67A, 67–78, 1985. 55. Yablon, I.G., Keller, F.G., and Shouse, L., The key role of the lateral malleolus in displaced fractures of the ankle, J. Bone Jt. Surg., 59A, 169–173, 1977. 56. Harper, M.C., Posterior instability of the talus: an anatomic evaluation, Foot Ankle, 10, 36–39, 1989. 57. Raasch, W.G., Larkin, J.J., and Draganich, L.F., Assessment of the posterior malleolus as a restraint to posterior subluxation of the ankle, J. Bone Jt. Surg., 74A, 1201–1206, 1992. 58. Harper, M.G. and Hardin, G., Posterior malleolar fractures of the ankle associated with external rotation-abduction injuries: results with and without internal fixation, J. Bone Jt. Surg., 70A, 1348– 1356, 1988. 59. Scheidt, K.B., Stiehl, J.B., Skrade, D.A., and Barnhardt, T., Posterior malleolar ankle fractures: an in vitro biomechanical analysis of stability in the loaded and unloaded states, J. Orthopaed. Trauma, 1992; 6, 96–101. 60. Hartford, J.M., Gorczyca, J.T., McNamara, J.L., and Mayor, M.B., Tibiotalar contact area. Contribution of posterior malleolus and deltoid ligament, Clin. Orthopaed., 320, 182–187, 1995. 61. Heim, U.F., Trimalleolar fractures: late results after fixation of the posterior fragment, Orthopedics, 12, 1053–1059, 1989. 62. Portis, R.B. and Mendelsohn, H.A., Conservative management of fractures of the ankle involving the medial malleolus, J. Am. Med. Assoc., 151, 102, 1953. 63. Herscovi, D. and Scaduto, J., Non-operative Treatment of Medial Malleolar Fractures, American Orthopaedic Foot and Ankle Society, Summer Meeting, San Diego, CA, July 19–21, 2001. 64. Limbird, R.S. and Aaron, R.K., Laterally comminuted fracture-dislocation of the ankle, J. Bone Jt. Surg. Am., 69A, 881–885, 1987. 65. Ebraheim, N.A., Lu, J., Yang, H., Mekhail, A.O., and Yeasting, R.A., Radiographic and CT evaluation of tibiofibular syndesmotic diastasis: a cadaver study, Foot Ankle Int., 18, 693–698, 1997. 66. Miller, S.D., Controversies in ankle fracture treatment: indications for fixation of stable Weber B fractures and indications for syndesmosis stabilization, Foot Ankle Clin., 5, 841–851, 2000. 67. Boden, S.D., Labropoulos, P.A., McCowin, P., Lestini, W.F., and Hurwitz, S.R., Mechanical considerations for the syndesmosis screw. A cadaver study, J. Bone Jt. Surg., 71A, 1548–1555, 1989. 68. Tornetta, P., Competence of the deltoid ligament in bimalleolar ankle fractures after medial malleolar fixation, J. Bone Jt. Surg., 82A, 843–848, 2000. 69. Miller, C.D. and Shelton, W.R., Deltoid and syndesmotic ligament injury in the ankle without fracture, Am. J. Sports Med., 23, 746–750, 1995. 70. Sorrento, D.L. and Mlodzienski, A., Incidence of lateral talar dome lesions in SER IV ankle fractures, J. Foot Ankle Surg., 40, 118–119, 2001. 71. Thordarson, D.B., Bains, R., and Shepherd, L.E., The role of ankle arthroscopy on the surgical management of ankle fractures, Foot Ankle Int., 22, 123–125, 2001. 72. Loren, G.J. and Ferkel, R.D., Arthroscopic assessment of occult intra-articular injury in acute ankle fractures, Arthroscopy, 18, 412–421, 2002. 73. van Dijk, C.N., Verhagen, R.A., and Tol, J.L., Arthroscopy for problems after ankle fracture, J. Bone Jt. Surg., 79B, 280–284, 1997. 74. Bray, T.J., Endicott, M., and Capra, S.E., Treatment of open ankle fractures. Immediate internal fixation versus closed immobilization and delayed fixation, Clin. Orthopaed., 240, 47–52, 1989. 75. Franklin, J.L., Johnson, K.D., and Hansen, S.T., Immediate internal fixation of open ankle fractures, J. Bone Jt. Surg., 66A, 1349–1356, 1984. 76. Wiss, D.A., Gilbert, P., Merritt, P.O., and Sarmiento, A., Immediate internal fixation of open ankle fractures, J. Orthopaed. Trauma, 2, 265–271, 1988. 77. Neer, C.S., Injuries of the ankle joint: evaluation, Conn. State. Med. J., 17, 580, 1953. 78. Charnley, J., Treatment of the Ten Common Fractures, 3rd ed., Williams & Wilkins, Baltimore, 1961. 79. Yde, J. and Kristensen, K.D., Ankle fractures: supination-eversion fractures stage II: primary and late results of operative and non-operative treatment, Acta Orthopaed. Scand., 51, 695–702, 1980. 80. van Laarhoven, C.J., Meeuwis, J.D., and van der Werken, C., Postoperative treatment of internally fixed ankle fractures: a prospective randomised study, J. Bone Jt. Surg., 78B, 395–399, 1996. 81. Eastwood, D.M., Irgau, I., and Atkins, R.M., The distal course of the sural nerve and its significance for incisions around the lateral hindfoot, Foot Ankle, 13, 199–202, 1992. 82. Lawrence, S.J. and Botte, M.J., The sural nerve in the foot and ankle: an anatomic study with clinical and surgical implications, Foot Ankle Int., 15, 490–494, 1994.


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83. Muller, M.E., Allgower, M., Schneider, R. et al., Manual of Internal Fixation, 3rd ed., Springer-Verlag, New York, 1991. 84. Schaffer, J.J. and Manoli, A., II, The antiglide plate for distal fibular fixation: a biomechanical comparison with fixation with a lateral plate, J. Bone Jt. Surg., 69A, 596–604, 1987. 85. Mattan, Y. and Segal, D., The use of small fragment sets in ankle fractures, Tech. Orthopaed., 6, 84, 1991. 86. Bucholz, R.W., Henry, S., and Henley, M.B., Fixation with bioabsorbable screws for the treatment of fractures of the ankle, J. Bone Jt. Surg., 76A, 319–324, 1994. 87. Coonrad, R.W., Fracture-dislocations of the ankle joint with impaction injury of the lateral weightbearing surface of the tibia, J. Bone Jt. Surg., 52A, 1337–1344, 1970. 88. Limbird, R.S. and Aaron, R.K., Laterally comminuted fracture-dislocation of the ankle, J. Bone Jt. Surg., 69A, 881–885, 1987. 89. Georgiadis, G.M. and White, D.B., Modified tension band wiring of medial malleolar ankle fractures, Foot Ankle Int., 16, 64–68, 1995. 90. Ostrum, R.F. and Litsky, A.S., Tension band fixation of medial malleolus fractures, J. Orthopaed. Trauma, 6, 464–468, 1992. 91. Baird, R.A. and Jackson, S.T., Fractures of the distal part of the fibula with associated disruption of the deltoid ligament: treatment without repair of the deltoid ligament, J. Bone Jt. Surg., 69A, 1346–1352, 1987. 92. Harper, M.C., The deltoid ligament: an evaluation of need for surgical repair, Clin. Orthopaed., 226, 156–168, 1988. 93. Shaffer, M.A., Okereke, E., Esterhai, J.L., Jr., Elliott, M.A., Walker, C.A., Yim, S.H., and Vanderborne, K., Effects of immobilization on plantar-flexion torque, fatigue resistance, and functional ability following an ankle fracture, Phys. Ther., 80, 769–780, 2000. 94. Tornetta, P., III, Spoo, J.E., Reynolds, F.A., and Lee, C., Overtightening of the ankle syndesmosis: Is it really possible?, J. Bone Jt. Surg., 83A, 489–492, 2001. 95. Thordarson, D.B., Samuelson, M., Shepherd, L.E., Merkle, P.F., and Lee, J., Bioabsorbable versus stainless steel screw fixation of the syndesmosis in pronation–lateral rotation ankle fractures: a prospective randomized trial, Foot Ankle Int., 22, 335–338, 2001. 96. Miller, S.D. and Carls, R.J., The bioresorbable syndesmotic screw: application of polymer technology in ankle fractures, Am. J. Orthoped., 31, 18–21, 2002. 97. McDaniel, W.J. and Wilson, F.C., Trimalleolar fractures of the ankle: an end result study, Clin. Orthopaed., 122, 37–45, 1977. 98. McLaughlin, H.L. and Ryder, C.T., Jr., Open reduction and internal fixation for fractures of the tibia and ankle, Surg. Clin. North Am., 29, 1523, 1949. 99. Macko, V.W., Matthews, L.S., Zwirkoski, P., and Goldstein, S.A., The joint-contact area of the ankle: the contribution of the posterior malleolus, J. Bone Jt. Surg., 73A, 347–351, 1991. 100. Wilson, F.C., Fractures and dislocations of the ankle, in Fractures in Adults, 2nd ed., Rockwood, C.A., Jr. and Green, D.P., Eds., Lippincott, Philadelphia, 1984, p. 1665. 101. Hughes, J.L., Corrective osteotomies of the fibula after defectively healed ankle fractures (abstract), J. Bone Jt. Surg., 58A, 728, 1976. 102. Harper, M.C. and Hardin, G., Posterior malleolar fractures of the ankle associated with external rotation-abduction injuries, J. Bone Jt. Surg., 70A, 1348–1356, 1988. 103. Cole, P.A. and Craft, J.A., Treatment of osteoporotic ankle fractures in the elderly: surgical strategies, Orthopaedics, 25, 427–430, 2002. 104. Perry, M., Taranow, W.S., and Manoli, A., Multiple Syndesmotic Fixation for Neuropathic Ankle Fractures with Failed Traditional Fixation, American Orthopaedic Foot and Ankle Society, 32nd Annual Meeting, February 16, 2002, Dallas, TX. 105. Konrath, G., Karges, D., Watson, J.T., Moad, B.R., and Cramer, K., Early versus delayed treatment of severe ankle fractures: a comparison of results, J. Orthopaed. Trauma, 9, 377–380, 1995.


2 Pilon Fractures Richard T. Laughlin Wright State University, Dayton, Ohio

CONTENTS I. Introduction .................................................................................................................... II. Fracture Classification..................................................................................................... III. Soft Tissue Classification ................................................................................................. IV. Temporary Fixation ........................................................................................................ V. Fixation of The Tibial Articular Surface ......................................................................... VI. Plate Fixation .................................................................................................................. VII. External Fixation............................................................................................................. VIII. Postoperative Care .......................................................................................................... IX. Results ............................................................................................................................. X. Complications.................................................................................................................. XI. Conclusion....................................................................................................................... Acknowledgment......................................................................................................................... References ...................................................................................................................................

I.

27 28 28 30 33 36 37 43 44 45 46 46 46

INTRODUCTION

Fractures of the distal tibial articular surface are some of the most challenging fractures to treat. They often involve soft tissue injury in an area that easily becomes compromised. The treatment of these complex injuries is fraught with potential complications and the surgeon should proceed with great caution as complications can often lead to infection, nonunion, and even amputation. The term pilon is often attached to this fracture type. This refers to fracture of the metaphyseal area extending to the articular surface. Pilon is a French term describing the distal tibial metaphysis because of its shape, which is similar to the pharmacist’s pestle. Plafond is another French term used to describe this position of the tibia and ankle as it means ceiling, referring to the horizontal distal tibial articular surface. A distinction must be made between the pilon fracture and the more common ankle fracture involving only the malleoli. The distinguishing characteristic of the pilon fracture is that it involves the supra-articular metaphysis, with varying degrees of impaction [1,2]. The impaction is related to the axial load mechanism of injury and includes primary articular cartilage damage, contributing to the uncertain outcome of these injuries, whereas the malleoli fractures (ankle fractures) are much more commonly caused by a twisting mechanism and have much less primary articular cartilage damage. Making the distinction between the pilon fracture and the malleoli fracture will affect treatment decisions as well as timing of surgery.

27


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Laughlin

Lateral

Anteroposterior

Axial

A

A

A

B

B

B

C

C

C

Figure 2.1 Ruedi–Allgo¨wer classification of pilon fractures [4,5].

II.

FRACTURE CLASSIFICATION

Many classification schemes have been proposed for this injury. The system of Ruedi and Allgo¨wer is one of the earlier classifications and is widely known (Figure 2.1). It is classified into three types based on displacement and comminution. Type 1 has minimal displacement, is of lower energy, and presumably causes less primary damage to the articular cartilage. Type 2 fracture has more displacement but the joint surface is not comminuted. Type 3 involves more comminution and impaction [3–5]. This classification is particularly helpful in understanding the pathology of the fracture. There are generally three main regions of the distal tibial articular surface that must be reconstructed. The relationship of these fragments to each other and their remaining attachment to the fibula will help determine the operative approach and fixation. This classification has spawned modifications by Ovadia and Beals [6], Maale and Seligson [7], and Mast et al. [8]. All of these authors attempt to further describe fracture patterns, but do not necessarily help direct treatment or predict outcome. The current AO classification uses the AO system of periarticular fractures in which A fractures are extra-articular; B fractures are partial articular, and C fractures are complete articular [9]. Each of these has three subtypes based on the amount of comminution and impaction (Figure 2.2). This classification system has further been expanded by the OTA Committee for Coding and Classification [10]. This system describes every fracture pattern in the same system of extraarticular, partial articular, and complete articular; but adds fibular fracture patterns and tibial fractures that extend into the diaphysis. All fractures are given an alphanumeric code, allowing for ease of database retrieval. The numeric code for pilon fracture is 43. This classification is very detailed and is primarily being used for academic purposes. It is all-inclusive, but may not be practical for easy use. All classification systems should help direct treatment and correlate with results. The common concepts of the classifications of the intra-articular fractures are that there are generally three regions: posterior, anterolateral, and anteromedial. Usually, some soft tissue attachment to the fibula is maintained. Understanding the ligamentous attachments and the fracture patterns will help the surgeon in planning the approach and fixation. Unfortunately, there has not been enough uniform use of the classification systems to truly relate fracture type with outcome. This will further be discussed in the section on results.

III.

SOFT TISSUE CLASSIFICATION

Soft tissue concerns are the major factor in decision making in the treatment of the pilon fracture. The ankle has thin skin, very little subcutaneous fat, and muscle coverage only on its posterior side.


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29

A

B

C

1

2

3

Figure 2.2 AO comprehensive classification for pilon fractures [9].

The skin is easily compromised, and incisions through this compromised tissue must be carefully planned and timed to minimize further injury. Soft tissue injuries accompanying closed fractures are often underestimated. Since there has been no open wound to dissipate energy from the injury, the skin can be intact but deeply contused or abraded. The main complication of these contusions and abrasions are necrosis, which predisposes tissue to infection. One must proceed with great caution when contemplating incisions in this compromised soft tissue component of the injury. Soft tissue injury around fractures has been characterized extensively for open fractures. It is important to note though that soft tissue injury occurs around closed fractures as well. This has been characterized by Oestern and Tscherne [11]. Closed fractures are classified into grades 0, I, II, and III (Figure 2.3). Grade 0 describes a simple fracture with little or no soft tissue injury. Grade I

G r a d e

Simple Fracture configuration with little or no soft tissue injury

0

G r a d e I

Deep, contaminated abrasion local contusional damage to skin/muscle moderately severe fracture configuration

G r a d e II

Figure 2.3

G r a d e III

Superficial abrasion (shaded area), mild to moderately severe fracture configuration

Extensive contusion or crushing of skin or destruction of muscle (shaded area), severe fracture

Tscherne [11] classification of soft tissue injury.


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involves superficial abrasion or contusion with mild to moderate fracture comminution. Grade II injuries have deep contaminated abrasions, local contusional damage to skin or muscle, and moderately severe comminution. Grade III injuries have extensive contusion or crushing of skin or distraction of muscle and severe fracture patterns. Understanding the magnitude of soft tissue injury will guide the surgeon in planning the surgical sequence. It is imperative to respect the level of injury and optimize the timing of surgery. Fractures with grade 0 soft tissue injury could be repaired early; however, most pilon fractures result in enough swelling to make delay of fixation prudent. Surgical windows for the timing of repair have been described for two periods. The early period is within 6 h of surgery and the late period is between 6 and 12 days [11]. In fractures with severe swelling and soft tissue contusion, one can easily wait 3 weeks before undertaking definitive fixation. In this author’s experience, it is unusual to have the opportunity to definitely fix these fractures in the first 6 h after injury. This is not to say that injuries should not be stabilized. The most important component in soft tissue healing is achieving stability of the underlying bone, along with elevation and a soft compressive dressing. One way to accomplish this is with a spanning external fixator. This can function as a traveling traction, providing stability, alignment, and length so that computed tomography (CT) can be obtained for preoperative planning [12]. The patient can then be transported easily, and have other more life-threatening injuries stabilized first. Once soft tissues have healed, definitive fixation can be undertaken [13–15]. In the case of open injuries or injuries with severe crushing of the skin the viability of the skin must be assessed and an early decision for flap coverage should be when possible. Where open injuries are involved the decision can often be made at the time of the initial debridement. The soft tissue defect is thoroughly assessed and if necessary a microvascular surgeon is consulted. If free-tissue transfer is required, best results are obtained when the flap is done in the first 7 to 10 days following the injury [16,17]. After this time, the wound becomes colonized and progresses to a chronic state where the tissues stiffen, there is chronic inflammation, and the vascular pedicles become less pliable [16]. Definitive fixation can be delayed until soft tissue coverage is obtained. In the cases with severe open injuries, fixation of articular fragments easily accessible through the wound can be done if soft tissue coverage will be obtained in the next few days; otherwise, it should be delayed until definitive soft tissue coverage is obtained [18]. Crushing injuries in which the skin is still intact can be more difficult to assess. It often may take more than 1 week for the skin to demarcate. In these cases, the fracture should be stabilized with a spanning external fixator until the soft tissues demarcate or heal. Definitive fixation can be delayed until this question is answered. Research has been done in the use of hyperbaric oxygen in these cases. If it is available and the patient can be safely transported to the chamber, it is useful to decrease the swelling and enhance the survival of the marginal tissue.

IV.

TEMPORARY FIXATION

Temporary spanning external fixation can be accomplished by fixing the fibula and placing a medial external fixator (Figure 2.4) or placing a fixator with a transfixion pin through the calcaneus, with medial or lateral bars connected to anterior half-pins in the tibia (Figure 2.5). This is easy to apply quickly in cases in which the patient may be too unstable for any extensive surgery [12,19]. Restoring alignment with only a medial fixator when both tibia and fibula are fractured is difficult. As traction is applied medially, the fracture is often pushed into valgus and cannot be adequately aligned (Figure 2.6). This method is suboptimal unless the fibula can be stabilized. Restoring alignment and length is essential for optimal soft tissue care and must be accomplished as soon as possible after the injury so that the soft tissues can begin recovering. Fixation of the fibula at this first surgical session is advantageous, as it restores length and helps greatly with alignment [13]. In the case of closed fractures, it also allows evacuation of hematoma from the fracture, thus decompressing the distal leg, which helps with management of the swelling and pain.


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31

B

C

D

Figure 2.4 (A and B) AO type 43C fracture, grade I open in a 50-year-old male who fell from a deer stand. (C and D) Radiographs showing provisional reduction with fibular plating and medial spanning external fixator. This restores alignment and length, allowing CT. Definitive fixation is delayed until soft tissues have recovered.

B

A

C

Figure 2.5 (A to C) The delta frame with a medial-to-lateral transfixion pin through the calcaneus and anterior half-pins in the tibia provides good stability when the fibula has not been fixed. A half-pin may be added to the first metatarsal base to control equinus.


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A

B

C

D

E

Figure 2.6 (A and B) Type 43C fracture in a 30-year-old male involved in a motor vehicle accident and initially treated with a medial spanning external fixator before transfer. (C) Valgus alignment and shortening with the first external fixator. (D) This was converted to a delta frame with fixation of the fibula, which restored alignment and length. (E) After soft tissue healing, formal open reduction and internal fixation was performed.

Once this is accomplished, CT is obtained [15]. The patient is placed in a compressive cotton dressing and kept with the foot elevated until the skin condition is favorable for an open procedure to reduce the joint. This may take up to 3 weeks. Even at 3 weeks, the articular pieces can still be manipulated and reduced. If the fibula was fixed initially, this incision usually heals by 3 weeks, giving the surgeon more options in choosing incisions for fixation of the tibia.


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FIXATION OF THE TIBIAL ARTICULAR SURFACE

Fixing the articular surface of the tibia requires careful planning. CT is essential, as it enables the surgeon to see the fragments in axial cuts [15]. The location of the fracture lines determines where the incisions should be made. The components of the articular surface usually occur in a predictable pattern. The regions that must be considered have been described by Waddell as the medial malleolus, the anterior tibial margin, the posterior malleolus, the tubercle of Chaput (anterolateral tibial tubercle), and the syndesmosis. When addressing the tibia, techniques for achieving indirect reduction are essential. The first technique is fibular fixation. Eighty-five percent of pilon fractures include a fibular fracture [20–23]. This fracture usually occurs above the syndesmosis and often is not extensively comminuted. Fixing the fibula fracture restores length, but more importantly, through ligamentotaxis, the posterior malleolus is usually brought back to the level of the true joint line [8,23]. This provides a starting or reference fragment for reduction of the remainder of the joint. When the fibula can be easily reconstructed, it is helpful in the reduction and prevents valgus drift of the ankle. Ruedi and Allgo¨wer [5] addressed the fibula first in 60% of their fractures. There are disadvantages to fixing the fibula. If it cannot be restored anatomically, it will interfere with subsequent reduction of the tibia; furthermore, once it is fixed, one cannot compress across the metaphyseal fracture in cases where external fixation is used [24]. By keeping the fibula out to length, the medial side of the ankle can collapse into varus alignment when not buttressed by internal fixation [19,25,26]. Finally, it requires an additional incision, which may compromise the tibial incision. In summary, fixing the fibula can be helpful in achieving reduction of the tibial articular surface, but does not necessarily need to be done universally. Another technique that should not be forgotten for achieving some indirect reduction is calcaneal traction. This can easily be done in surgery by placing a 1.8-mm wire through the calcaneal tuberosity, attaching it to a half-ring, and tensioning. Ten to 15 pounds is then attached by a sterile rope and hung over the edge of the table. This provides in-line traction and does not limit any medial access to the leg. Finally, a medial external fixator or the universal AO distractor can provide traction to indirectly reduce the fracture [9]. When fragments have remaining soft tissue attachments, they can be reduced via ligamentotaxis, which occurs during distraction. This also can provide distraction of the joint itself so that the quality of the reduction can be assessed. The AO universal distractor is applied by placing 5-mm half-pins in the tibia above the fracture, remote enough to allow plate fixation, if that is chosen. The pins in the foot can be placed either in the talar neck or in the calcaneal tuberosity. The author’s preference is to put the pin in the superior, posterior portion of the calcaneal tuberosity, as it is safe and easily placed. A pin in this location rarely gets in the way of the surgeon working on the articular surface. In cases where the fibula is not fixed, care must be taken not to overdistract medially, as this will angulate the fracture into a valgus orientation (Figure 2.6). After indirect reduction techniques have been employed, joint reduction must be assessed. Image intensifier radiography is used to assess the reduction. A mortise and especially a good lateral view are essential. In some cases, closed reduction can be obtained. Fragments may be manipulated with percutaneously placed pins or pointed reduction clamps. This is best done in the first few days after injury. If the articular fracture is to be treated percutaneously with a medial external fixator, the joint must be reduced early, as after 1 week it becomes increasingly difficult to manipulate the fragments without exposing them [24,27]. If anatomic reduction is obtained in this manner, screws can be placed percutaneously as well. Smaller screws placed in lag fashion are preferred for joint fixation. Usually, 2.7-, 3.5-, and 4-mm screws are of sufficient size to lag the articular fragments back together. In most cases, an open reduction will be required. The incision for the open procedure usually is anterolateral or anteromedial. Rather than following traditional bony landmarks, such as the anterior tibial crest, it is best to make incisions over a major fracture line. By doing this, the fracture can be opened up like a book, providing access to the rest of the joint. Extreme care must be taken not to strip the joint capsule or periosteum off of the metaphyseal shell.


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Most fractures are addressed by regions. They usually include the anterolateral region (tubercle of Chaput), the posterior malleolus, and the medial malleolus. When comminution exists, it usually involves the central portion of the articular surface where these three regions meet; thus even in the comminuted fracture, these three regions can be delineated. The anterolateral and posterolateral fragments usually have some attachment to the fibula by the anterior and posterior tibiofibular ligaments. Thus restoring the fibula aids in restoring the lateral fragments of the tibia. A standard way to approach this is to restore fibular length, which usually puts the posterior malleolus at its proper position (Figure 2.7). Then the central portion of the joint is approached through an incision on the fracture line that divides the anterolateral fragment and the medial malleolus. Central comminuted fragments are then reduced to the posterior fragment. The anterolateral fragment can then be reduced, which reconstitutes the lateral column of the tibia. Finally, the medial side is reduced to this. Provisional reduction is held with 1.25- or 1.6-mm wires, followed by lag screw fixation. Generally, two screws are placed connecting the anterolateral fragment to the posterolateral fragment. The medial malleolus should have one screw going into each of the lateral fragments. Screws should be placed perpendicular to the fracture lines and as close to the joint line as possible. The strongest bone lies in the area of the epiphyseal scar. Also, if a small wire circular fixation is chosen for neutralization, the surgeon must keep the interfragmentary screws clear of the transfixion wires [14]. Bone grafting is the third step of reconstruction described by the traditional approach of the AO group. The injury is predominantly produced by an axial load, so articular fragments are impacted into the softer metaphyseal cancellous bone. When they are reduced, defects in the metaphysis that need to be supported are left behind. The defects should be filled with cancellous bone graft taken from the iliac crest, distal femur, or proximal tibia. Many bone graft substitutes are available to extend the bone graft, but these should be used as supplements and not as the sole bone graft. In defects that are completely contained, one may choose to use only the bone graft substitutes, but there has not been enough research to fully endorse this.

Figure 2.7 Type 43C fracture with a grade III open wound requiring free-flap coverage in a 35-year-old male who fell from a roof. Initial fixation involved open reduction of the fibula with a medial spanning external fixator. The joint was reconstructed before placement of the free flap. Once the free flap healed, the metaphysis was bone grafted and the fixation converted to a ring external fixator.


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Supporting the articular fragments with bone graft and filling cancellous defects in the metaphysis enhances the stability of the fixation as it provides substance for the lag screws to compress against. Timing of the bone graft must be considered when addressing the open pilon fracture. In cases where there has been gross contamination and compromised soft tissue, the soft tissue envelope should be stable before bone grafting. In cases treated with external fixation because of soft tissue compromise, one may consider waiting 4 to 6 weeks before bone grafting. At this point, the soft tissues are stabilized, and chances of the bone graft becoming infected are lower. Similar concerns exist in cases where free-flap coverage is used. The final step in reconstruction of the pilon fracture is the reattachment of the articular segment to the tibial shaft. One must consider the comminution of the metaphysis and the status of the fibula when deciding how to address this stage. This area of treatment holds the most controversy, but the goals are the same regardless of the method chosen. Fixation must be stable to allow fracture and soft tissue healing and, in some cases, early weight-bearing. The choices for fixation are numerous and include both internal and external fixation. Table 2.1 lists the options for fixation. When choosing the method of fixation, one must address the personality of not only the fracture, but also that of the soft tissue injury. In all cases, the articular surface should be reduced anatomically. If there are no depressed, impacted articular segments, this may be accomplished with minimal incisions. When there are impacted fragments, the fracture needs to be opened, as previously described. Fixation of the fibula is easy to perform when it is not comminuted. This can help to restore length and reduce the articular surface of the tibia. The only disadvantage is that it prevents compression of the metaphyseal region if external fixation is chosen. Fixation of the tibial articular surface to the metaphyseal area can be done with plate fixation or external fixation. Plate fixation is best chosen when the surgeon can get good screw purchase in the articular segments and the metaphyseal area can be lagged together as well. If this can be accomplished with stable soft tissue coverage, plate fixation provides rigid stabilization, allowing early motion [23,28] (Figure 2.8). The main disadvantages to open reduction and internal fixation are the soft tissue concerns [18,19,25]. With the amount of swelling that occurs, the added space that a plate occupies can make it difficult to achieve a tension-free closure of the skin, increasing the risk of wound breakdown. Many of the newer plates have a lower profile and are easier to get into the soft tissue envelope, but it must be remembered that their strength is lower as well. The second disadvantage to plating is the amount of bone graft required to fill metaphyseal defects. As stated earlier, the metaphyseal fragments can be lagged together without excessive soft tissue stripping, then a plate is an effective way to neutralize the fracture. When there is extensive comminution, the plate functions as a buttress, maintaining length of the tibia and preventing varus collapse. When restoring normal length, the gap created can require a large amount of bone graft, and the surgeon must be prepared to harvest this amount. Plate fixation is the method of choice in most B type (partial articular) fractures, where a portion of the joint surface is still attached to the metaphyseal regions (Figure 2.9). In these fractures, the joint is reduced, the impacted areas bone grafted, and a buttress plate is applied to support the reduced articular segment.

Table 2.1 Fixation Methods for Pilon Fractures Internal fixation

External fixation

Traditional buttress plating Locking screw or plate systems Precontoured, percutaneous plates

Joint or rigid spanning Joint-spanning or articulated Non-joint-spanning Small wire — hybrid Small wire — Ilizarov


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B

A

Figure 2.8 (A and B) Rigid internal fixation of a type 43C fracture with minimal metaphyseal comminution. There was no fibula fracture, thus it was safer to make the medial incision.

When the entire articular surface is detached from the metaphysis and the metaphyseal region is extensively comminuted beyond what can be safely reconstructed anatomically, the decision must be made to span the defect with internal or external fixation and bone graft; or in some cases, the comminuted area can be compressed and shortened, decreasing the amount of bone needed to fill the defect. Compressing the fracture also adds stability to the fixation construct. If the fibula is not fixed, the relationship of the mortise must be maintained. This is more difficult, but can be done with external fixation. The final option for reconstructing the metaphyseal defect is to maintain the length and use bone transport to fill the defect. This can be done using ring external fixation and transporting a segment of tibia through a proximal corticotomy (Figure 2.10).

VI.

PLATE FIXATION

Plate fixation is very effective for the fractures described previously. Plates are usually applied to the medial surface of the tibia, but may be applied anteriorly or posteriorly (Figure 2.11), depending on the side of the tibia that needs buttressing. The implants chosen currently tend to be lower profile and less bulky than the original plates used by the AO group. Small implants, such as the cloverleaf plate and the recently released locking plates, are less bulky and thus easier to place in the soft tissue envelope. Plates are placed medially to buttress the sagittal plane fractures. This prevents late varus deformity and allows lag screw fixation through the plate. This can be done with the cloverleaf plate, cutting off the posterior arm of the plate. These smaller plates are easy to contour and generally are well tolerated by the soft tissues. Locking plates are now available, introducing many new concepts in internal fixation. By providing screws with threaded heads that lock into the plate, the construct becomes a fixed-angle device, which theoretically provides better control of the distal fragment, especially in cases where comminution precludes lag screw fixation of all the metaphyseal fragments. Very little has been published on clinical results with locking plates; however, it seems like a natural evolution in plate fixation as efforts are made to avoid extensive exposures and use plates as bridging devices rather than strictly neutralization or buttress devices.


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A

C

B

Figure 2.9 (A and B) Closed type 43B fracture in a 22-year-old male involved in a motorcycle accident. (B) CT scan demonstrates the displaced anterior articular segment. (C) This was treated with lag screw fixation and a buttress plate.

VII.

EXTERNAL FIXATION

When soft tissue concerns preclude internal fixation, external fixation should be considered (Figure 2.12). External fixation is an important technique as it is the least invasive and safest technique. The first type of fixator to be considered is a simple frame that spans the joint. This can be placed when the patient first presents and allows realignment of the joint and immobilization, which are essential for ‘‘resuscitating’’ the soft tissues. By doing this, definitive fixation can be delayed until the soft tissues recover. Two types of spanning frames are generally used. The first is a delta or triangle frame, which provides meal or lateral stability and should be used when both the tibia and the fibula are fractured and no other fixation is used. It is very simple to apply and consists of two 5mm half-pins in the anterior tibia, well above the zone of injury, and a centrally threaded transfixion pin through the calcaneus (Figure 2.5). When the fibula is intact or has been fixed, one can span the joint with the above frame or use a medial frame only (Figure 2.4). Using only a medial frame when the fibula is not intact or fixed makes obtaining alignment more difficult. When the medial frame is distracted to obtain reduction, the fracture tends to drift into valgus, which is not acceptable even when the fixator is only temporary (Figure 2.6). One of the keys to soft tissue recovery is reduction of the fracture. These fixators are usually a temporary means for stabilizing the fracture until the soft tissue will allow definitive fixation. Other types of external fixation are used for definitive treatment. Marsh [24] and Bonar and Marsh [27] have written extensively on the one-piece articulated fixator as a definitive method of treatment. This consists of a fixator that has two half-pins above the


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fracture, a pin in the talus neck, and a pin in the calcaneus (Figure 2.13). The articulation is at the level of the ankle joint. Additionally, there are joints in the fixator that allow correction of alignment once the fixator is attached to the half-pins. Initial use of these fixators recommended fixation of the fibula, lag screw fixation of the articular surface, and neutralization with the external fixator. This can work in the lower-energy fractures when there is still bony contact between the major fracture fragments. Since there is no direct connection between the articular segment and the metadiaphysis, stability is only possible through contact of the bony fragments. In addition, the tendency is to distract the fracture to maintain alignment, which can delay healing; or if healing does occur, there is a tendency to varus collapse with removal of the frame [29]. These concerns have given rise to recommendations not to automatically fix the fibula in order to allow compression of the metaphysis. As long as the relationship of the mortise can be maintained, the fibula can be left alone, allowing compression of the metaphysis to promote healing. This is an acceptable method provided there is not more than 1 to 2 cm of shortening planned. If the fracture gap is larger than this, it should be bone grafted or bone transport should be used and another fixator chosen.

S.C.

S.C. A

B

S.C. C

Figure 2.10 (A and B) Closed type 43C fracture with central comminution of the articular surface in a 32-year-old male. (C) CT scan showing the central comminution.


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S.C. D

E

Figure 2.10 Continued (D) Treatment consisted of lag screw fixation of the joint with ring external fixation of the metaphyseal area and bone transport to fill the metaphyseal defect. (E) Bone transport allowed compression of the metaphyseal fracture. The fibula was not fixed out to length, which allowed the compression in the metaphyseal segment.

The one-piece articulated fixator has been used with acceptable results and low infection rates [24]. The main disadvantages include the lack of fixation at the level of the articular segment. Also, if there is a pin infection of either the talar or the calcaneal pin, there are very few options for pin exchange, and an alternate means of fixation may need to be chosen. These fixator half-pins commonly start to loosen at 3 to 4 months, so if longer fixation is needed perhaps another fixator should be chosen. The next type of fixator category is the ring external fixators. The Ilizarov type of fixators fix each level of the fracture with one or two rings. The hybrid fixators place a ring at the level of the articular segment with a unilateral bar or articulated segment attached to the tibial shaft with halfpins (Figure 2.14). External fixation is also preferable when the fracture extends up the tibial shaft where internal fixation would require an excessively long plate. The Ilizarov fixators are very modular and can be adapted to any fracture pattern. They can be rigid enough to allow full weight-bearing (Figure 2.15), which is advantageous in the multipletrauma patient. They can also be extended onto the foot, crossing the ankle joint. This allows immobilization for soft tissue healing. It also allows distraction across the joint to unload the cartilage, which some feel promotes healing of the articular cartilage. The ring external fixators provide multiplane fixation with wires that are tensioned. Tensioned wires provide very rigid fixation and can be placed in multiple planes. Usually 1.8-mm wires are used. If only wires are used on the metaphyseal or the epiphyseal area, three wires should be placed. The reference wire is placed parallel to the articular surface of the tibia in the coronal plane. A smooth wire is used to allow adjustment of the ring in relation to the leg so it can be properly centered. Another wire is placed transfibular, and a third wire is placed from posteromedial to anterolateral. Care must be taken to keep this wire free from the anterior and posterior tibial tendons. These three wires act as a trampoline and provide good fixation. If the metaphyseal fragment is large enough, a half-pin can be added to the distal ring. The advantage of this is that it adds an additional level of fixation. The disadvantage is that half-pin fixation in soft metaphyseal bone can be suboptimal, leading to early loosening. In addition, the half-pin alters the biomechanics of the construct. Half-pin fixation causes a shearing motion of the fracture when an axial load is applied. This shearing motion is significant when using hybrid fixation [30]. When an axial load is applied, the segment of bone with the half-pin translates away from the other segment [30]. This may possibly explain nonunion rates reported in hybrid fixation.


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P.C. A

P.C. B

P.C. C

Figure 2.11 (A and B) An unusual fracture pattern with a large posterior fragment that had disruption of the posterior tibiofibular ligaments in a 55-year-old female. (C) CT scan demonstrates displacement at the posterior tibiofibular joints.


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P.C. D

P.C. E

Figure 2.11 Continued (D and E) This was addressed with a posterior buttress plate on the tibia through a posterolateral incision that allowed direct reduction of the posterior fragment. The fibula was plated through this incision. A medial plate was used percutaneously to buttress the nondisplaced fracture of the medial malleolus.

This phenomenon is avoided with multilevel ring fixation. When there is multiple-plane fixation above and below the fracture, the angular forces are neutralized. The basic Ilizarov configuration consists of a ring at the level of the metaphyseal shell, two rings above the fracture, and a foot plate when there is severe comminution of the articular surface or soft tissue injury that requires distraction and immobilization for healing. The ring at the level of the metaphyseal shell should have three wires or two wires and a halfpin. The rings above the fracture should have one wire as a reference on the top ring, and at least two half-pins on each ring. The half-pins should be maximally divergent. Ninety degrees of divergence is optimal; however, due to soft tissue constraints, it can be difficult to achieve more than 608 of divergence. The foot piece is attached with two calcaneal wires, and two wires through the midfoot at the cuneiform level. Once the frame is complete, the ankle joint can be distracted 2 to 3 mm to allow for healing of the articular cartilage. This also maintains the foot in a plantigrade position, preventing an equinus contracture.


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Figure 2.12 Extensive soft tissue injury after sustaining a patella, tibial plateau, pilon and talus fracture dislocation all on the same extremity in a 33-year-old truck driver. The fractures were temporarily spanned with external fixation until the soft tissues recovered.

A newer modification of the Ilizarov construct is the Taylor spatial frame. The rings on this frame are stronger and, thus, one ring per level is probably adequate. The rings are connected with diagonal struts that allow for easy adjustment. The adjustments are made through a computer program that takes into account the position of each bone segment within the ring and then moves the rings in relation to each other. This frame is quite strong and is gaining popularity due to its adjustability. When a hybrid fixator is used, two to three half-pins are placed above the fracture. Because these frames have only a bar or articulated piece extending off the ring, it is more difficult to place the half-pins at widely divergent angles. When the pins are predominantly in one plane, the amount of shearing motion introduced to the fracture increases [30]. The increased sheer force at the fracture is detrimental to healing. Though these frames can maintain length and alignment, there may often be a need for a secondary procedure, such as bone grafting.

A

B

Figure 2.13 (A and B) A closed fracture treated with minimal internal fixation and an articulated external fixator in a 45-year-old alcoholic male.


Pilon Fractures

A

43

B

Figure 2.14 (A and B) A comminuted type 43C fracture in a 42-year-old male involved in a motor vehicle crash. Treatment with minimal internal fixation and neutralization with a hybrid external fixator.

Figure 2.15 Ring external fixator for pilon fracture. Patients can weight-bear on these frames. This is advantageous in patients who have multiple injuries when it may be difficult to keep them non-weightbearing.

VIII.

POSTOPERATIVE CARE

Postoperative care of the pilon fracture is equally as important as fixation. First, tension-free closure of incisions should be performed. When using small wire fixation, wounds need to be closed before placing the transfixion wires. If a tension-free closure cannot be obtained, the lateral incision should be left open and skin grafted [31,32].


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A

B

Figure 2.16 (A and B) Postoperative dressing for internal fixation consists of gauze over the wounds wrapped with a roll of Red Cross cotton and then placed in a plaster splint and wrapped with an elastic bandage. This provides gentle compression and keeps the foot in a neutral position until the wound is sealed and the pain decreased enough to allow active range of motion.

Generally, weight-bearing is restricted until the wound has sealed and is dry. When a ring external fixator is used, patients may fully weight-bear, and this is encouraged. Weight-bearing stimulates bone healing and aids in the overall rehabilitation of the foot and the ankle. It is also quite helpful when patients have multiple injuries to allow them to weight-bear on the affected extremity. Hybrid fixators do not allow such an aggressive progression in weight-bearing, and patients will generally need to stay at the touchdown weight-bearing for 2 to 3 months before progressing. Finally, patients treated with open reduction and internal fixation should be kept non-weightbearing for a total of 3 months. Initially, they should be placed in a plaster splint that maintains the ankle at 908 and is kept elevated to allow swelling to decrease. The elevation and a soft bulky cotton dressing, supplemented by plaster splints, are critical to edema control (Figure 2.16). This should be maintained until the wound is dry, which can easily take 2 to 3 weeks. When the wound is dry, the patient can be advance to a range of motion exercises, and be given an elastic compression stocking with a compression gradient of 15 to 30 mmHg. Union of a pilon fracture takes 12 to 16 weeks. Fractures must be followed closely in the first 2 to 3 months to assess wound healing. As fracture union is demonstrated on x-rays, weight-bearing can be progressed. In cases where external fixation has been used, one must be sure there is adequate healing before removal of the frame. Premature removal can lead to nonunion, but more commonly, there may be varus collapse as the medial buttressing effect of the fixator is removed. The fracture will often heal, but only after it has collapsed into varus angulation.

IX.

RESULTS

The results of treatment for pilon fractures seem to correlate with the severity of the injury, but more importantly, correlate with the treated fractures that avoided complications. Some have argued that the quality of reduction of the articular surface does not necessarily correlate with the clinical result [24]. Alignment, though, is crucial to maintaining the function of the foot. In the extra-articular injuries and injuries with minimal comminution, with modern reconstructive techniques, one should expect good to excellent results in 75 to 80% of the cases. Injuries that involve higher levels of comminution, namely the C-3 injuries, are increasingly difficult to treat. Even with modern techniques and equipment, the results are still, at best, fair. This is attributed to the crushing injury to the articular cartilage that occurs at the time of injury [33]. Furthermore, extensive scarring affects the soft tissues crossing the joint, often leads to ankle and foot stiffness.


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In these difficult cases, the primary goal of treatment should be to maintain alignment and preserve bone stock for subsequent reconstructive procedures.

X.

COMPLICATIONS

Complications with this injury are common. They must be anticipated so that every possible means can be employed to avoid them. The first event that can lead to many of the soft tissue complications is massive swelling and fracture blisters. These must be addressed as soon as the patient arrives [34]. Early reduction with splinting in a compression dressing can help control swelling. Once massive swelling occurs, it becomes increasingly difficult to manage and necessitates longer delays for fixation. Excessive swelling leads to wounds that tend to drain more, and prolonged drainage can lead to deep infection. All this must be avoided by controlling the swelling in a bulky dressing. The next complication that occurs is wound-edge necrosis or slough. When this is superficial it can be treated with antibiotics and edema control with wound care. It is important to be vigilant and to proceed to flap coverage if drainage persists or the necrosis becomes wet. Stable soft tissue coverage is critical to successful treatment, and early aggressive intervention to achieve coverage using free-flap techniques is often preferable to hoping for resolution with dressing changes and local wound care [17]. This is particularly true when there is internal fixation in the form of plates. Varus and valgus malunions are related to the methods of fixation chosen. Obviously, in cases of internal fixation proper alignment must be achieved at the time of surgery, and when defects exist, they must be bone grafted. When external fixation is used, alignment can be maintained and even adjusted, but one must gradually dynamize the frame before removal to minimize the chances of late changes in alignment. Other than amputation, infection is the most devastating complication [35]. It originates in the soft tissues and extends to the bone when the soft tissues have not healed and continued to drain. Other contributors are devitalized bone that is not removed. When cortical bone has all its soft tissue removed, either by the injury or by surgical dissection, it should generally be removed unless its presence is absolutely necessary for gaining stable fixation of the fracture. If devitalized bone is left in the wound, one must be even more aggressive in achieving durable tissue coverage in the form of free-muscle flaps. Superficial infection rates have been reported in the range of 8 to 20%; whereas, deep infections have been reported to be up to 55% [19]. Even in a modern series with staged fixation of the tibia, an infection rate of 14% was reported in the C-3 group [13]. Whether or not the fracture was open does not seem to correlate with the infection rate. The single most important factor is the amount of soft tissue damage at the time of injury and the ability to obtain durable soft tissue coverage during the acute phase of wound healing. Pin tract infections in cases treated by external fixation are quite common and usually can be treated with orally administered antibiotics. Pins that do not go through the zone of injury and that have a stable bony construct rarely become infected. If a pin becomes inflamed, the soft tissues should be examined to relieve any tension that may be the source. Then antibiotics should be administered with the expectation of resolution in 2 to 3 days. If inflammation and drainage persist, the pins should be exchanged. This is another complication that is greatly reduced with meticulous edema control. Drainage and inflammation generally subside with pin removal. Late complications are those of malunion, nonunion, and osteoarthritis [19,28]. Nonunion is often a result of overdistraction, and should be recognized and bone grafted early. In the cases where internal fixation is used, this may avert hardware failure. Patients with severe comminution in the metaphyseal–diaphyseal junction are at highest risk, and consideration should be given to early bone grafting. Posttraumatic arthritis is common and occurs to varying degrees, depending on the amount of articular damage at the time of injury [33]. It has been noted that even anatomically reduced fractures go on to develop arthrosis. It does not universally lead to arthrodesis, but certainly decreases function [24]. This has been reported in 13 to 54% of patients, and leads to low functional scores in patients who have been followed with this injury [28]. Finally, in all severe injuries of the lower leg, ankle, and foot, amputation is a subject that must be discussed with patients and their families. In cases where there is division of the neurovascular


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bundle, and the foot is ischemic, immediate amputation is often necessary. In cases with multiplejoint involvement or severe ipsilateral crushing injuries of the foot, early amputation should be considered, as reconstruction often leaves the patient with a foot that functionally is not better than a below-knee amputation, and is often chronically painful. Functional outcome studies have shown that patients that require a free flap and ankle fusion function at a level below that of a transtibial amputee, and this may be a better option for some patients.

XI.

CONCLUSION

The pilon fracture is a challenging injury that significantly alters the function of the foot and ankle, even in cases in which anatomic reconstruction is achieved. Its treatment can be fraught with complications, necessitating a cautious approach. The goals of treatment should be directed to avoid complications, maintain alignment, and reconstruct the articular surface to achieve motion at the ankle. In these cases, one must pay close attention to the soft tissue envelope and take great care to preserve it, as soft tissue coverage will often determine the health and healing potential of the underlying bone. Choice of fixation should be guided by the surgeon’s experience and should not exceed what the soft tissues will tolerate, as the status of the soft tissues often determines the rate of complication.

ACKNOWLEDGMENT I would like to thank Peggy Baldwin and Lisa Harlett for their work in manuscript preparation and Ben Kleinhenz for preparing the photographs.

REFERENCES 1. Carr, J.B., The pilon fracture, in Complex Foot and Ankle Trauma, Adelaar, R.S., Ed., Lippincott-Raven, Philadelphia, 1999, pp. 45–63. 2. Hein, U., The Pilon Tibial Fracture: Classification Surgical Techniques, Results, W.B. Saunders, Philadelphia, 1995, pp. 244–245. 3. Ruedi, T., Fractures of the lower end of the tibia into the ankle joint: results 9 years after open reduction and internal fixation, Injury, 5, 130–134, 1973. 4. Ruedi, T.P. and Allgo¨wer, M., Fractures of the lower end of the tibia into the ankle-joint, Vol 1, Injury, 92–99, 1969. 5. Ruedi, T.P. and Allgo¨wer, M., The operative treatment of intra-articular fractures of the lower end of the tibia, Clin. Orthopaed., 138, 105–110, 1979. 6. Ovadia, D.N. and Beals, R.K., Fractures of the tibial plafond, J. Bone Jt. Surg., 68A, 543–551, 1986. 7. Maale, G. and Seligson, D., Fractures through the distal weight-bearing surface of the tibia, Vol 3(6), Orthopedics, 517–521, 1980. 8. Mast, J.W., Spiegel, P.G., and Pappas, J.N., Fractures of the tibial pilon, Clin. Orthopaed., 230, 68–82, 1988. 9. Sommer, C. and Ruedi, T.P., Tibia: distal (pilon), in AO Principles of Fracture Management, Ruedi, T.P. and Murphy, W.M., Eds., Thieme, New York, 2000, pp. 539–556. 10. OTA Committee for Coding and Classification, J. Orthopaed. Trauma, 10 (Suppl. 1), 56–60, 1996. 11. Oestern, H.J. and Tscherne, H., Pathophysiology and classification of soft tissue injuries associated with fractures, in Fractures with Soft Tissue Injuries, Tscherne, H. and Gotzen, L., Eds., Springer-Verlag, Berlin, 1984. 12. Tornetta, P., III and Gorup, J., Axial computed tomography of pilon fractures, Clin. Orthopaed., 323, 273–276, 1996. 13. Bone, L., Stegemann, P., McNamara, K., and Seibel, R., External fixation of severely comminuted and open pilon fractures, Clin. Orthopaed., 292, 101–107, 1993. 14. Herscovici, D., Devinney, S., Jenkins, M.A., DiPasquale, T.G., Infante, A.F., and Sanders, R.W., The functional outcomes of type C3 tibial plafond fractures with use of a staged protocol, Orthopaedic Trauma Association 18th Annual Meeting, Toronto, Canada, October 12, 2002. 15. Tornetta, P., III, Weiner, L., Bergman, M., Watnik, N., Steuer, J., Kelley, M., and Yang, E., Pilon fractures: treatment with combined internal and external fixation, J. Orthopaed. Trauma, 7, 489–496, 1993.


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16. Cierny, G., Byrd, H.S., and Jones, R.E., Primary versus delayed soft tissue coverage for severe open tibial fractures, Clin. Orthopaed., 178, 54–63, 1983. 17. Trumble, T.E., Benirschke, S.K., and Vedder, N.B., Use of radial forearm flaps to treat complication of closed pilon fractures, J. Orthopaed. Trauma, 6, 358–365, 1992. 18. Bosse, M.J., Castillo, R.C., Herscovici, D., DePasquale, T.G., and Mackenzie, E.J., The mangled foot and ankle: the role of soft tissue coverage, Orthopaedic Trauma Association 18th Annual Meeting, Toronto, Canada, October 12, 2002. 19. Dillin, L. and Slabough, P., Delayed wound healing, infection and nonunion following open reduction and internal fixation of the tibial plafond fractures, J. Trauma, 591–596, 1983. 20. Bourne, R.B., Rorabeck, C.H., and MacNab, J., Intra-articular fractures of the distal tibia: the pilon fracture, J. Trauma, 23, 591–596, 1983. 21. Brumback, R.J. and McGarvey, W.C., Fractures of the tibial plafond: the pilon fracture. Evolving treatment concepts, Orthoped. Clin. North Am., 26, 273–285, 1995. 22. Hansen, S.T., Functional Reconstruction of the Foot & Ankle, Lippincott Williams & Wilkins, Baltimore, 2000, pp. 53–64. 23. Helfet, D.L., Koval, K., Pappas, J., Sanders, R.W., and DiPasquale, T., Intraarticular ‘‘pilon’’ fracture of the tibia, Clin. Orthopaed., 298, 221–228, 1994. 24. Marsh, J.L., Pilon fracture case presentations, Orthopaedic Trauma Association 18th Annual Meeting, Toronto, Canada, October 13, 2002. 25. McFerran, M.A., Smith, S.W., Boulas, H.J., and Schwartz, H.S., Complications encountered in the treatment of pilon fractures, J. Orthopaed. Trauma, 6, 195–200, 1992. 26. Teeny, S.M. and Wiss D.A., Open reduction and internal fixation of tibial plafond fractures: variables contributing to poor results and complications, Clin. Orthopaed., 292, 108–117, 1993. 27. Bonar, S.K. and Marsh, J.L., Unilateral external fixation for severe pilon fractures, Foot Ankle, 14, 57–64, 1993. 28. Etter, C. and Ganz, R., Long-term results of tibial plafond fractures treated with open reduction and internal fixation, Injury, 130–134, 1973. 29. DiChristina, D., Riemer, B.L., Butterfield, S.L., and Burke, C.J., III, Pilon fractures treated with an articulated external fixator: a preliminary report of significant complication, Orthoped. Trans., 719–721, 1994. 30. Vitello, W., Laughlin, R.T., and Lakatos, R., Biomechanics of four hybrid external fixators, Mid-America Orthopaedic Association Annual Meeting, Scottsdale, AZ, April 27, 2002. 31. DiStasio, A.J., II, Dugdale, T.W., and Deafenbaugh, M.K., Multiple releasing skin incisions in orthopedic lower extremity trauma, J. Orthopaed. Trauma, 7, 270–274, 1993. 32. Salmon, N., Arteries of the Skin, Churchill Livingstone, New York, 1988, pp. 62–67, pp. 151–154. 33. Borrelli, J., Jr., Torzilli, D.A., Grigiene, R., and Helfet, R., Effect of impact load on articular cartilage: development of an intra-articular fracture model, J. Orthopaed. Trauma, 11, 319–326, 1997. 34. Kaplan, F.T.C. and Koval, K.J., Treatment of fracture blisters about the foot and ankle, in Concepts of Foot and Ankle Trauma, Sanders, R., Ed., 1999, pp. 487–497. 35. Stasikelis, P.J., Calhoun, J.H., Ledbetter, B.R., Anger, D.M., and Mader, J.T., Treatment of infection pilon nonunions with small pin fixators, Foot Ankle, 14, 373–379, 1993.



3 Talar Fractures and Dislocations Saul G. Trevino and Vinod K. Panchbhavi University of Texas Medical Branch, Galveston, Texas

CONTENTS I. Introduction .................................................................................................................... II. History............................................................................................................................. III. Anatomy.......................................................................................................................... A. The Head of the Talus ............................................................................................. B. The Neck of the Talus.............................................................................................. C. The Body of the Talus ............................................................................................. D. Blood Supply ........................................................................................................... 1. Posterior Tibial Artery ...................................................................................... 2. Dorsalis Pedis Artery and Peroneal Artery ....................................................... 3. Intraosseous Circulation.................................................................................... IV. Fractures of the Talar Neck ............................................................................................ A. Clinical Features ...................................................................................................... B. Classification ............................................................................................................ C. Imaging Studies........................................................................................................ D. Categories ................................................................................................................ 1. Group I Fractures ............................................................................................. 2. Group II Fractures ............................................................................................ 3. Group III Fractures........................................................................................... V. Surgical Techniques ......................................................................................................... VI. Hawkins III Open Fractures............................................................................................ VII. Hawkins Type IV Injuries ............................................................................................... VIII. Total Dislocation of the Talus......................................................................................... IX. Shear Fractures of the Talar Body .................................................................................. X. Complications.................................................................................................................. A. Skin Problems .......................................................................................................... B. Osteomyelitis............................................................................................................ C. Avascular Necrosis (AVN)....................................................................................... D. Nonunion................................................................................................................. E. Malunions of the Talar Neck................................................................................... F. Posttraumatic Arthritis ............................................................................................ XI. Surgical Treatment .......................................................................................................... A. Principles of Arthrodesis.......................................................................................... 1. Ankle Arthrodesis .............................................................................................

50 50 51 51 51 52 52 54 54 54 55 56 56 56 58 58 59 61 62 65 67 68 70 70 70 71 75 75 76 76 76 76 77

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B. Tibiotalar Fusion with Partial Talectomy................................................................ C. Talectomy and Tibiocalcaneal Fusion ..................................................................... XII. Osteochondral Lesions (OCLS) of the Talus ................................................................... A. Treatment................................................................................................................. B. Prognosis.................................................................................................................. XIII. Fractures of the Posterior Process ................................................................................... A. Anatomy .................................................................................................................. B. Mechanism of Injury................................................................................................ C. Clinical Features ...................................................................................................... D. Treatment................................................................................................................. XIV. Fracture of the Medial Tubercle (Cedell’s Fracture) ....................................................... XV. Fractures of the Lateral Process ...................................................................................... A. Clinical Evaluation................................................................................................... B. Mechanism of Injury................................................................................................ C. Clinical Evaluation................................................................................................... D. Treatment................................................................................................................. XVI. Conclusion....................................................................................................................... References ...................................................................................................................................

I.

78 78 79 82 84 84 84 84 85 85 85 87 87 87 89 89 89 89

INTRODUCTION

Injuries to the talus account for only 1% of all fractures, but are among the most challenging to treat because of the bone’s unique anatomic characteristics. The talus has no muscle or tendon attachment and most of its surface is covered with articular cartilage, which leaves a limited area for blood supply in and out of the bone. Fractures and fracture dislocations in the talus are caused by high-energy trauma and result in comminution. Such injuries are an emergency due to the risk of compromise to the blood supply to the talus and also due to pressure on the local skin and soft tissue from displaced parts of the talus. This area of the blood supply is vulnerable to further injury during surgical exposure. The small nonarticular surface area limits the choice of internal fixation devices that can be used to achieve rigid or stable fixation. Through its articulation with adjacent bones, the talus plays an important role in the biomechanics of gait, and becomes deranged if the joint surfaces and bony contour and alignment are not restored. Avascular necrosis (AVN) and posttraumatic arthritis are common outcomes following talar injuries and lead to long-term disability.

II.

HISTORY

The origin of the names for the talus and astragalus dates back to pre-Christian times. Both were related to the use of animal bones as a die in gambling. The Romans used the heel bone of a horse to fashion the material for dice. They called this bone the taxillus. The Greeks, playing a similar game, used the second vertebrae of the cervical spine, which was called the astragalus. The original game was played with either four tali or four astragali. The best combination was considered four different numbers and this was called a Venus. The worst combination was called a canis, which represented the number one on all four dice [1,2]. Herodotus reported the first case of fracture/dislocation of the talus in approximately 500 BC when an Egyptian surgeon treated King Garious I [1], but the exact treatment is unknown. In 1608, Fabricius of Hildon reported a fracture/dislocation of the talus, which was treated with a talectomy [3]. The early 19th-century treatment of these severe injuries often resulted in death due to secondary infection. Syme [4] recommended below-knee amputation; however, there was still a 25% mortality. Most of the foundation of the knowledge on talar injuries originated from World War I and II [3,5]. In 1919, Anderson reported 18 cases of ‘‘aviator’s astragalus.’’ The name derives from the


Talar Fractures and Dislocations

51

dorsiflexion injury pilots sustained when their foot impacted the rudder of the plane. There were inadequate brakes and no parachutes at that time [5]. A review article on World War II injuries by Coltart [3] in 1952 reported on 106 talar neck injures in a series of 228 talar fractures. These cases were extracted from over 25,000 fractures, of which 4,000 were foot fractures. This large series forms the statistical basis that talar neck injuries comprise 50% of all talar fractures. In 1970, Hawkins [6] proposed the first significant radiographic classification on vertical talar neck injuries. These fractures were grouped into three categories that were useful for predicting the prognosis and potential for AVN. In 1978, Canale and Kelly [7] reviewed a series of cases by Hawkins and added a type IV fracture that was associated with either a subluxation or dislocation of the talonavicular joint. Although talar injuries are relatively uncommon, their importance is due to their propensity toward disability and multiple complications. Due to the interarticular nature of most of these fractures and frequent occurrence of AVN there is a high association with disability due to infection, arthritis, malalignment, and bone loss [7–11].

III.

ANATOMY

The talus is divided into three regions: the head, neck, and body. There are no tendinous insertions or muscle origins on this bone. The talus consists of approximately 60 to 70% articular surface that is weight-bearing. There are five articular surfaces: the tibiotalar joint, the talonavicular joint, and the posterior, anterior, and middle facets of the subtalar joint. The tibiotalar joint has both medial and lateral facets, as well as a trochlear portion. The undersurface of the talus consists of three individual facets: the posterior, anterior, and medial facets. The anterior and medial facets can be continuous in 60% of patients [12,13]. The trochlear articulation is encased between the medial malleolus and the fibula. The radius of its surface is 20 mm and represents one third of the arc of the circle. The medial side is smaller than the lateral side so that it is somewhat similar to a frustrum. A frustrum is described as two parallel lines that bisect a cone. The concept that the trochlea is similar to a frustrum was described by Inman [14] (Figure 3.1). However, this analogy is incorrect due to the fact that the talar planes are tangential rather than parallel, while a frustrum has parallel lines. This lack of parallelism confirms the difficulty in taking a mortise view of the ankle that presumes two parallel surfaces [15].

A.

The Head of the Talus

Sarrafian [12] described the talonavicular articulation as the acetabulum pedis or the foot socket. This socket is encased by the inferior and superomedial calcaneal navicular ligaments. It is hinged laterally by the lateral calcaneal navicular component of the bifurcate ligament, medially by the posterior tibial tendon, and inferiorly by the spring ligament [12]. The anterior calcaneal articular facet is an extension of the head on its anterior inferior surface, and provides articulation with the anterior facet of the calcaneus (Figure 3.2).

B.

The Neck of the Talus

The neck of the talus is the region between the body and the head of the talus. The overall alignment of the neck has been described as being medially deviated 248 (10 to 448). There is also a plantardirected deviation of the talar neck that averages approximately 248(5 to 508) [16]. Thus, the angles of inclination and declination vary greatly from one individual to another (Figure 3.3). This variability creates difficulty when aligning fractures of the neck without adequate radiographic verification and direct visualization of the fracture from two different exposures [7,17]. The medial neck of the talus is shorter than its lateral column. Medial comminution in talar neck injuries is common, and lack of surgical correction is associated with varus malunions [18]. A cadaveric study by Ebraheim et al. [19] described the structural characteristics of the talar neck. By taking serial radiographs of 13 dry tali and comparing them with cadaveric sections in the coronal, sagittal, and axial planes, the trabecular content of the neck of the talus was less than the


52


Figure 3.1 A frustrum is an area that results from two parallel lines that bisect a cone. The ankle joint has been described as a frustrum but its medial and lateral surfaces are not parallel. (From Inman, V.T., The Joints of the Ankle, Williams & Wilkins, Baltimore, 1976, Figure 8.4. With permission.)

head or the body. The trabecular orientation was different in the neck from the talar body [19]. This difference in trabecular pattern was thought to be due to the weight-bearing function of the talar head and body.

C.

The Body of the Talus

The body is the most proximal portion of the talus. Its projections consist of the posterior, lateral, and medial processes. The posterior process of the talus is the most frequently damaged portion. It consists of two landmarks: a posteromedial tubercle and a larger posterolateral tubercle. The groove between these tubercules is stabilized by a posterior pulley for the flexor hallucis longus (FHL) tendon. The posterolateral tubercle provides the attachment point for the posterior talofibular ligament as well as the posterior talocalcaneal ligament. The posterolateral process may be segmented, and this accessory bone is called the os trigonum. If it is elongated it is described as the Stieda process. Anchoring the talus to the calcaneus are three talocalcaneal ligaments (lateral, posterior, and medial), the cervical ligament that attaches to the neck of the talus, and the interosseous ligament (Figure 3.3). There is an extensor retinaculum that has three divisions (lateral, medial, and middle) that extend onto the lateral surface of the talus. The last anchoring ligament attachment is the bifurcate ligament that extends its medial portion to the talus from the calcaneus. The medial ligaments of the talus consist of the superficial and deep deltoid ligaments. The deep portion originates from the posterior colliculus and attaches to the posteromedial process. It also can attach to the undersurface of the talus anteriorly. The superficial deltoid ligament has multiple reflections. It attaches to the spring ligament, the sustentaculum tali, and the medial calcaneus (Figure 3.4).

D.

Blood Supply

The extensive cartilaginous surface of the talus permits limited areas for perforating arteries. The blood vessels, their entry points, and the distribution of blood flow have been well described by



53

Figure 3.2 (A) Angle of inclination. The angle of inclination is medially deviated in the frontal plane, on an average, at 248 (10 to 448). (B) Angle of declination. The angle of declination is plantar directed, on an average, at 248 (5 to 508). (From Sarrafian, S.K., Anatomy of the Foot and Ankle, Lippincott, Philadelphia, 1983, pp. 47–48. With permission.)

Figure 3.3 Lateral ligaments of the ankle. The specimen shows the relationship of the ATFL and the cervical ligament. The cervical ligament attaches to the neck of the talus as well as to the interosseous ligament.


54


Figure 3.4 Medial ligaments of the ankle. The deltoid ligament is divided into both superficial and deep portions. The superficial deltoid ligament originates from the anterior colliculus, while the posterior colliculus originates from the posteromedial process.

multiple authors including Haliburton [20], Mulfinger and Truetta [21], and Wildenauer [22] . The limited entrance points for these vessels place the talus at risk for osteonecrosis, especially with talar body and neck fractures. The talus, like the scaphoid, has retrograde blood flow. The talar body receives a significant amount of blood from the inferior surface of the neck of the talus. Three main vessels — the posterior tibial, the peroneal artery, and the dorsalis pedis — provide the arterial supply of the talus through a periosteal network. 1.

Posterior Tibial Artery

The posterior tibial artery is significant because it supplies three main branches. The artery of the tarsal canal originates just proximal to the division of the medial and lateral plantar arteries. It forms an anastomotic sling with the artery of the sinus tarsi underneath the talar neck. This confluence is probably the main source of circulation to the talar body. Approximately 5 mm past its origin, the artery of the tarsal canal has a deltoid branch. This branch passes between the talotibial and talocalcaneal portion of the deltoid ligament and supplies the medial periosteal surface of the talar body [20,21,23]. This branch is significant because it may be the only vessel remaining in the typical displaced talar neck fracture. There are also small calcaneal vessels that supply the posterior aspect of the talus via the posterolateral process. Unfortunately, the anastomotic sling is also vulnerable to injury from surgical procedures like subtalar or triple arthrodeses (Figure 3.5). 2.

Dorsalis Pedis Artery and Peroneal Artery

The peroneal artery provides the extraosseous circulation on the surface as well as on a communicating branch with the dorsalis pedis. The artery of the sinus tarsi is formed with its branches and other communicating vessels and forms a communication with the artery of the tarsal canal to form the lateral portion of the tarsal sling. 3.

Intraosseous Circulation

The superomedial half of the talar head is supplied by the dorsalis pedis or the anterior tibial artery, which penetrates the dorsum of the neck. A branch of the sinus tarsi artery supplies the inferior lateral aspect. The artery of the tarsal canal, which provides four or five major branches that enter posterolaterally into the talar body, supplies predominantly the body. The body is also supplied by



55

Anterior tibial artery Posterior tubercle artery Deltoid branches

Posterior tibial artery Deltoid branches

Artery of the tarsal canal

Tarsal sinus branches

Medial plantar artery

Posterior tibial artery

Lateral plantar Artery of artery the tarsal canal

A Posterior tubercle vessels Artery of the tarsal canal Deltoid branches Tarsal sinus branches Lateral

B

Medial

Superior neck vessels (dorsalis pedis artery)

Figure 3.5 Intra- and extraosseous circulation. (A) Extraosseous blood to the talus. (B) The region’s blood supply to the talus. (From Kelikian, A.S., Operative Treatment of the Foot and Ankle, Appleton & Lange, New York, 1999, Figure 26.2. With permission.)

the anastomotic sling in the sinus tarsi, which supplies the lateral inferior segment and the posterior facet. The medial third of the talar body is supplied by the deltoid branch of the posterior tibial, and the posterior aspect of the body of the talus is supplied by the calcaneal branch of the posterior tibial artery as well as the peroneal artery. It has been reported by Gelberman and Mortensen [24] that ‘‘the single major arterial supply to the body of the talus is the artery of the tarsal canal’’ and ‘‘the deltoid vessel constitutes the most significant minor blood supply to the body.’’ In summary, the main supply of the talus is through the posterior tibial artery via the tarsal canal branch. It also supplies the medial process and the medial portion of the body via the deltoid branch. Unfortunately, the retrograde flow beneath the neck is vulnerable to talar neck injuries as well as surgical procedures that violate this area. In general, the talus, however, has a rich anastomotic interosseous circulation, which allows for revascularization with the minor arteries and can prevent complete osteonecrosis. This premise supports early open reduction and rigid fixation.

IV.

FRACTURES OF THE TALAR NECK

Fractures of the talar neck constitute 50% of major talar fractures; 64% of these are associated with other fractures. The literature reports that 16 to 44% of talar neck fractures are open injuries and up to 28% have associated fractures of the medial malleolus. These are significant injuries due to their interarticular nature. These fractures have a high rate of malunion, AVN, nonunion, infection, and posttraumatic arthritis of the ankle and subtalar joint. From an anatomic point of view, the neck is the weakest portion of the talus. The vulnerability of the neck relates to the small cross-sectional area, its local porosity, as well as the trabecular pattern [19]. The initial theory of the mechanism of injury was believed to be a dorsiflexion injury of the neck against the anterior tip of the tibia. Peterson and Romanus [25] doubted this concept due to the fact that the anterior rim of the tibial plafond was seldom damaged in this fracture. In their


56


classic cadaveric experiment, they were initially unable to reproduce the classic talar neck fracture with a dorsiflexion force to the foot and the ankle constrained. They redesigned their study by restricting dorsiflexion of the ankle. Thus, they were able to reproduce the fracture in the talar neck on 20 fresh cadaveric feet by a cantilever effect. The talus acted as a cantilever between the plantar aspect of the foot and the tibia. This experiment is similar to a head-on collision in which an individual holds his or her leg in an extended position against the floorboard of a vehicle with the calf muscle contracted. The stages of this injury were initially proposed by Coltart [3] and later modified by Penny and Davis [26]. Familiarity with these stages facilitates understanding this complex fracture. Anatomically, the interosseous ligament lies between the posterior and middle facets. Stage I occurs with rapid dorsiflexion of the foot while the heel is fixed, allowing the talus to act as a cantilever. The initial injury consists of rupture of the posterior capsule followed by either impaction or breakage of the talar neck, with associated injury to the interosseous and cervical ligaments. Without these two stabilizing ligaments, the talar body flexes into equinus, and the fractured neck points downward onto the superior surface of the calcaneus. With additional force, stage II involves injury to the posterior ankle, disrupting the capsule, the posterior ligaments, and parts of the deltoid ligament. Stage III results with the talar body dislocating out in a posteromedial direction. This part has been described as a melon seed squeezed between two fingers [27]. The talar body is restrained by the remnants of the deltoid ligament and rests inferior to the medial malleolus. The fractured neck is now facing superolaterally. Stage IV is the total extrusion of the body of the talus.

A.

Clinical Features

Talar neck fractures are more common in young adult males, with a ratio of 3:1 males to females. The usual presentation is severe pain and swelling, with associated deformity of the foot and ankle. Late presentation with an untreated dislocation will reveal ecchymosis over the medial and lateral aspects of the ankle, as well as potential pressure necrosis of the skin. With posterior protrusion of the body of the talus, the toes of the foot will be in a flexed position due to tethering of the FHL. Urgent management is indicated to avoid the complications of osteonecrosis and skin necrosis. Historically, Bonnen [28] reported a 73% slough rate in irreducible talar neck fractures. Other authors have noted a high association of skin necrosis with wound infection and subsequent osteomyelitis [29]. Between 16 and 44% of these injuries are reported to be open [7,11].

B.

Classification

Hawkins, in his original article, placed fractures of the neck of the talus into three groups: group I were nondisplaced fractures, group II were fractures associated with subtalar displacement with a congruous ankle, and group III had both an ankle dislocation and a subtalar joint displacement with either medial or lateral dislocation of the talar body. In 1978, Canale and Kelly [7] added a group IV consisting of patients who had a talonavicular dislocation or subluxation (Figure 3.6A to Figure 3.6D). Troublesome presentations consist of four categories: (1) nondisplaced fractures with questionable subluxation, (2) late presentations with massive swelling or skin slough, (3) open fractures, and (4) open fractures with extruded talar fragments.

C.

Imaging Studies

Routine radiographs of the ankle and foot are necessary. Usually, the lateral radiograph of the ankle best demonstrates the coronal fracture line of the talar neck, although oblique views can be helpful. There is a high association of both medial malleolar and calcaneal fractures, with a lesser degree of navicular and cuboid fractures [7,30,31]. In order to judge the postreduction alignment, Canale and Kelly [7] described a pronation view of the talar neck that allows the evaluation of both the medial and lateral aspects of the neck for overall frontal plane malalignment. To achieve this view, the ankle is positioned in maximum equinus and the foot is pronated 158. The x-ray beam is directed 758 cephalad from the horizontal (Figure 3.7).



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Figure 3.6 (A) Group 1 talar neck fracture. The radiograph reveals a vertical fracture line with no visible displacement. CT scan is recommended to verify the lack of displacement. (B) Group II talar neck fracture. The talar body is subluxed from the subtalar joint. The degree of subluxation can be quite subtle. (C) Group III Hawkins talar neck fracture. The talar body is dislocated from the ankle joint with the posterior aspect of the talar body on the medial aspect of the hindfoot.


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Figure 3.6 Continued (D) Group IV Hawkins talar neck fracture. The dislocated talar body is associated with a fracture dislocation of the talar head from the naviculum.

Computed tomography (CT) scans in the acute setting are also useful to determine the presence or absence of comminution of the neck and associated injuries. The CT scan protocol should use 1-mm acquisition for optimal evaluation [32]. Magnetic resonance imaging (MRI) studies are rarely needed in the acute setting, but may be useful in later evaluations for osteonecrosis. For the least interference with MRI resolution, Baumhauer and Alvarez [30] have recommended the use of titanium screws.

D. 1.

Categories Group I Fractures

Group I injuries are nondisplaced fractures without any subluxation. However, due to the high energy associated with these fractures, it is unusual to have a completely nondisplaced fracture. For

Figure 3.7 Canale view. It is used to assess the congruity of the medial border of the neck of the talus. The foot is positioned in maximum ankle equinus with the foot in 158 of pronation with the x-ray beam directed 758 cephalad from the horizontal.



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this reason, CT scan is recommended to rule out any subtle displacements or associated fractures. Although group I fractures have minimal displacement, osteonecrosis can still occur. Damage to the dorsal and lateral circulation of the neck can also occur. Hawkins’s [6,33] original series had zero cases of osteonecrosis; however, Canale and Kelly’s [7] later series had 13% incidence. Group I injuries are frequently missed by the nonorthopedist evaluating a sprained ankle [34]. O’Brien was also concerned that minimally displaced fractures would be treated as group I injuries. These minimally displaced fractures can result in malunion and subtalar arthritis. If in doubt, it is best to use a CT scan to differentiate these groups. Treatment for group I fractures. Group I fractures should be treated for a minimum of 6 weeks in a non-weight-bearing short leg cast (SLC), which is appropriate if there is no initial displacement seen on a CT scan. Weight-bearing is allowed when there is radiographic evidence of healing. The danger with early weight-bearing is that the fracture can become displaced [26,33]. Consolidation of the fracture usually occurs between 6 and 16 weeks. There is still some controversy regarding whether or not the foot should be in equinus or neutral [8,34]. The equinus position is recommended since it allows for more ankle stability compared with the neutral position. Additionally, the patient is likely to be more compliant with non-weight-bearing if the ankle is in equinus. It is believed that the 13% incidence of AVN found in this group probably indicates that these injuries were actually group II fractures that reduced spontaneously [33]. In pediatric cases, there is a higher incidence of AVN compared with that in adults. However, the recovery is certainly better [35]. 2.

Group II Fractures

Group II fractures are characterized by incongruity of the subtalar joint with either subluxation or frank dislocation. The mechanism of this injury damages the arterial sling underneath the talar neck, increasing the potential for osteonecrosis. This injury pattern affects the artery of the tarsal canal, the major source of circulation to the talar body. Treatment for group II fractures. Closed reduction should be performed promptly to allow for revascularization. With the use of intravenous sedation and ankle block, adequate anesthesia can be achieved for a closed reduction if there are no other associated fractures. Most authors recommend at least one attempt at a closed reduction in the acute setting [30,33]. The reduction maneuver is performed with the knee in flexion. The foot is then plantar flexed to realign the dorsally subluxed talar head with the proximal neck. The foot is then displaced posteriorly to allow reduction of the subtalar joint. As a final maneuver, the forefoot can be manipulated in a rotational fashion to correct any varus or valgus malalignment. Adequacy of the reduction is confirmed with lateral radiographs for sagittal alignment, a Canale pronation view for varus and valgus alignment, and a Broden view for subtalar alignment [30,36,37]. If the initial radiographic evaluation is acceptable, the patient can be treated in a short leg cast or can be scheduled for pinning in situ or open reduction and internal fixation (ORIF). To minimize residual stiffness and varus malalignment, most recent recommendations have been for anatomic reduction with ORIF. Adelaar [36] recommends no acceptance of rotational malalignment, but does allow for 3 to 5 mm of dorsal displacement. Grob et al. [38] would only accept anatomic reduction, otherwise they would proceed to surgery. Unfortunately, at reduction time, motion at the fracture can confuse adequate rotational alignment so that exact positioning cannot be relied on without some form of fixation. For this reason, preliminary pin fixation in the operating room and then testing the arc of motion of the subtalar joint is recommended. Rotational malalignment can be changed by remanipulation and reapplication of the pins for fixation. Percutaneous screw fixation can be performed after confirming the biomechanical exam (Figure 3.8A to Figure 3.8D). If the initial closed reduction is inadequate, the patient should be taken to the operating room for further manipulation or ORIF. Unfortunately, there are no prospective studies that mandate this approach, but it is logical in these high-risk cases to attempt to get the earliest closed reduction and fixation possible. Because of the limitations of closed treatment, many authors advocate ORIF for all Group II fractures [11,30,36]. Surgical technique and postoperative management will be discussed in the next section since groups II and III are a continuum in treatment.


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Figure 3.8 Steps in percutaneous fixation of a group II talar neck fracture. (A) The patient was initially treated for a subtalar dislocation. (B) Shows the postreduction lateral x-ray with evidence of a talar neck fracture with minimal displacement.



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Figure 3.8 Continued (C) Shows the surgical technique of preliminary wire fixation. (D) Lateral radiograph of the preliminary wire fixation. Biomechanical examination to check for proper rotational alignment should be the next step.

3.

Group III Fractures

Group III fractures involve dislocation of the talar body from both the subtalar and the ankle joints, leading to an almost 100% potential for osteonecrosis. These high-energy injuries are associated with approximately 50% open fractures, with frequent skin, vascular, and neural compromise. This presentation is considered a medical emergency since successful closed reductions are rare even with the use of general anesthesia. Treatment for group III fractures. The prudent course is to attempt a closed reduction under general anesthesia and if unsuccessful, perform an emergent open reduction with or without a medial malleolar osteotomy [30,37]. Anatomically, the deep deltoid ligament tethers the body fragment. Potential residual blood flow is limited by the patency of the deltoid branch. Care is taken not to violate this vessel and ligament during open reduction. Axial traction with a threaded calcaneal pin is useful in attempted closed reductions. After application of the traction, the foot is placed in a dorsiflexed position to open the posteromedial portion of the ankle joint. Using either direct pressure or a pin as a joystick the fracture can be manipulated back into place [30]. Unfortunately, the neurovascular bundle is in close proximity to the body, so utilization of a pin for manipulation is dangerous. A limited incision is recommended to avoid impaling the vessel and nerves. If a closed reduction is still not possible after one or two attempts, an open reduction should be done. The incision is made directly over the


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talar body to facilitate manipulation and protection of the neurovascular bundle (Figure 3.9A to Figure 3.9D). If the attempt at reduction fails, then a medial malleolar osteotomy may be indicated. Incisions can be left open to accommodate excessive swelling followed by delayed primary closure.

V.

SURGICAL TECHNIQUES

Potential complications can be minimized with proper surgical techniques. The most important goal is to obtain anatomic reduction without jeopardizing the residual circulation. Precise reduction is complicated by medial and lateral comminution. Varus angulation of the neck is associated with an inverted posture and loss of eversion [18]. There are two standard surgical approaches for exposure of the anterior aspect of the ankle and talus. Depending on the degree of comminution, one or two incisions may be used. For Hawkins type II fractures with minimal comminution, it is feasible to attempt percutaneous internal fixation with an adequate closed reduction. If percutaneous reduction is not acceptable, then an anteromedial approach is recommended. The incision is placed parallel to the anterior tibialis tendon and extended from the dorsal tuberosity of the navicular to the tip of the medial malleolus. Dissection is limited, and an attempt is made to follow the soft tissue plane of the fracture so as to avoid vascular compromise. If a medial malleolar fracture is present or if a medial malleolar osteotomy is entertained, then this incision is extended proximally over the midportion of the medial malleolus. Numerous osteotomy techniques have been advocated. Accessible techniques can be a Chevron approach (Sanders [2]) or a step-cut technique [39]. Care is taken to access both the anterior and posterior aspects of the talus to protect the posterior tibial tendon, which can be injured especially with a straight oblique cut. This osteotomy allows for excellent exposure of complicated talar body fractures and allows for multidirectional internal fixation. If medial comminution of the talar neck makes assessment of the reduction difficult, a second incision on the anterolateral aspect of the talus can be made since this side is frequently not comminuted. This incision is made between the extensor digitorum longus and the peroneus teritus. Blunt dissection is used in the subcutaneous tissue to identify the branch of the superficial peroneal nerve. Exposure of the sinus tarsi and the subtalar joint by dissecting the extensor digitorum brevis off the calcaneal cuboid joint (CCJ) should be facilitated. This bilateral exposure lessens the risk of malreduction and shortening of the medial column. This incision can also be extended proximally to expose the lateral process or any talar body fragments. If more exposure of the lateral body is needed, a distal fibular osteotomy can be performed through this incision or through a separate lateral fibular approach. The fibular osteotomy is also indicated for treatment of osteochondral fractures of the body of the talus. Thus, a comprehensive approach is possible for all variations of a talar neck fracture. The entire subtalar joint is easily accessible for adequate bony debridement and for the prevention of subtalar arthritis (Figure 10A and Figure 10B). Preliminary fixation is achieved with multiple 0.62 Kirschner wires. After fluoroscopic confirmation of adequate reduction using the Canale, Broden, and lateral views, subtalar motion is assessed. This confirms the arc of motion and the ability to have adequate eversion relative to any tibia vara. For this reason, it is advisable to prep the lower leg up to the knee for adequate visualization. The most common error is loss of eversion ability either by shortening of the medial neck of the talus or by incorrect rotational alignment or comminution [18,27]. If motion is acceptable, then any grafting needed is obtained from the calcaneus or from Gerdy’s tubercle at the proximal tibia. The location of the fracture determines the type of internal fixation and location of the screws. Fractures at the base of the neck allow for better purchase with both medial and lateral longitudinal compression screws. However, with true neck fractures, the amount of surface in the distal neck is minimal and for this reason, either the headless or countersunk screws are used. Mallon et al. [40] suggest the use of a headless Herbert screw in antegrade fixation for better compression. Unfortunately, there is no scientific basis on what percent of the cartilaginous surface can be violated with countersinking and its effect on subsequent arthritis of the talonavicular joint. Controversy also exists regarding the use of antegrade compression screws with comminuted talar neck fractures. An opposing school of thought recommends using either a posterolateral



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Figure 3.9 Sequence of ORIF for group III talar neck fracture. (A) Preoperative radiograph showing dislocation of the talar body. (B) Intraoperative picture showing a limited medial incision over the dislocated fragments. Care is taken to avoid damage to the neurovascular bundle. (C) Instrument is displacing the neurovascular bundle to allow for an attempted open reduction. (D) Postreduction clinical picture without the need for a medial malleolar osteotomy.


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Extensor digitorum longus retracted Extensor digitorum longus

Talar neck tracture

Incislon Talonavicular joint

Superficial peroneal nerve

Extensor digitorum brevis

B

Figure 3.10 (A) The anteromedial incision is made parallel to the anterior tibial tendon extending from the tuberosity of the navicular to the tip of the medial malleolus. The incision is extended over the medial malleolus in order to perform a malleolar osteotomy. (B) The anterolateral incision is made in the interval between the extensor digitorum longus and the peroneus teritus. This incision is extended proximally to expose the lateral process of the talus. A fibular osteotomy can be performed for a body fracture if indicated. (From Kelikian, A.S., Operative Treatment of the Foot and Ankle, Appleton & Lange, New York, 1999, p. 509, Figure 20.) With permission.

approach or an anterior plating. Trillat et al. [41] were the first to describe the use of the posterolateral approach of the ankle for this fixation. A posterolateral incision allows for retrograde fixation from the posterior aspect into the head of the talus. Historically, biomechanical studies by Swanson et al. [42] reported that superior fixation was achieved using this retrograde fixation method compared with the antegrade use of pins or screws, or the combination of both. Only the posterior-to-anterior screws were able to withstand 1129 neutrons of sheer force across the talar neck with active motion.



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In order to use the posterolateral incision, the patient is placed in the lateral decubitus position. The leg is positioned so that either an anteromedial or a posterolateral incision can be performed. Fluoroscopy is positioned before the start of the procedure. The posterolateral incision is placed lateral to the Achilles tendon in an interval between the FHL and the peroneal tendons. This incision is carried down to the posterior capsule, exposing the FHL tendon and its muscle belly as well as the posterolateral tubercle of the talus. Both Sanders [2] and Swanson et al. [42] recommend screw placement into both medial and lateral tubercles on each side of the flexor hallucis tendon. Ebraheim et al. [19] suggest using the lateral tubercle of the posterior process, but advise avoiding violation of the sinus tarsi or the lateral wall of the talus. The screw should be placed in an anteromedial and inferior direction. Unfortunately, the wafer shape of the posterior aspect of the talus limits the size of the screw, so the screw heads may impinge on either the posterior aspect of the ankle joint in maximum plantar flexion or on the subtalar joint surface. A solution is to use a headless screw system that avoids the problems with prominent screw heads. In acute traumatic injuries, this approach can appear to be a dark hole requiring excellent assistance to carry out the procedure. Since this fracture is usually treated in an emergent setting, the assistive capacities of the operating room can be strained. Other challenges are the variation in shape and alignment of a normal talar neck in the sagittal and transverse planes and the fact that adequate reduction has to be achieved before placement of the screw. The greatest challenge is judging rotational malalignment in the lateral decubitus position. For all the above reasons, the posterolateral approach has significant limitations. It is most useful in elective reconstructive procedures such as malalignment of the talar neck or in cases where the talar neck fracture is minimally displaced so alignment is not a significant problem (Figure 3.11A to Figure 3.11C). Recent studies by Fleuriau-Chateau et al. [43] and Westbrook et al. [44] advocate the use of single- or dual-minifragment plates along the talar neck side using 2.0 plates. They felt that the rigid plate fixed along the axis of the neck protected the residual blood supply and allowed for better revascularization and avoided the potential for overcorrection with compression. The plate is positioned to neutralize the stress on the compression screws. In some cases compression screws were not used with this technique. The plate is placed either dorsally or plantarly, preventing sagittal malalignment and loss of reduction. Fleuriau-Chateau et al. reported 17% hardware removal cases compared with a 26% incidence in the study by Westbrook et al. that used longitudinal screws. The plate method is limited by the minimal nonarticular surface on the medial side (Figure 3.12A and Figure 3.12B). The relatively high occurrence of hardware removals is significant, and further studies will be necessary to prove the efficacy of this procedure.

VI.

HAWKINS III OPEN FRACTURES

Open fractures associated with Hawkins III fractures are devastating injuries. Appropriate treatment includes debridement and irrigation followed by empiric intravenous antibiotics. Due to extensive vascular damage the prognosis for these fractures is fair to poor. If there is any residual soft tissue remaining on the talar body fragment, the recommended treatment is an ORIF after adequate incision and drainage [30,36]. Other authors have proposed primary tibiotalar fusion or subtalar fusion [38,45]. These fusion techniques are used to promote vascularity through the fusion site. Pennal [45] reported on three cases with the use of primary subtalar fusion. However, 100% of his cases developed AVN. The more controversial issue is what to do with rare talar body dislocations that are completely extruded and have no attached soft tissue. Most authors have only one or two cases to form the basis of their opinion. Hawkins [33] had a series of five cases that he treated with primary talectomy, and four of the five had poor results. Pennal [45] had three cases of partial talectomy — one of which did well with a tibiocalcaneal fusion. Other options include a partial talectomy followed 6 weeks later by a Blair type arthrodesis [26,46,47]. Dennis and Tullos’s [46] series of seven patients resulted in five out of seven good results; however, a third of these patients had pseudoarthrosis. Another alternative is a total talectomy followed by tibiocalcaneal fusion [48]. Sanders [2] had two cases treated with delayed fusion using iliac crest bone graft and a pantalar arthrodesis, all of which had poor results. The largest series was reported by Marsh et al. [49] who had 18 open fractures; 12 of the 18 fractures were partial or


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Figure 3.11 Posterolateral approach to the ankle. (A) The dissected fresh cadaver displays an extensile approach to the posterolateral aspect of the hindfoot. Such an extensile approach is less used now due to cannulated screw fixation. (B) Shows the limited area for placement of a posterior-to-anterior cannulated screw fixation on the posterior process of the talus. (C) This approach was utilized to correct a rotational malalignment that was corrected with an osteotomy of the talar neck via an Ollier incision.

Figure 3.12 Utilization of miniplates for ORIF of talar neck fractures. (A) The medial aspect of the talus reveals the majority of the surface to be cartilaginous in nature. Plate placement is limited to this limited area and will interfere with motion.



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Figure 3.12 Continued (B1 and B2) A miniplate is placed on the medial and lateral aspects of the talus to add improved stabilization and avoidance of talar articular surface.

extruded fragments; 38 infections occurred with a 71% failure rate. His conclusion was that it was best to discard the extruded and contaminated fragment if there was no soft tissue attachment. The functional outcome of these particular injuries correlated best with absence of infection. Only one out of seven infected cases resulted in a successful treatment.

VII.

HAWKINS TYPE IV INJURIES

Hawkins type IV injuries are extremely rare. In 1978, Canale and Kelly [7] reported on three cases of type IV talar injuries. They were all open fractures. All three cases were treated by total talectomy, and the results were two fair and one poor. Canale and Kelly thought that type IV injuries needed pin stabilization of the talonavicular joint and that these had a higher potential for developing AVN of the talar head.


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VIII. TOTAL DISLOCATION OF THE TALUS Total dislocation of the talus is also an extremely rare injury (Figure 3.13A to Figure 3.13C). The mechanism of injury is different than Hawkins type fractures. The dislocation is usually a consequence of either a sustained medial or lateral subtalar displacement. Most of the papers reporting these injuries refer to just one case due to the rare occurrence. If the dislocation is closed, usually

Figure 3.13 Total dislocation of the talus. (A1 and A2) Preoperative radiograph — the radiograph shows a complete open lateral dislocation of the talus. The fragment has only a small amount of soft tissue attachment.



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Figure 3.13 Continued (B1 and B2) Initial fixation was that of a tibiotalar pin fixation with accompanying local wound care. (C) Reveals complete AVN of the talus with posttraumatic arthritis at 12 months after surgery.

these patients will present with a very tense skin with possible tissue necrosis. One can attempt a closed reduction of this dislocation; however, it is recommended that if the closed reduction fails, an ORIF should be attempted, which may or may not need skeletal traction. The results with these injuries are good if there is no occurrence of infection or AVN. If the talus is completely extruded, the standard treatment is incision and drainage and the question whether to reimplant or not. There have been multiple small reports on this condition [3,10,45,49–53]. In the largest published series, Coltart [3] treated seven out of nine patients with total talectomy. The two cases that were reduced both developed AVN. Ritsema [52] reported on five cases. Two of these cases were open, but neither developed AVN or infection. In the treatment of the above injuries, the most recent literature recommends resection and fusion [2]. Jaffe et al. [54]


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presented four cases, of which three out of four fused. One of the cases was lost to follow-up. Sanders [2] reported mixed results with talectomy and, unfortunately, fusion only gave a fair to good result.

IX.

SHEAR FRACTURES OF THE TALAR BODY

Shear fractures of the talar body are relatively common, representing somewhere between 13 and 20% of all talar injuries. Inokuchi et al. [55] distinguished fractures of the talar body from the talar neck by the location of the fracture line. If the fracture line extended proximal to the lateral process of the talus, it would be considered a body fracture instead of a proximal neck injury. In the original article by Hawkins using these criteria, some of the talar neck fractures were actually body fractures. Although Boyd and Knight [56] devised a classified scheme for this fracture pattern, it is seldom used due to its complexity. By their classification, a type I fracture is a coronal or sagittal fracture and a type II fracture is a horizontal fracture. They divide type I fractures into four types similar to talar neck fractures: type IA is a simple nondisplaced fracture; type IB has displacement at the trochlea; type IC is a trochlear fracture with dislocation of the subtalar joint; and type ID is a trochlear fracture with dislocations of both the subtalar and the tibiotalar joint. Type II fractures are divided into two categories: type IIA fractures consist of displacements less than 3 mm and type IIB fractures have displacements greater than 3 mm (Figure 3.14). The mechanism of these fractures is similar to the dorsiflexion injuries of Hawkins classification. The treatment of these fractures is basically similar to that of talar neck fractures, with the same surgical techniques and preliminary fixation. Nondisplaced fractures can be managed conservatively (Figure 3.15A and Figure 3.15B). Due to the complex nature of the fracture pattern and its intra-articular location, exposure recommendations are accomplished by either medial malleolar osteotomies or, if necessary, medial and lateral osteotomies (Figure 3.16A to Figure 3.16E). Crush injuries, due to their high-energy nature, are associated with a high incidence of osteoarthritis as well as AVN. Early articles recommend the use of a talectomy along with a tibiocalcaneal fusion or Blair type fusion [8,45,56]. Currently, the experienced orthopedist can consider ORIF using extensile exposure-absorbable pins and headless screws [11,38]. Bone graft can be taken from the Gerdy’s tubercle at the knee level to augment any defects. The patient is then immobilized until wound healing and then early range of motion is followed by off-loading with a boot until bony union occurs.

X.

COMPLICATIONS

A.

Skin Problems

Pressure necrosis secondary to displaced fragments is a common complication of these high-energy injuries. The additional trauma of an open fracture leads to increased probability of infection, especially with the association of diminished circulation or contamination. Primary closure is difficult due to the intense swelling involved in these acute injuries. Although early ORIF is

Figure 3.14 Boyd’s classification of talar body fractures. (From Coughlin, M.J. and Mann, R.A., Surgery of the Foot and Ankle, Mosby, St. Louis, MO, 1999, Figure 35.25. With permission.)



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Figure 3.15 (A) Lateral radiograph showing a coronal fracture of the talus that represents a type A fracture. (B) Lateral radiograph of same fracture at 9 months post injury showing healing of the fracture treated conservatively.

recommended, after this is accomplished, it is better to leave the wound open rather than jeopardize viability of the wound edges. A delayed primary closure is usually performed 5 to 7 days later. In difficult cases, one can consider the use of vacuum-assisted wound closure (VAC). Skin necrosis is more common on the anterior and medial aspects, therefore LeMaire and Bustin [57] and Szyszkowitz et al. [11] recommend using a posterolateral incision for these fractures . The difficulty with a posterolateral incision is that exposure is limited and the adequacy of the reduction is difficult to confirm. The usual treatment for skin necrosis is immediate consultation, with plastic surgery for temporary coverage with an allograft or local wound care. Wound coverage should ideally be performed 5 to 7 days post operation in order to decrease the risk of infection. Definitive procedures can consist of fasciocutaneous free flaps or skin grafts (Figure 3.17A to Figure 3.17E).

B.

Osteomyelitis

Osteomyelitis is common with open injures. Infections are accompanied by systemic symptoms along with draining wounds and increasing pain due to pressure from the underlying infection. Appropriate treatment consists of repeated incision and drainage every 48 hours until cultures are


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Figure 3.16 (A) Lateral radiograph showing displaced fracture of the talus. (B and C) CT scans showing the fracture in the sagittal and coronal planes. (D and E) Final AP and lateral radiographs showing good radiographic union.



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negative. Culture-specific antibiotics are then used. In cases of bone loss from partial or complete talectomy, antibiotic bead pouches or spacers are used. At the authors’ institution, the usual recommendation is 4 g vancomycin, 3.6 g tobramycin, and 6 g cefoxitin mixed with 50 g of bone cement [58]. External fixation can be considered if the wound is unstable. The wound should be off-loaded. Once the infection has been cleared, salvage is with a fusion. A below-knee amputation

Figure 3.17 Soft tissue complications. (A) Lateral radiograph of a type III fracture dislocation of the talar neck. (B) Anterior exposure of recently reduced fracture without medial malleolar osteotomy.


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Figure 3.17 Continued (C) Postreduction lateral x-rays with good alignment and position. (D) Wound slough 3 days post fracture with exposed anterior tibialis tendon. (E) Utilization of a forearm free flap for coverage.



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is a reasonable alternative to a fusion due to its relatively short recovery time and improved function with a prosthesis compared with talectomies with fusions.

C.

Avascular Necrosis (AVN)

One of the most common characteristics of talar neck fractures is varying degrees of AVN. Hawkins reported a 58% overall incidence of AVN. Even with group I nondisplaced talar neck fractures, Canale and Kelly [7] reported 13% occurrence. Radiographic evidence of AVN occurs usually within the first 8-week period [3]. A positive Hawkins sign is the presence of disuse osteoporosis on the anteroposterior (AP) ankle view approximately 6 to 8 weeks after injury (Figure 3.18). This finding is indicative of normal vascularity. The most comprehensive series regarding prognosis after the onset of AVN was by Canale and Kelly [7]. They reported on 49 cases, of which 23 had positive Hawkins signs. Only one case with a positive Hawkins sign developed AVN. Of the 27 cases that did not have a positive Hawkins signs, 77% had AVN. In addition to routine radiographs, MRI is useful for clarifying the extent of AVN. It has been reported by several authors that MRI changes can be noted at 3 weeks after injury [36,59,60]. Thordarson’s [60] prospective study of 21 consecutive cases of talar neck fractures showed a positive correlation of AVN with MRI if the plain films demonstrated greater than 50% involvement of the talar dome; if less than 50% AVN of the talar body, MRI correlated poorly. It should be emphasized that these fractures can heal even with the presence of AVN. However, the ability of the dead bone to be replaced can take up to 36 months [34]. The controversy is how to avoid collapse of the talus with the presence of AVN. The majority of studies show that non-weight-bearing for a prolonged period gives the best results. It is unknown whether non-weight-bearing will prevent talar body collapse. Mindell et al. [10] reported on 6 out of 13 patients who had collapse even though they were non-weight-bearing. Pennal [45] developed a patella-bearing caliper for off-loading during ambulation. Canale and Kelly [7] reported the best results with patients who were non-weight-bearing for 8 months. However, patient compliance with such an extended period of non-weight-bearing is an issue. The use of non-weight-bearing calipers is poorly tolerated and is seldom practiced. Custom-fabricated patella tendon bearing orthosis (PTB) braces are a better alternative than the caliper.

D.

Nonunion

This is a relatively uncommon finding in talar neck and body injuries. A nonunion, as defined by Peterson et al. [61], is a lack of radiographic evidence of healing within a 6-month period. In their

Figure 3.18 AP radiograph 6 weeks after talar neck fracture. The juxtarticular subchondral resorbtion represents evidence of adequate blood supply of the talar body.


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series, 13% were classified as delayed unions, but none of these cases went to nonunion. Other authors record an incidence of nonunion between 2.5 and 4% [31,62]. The recommended treatment for the above is an ORIF with bone grafting. There are no large series on this particular treatment.

E.

Malunions of the Talar Neck

Malunions of the talar neck are common, and an important cause of posttraumatic arthritis of the ankle and subtalar joints. Canale [7] was the first one to raise the importance of varus angulation at the talar neck in the acute treatment. He reported on 71 fractures of the talar neck, of which roughly 25% (18 of 71) had malunions. He described a special radiographic view of the neck to determine varus and valgus angulation. The foot is maximally plantar flexed with 158 of pronation. The beam is directed cephalad and 758 from the horizontal. Varus malalignment occurred in 77% of cases (14/ 18 cases) and was most commonly associated with closed reduction. In contrast, type III injuries had only 28% occurrence due to the fact that ORIF was performed. The definition of a malunion has changed dramatically. The initial acceptable limits for reduction were 5 mm of displacement or 58 of varus. Not until 1991 did King and Powell [63] recommend anatomic reduction. They felt that anatomic reduction was required due to the fact that the talus bridges three joints. Sangeorzan’s [64] cadaver studies confirmed the need for anatomic alignment. His data showed that the anterior and middle facets were significantly unloaded by any displacement of the talar neck. In their classic article, Daniels and Smith [18] took a series of cadaver feet and created a shortening of the medial column of the talar neck by removing a medial wedge. The results showed loss of eversion ability of the foot with varus inclination. A common surgical error is the use of compression screws over the medial column or the inability to judge correct reduction of a comminuted medial column. This error can be minimized by the use of dual incisions, noncompression screws medially, and local bone graft. More importantly, at the time of preliminary wire fixation during either open or closed reduction, the passive range of motion should be checked for eversion capability. If there is loss, the reduction should be rotated in the desired direction to allow for at least 5 to 108 of eversion. The treatment for malalignment can consist either of a closing wedge osteotomy of the neck or an opening wedge osteotomy, depending on the nature and location of the injury (Figure 3.19A to Figure 3.19D).

F.

Posttraumatic Arthritis

Since the talar surface is roughly 70% articular, it is a common finding to have intra-articular extension from these injuries. The incidence of posttraumatic arthritis is from 50 to 97% [31,61]. Fortunately, the traumatic radiographic changes do not correlate 100% with the clinical picture. For this reason selective analgesic blocks are used preoperatively to distinguish between subtalar and ankle arthritis. To ensure that the block is properly located, fluoroscopic control is recommended. The use of the posterolateral portal site used for subtalar arthroscopy is recommended for this evaluation.

XI.

SURGICAL TREATMENT

A.

Principles of Arthrodesis

The general rule for hindfoot arthrodesis is to fuse as few joints as possible. Precise diagnosis is by the utilization of fluoroscopy-assisted analgesic injections. If there is a suspected associated regional pain syndrome, the patient should have a trial of cast immobilization before arthrodesis. An alternative to surgery can consist of simple bracing or at least a means to delay an ankle arthroplasty in the younger patient. A new alternative for orthotic management is the so-called Arizona brace, which limits both subtalar and ankle motion. A varus hindfoot deformity can be stabilized with the use of a lateral outflare to the sole of the shoe, which decreases the lateral thrust at the knee. Structural hindfoot malalignments may require associated osteotomies and soft tissue releases. In complex injuries, amputation is still an alternative to an arthrodesis.



1.

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Ankle Arthrodesis

Ankle arthrodesis is one of the established means of relieving arthritis of talar neck and body fractures. Stabilization of the arthrodesis can be achieved with screw fixation, plate fixation, or intramedullary nail. In the presence of an active or prior infection, the use of an external fixator

Figure 3.19 (A) Preoperative clinical examination reveals the patient with classic equinovarus deformity of the foot due to varus malalignment. He is now 6 months since his injury. (B) Preoperative CT scan reveals the varus malalignment on the transverse views. (C) Operative technique was performed with an Ollier incision to perform a biplane derotational closing lateral wedge.


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Figure 3.19 Continued (D) Postreduction radiograph displays the posterior-to-anterior screw placement.

such as an Ilizarov frame is acceptable. Talectomy is an alternative to an ankle arthrodesis. This was recommended in the early history of treatment of these disorders due to the frequent association of infection. The standard talectomy has frequently given mixed reviews with frequent residual pain or limping and shortness [6,49,65,66]. Talectomy results with at least 1 inch of shortening, abnormal motion, which has a guarded long-term prognosis. Itokazu [66] recommends a subtotal talectomy with 1-cm shortening of the fibula as an improved modification for total talectomy. Unfortunately, his only case went to an auto fusion. Gunal [65] did an osteotomy of the medial malleolus and displaced it laterally so as to bring the foot forward. He reported on four cases that had good to excellent results after a 3-year follow-up.

B.

Tibiotalar Fusion with Partial Talectomy

Due to the marked loss of motion that results from fusion of both the tibiotalar and subtalar joints, alternative methods have been used to avoid this problem. In 1943, Blair [67] performed a partial talectomy associated with a sliding anterior tibial graft into the slot of the talar head. His method allowed for preservation of length, motion, and cosmesis. This technique lacked internal fixation for the tibial graft, so complications of nonunion or subsequent resorptive breakdown of the autogenous graft were common. In 1971, Morris [47] modified the technique with the use of internal fixation (Figure 3.20A and Figure 3.20B). The technique consisted of a 2.5 5.0-cm sliding graft into a 2-cm slot and holding of the foot in 108 of plantar flexion. The anterior tibial graft was stabilized with a lag screw into the posterior cortex of the tibia and the subtalar joint with a pin through the calcaneus and tibia. He performed ten cases in which he reported that seven cases had adequate motion and painless feet. In a more scientific study, Dennis and Tullos [46] performed a similar procedure on seven patients, in which five out of seven had good results. However, two of the seven had pseudoarthroses and had a nonunion rate of 43%. In 1982, Lionberger [68], at the same institution, condemned the Blair fusion and recommended the use of a cannulated pediatric hip screw without an anterior tibial graft. He placed the anterior border of the tibia next to the neck, and he had five out of five patients with excellent results.

C.

Talectomy and Tibiocalcaneal Fusion

The tibiocalcaneal fusion is a reasonable salvage procedure for patients who have had total talectomy. Reckling [48] performed this procedure along with resection of both malleoli, using a



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Figure 3.20 Blair type arthrodesis post partial talectomy. (A) Oblique view of the tibiotalar fusion using a sliding tibial graft. (B) Lateral view of the same procedure, which demonstrates a solid arthrodesis but evidence of subtalar arthritis.

Charnley compression device to help the fusion. He had 15 out of 16 successful fusions, but they were associated with at least a 1.25-in. leg length difference. Mann and Chou [69] reported a case of AVN that was treated with screw fixation from the calcaneus into the tibia. This is indicated for arthritis and partial AVN. Recent literature supports the use of screw fixation [69,70]. The standard approach to this fusion is with a lateral incision over the fibula. For exposure of the tibiotalar joint, an osteotomy of the fibula is performed approximately 7 cm above the ankle with wedge osteotomies of the tibiotalar joint to correct whatever deformity is present. Autogenous graft can supplement the fusion and can be taken from the lateral malleolus with a small acetabular reamer. In special circumstances a posterior approach is indicated, which was popularized by Johnson [71] using the Calandruccio clamp. He reported success in 14 out of 21 cases; four of these cases had AVN. Cases without the use of the compression clamp led to four out of six having poor results. In 1994, the technique was improved with the use of retrograde nailing. Kile et al. [72] reported on 30 cases using an intramedullary rod (Figure 3.21A to Figure 3.21D). They had 86% satisfactory cases (26/30), of which three cases had AVN. The complications consisted of two deep infections and one nonunion that led to an amputation. These are salvage procedures, so the goal is to relieve pain and improve gait. Sanders et al. [73], who used an anterior plate technique with 100% fusion rate, still thought that in these complex injuries an amputation may result in a more favorable overall function.

XII.

OSTEOCHONDRAL LESIONS (OCLS) OF THE TALUS

OCLs of the talus were first described in 1888 by Konig [74]. He described these lesions that lead to loose bodies of joints. Kappis [75] was the first to describe these lesions in the ankle in 1922. By definition, it is an injury that results in separation of an osteochondral fragment from a portion of the talus. These lesions have been given multiple names, including osteochondritis dissecans, transchondral fractures, juvenile osteonecrosis, and osteochondral defects. Currently, the most proper descriptive term is acute or chronic OCLs of the talus, as described by Ferkel and


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Figure 3.21 (A and B) AP and lateral radiographs of an elderly patient who was treated nonoperatively for a group II talar neck fracture that presents with a malunion and AVN of the talar body. (C and D) AP and lateral radiographs show intramedullary fixation for a tibio–talo–calcaneal fusion associated with a derotational osteotomy.

Fasulo [76]. Approximately 1% of all talar injuries are osteochondral. If one considers solely chondral lesions of the talus, they are quite common, occurring in up to 50% of ankle fractures [77,78] (Figure 3.22A and Figure 3.22B). It has been noted that ankle sprains have OCL lesions of approximately 2 to 6% [79–81]. The typical patient is male and he can present either with a posttraumatic or nontraumatic type of lesion. It is felt that the majority of these lesions are related to trauma. However, it is possible that an avascular segment of bone can also cause a similar lesion, and this has been reported in metabolic and genetic disorders.



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Figure 3.22 (A) AP radiograph of the ankle demonstrates the arthroscope in the anteromedial portal for examination of a fractured ankle. (B) Demonstrates the multiple osteochondral fragments from the fractured ankle.

The lesion can be either medial or lateral. In general, medial lesions are located on the posterior aspect of the talar dome while the lateral lesions tend to occur anterolaterally. The majority of the lateral lesions are traumatic, while the opposite can be said of the medial side, but certainly some of them are related to trauma. The symptoms associated with medial lesions are usually described as a deep pain without focal tenderness but aggravated by activity. On physical examination there is seldom any synovitis or loss of motion. With medial lesions, pain can be elicited over the posteromedial aspect of the ankle if the ankle is maximally dorsiflexed with deep palpation of the posteromedial edge of the talus. The lateral lesions are rarely seen without a history of trauma. The patient will complain of loss of motion and swelling. Pain is usually positive over the anterolateral aspect of the ankle and is commonly associated with joint laxity. In both types with loose joints the anterior drawer maneuver produces clicking or crepitation. Historically, in the early 1980s, diagnosis was often missed due to the lack of tomography or CT scan. Since the advent of MRI, lesions are easy to see as well as obscure lesions in the tibia and inferior surface of the talus. Unfortunately, there are now multiple classifications specifically for radiographs, CT, and MRI. Routine ankle radiographs frequently show small but specific lesions; however, there are many that are not easily seen or are misread. The accuracy of radiographs can be improved, especially with posterior lesions of the talus, by taking an AP view with the heel raised


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approximately 4 cm so as to visualize the posterior aspect of the talus. Berndt and Harty [79] have proposed the standard radiographic classical description for OCL. Stage I has no radiographic changes and is considered a contusion of the surface of the talus. Stage II consists of a stable partial fissure of the osteochondral surface. Stage III is an OCL that is separated from the talus but is stable, while stage IV is felt to be unstable. It can be difficult to determine whether the fragment identified is an active one and for this reason, a technetium bone scan can help to determine the difference between an active and a nonactive lesion. If the bone scan is positive, then a subsequent CT scan can determine the size and exact location of the lesion. A CT scan provides excellent bone detail and also determines the extent of related cystic cavities. However, the visualization of articular cartilage is poor without a contrast agent. Requests for the CT scan should be for 2-mm cuts in both the coronal and axial planes with contrast. Ferkel and Sgaglione [77] utilized arthroscopic procedures to confirm the Berndt and Harty classification scheme. Their four-part classification scheme is the following: stage I is a cystic lesion within the dome of the talus with intact roof on all views; stage IIA is a cystic lesion with communication to the talar dome surface; stage IIB is an open articular surface lesion overlying the nondisplaced fragment; stage III is an undisplaced lesion with a lucency; and stage IV is a displaced fragment. An MRI classification was developed by Anderson et al. [82] in 1989. The advantage of the MRI scan is that it is easy to confirm stage I lesions, which correlate with a positive bone scan and bone marrow edema. The exact mechanism of injury is unknown. Berndt and Harty described that with internal rotation of the tibia associated with inversion and dorsiflexion of the ankle, the lateral surface is abutted against the medial articular surface of the fibula, thus causing a lateral lesion. The posteromedial lesion was postulated to occur with external rotation, plantar flexion, and inversion impacting the medial talus against the posteromedial tibia. Persistent pain with an ankle sprain should make one suspicious of an OCL. Slow response to conservative management is an indication for MRI. The usual signal changes seen with an MRI is a high-signal line on T2 pulse sequences at the talar fragment interface that represents loose granulation tissue. Detached fragments are identified by the presence of a smooth high-signal intensity fluid line encircling the fragments. The MRI has the advantages of no irradiation and the ability to distinguish between stable and unstable lesions. However, for staging, arthroscopic diagnosis is the most definitive due to the ability of direct inspection and probing of the lesion.

A.

Treatment

The treatment of OCL depends on the size, location, and quality of the attached cartilage and bone. In grade I lesions, treatment consists of off-loading with an ankle brace and restricted activity for 6 weeks or when asymptomatic. For grade II lesions, the patient is protected in a short leg cast for a 6-week period to see if the lesion can heal. Pettine and Morrey [83] reported a 90% success rate with this method. Recommendations are different for the different locations of grade III lesions. Lateral lesions are treated aggressively with immediate arthroscopic debridement and curettage to subchondral bone. Attempts for reattachment in acute lesions can be entertained if there is good quality of subchondral bone and articular cartilage (Figure 3.23A to Figure 3.23D). The lesion can be drilled and screws or absorbable pins can be used for fixation. The most suitable lesions for reduction are transchondral lesions that have substantial bony components. If there is minimal subchondral bone, then it is best to debride and drill the base, so as to promote fibrocartilage. Grade III medial lesions can be treated initially with a 6-week period of casting. This is more commonly done with younger patients because AVN may be the actual cause and because younger patients have a higher potential for healing. In acute grade IV lesions, the osteochondral fragment can be reattached in the ideal case. In late cases with chronic locking, removal and drilling of the lesion is the preferred treatment. Lesions greater than 1 cm have a poorer prognosis for curettage and drilling. One option is to use fresh frozen cadaver allografts [84]. Another option is osteochondral autograft using donor material from the patient’s knee or ipsilateral ankle. Mosaicplasty is a surgical technique that consists of single or multiple osteochondral cylindrical grafts from the ipsilateral knee. Indications for these grafts are grade III or IV OCL that have failed conservative and surgical management, or similar lesions that are larger than 1 cm.



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Figure 3.23 (A and B) AP and lateral radiographs demonstrate a compression fracture of the anterolateral portion of the tibial plafond associated with a Weber C fracture. (C) Coronal CT scan confirms the tibial plafond fracture as well as an osteochondral fracture of the lateral dome of the talus. (D) Postreduction x-rays demonstrate excellent alignment of the tibial plafond fracture that was facilitated by the use of a fibular osteotomy. Bioabsorbable pins were used for the fixation of the talus.

With regard to internal fixation, the most easily repaired are lateral talar dome lesions. Bioabsorbable pins are useful in smaller lesions. However, headless screws such as the Herbert screw provide better fixation. Medial lesions are much more difficult to approach and frequently require a medial malleolar osteotomy [85]. Postoperative management for acute OCLs is cast immobilization without weight-bearing for a 3- to 6-week period followed by physical therapy and clinical evaluations until healing appears. The postoperative care for grade I and II lesions is 3 weeks non-weight-bearing, but no casting so as to allow range of motion. Swimming and lowresistance cycling are also encouraged. Grade III and IV lesions are treated with 6 weeks of


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immobilized non-weight-bearing followed by swimming and biking for 6 weeks and physical therapy. The surgical technique for debridement starts with comprehensive arthroscopic examination of the ankle joint. The loose fragment is lifted from the bed. The necrotic bone is debrided to a bleeding base and stable edges are identified with the use of straight and angled curettes. Debridement should be complete, especially in the medial and lateral gutters because one of the frequent causes of poor results is due to inadequate debridement in these areas [85]. At completion of the debridement, the rim of remaining cartilage should be well attached to the subchondral bone. The exposed base is perforated with a bony awl or burr to achieve bleeding, which is observed after release of the tourniquet. Drilling can also be performed with Kirschner wires. One should avoid transmalleolar drilling as much as possible, as this encourages tibial lesions. Subchondral cysts are controversial in diagnosis and treatment. There are varying interpretations of whether these cysts are degenerative or related to OCL. A new proposed classification scheme adding this subgroup to the Berendt and Harty classification has been recently published. If there is no motion of the subchondral bone it is possible to create vascular channels with retrograde drilling of intact lesions. The cartilaginous surface is not violated [86]. However, this is presently experimental. These lesions are usually drilled either from the anterolateral portal or accessory anterior portal while viewing from the anteromedial portal. The Kirschner wire can be used to make multiple drill holes to a depth of 1 to 1.5 cm. One can also use a transtalar approach through the sinus tarsi using a guidewire for a 3.5 drill. The drilling of the cyst is confirmed by fluoroscopic dye technique. Grafting is applied through the drill hole and confirmed radiographically [86]. There have been very few isolated reports on acute injuries treated with immediate fixation. Kristensen et al. [87] reported of a stage IV lesion treated with PGA pins in only one patient. Angermann and Riegels [88] reported use of a fibrin sealant in five patients; all of them healed and 75% returned to sports. Debridement for chronic lesion along with curettage is more common and up to 80 to 90% good results with smaller lesions has been reported [88]-.

B.

Prognosis

It should be noted that arthritic changes are proportional to the size and location of the lesion. Usually when lesions are greater than 1 cm and especially if the patient is heavy or highly active, it is very likely that degenerative changes will occur over a period of time. The report of Flick and Gould [89] found that 84% of patients in long-term follow-up did not develop arthrosis. Canale and Belding [90] reported 22% of cases that developed arthrosis and 75% in stage III and IV lesions.

XIII. A.

FRACTURES OF THE POSTERIOR PROCESS Anatomy

The posterior process of the talus comprises two tubercles: the posterolateral and the posteromedial. There is a sulcus dividing these two tubercles that encases the FHL tendon and has multiple ligamentous attachments. The superior surface of the posterolateral tubercle is nonarticular; however, it provides insertion of the posterior talofibular ligament and the talar component of the ligament of Rouviere. The inferior surface is part of the posterior facet of the subtalar joint [12]. Burman and Lapidus [91] reported the presence of accessory bones in 15% of their cases. Sarrafian [12] reported 11% had separate ossicles, the so-called os trigonum. However, when this bone was fused to the posterior tubercle, he described it as a trigonal process or the Steida’s process. The os trigonum is unilateral in two thirds of the cases. It originates as a synchondrosis between these two bones. In contrast, the medial tubercle is a much smaller bone. It provides attachment for the deep and superficial layers of the talotibial component of the deltoid ligament.

B.

Mechanism of Injury

The injury to the os trigonum can occur either in compression or in distraction. The compressive force is caused by plantar flexion of the foot, which causes impingement of the posterolateral



85

tubercle on the tibial plafond. This collision results in either fracture or displacement of the os trigonum from its synchondrosis. These repetitive injuries are commonly seen in ballet dancers and soccer players [92]. The opposite mechanism can also occur with excessive dorsiflexion of the foot, which causes an avulsion fracture similar to an accessory navicular, or the attachment of the patellar tendon.

C.

Clinical Features

Common plantar flexion mechanisms are seen in ballet en pointe, kicking a football, or accidentally missing a step and landing on the heel, causing a sudden plantar-flexed lesion. Tenderness is usually localized over the posterolateral aspect of the ankle. A supportive test is to provocate pain by moving the great toe passively or actively, which moves the FHL in the groove between the two tubercles. This complex of signs and symptoms has been described as the os trigonum syndrome [92]. Crepitation can be felt with plantar flexion, although this is more common in the chronic lesion. Plain radiographs that show a detached fragment from the posterior tubercle with a rough, irregular surface are suggestive of a fractured tubercle. However, it should be noted that this os trigonum is unilateral in two thirds of the cases. In order to improve diagnostic accuracy, Paulos et al. [93] described a 308 subtalar oblique view. When one is in doubt, a bone scan can be utilized to show if it is an active lesion, and a CT scan can help determine its anatomic features.

D.

Treatment

If the fragment is nondisplaced, a short leg cast in approximately 58 of equinus for a 4- to 6-week period is satisfactory. The patient is observed for a 4- to 6-month period to see if symptoms reoccur. If conservative treatment fails, surgical excision of the fragment is recommended [93,94]. With regard to surgical approaches, it has been shown that one can approach this either from a posterolateral or from a posteromedial aspect as described by Paulos et al. [93] (Figure 3.24A to Figure 3.24E). However, the main disadvantage of the posteromedial approach is the potential for tibial nerve damage. The posterolateral approach can damage the sural nerve. The most direct approach is to have the patient either in the prone or in the posterolateral position, utilizing an incision just lateral to the Achilles tendon and extending through both the superficial and deep fascia. The FHL tendon is retracted medially to expose the fragment. Surgical excision is effective in these cases however; Amendola [95] has recently reported utilizing arthroscope-assisted fixation of a posterior process fracture. Results of treatment of acute fractures are meager. Multiple papers do exist on the outcome of treatment of chronic posterior ankle impingement, which is treated in a similar fashion. In the treatment of the chronic condition of posterior impingement, the results have been good. Hedrick and McBryde [96] reported 30 cases. In 28 patients of posterior impingement, 60% improved nonsurgically and 40% required excision. Marotta and Micheli [97] reported 16 patients in whom the posterolateral approach was utilized, and in their retrospective study, all had improvement; however, they still had some residual symptoms. Brodsky and Khalil [98] and Wredmark et al. [99] reported similar findings.

XIV.

FRACTURE OF THE MEDIAL TUBERCLE (CEDELL’S FRACTURE)

This is an extremely uncommon fracture. The eponym Cedell [100] was given for this fracture when he reported on four cases, which he felt resulted from trauma from a dorsiflexion-pronated injury. These cases presented with a firm mass over the posterior aspect of the medial malleolus. He attempted to treat these four causes conservatively; however, three of the four required surgery. Complications from this fracture can result in a tarsal tunnel syndrome, as reported by Stefko et al. [101]. Ebraheim et al. [102] reported four cases of this. One case was treated acutely with an ORIF and two resulted with late nonunions. These cases can be treated conservatively if the fragment is small and it does not interfere with ankle or subtalar motion (Figure 3.25). They can be treated in a


86


Figure 3.24 (A and B) Prereduction AP and lateral radiographs of the foot demonstrate a talonavicular dislocation associated with a posterior process fracture. (C) Postreduction radiograph demonstrates incomplete reduction of the posterior process. (D) Operative intervention was performed with an anteromedial incision centered on the flexor digitorum longus tendon. This tendon was manipulated in order to see the distal extent of the fracture as well as facilitation of screw placement. (E) Postreduction radiograph demonstrates good anatomic reduction with a cancellous screw.



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Figure 3.25 Coronal CT section demonstrates a medial process fracture with minimal displacement. This fracture was treated conservatively since subtalar motion was not affected.

non-weight-bearing short leg cast for a 6-week period. If the fragment is larger and interferes with motion, consideration either for excision or ORIF can be performed.

XV.

FRACTURES OF THE LATERAL PROCESS

Lateral process fractures of the talus have become more common with the advent of snowboarding as a popular pastime [103]. This fracture is described as ‘‘snowboarder’s ankle’’ or ‘‘snowboarder’s fracture’’ [104]. Mukherjee and Young [105] found 13 cases among 1500 cases of fractures and sprains around the ankle.

A.

Clinical Evaluation

There needs to be a high index of suspicion due to the fact that this fracture, if untreated, frequently leads to both ankle and subtalar arthritis due to its dual articulation with the distal fibula and posterior facet. Patients with an ankle sprain who have poor range of motion or persistent pain distal to the fibula should be evaluated for the above. From an anatomic basis, the lateral process serves as the point of attachment for the lateral talocalcaneal ligament, cervical, bifurcate, and anterior talofibular ligament (ATFL) and, therefore, is important in lateral stability of the ankle.

B.

Mechanism of Injury

It is believed that this injury results from acute dorsiflexion and inversion of the foot. This classically occurs when an individual who is snowboarding hits a mogul with the foot inverted


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and sustains an acute dorsiflexion force of the ankle. Due to the length of the snowboard, the bending moment of the foot is exaggerated. Other factors are the use of soft-shelled boots and aerial maneuvers, which accentuate the forces on the ankle. It is also associated with fractures of the talar neck (Figure 3.26A to Figure 3.26C).

Figure 3.26 (A) Coronal CT scan shows a two-part joint-depression fracture of the lateral process of the talus. (B) An Ollier incision allows for adequate visualization of the subtalar joint as well as the medial fragment. (C) Postreduction x-rays reveal adequate reduction of this comminuted fracture with cancellous screws.



C.

89

Clinical Evaluation

Lateral talar process fractures should be part of the differential for every patient with an ankle sprain who has persistent pain or loss of motion. Acutely, local tenderness is distal to the tip of the fibula and x-rays should be taken to rule out this entity. Commonly, a radiographically suspicious sign is any comminution or fragmentation lateral to the lateral process. A special AP view was described by Mukherjee and Young [105], who recommended an AP view with the foot in 458 of internal rotation and 308 of equinus. Once a suspicious lesion is noted, a CT scan best determines the exact size and location and the feasibility for surgical reconstruction. Hawkins [33] described the classification scheme for these fractures. He divides them into a simplistic three-part staging system. Type I is a simple fracture, type II is a comminuted fracture, and type III is a chip fracture of the anterior or inferior portion of the posterior process with no extension into the talofibular articulation [33].

D.

Treatment

Determination for ORIF would be dependent on the size of the fragment, the degree of comminution, and the displacement. With a small fragment that is nondisplaced, conservative treatment that is non-weight-bearing can be recommended for a 4-week period followed by early range of motion. If pain is elicited with motion, delayed open reduction and internal fixation can be considered. If the fragment is large or displaced more than 2 mm, an ORIF is indicated [103,105]. Due to the articular nature of this fragment, either a headless screw should be used or the fragment should be excised [40]. The main proponent for operation was by Mukherjee [105] who recommended fixation of large fragments. Unfortunately, his reports of late excision of fragments had only mixed results. In conclusion, it is felt that a high index of suspicion is useful in diagnosing these fractures early so that a definitive procedure can be done in the early stage of the injury, so as to allow for a better prognosis. For patients who have a significant problem, consideration for a subtalar fusion should be entertained, as well as decompressing the talofibular joint. It is possible that in some cases a fusion of both the ankle and the subtalar joint may be entertained, although this is an uncommon outcome.

XVI.

CONCLUSION

Injuries to the talus, although challenging, are rare, reflecting paucity of significant scientific objective data on management of these fractures. A through understanding of anatomy and biomechanics and experience in dealing with these injuries is invaluable to the treating surgeon to obtain the best possible results. Even after accurate reduction and stable fixation, there is a high incidence of osteonecrosis, collapse, and posttraumatic arthritis. It is imperative that the patients are made aware of potential complications and long-term disability that can follow these devastating injuries. Isolated fractures in the lateral, medial, and posterior processes are also rare and high index of suspicion and special imaging techniques may be required to detect these fractures, which if left untreated can be disabling. New techniques are available such as arthroscope-assisted internal fixation and use of bioabsorbable implants. A great deal of progress has been made in our understanding and management of the OCLs of talus in the recent past, such as with the autologous chondrocyte replacement technique that aims to restore hyaline cartilage.

REFERENCES 1. Goldie, I., Talar and peritalar injuries, in The Foot, 1st ed., Helal, B. and Wilson, D.W., Eds., Churchill Livingstone, New York, 1988, pp. 916–931. 2. Sanders, R., Fractures and fracture-dislocations of the talus, in Surgery of the Foot and Ankle, 7th ed., Coughlin, M.J. and Mann, R.A., Eds., Mosby, St. Louis, MO, 1999, pp. 1465–1518.


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Ebraheim, N.A., Mekhail, A.O., Salpietro, B.J., Mermer, M.J., and Jackson, W.T., Talar neck fractures: anatomic consideration for posterior screw application, Foot Ankle Int., 17, 541–547, 1996. Haliburton, R.A., Sullivan, C.R., and Kelly, R.J., The extra-osseous and intra-osseous blood supply of the talus, J. Bone Jt. Surg., 40A, 1115–1120, 1958. Mulfinger, G.L. and Truetta, J., The blood supply of the talus, J. Bone Jt. Surg., 52B, 160–167, 1970. Wildenauer, E., Die Blutversorgung der Talus, Z. Anat., 115, 32, 1950. Kelly, P.H. and Sullivan, C.R., Blood supply of the talus, Clin. Orthopaed., 30, 37–44, 1963. Gelberman, R.H. and Mortensen, W.W., The arterial anatomy of the talus, Foot Ankle, 4, 64–72, 1983. Peterson, L. and Romanus, B., Fractures of the collum tali: an experimental study, J. Biomech., 9, 277–279, 1976. Penny, J.N. and Davis, M.L., Fractures and fracture-dislocation of the neck of the talus, J. Trauma, 20, 1029–1037, 1980. Daniels, T.R. and Smith, J.W., Talar neck fractures, Foot Ankle, 14, 225–232, 1993. Bonnin, J.G., Dislocations and fracture-dislocations of the talus, Br. J. Surg., 28, 88–100, 1840. McKeever, F.M., Fractures of the tarsal and metatarsal bones, Surg. Gynecol. Obstet., 90, 735–745, 1950. Baumhauer, J.F. and Alvarez, R.G., Controversies in treating talus fractures, Orthoped. Clin. North Am., 26, 335–351, 1995. Lorentzen, J.E., Christensen, S.B., Krogsoe, O., and Sneppen, O., Fractures of the neck of the talus, Acta Orthopaed. Scand., 48, 115–120, 1977. Wechsler, R.J., Schweitzer, M.E., Karasick, D., Deely, D.M., and Glaser, J.B., Helical CT of talar fractures, Skeletal Radiol., 26, 137–142, 1997. Hawkins, J.L., Fractures of the lateral process of the talus, J. Bone Jt. Surg., 47A, 991–1002, 1970. O’Brien, E.T., Howard, J.B., and Shepard, M.J., Injuries of the talus, J. Bone Jt. Surg., 54, 1575–1576, 1972. Rammelt, S., Zwipp, H., and Gavlik, J.M., Avascular necrosis after minimally displaced talus fracture in a child, Foot Ankle Int., 21, 1030–1036, 2000. Adelaar, R.S., Complex fractures of the talus, Instr. Course Lect., 46, 323–338, 1997. Alvarez, R.G., Talar neck fractures, in Current Therapy in Foot and Ankle Surgery, Myerson, M.S., Ed., Mosby, St. Louis, MO, 1993, pp. 243–248. Grob, D., Simpson, L., Weber, B.G., and Bray, T., Operative treatment of displaced talus fractures, Clin. Orthopaed., 199, 88–96, 1985. Alexander, I.J. and Watson, J.T., Step-cut osteotomy of the medial malleolus for exposure of the medial ankle joint space, Foot Ankle, 11, 242–243, 1991. Mallon, W.J., Wombwell, J.H., and Nunley, J.A., Intra-articular talar factures: repair using the Herbert bone screw, Foot Ankle, 10, 88–92, 1989. Trillat, A., Bousquet, G., and Lapeyre, B., Displaced fractures of the neck and body of the talus: value of screwing by posterior surgical approach, Rev. Chir. Orthoped., 56, 529–536, 1970. Swanson, T.V., Bray, T.J., and Holmes, G.B., Fractures of the talar neck. J. Bone Jt. Surg., 74A, 544–551, 1992. Fleuriau-Chateau, P.B., Brokaw, D.S., Jelen, B.A., Scheid, D.K., and Weber, T.G., Plate fixation of talar neck fractures: preliminary review of a new technique in twenty-three patients, J. Trauma, 16, 213–219, 2002.



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44. Westbrook, A.P., Hutchinson, J.W., and Moran, C.G., Internal Fixation with Lag Screws for Displaced Talar Neck Fractures, paper presented at the OTA Meeting, San Antonio, TX, 2002. 45. Pennal, G.F., Fractures of the talus, Clin. Orthopaed., 30, 53–63, 1963. 46. Dennis, M.D. and Tullos, H.S., Blair tibiotalar arthrodesis for injuries of the talus, J. Bone Jt. Surg., 62A, 103–107, 1980. 47. Morris, H., Hand, W., and Dunn, W., The modified Blair fusion for fractures of the talus, J. Bone Jt. Surg., 53A, 1289–1297, 1971. 48. Reckling, F.W., Early tibiocalcaneal fusion in the treatment of severe injuries of the talus, J. Trauma, 12, 390–396, 1972. 49. Marsh, J.L., Saltzman, C.L., Iverson, M., and Shapiro, D.S., Major open injuries of the talus, J. Orthopaed. Trauma, 9, 371–376, 1995. 50. Brewster, N.T. and Maffulli, N., Reimplantation of the totally extruded talus, J. Orthopaed. Trauma, 11, 42–45, 1997. 51. Hiraizumi, Y., Hara, T., Takahshi, M., and Mayehiyo, S., Open total dislocation of the talus with extrusion (missing talus): report of two cases, Foot Ankle, 13, 473–477, 1992. 52. Ritsema, G.H., Total talar dislocation, J. Trauma, 28, 692–694, 1988. 53. Sneed, W.L., The astragalus: a case of dislocation, excision, and replacement — an attempt to show the circulation in this bone, J. Bone Jt. Surg., 7, 384–399, 1925. 54. Jaffe, K.A., Conlan, T.K., Sardis, L., and Meyer, R.D., Traumatic talectomy without fractures: four case reports and review of the literature, Foot Ankle Int., 16, 583–587, 1995. 55. Inokuchi, S., Ogawa, K., and Usami, N., Classification of fractures of the talus: clear differentiation between neck and body fractures, Foot Ankle Int., 17, 748–750, 1996. 56. Boyd, H.B. and Knight, R.A., Fractures of the astragalus, South. Med. J., 35, 160–167, 1942. 57. LeMaire, R.G. and Bustin, M., Screw fixation of fractures of the neck of the talus using a posterior approach, J. Trauma, 20, 669–673, 1980. 58. Calhoun, J.H. and Mader, J.T., Musculoskeletal Infections, Marcel Dekker, New York, 2003. 59. Delanois, R.E., Mont, M.A., Yoon, T.R., Mizell, M., and Hungerford, D.S., Atraumatic osteonecrosis of the talus, J. Bone Jt. Surg., 80A, 529–536, 1998. 60. Thordarson, D.B., Triffon, M.J., and Terk, M.R., Magnetic resonance imaging to detect avascular necrosis after open reduction internal fixation of talar neck fractures, Foot Ankle Int., 17, 742–747, 1996. 61. Peterson, L., Goldie, I., and Irstam, L., Fractures of the neck of the talus: a clinical study, Acta Orthopaed. Scand., 48, 696–706, 1977. 62. Migues, A., Solari, G., Carrasco, N.M., and Gonzalez-Della, V.A., Repair of neck nonunion with indirect corticocancellous graft technique: a case report and review of the literature, Foot Ankle Int., 17, 690–694, 1996. 63. King, R.E. and Powell, D.F., Injury to the talus, in Disorders of the Foot and Ankle, Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1991, pp. 2293–2325. 64. Sangeorzan, B.J., Wagner, U.A., Harrington, R.M., and Tencer, A.F. Contact characteristics of the subtalar joint: the effect of talar neck misalignment, J. Orthopaed. Res., 10, 544–551, 1992. 65. Gunal, I., Atilla, S., Arac, S., Gursoy, Y., and Karagozlu, H., A new technique of talectomy for severe fracture dislocations of the talus, J. Bone Jt. Surg., 75B, 69–71, 1993. 66. Itokazu, M., Matsunaga, T., and Tanaka, S., Ankle arthroplasty by excision of the talar body: subtotal talectomy, Foot Ankle Int., 15, 191–196, 1994. 67. Blair, H.C., Comminuted fractures and fracture dislocations of the body of the astragalus, Am. J. Surg., 59, 37–43, 1943. 68. Lionberger, D.R., Bishop, J.O., and Tullos, H.S., The modified Blair fusion, Foot Ankle, 13, 60–62, 1982. 69. Mann, R.A. and Chou, L.B., Tibiocalcaneal arthrodesis, Foot Ankle Int., 16, 401–405, 1995. 70. Papa, J.A. and Myerson, M.S., Pantalar and tibiotalocalcaneal arthrodesis for posttraumatic osteoarthrosis of the ankle and hindfoot, J. Bone Jt. Surg., 74A, 1042–1049, 1992. 71. Johnson, K., Surgery of the Foot and Ankle, Raven, New York, 1989, pp. 151–176. 72. Kile, T.A., Donnely, R.E., Gehrke, J.C., Werner, M.E., and Johnson, K.A., The results of ankle arthrodesis, J. Bone Jt. Surg., 72A, 141–143, 1990. 73. Sanders, R., Helfet, D.L., Pappas, J., and Mast, J., The salvage of grade IIIB open ankle and talus fractures, J. Orthopaed. Trauma, 6, 201–208, 1992. 74. Konnig, F., Veber freie Korper in den Gelenken, Dtsch. Z. chir., 27, 90, 1888. 75. Kappis, M., Weitere Beitrage zu traumtisch-mechanischen Entsehung der ‘‘spontanen’’ Knorpelalblosungen sogen (Osteochondritis dissecans), Dtsch. Z. Chir., 171, 13, 1922. 76. Ferkel, R.D. and Fasulo, G.H., Arthroscopic treatment of ankle injures, Orthoped. Clin. North. Am., 25, 17–32, 1994. 77. Ferkel, R.D. and Sgaglione, N.A., Arthroscopic Surgery: The Foot and Ankle, Lippincott-Raven, Philadelphia, 1996, pp. 145–184. 78. Ferkel, R.D. and Sgaglione, N.A., Arthroscopic treatment of osteochondral lesions of the talus: longterm results, Orthoped. Trans., 17, 1011, 1993–1994.


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79. Berndt, A.L. and Harty, M., Transchondral fractures (osteochondritis dissecans) of the talus, J. Bone Jt. Surg., 41A, 988–1020, 1959. 80. Smith, G.R., Winquist, R., Allan, N.K., and Northrop, C.H., Subtle transchondral fractures of the talar dome: a radiological perspective, Diagn. Radiol., 124, 667–673, 1977. 81. Van Buecken, K., Barrack, R.L., Alexander, A.H., and Ertl, J.P., Arthroscopic treatment of transchondral talar dome fractures, Am. J. Sports Med., 17, 350–356, 1989. 82. Anderson, I.F., Chrichton, K.J., Grattan-Smith, T., Cooper, R.A., and Brazier, D., Osteochondral fractures of the dome of the talus, J. Bone Jt. Surg., 71A, 1143–1152, 1989. 83. Pettine, K.A. and Morrey, B.F., Osteochondral fractures of the talus: a long-term follow-up, J. Bone Jt. Surg., 69B, 89–92, 1987. 84. Tasto, J., Ostrander, R., Bugbee, W., and Brage, M., The Diagnosis and Management of Osteochondral Lesions of the Talus: Osteochondral Allograft Update, paper presented at the AOFAS Annual Winter Meeting, Dallas, TX, 2002. 85. Easley, M.E., Scranton, P.E., Jr., Osteochondral autologous transfer system, Foot Ankle Clin., 8, 275–290, 2003. 86. Berlet, G.C., Raissi, A., and Lee, T.H., Retrograd Drilling of Osteochondral Lesions of the Talus, paper presentation at the AAOS Annual Meeting, New Orleans, LA, 2003. 87. Kristensen, G., Lind, T., Lavard, P., and Olsen, P.A., Fracture stage 4 of the lateral talar dome treated arthroscopically using Biofix for fixation, Arthroscopy, 6, 242–244, 1990. 88. Angermann, P. and Riegels, N.P., Fibrin fixation of osteochondral talar fracture, Acta Orthopaed. Scand., 61, 551–553, 1990. 89. Flick, A.B. and Gould, N., Osteochondritis dissecans of the talus: review of the literature and new surgical approach for medial dome lesions, Foot Ankle, 5, 165–185, 1985. 90. Canale, S.T. and Belding, R.H., Osteochondral lesions of the talus, J. Bone Jt. Surg., 62A, 97–102, 1980. 91. Burman, M.S. and Lapidus, P.W., The functional disturbances caused by inconstant bones and sesamoids of the foot, Arch. Surg., 22, 936–975, 1931. 92. Hamilton, W.G., Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the os trigonum in ballet dancers, Foot Ankle, 3, 74–80, 1982. 93. Paulos, L.E., Johnson, C.L., and Noyes, F.R., Posterior compartment fractures of the ankle: a commonly missed athletic injury, Am. J. Sports Med., 11, 439–443, 1983. 94. Ihle, C.L. and Cochran, R.M., Fractures of the fused os trigonum, Am. J. Sports Med., 10, 47–50, 1982. 95. Sitler, D., Amendola, A., Bailey, C.S., Thain, L., and Spouge, A., Posterior ankle arthroscopy, J. Bone Jt. Surg., 86A, 763–769, 2002. 96. Hedrick, M.R. and McBryde, A.M., Posterior ankle impingement, Foot Ankle Int., 15, 2–8, 1994. 97. Marotta, J.J. and Micheli, L.J., Os trigonum impingement in dancers, Am. J. Sports Med., 20, 533–536, 1992. 98. Brodsky, A.E. and Khalil, M.A., Talar compression syndrome, Foot Ankle, 7, 338–344, 1987. 99. Wredmark, T., Carlstedt, C.A., Bauer, H., and Saartok, T., Os trigonum syndrome: a clinical entity in ballet dancers, Foot Ankle, 11, 404–406, 1991. 100. Cedell, C.A., Rupture of the posterior talotibial ligament with avulsion of a bone fragment from the talus, Acta Orthopaed. Scand., 45, 454–461, 1974. 101. Stefko, R.M., Lauerman, W.C., and Heckman, J.D., Tarsal tunnel syndrome caused by an unrecognized fracture of the posterior process of the talus (Cedell fracture): a case report, J. Bone Jt. Surg., 76A, 116–118, 1994. 102. Ebraheim, N.A., Padanilam, T.G., and Wong, F.Y., Posteromedial process fractures of the talus, Foot Ankle Int., 16, 764–739, 1995. 103. Fehnel, D.J., Baumhauer, J.F., Huber, B. et al., Fractures of the Lateral Process of the Talus: A Functional Outcome Study, paper presented at the Annual Summer Meeting of the American Foot and Ankle Society, Ashville, NC, 1994. 104. McCrory, P. and Bladin, C., Fractures of the lateral process of the talus: a clinic review — ‘‘snowboarder’s ankle,’’ Clin. J. Sports Med., 6, 124–128, 1996. 105. Mukherjee, S.K. and Young, A.B., Dome fracture of the talus, J. Bone Jt. Surg., 55B, 319–326, 1973.


4 Calcaneal Fractures* Paul J. Juliano and Hoan-Vu Nguyen Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey, Pennsylvania

CONTENTS I. History............................................................................................................................. 94 II. Anatomy.......................................................................................................................... 94 III. Mechanism of Injury ....................................................................................................... 95 IV. Classification ................................................................................................................... 98 V. Initial Presentation ......................................................................................................... 101 VI. Initial Management ........................................................................................................ 101 VII. Radiographic Examination............................................................................................. 101 VIII. Definitive Management .................................................................................................. 104 A. Extra-Articular Fractures ....................................................................................... 104 B. Intra-Articular Fractures ........................................................................................ 106 IX. Surgical Approach .......................................................................................................... 108 A. Lateral Approach.................................................................................................... 108 B. Medial Approach .................................................................................................... 108 X. Preferred Method of Treatment...................................................................................... 108 XI. Postoperative Management ............................................................................................ 109 XII. Complications................................................................................................................. 109 XIII. Open Calcaneal Fractures .............................................................................................. 114 XIV. Salvage Procedures ......................................................................................................... 114 XV. Conclusions .................................................................................................................... 114 References .................................................................................................................................. 115

Fractures of the calcaneus (os calcis) are the most common of tarsal bone fractures, with an overall incidence of approximately 2%. Despite increased experience with these types of fractures, however, there is considerable debate regarding their treatment and overall management. Controversies remain regarding the most appropriate classification system, treatment options, indications for surgery, surgical approaches, and postoperative management. This chapter presents a rational approach on the treatment of calcaneus fractures, based on current and past literature as well as the authors’ preferred treatment.

*Modified from Juliano, P.J. and Nguyen H.-V., Fractures of the calcaneus, Orthoped. Clin. North Am., 32, 35–51, 2001. With permission from Elsevier.

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HISTORY

The first accurate description of treatment for calcaneus fractures was given in 1720 by Petit and DeSault in France. They recommended ‘‘rest until the fragments consolidated’’ [1,2]. Conservative management through rest and elevation remained the mainstay of treatment until the 1900s. In 1908, Cotton and Wilson described their closed reduction technique in an attempt to restore normal anatomy and reduce the disabilities previously associated with calcaneus fractures. They proposed closed manual molding of the fracture fragments after disimpaction with a mallet, followed by casting. In 1931, Bohler modified this technique using pin traction and clamps in an attempt to restore normal anatomy. He emphasized the need to restore the tuber angle (Bohler’s angle). In 1902, Morestin was the first to advocate open reduction. In 1913, Leriche was the first to use plates and screws for osteosynthesis. In 1948, Palmer popularized his method of open reduction using a lateral approach with bone grafting. Used extensively in Europe, Palmer’s method was slow to catch on in the United States. Operative fixation of calcaneal fractures in the United States focused on primary subtalar arthrodesis alone or triple arthrodesis. In 1943, Gallie first described primary subtalar arthrodesis [1]. These four treatment options — conservative management, closed reduction, open reduction, and primary arthrodesis continue to be viable treatment alternatives today.

II.

ANATOMY

The calcaneus is the largest of the tarsal bones, with articular surfaces for the talus and the cuboid bone (Figure 4.1). The calcaneus can be divided into an anterior half and a posterior half. The anterior half contains the four articular facets — the articulating surface for the cuboid bone and the anterior, middle, and posterior facets for the talus. The posterior facet is the largest of these surfaces. It is convex in shape and is the major weight-bearing surface of the calcaneus. The middle facet is located on the sustentaculum tali, a broad process that projects from the medial portion of the calcaneus toward the talus. The middle facet is concave in shape and usually is contiguous with the anterior facet, also concave in shape and usually located just lateral to the middle facet. The calcaneus has important ligamentous and tendinous relationships. Laterally, the peroneal tendons run between the calcaneus and the lateral malleolus. These tendons can be impinged on by the lateral wall fragment after fracture of the calcaneus. The flexor hallucis longus tendon runs on the undersurface of the sustentaculum tali and can be damaged during repair of the fracture. The tibial nerve, artery, and tendon also are associated with the medial wall, making internal fixation from a medial approach difficult. The interosseous ligament lies in the interosseous sulcus (calcaneal groove), which is located between the posterior and middle facets. Together with the thick medial talocalcaneal ligaments, the interosseous ligament persistently holds the sustentaculum tali in position during calcaneus fractures [3,4]. The calcaneus has a thin cortical shell and is composed mostly of cancellous bone. The exceptions include the cortical thickening that supports the posterior facet (known as the thalamic portion), the dense cortical bone in the sustentaculum tali, and the thick cortex in the angle of Gissane [5]. The pattern of trabeculae reflects the static and dynamic strains to which the bone is exposed repeatedly. Traction trabeculae radiate from the inferior cortex, whereas compression trabeculae converge to support the posterior and anterior facets. The middle or neutral triangle of sparse trabeculae is the area through which the blood vessels traverse [6]. The normal anatomy of the calcaneus contributes to the primary functions of the calcaneus. Normal calcaneal structure provides a foundation for transmission of the body’s weight down through the tibia, ankle, and subtalar joints. The normal vertical-support function of the calcaneus depends on its normal alignment beneath the weight-bearing line of the tibia. Displacement of the body of the calcaneus can result in eccentric weight distribution in the foot and deformities about the ankle joint. Normal anatomy also provides structural support for the maintenance of normal lateral column length. Lateral column length affects abduction and adduction of the midfoot and forefoot and assists in supination of the foot to provide strong push-off during gait. The calcaneus also provides a lever arm to increase the power of the gastrocnemius–soleus mechanism [7].


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Right foot Posterior articular surface for talus

Anterior articular surface for talus

Middle articular surface for talus Anterior articular surface for talus

Body

Articular surface for cuboid bone

Middle articular surface for talus Posterior articularr surface for talus


Peroneal trochlea

Tuberosity Lateral process of tuberosity

Peroneal trochlea

Sustentaculum tali

Groove for peroneus longus tendon

Body

Lateral view Anterior articular surface for talus

Middle articular surface for talus

Tuberosity

Posterior articular surface for talus


Superior view Middle articular surface Tuberosity

Posterior articular surface

Sustentaculum tali Sustentaculum tali

Tibia

Groove for flexor hallucis longus tendon Medial view

Groove for flexor hallucis longus tendon

Medial process of tuberosity

Medial process of tuberosity

Fibula

Posterior tibiofibular ligament

Deltoid ligament

40⬚

Posterior view

33⬚ to

Posterior talofibular ligament

Lateral process of tuberosity

Tuberosity

Interosseous membrane

Talus

Peroneal trochlea

Tube r angle

Calcaneofibular ligament Peroneal tendons in inferior peroneal retinaculum

Posterior talocalcaneal ligament

Posterior view with ligaments

Critical angle Functional relations of calcaneus

Figure 4.1 Anatomy of the calcaneus. (From Netter, F.H., Atlas of Human Anatomy, Ciba-Geigy Corporation, Summit, NJ, 1994, p. 494. With permission. Reprinted from Orthoped. Clin. North Am., 32, 2001.)

III.

MECHANISM OF INJURY

Fractures of the calcaneus can have many possible configurations, which is a major reason for the inability to develop one consistent classification system. Certain fracture patterns do consistently develop, however, and have been described in the past. Low-energy injuries result in nondisplaced


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or minimally displaced fractures. High-energy injuries result in more comminuted and intraarticular fractures [8]. These fractures result from shear and compressive forces. Intra-articular fractures occur after eccentric axial loading of the talus on the calcaneus. A primary shear fracture line parallel to the posterolateral edge of the talus is produced [9]. This line divides the calcaneus into two parts — a posterolateral (tuberosity) fragment and an anteromedial (sustentaculum or constant) fragment (Figure 4.2). The fracture line varies in location from the calcaneal sulcus to the lateral portion of the posterior facet but is always posterior to the interosseous ligament. This position allows the anteromedial fragment to remain connected to the talus, which is an important concept for reconstruction [10]. The exact position of the fracture line depends on the position of the foot at impact. If the foot is in valgus, the fracture occurs more laterally. As the foot becomes more varus, the fracture line tends to shift medially [3]. Secondary fracture lines may develop off of this primary line. The most common is the posterior fracture line, which divides the calcaneus into anterior and posterior fragments. This secondary line is a result of

Figure 4.2 Mechanism of injury. (A) Application of force. (B) Displacement with the sustentaculum tail (the constant fragment) following the talus and the tuberosity fragment shifting laterally. Classic fracture patterns of Essex–Lopresti: (C) joint depression; (D) tongue type. (From Sanders, R., Hansen, S.T., and McReynolds, I.S., Fractures of the calcaneus, in Disorders of the Foot, Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1991, p. 2328. With permission. Reprinted from Orthoped. Clin. North Am., 32, 37, 2001.)


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axial loading of the anterolateral process of the talus on the calcaneus. The compressive force usually starts at the angle of Gissane and continues medially. The thalamic fragment, which is the depressed portion of the posterior facet, is created. This fragment varies in size depending on the posterior exit point of the secondary line and whether the loading is more horizontal or vertical. In the horizontal type, the fracture line exits superiorly just behind the posterior facet. This mechanism is believed to be responsible for the central depression type of fracture proposed by Essex–Lopresti. In the vertical type, the line exits posteriorly above the Achilles tendon insertion, producing the tongue type fracture proposed by Essex–Lopresti [3,8–11]. With more severe intra-articular fractures, the talus can drive the thalamic fragment into the cancellous bone of the calcaneus body fragment, shearing the attachment of the thalamic fragment from the lateral wall and causing a blowout fracture. The resultant lateral wall bulge impinges on the fibulocalcaneal space, predisposing it to fibulocalcaneal impingement and peroneal tendon entrapment [9]. The fracture pattern on the lateral wall in the sagittal plane typically produces an inverted Y pattern, with the exact orientation of the posterior limb varying among fractures (Figure 4.3). It can project horizontally toward the tuber as in the tongue type fracture, or it can extend vertically as in the joint depression type fracture [3]. The calcaneus loses length as a result of the muscular attachments to the various fragments. The body fragment, released from its attachment anteriorly, loses it alignment and pitch as it tilts into varus and is pulled proximally by the Achilles tendon. As the calcaneal pitch collapses, the calcaneal length and Achilles tendon fulcrum shorten. Secondary fracture lines extending anteriorly may enter the plantar aspect of the calcaneus or penetrate the calcaneocuboid joint, allowing the arch to collapse further [9]. The forces that produce the fracture patterns also are responsible for the various soft tissue injuries incurred with calcaneus fractures. A stretch, shearing injury usually is sustained on the medial side, and a compression injury usually occurs on the plantar aspect. The lateral soft tissues are relatively spared. The fracture blisters are seen more commonly on the medial side, and hemorrhage is seen more commonly on the plantar aspect [9]. The fracture patterns lead to many problems that become the goals of treatment. The posterior facet is depressed, resulting in a flattening of Bohler’s angle and an overall loss of height of the calcaneus. The superomedial border, which may include a portion of the posterior facet, is avulsed. The lateral wall is spread apart, which leads to an overall increase in calcaneal width. The calcaneal length is also shortened secondary to the above-described reasons [9,12].

Anterolateral fragment

Calcancocuboid joint

Figure 4.3 Continuation of the anteroposterior dividing fracture line on the lateral wall. Note the anterolateral fragment. This inverted ‘‘Y’’ pattern was also noted by Soeur and Remy. The dotted line depicts a variation commonly seen with joint depression fractures. (From Carr, J.B., Hamilton, J.J., and Bear, L.S., Foot Ankle, 10, 85, 1989. With permission. Reprinted from Orthoped. Clin. North Am., 32, 38, 2001.)


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CLASSIFICATION

There have been many attempts to develop a universally accepted classification scheme for calcaneus fractures. An ideal classification system would incorporate fracture anatomy and the mechanism of injury and predict the correct course of treatment and outcome. Because controversies remain regarding the most appropriate treatment courses and their respective outcomes, debate continues over the most appropriate classification system. The first widely accepted classification system was proposed by Essex–Lopresti in 1952 (see box below). Fractures were divided into those that involved the subtalar joint and those that did not. Of the fractures that involved the subtalar joint, the two main types were the tongue type fractures and the joint depression fractures described previously.

Essex–Lopresti classification 1.

2.

Not involving subtaloid joint A. Tuberosity fracture . Beak type . Avulsion medial border . Vertical . Horizontal B. Involving calcaneocuboid joint . Parrot nose type . Various Involving subtaloid joint A. Without displacement B. With displacement . Tongue type, with displacement . Centrolateral depression of joint . Sustentaculum tali fracture alone . With comminution from below (including severe tongue and joint depression type) . From behind forward with dislocation subtaloid joint

Soeur and Remy [13] devised a classification system for intra-articular fractures in 1975 based on the mechanism of injury. They believed that the thalamic fragment was the key to repair. The thalamic portion of the calcaneus was the part of the bone, formed of a layer of compact bone tissue, that supports the posterior articular facet and continues forward, becoming thinner toward the groove of the sinus tarsi. Fractures were divided into those caused by direct vertical compression and those caused by shearing or a combination of shearing and compression. Stephenson [14,15] modified the classification system initially proposed by Warrick and Bremner in 1953. This system is based on the mechanism of injury, the location of a primary sagittal fracture line that divides the bone, and the number of major fracture fragments that are displaced (Figure 4.4). The mechanism of injury is a result of shear or compressive forces or a combination of the two. With the advent of the computed tomography (CT) scan, new classification systems were developed to assist in the diagnosis of calcaneus fractures. Crosby and Fitzgibbons [16] initially proposed a simple three-level CT classification based on the posterior facet. Type I fractures were those in which the posterior facet fragments were nondisplaced or minimally displaced. The intraarticular fracture extended through the posterior facet, and there was less than 2 mm of diastasis or depression of the fragments or both. Type II fractures were those in which the facet fragments were displaced but not comminuted. The intra-articular fracture extended through the posterior articular facet, and there was 2 mm or more of diastasis or depression of the fragments or both. Type III fractures had a comminuted posterior facet. Crosby and Fitzgibbons [16] believed this classification system could predict the prognosis accurately. Type I fractures generally did well with closed treatment, type II had mixed results, and type III generally did poorly.


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Primary fracture Superior

Lateral

Two-part fracture Shear Lateral

Coronal

Compression Superior

Coronal

T

Lateral

T

1

T

1

1 Joint depression

2

Extra-articular

Coronal

2

3 2

Intra-articular

Tongue

Three-part fracture Shear−compression Lateral

Coronal

T Joint depression

1

3 2

Tongue

Figure 4.4 Types of fractures. The differences in the patterns of the fractures, moving from the top to the bottom of the figure, are the result of increasing injuring forces. The heavy solid lines show the primary fracture, as described by Essex–Lopresti. This is an intra-articular fracture that involves the posterior facet. The heavy dashed lines show the other paths that the primary sagittal fracture may take, either lateral to the posterior facet or along the calcaneal sucus medial to the facet. The fracture line that goes thorough the calcaneal sulcus is through a nonarticulating portion of the subtalar joint, but this fracture is considered to be intra-articular. The narrow dashed lines show the outlines and positions of the displaced fragments in the two- and three-part fractures. Note that the two- and three-part shear– compression fractures (shown only as lateral views and as coronal sections through the posterior facet of the talus and the posterior facet of the calcaneus) may be one of two types, either a joint depression or a tongue fracture. In the two-part compression fracture, the superomedial fragment (1) and the fragment of the tuberosity (2) are present, separated by the undisplaced sagittal fracture that is visible only in the coronal plane. However, they are considered as one fragment (of a two-part fracture) for purposes of classification and treatment. If greater force is applied to a supinated foot, the fragment of the tuberosity (2) may be displaced superiorly with respect to the superomedial fragment (1), and then there is a threepart compression fracture (not illustrated). T, talus; 1, superomedial fragment; 2, fragment of the tuberosity; and 3, the fragment of the posterior facet. (From Stephenson, J.R., J. Bone Jt. Surg. — U.S. edition, 69, 117, 1987. With permission. Reprinted from Orthoped. Clin. North Am., 32, 39, 2001.)


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Sanders et al. [17] proposed a classification system based on coronal and axial CT scan sections (Figure 4.5). Using the section with the widest undersurface of the posterior facet of the talus, the talus is divided into three equal columns by two lines, A and B. These two lines separate the posterior facet of the calcaneus into three potential pieces: a medial, a central, and a lateral column. A third fracture line, C, corresponding to the medial edge of the posterior facet of the talus, separates the posterior facet from the sustentaculum and results in a total of four potential pieces. The lines are named A, B, and C from lateral to medial because as the fracture line moves medially, intraoperative visualization of the joint becomes more difficult, and the ability to obtain an anatomic reduction decreases. All nondisplaced articular fractures, regardless of the number of

A B C

C

A

Type IIA

A B

III AB

B

Type IIB

A

C

III AC

Type IIC

B C

III BC

A B C

Type IV

Figure 4.5 CT scan classification of intra-articular calcaneal fractures. (From Sanders, R., Fortin, P., DiPasquale, T. et al., Clin. Orthoped., 290, 89, 1993. With permission. Reprinted from Orthoped. Clin. North Am., 32, 41, 2001.)


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fracture lines, are considered type I fractures and benefit from early motion without the need for operative intervention, unless there is an extra-articular component that is severely displaced. Type II fractures are two-part fractures of the posterior facet, similar in appearance to a split fracture of the tibial plateau. Three types — IIA, IIB, and IIC — exist, based on the location of the primary fracture line. Type III articular fractures are three-part fractures that feature a centrally depressed fragment, similar to a split-depressed tibial plateau or die-punch distal radial fracture. Types include IIIAB, IIIAC, and IIIBC. Type IV articular fractures are highly comminuted. Often, more than four articular fragments exist [8,17,18].

V.

INITIAL PRESENTATION

Fractures of the calcaneus usually are a result of direct axial loading onto the calcaneus by the talus. A small percentage may result from twisting forces. In most series, the cause of these fractures is a fall from a height, although motor vehicle accidents as a cause is increasing in incidence. The most common symptom indicating a fracture is pain over the heel region. The most common signs of a fracture include tenderness, swelling, ecchymosis, and distortion of the normal anatomy around the heel. Although not pathognomonic for calcaneal fractures, plantar ecchymosis is specific for these fractures [19]. The skin blistering that commonly is seen usually occurs within the first 36 hours after injury [20]. Because of the powerful forces required to produce fractures of the calcaneus, associated injuries are frequent, with fractures of the extremities being the most common. Ten percent of cases have associated spinal injuries, with most occurring in the lumbar region [21]. Approximately 10% of calcaneal fractures also develop compartment syndromes, and of these, half develop clawing of the lesser toes and other foot deformities, including stiffness and neurovascular dysfunction [22].

VI.

INITIAL MANAGEMENT

At the time of initial presentation, the patient’s foot should be placed in a Jones dressing and foot pump to reduce the amount of swelling. A posterior splint should be applied and the leg elevated to minimize swelling and prevent blister formation. Surgery should be postponed in the event of blister formation or excessive swelling until the wounds epithelialize and the skin passes the wrinkle test. The skin on the lateral surface of the heel should wrinkle along the normal skin creases on dorsiflexion and eversion of the foot. Historically, it takes approximately 1 week for the edema to decrease and for the patient to pass the wrinkle test. In some patients, it may take 2 to 3 weeks for the skin to wrinkle. The use of a pneumatic compression device has been reported to decrease the time to surgery [23,24] 47. Open fractures require immediate irrigation and debridement. Compartment syndrome recognition requires immediate surgical release. After irrigation and debridement of an open fracture, an external fixator is placed. The external fixator frequently can restore the length, width, and height of the calcaneus. The articular reduction is not usually corrected at this time, however. Depending on the soft tissue damage, a staged open reduction may be planned. In the event of a massive contaminated wound, it may be prudent to close the soft tissue over antibiotic beads in preparation for a staged reconstruction.

VII.

RADIOGRAPHIC EXAMINATION

When a fracture of the calcaneus is suspected, standard radiographs usually are obtained. These include a lateral view of the hindfoot, a dorsal plantar anteroposterior projection, and an axial view of the heel. The lateral view usually confirms a fracture and is used to measure Bohler’s and Gissane’s angles. The anteroposterior view of the foot can show a fracture into the calcaneocuboid joint or a lateral wall bulge. The axial view shows the calcaneal tuberosity, the sustentaculum tali, and, to variable degrees, the posterior facet (Figure 4.6).


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Figure 4.6 (A) Lateral view of the calcaneus shows loss of Bohler’s and Gissane’s angles. (B) Axial view of the calcaneus. (C) Mortise view of the calcaneus shows the posterior facet of the calcaneus. (Reprinted from Orthoped. Clin. North Am., 32, 43, 2001. With permission.)

Additional radiographic views can be obtained to visualize individual joint surfaces. Of these, Broden’s view, used to visualize the posterior facet, is the most common (Figure 4.7) [9]. It is obtained in the following manner. The patient is placed supine, with the foot placed in neutral flexion with the leg internally rotated 30 to 408. The x-ray beam is centered over the lateral malleolus, and four views are taken with the tube angled 40, 30, 20, and 108 toward the head. The pictures result in views that show the posterior facet as it moves from posterior to anterior, with the 108 view showing the posterior portion of the facet and the 408 view showing the anterior portion. Although no longer routinely obtained preoperatively, Broden’s view can be used intra-


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X-ray

10⬚ 20⬚ 30⬚ 40⬚

Cassette

Figure 4.7 Technique of obtaining Broden’s views of the calcaneus. The foot is rotated 458 inward and films are obtained at 10, 20, 30, and 408 distal to the perpendicular, with the beam centered on the sinus tarsi. (From Burdeaux, B.D., Clin. Orthoped., 177, 87–103, 1983. With permission. Reprinted from Orthoped. Clin. North Am., 32, 44, 2001.)

operatively to assess realignment of the posterior facet using intraoperative fluoroscopy [25]. Another standard radiograph that is obtained easily is the mortise view of the ankle. This view shows the posterior facet of the calcaneus well (Figure 4.8). The authors rely on the lateral radiograph of the foot and mortise view of the ankle as the plain radiographs of choice. The lateral view gives adequate information about Bohler’s and Gissane’s angles. The mortise view shows the posterior facet nicely. Both can be taken without much discomfort for the patient. Bohler’s angle, usually between 20 and 408 is formed by two lines. The first line is drawn from the highest point of the anterior process of the calcaneus to the highest point of the posterior facet. The second line runs tangential to the superior edge of the tuberosity (Figure 4.9). The crucial angle of Gissane is formed by two strong cortical struts that extend laterally and form an obtuse angle. The first strut extends along the lateral border of the posterior facet, and the second extends anteriorly to the beak of the calcaneus [18,23] (Figure 4.10). Because of the positioning required in multiple planes in the setting of acute pain, these standard radiographs sometimes can be difficult to obtain. The ability to visualize adequately the joint surfaces was also a major limitation of standard radiographs. The CT scanning is a crucial adjunct to standard radiographs in the diagnosis and treatment of calcaneal fractures. The CT scan allows for better visualization of joint alignment, number, and positioning of fracture fragments, and injuries to the nearby soft tissues. A CT scan of the fracture can be obtained in the following manner. The patient is placed in the supine position with the hips and knees flexed. The feet are kept together with both feet routinely scanned for comparison. A lateral scout film can be obtained to position the patient until the coronal sections are perpendicular to the posterior facet. An oblique 308 coronal plane usually is required because of the angles of the facets. The posterior facet usually forms an angle of 508 with the longitudinal axis of the calcaneus, whereas the middle facet forms a slightly steeper angle of 608. This coronal view not only gives information about the posterior facet, but also the sustentaculum tali, the shape of the heel, and the position of the peroneal and flexor hallucis tendons. The second view obtained is the transverse view, which is 908 to the coronal view and parallel to the long axis of the foot. This view provides information about the calcaneocuboid joint, the anteroinferior aspect of the posterior facet, the sustentaculum tali, and the lateral wall [25,26].


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Figure 4.8 (A) Lateral, (B) Harris axial, and (C) mortise views clearly demonstrating the posterior facet reduction of the calcaneus. (Reprinted from Orthoped. Clin. North Am., 32, 45, 2001. With permission.)

VIII. DEFINITIVE MANAGEMENT The optimal management for calcaneal fractures has been difficult to determine in the past. Without a consistent classification system and a uniform system for comparing results, comparisons of the various treatment modalities could not be undertaken. Most physicians have agreed on the treatment of extra-articular fractures, which generally have a more favorable result than the treatment of intra-articular fractures [27].

A.

Extra-Articular Fractures

The most common types of extra-articular fractures are those that involve the anterior process and those that involve the tuberosity. The anterior process fractures can be divided further into avulsion


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Figure 4.9 Bohler’s angle. (Reprinted from Orthoped. Clin. North Am., 32, 47, 2001. With permission.)

fractures and compression fractures. Avulsion fractures are the more common of the anterior process fractures. They frequently are misdiagnosed as ankle sprains because the point of maximum tenderness is located over the sinus tarsi adjacent to the anterior talofibular ligament. The mechanism of injury also is similar to the mechanism that produces a lateral ankle sprain. These fractures occur as a result of adduction and plantar flexion of the foot, which places stress on the bifurcate ligament that connects the anterior process to the cuboid and navicular bones. The options for treatment of avulsion fractures are various, but most clinicians agree that optimal treatment is nonoperative. Recommendations include a woven elastic (Ace) bandage and crutches for 2 weeks, non-weight-bearing and short leg cast for 4 weeks, and non-weight-bearing for 8 weeks. The authors usually place patients in a short leg cast for 4 weeks followed by range-of-motion exercises.

Figure 4.10 permission.)

Gissane’s angle. (Reprinted from Orthoped. Clin. North Am., 32, 47, 2001. With


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These fractures may take 1 year to become asymptomatic [28,29]. The criteria used for operative treatment, which includes excision or open reduction and fixation, is the size of the avulsed fragment and the degree of symptoms. Fragments greater than 2 cm generally require operative treatment. Fractures of the tuberosity classically were divided into beak fractures and avulsion fractures. Watson Jones initially described direct trauma as the cause of beak fractures and the strong pull of the Achilles tendon as the cause of avulsion fractures. This theory was supported by the belief that the Achilles tendon did not insert on the most superior aspect of the tuberosity where beak fractures occurred. More recently, it has been shown that in some individuals, the Achilles tendon can insert into the superior aspect of the tuberosity [30,31]. Avulsion is believed to be the mechanism for any part of the tuberosity, including beak fractures. Treatment of tuberosity fractures depends on the amount of displacement of the fracture fragment. Minimally displaced fractures can be treated by nonoperative means, whereas displaced fractures require open reduction and fixation [30,31]. Displaced tuberosity fractures with skin tenting can lead to skin necrosis and sloughing as a result of the strong pull of the Achilles tendon on the bone. These fractures should be treated emergently with an external fixator to counter the pull of the Achilles tendon.

B.

Intra-Articular Fractures

The treatment of intra-articular fractures is controversial. Nonoperative treatment continues to be the preferred method for undisplaced fractures. Displaced and comminuted fractures can be treated conservatively without reduction and early range of motion, with closed reduction, with primary arthrodesis — subtalar or triple — or with open reduction and internal fixation (ORIF). The authors routinely use as indications for operative treatment Sanders types II through IV. Type II and III fractures require ORIF as described subsequently. Type IV fractures require primary arthrodesis or a salvage procedure. Patients with relative contraindications for primary reduction and fixation include patients with open fractures, smokers, diabetics, and patients with severe osteopenia. The outcomes of the different treatment methods have been examined with differing opinions. Lowery [32] examined the results of the different treatment options from various authors with the percentages of satisfactory and unsatisfactory results (Table 4.1). ORIF has become an increasingly popular method for treatment of intra-articular fractures. The difference in outcomes between operative and nonoperative treatment has yet to be shown fully, however. Kundel et al. [33] examined two groups of matched cohorts based on plain films and the Essex–Lopresti classification. They found no difference between the groups with regard to pain, gait, or footwear. The only significant advantage of operative treatment was return to previous occupation. Buckley and Meek [34] examined two matched groups according to the Essex–Lopresti classification system. They found no difference in pain, subtalar motion, and return to work. The overall result was better, however, in the operative fractures if the posterior facet was anatomically reduced. Thordarson and Krieger [24], using the Sanders CT classification system in a prospective, randomized study, showed superior results in operative vs. nonoperative treatment. The operative group had less pain, fewer restrictions in daily activity, walking ability, exercise ability, and ability to work. The most recent study examining the results of operative and nonoperative treatment is Buckley et al. [35]. In a prospective, randomized, controlled multicenter trial, they assessed the results from 309 patients after a 2-year follow-up. Patients were randomized to either nonoperative or operative treatment. Nonoperative treatment involved no attempts at closed reduction, and the patients were treated only with ice, elevation, and rest. Operative treatment involved a standard protocol of a lateral approach and rigid internal fixation. The outcomes as measured on the Short Form-36 (SF-36) and a visual analog scale (VAS) were not found to be different between the two groups. The score on the SF-36 was 64.7 and 68.7, respectively, and the score on the VAS was 64.3 and 68.6, respectively. However, if the patients receiving Workmen’s Compensation (157 patients — 37%) were removed, the outcomes of certain groups were improved with operative intervention. The groups that did better with surgery included women, younger patients, and patients with a light-tomoderate workload.


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Table 4.1 Results of Calcaneal Fracture Treatment* Treatment and First Authory Primary arthrodesis Zayer65 Subtalar Triple Pennal40 Thompson60, 61 Triple Noble37 Lindsay30 Hall20 No reduction Zayer65 Pozo43 Bertelsen3 Lindsay30 Closed reduction Omoto38 Herman24 Aitken1 Bertelsen3 Cotton12 Reuter14 Crosby (all types)13 Percutaneous reduction Pescatori (llizarov)42 Essex-Lopresti15 Reuter (Essex-Lopresti)44 Open reduction Zayer65 Harding21 Stephenson59 Stephenson58 Ross4 Tongue type Joint depression Romash45 Palmer39 Reuter44 Lateral approach Medial approach Beze4 Letronel29 Zwipp67 Sanders50 Type II Type III Type IV Hutchinson25 Eberle14

% Satisfactory

% Unsatisfactory

0 50 76

100 50 24

95 56 60 74

5 44 40 26

22 67 100 76

78 33 0 24

91 73 75 100 50 45 13

9 27 25 0 50 55 47

78 60 58

22 40 42

43 75 77 86

57 25 23 14

87 67 70 96

13 33 30 4

88 57 85 90 93

12 43 15 10 7

73 70 11 76.6 73

27 30 89 22.4 27

*Treatment results are listed according to treatment method; Subclassifications are noted below the author’s name. y See original source of table for complete references for authors listed. From Lowury RB: Fractures of the calcaneus. Foot Ankle Int 17:230-235, 1996; with permission.


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Independent predictors of satisfaction, regardless of the treatment, included patients with a Bohler’s angle of 15 to 368, no subsequent arthrodesis, a non-work-related injury, and a unilateral injury. Patients who required a subtalar arthrodesis were not included in the study. However, it was found that a nonoperatively treated patient was 5.5 times as likely than an operatively treated patient to require a subtalar arthrodesis.

IX.

SURGICAL APPROACH

A.

Lateral Approach

An extensile L- or J-shaped lateral approach is made with the patient in the lateral position. The surgery involves elevating the entire soft tissue envelope off the lateral aspect of the calcaneus with the flap containing the peroneal tendons, sural nerve, and calcaneofibular ligament. It allows visualization of the entire wall of the calcaneus and the posterior facet of the subtalar joint. Kirschner wires, size 0.062, are placed as retractors in the fibula, the talar neck, and the cuboid bone to maintain the notouch technique of flap retraction. The medial wall is not visualized directly using this technique, but the authors have used this approach with greater than 0% effectiveness. The medial approach (as noted subsequently) is used for isolated sustentacular fractures [10].

B.

Medial Approach

Burdeaux [36,37,45] recommended a medial approach initially popularized by McReynolds in 1958. This approach is based on the principle of restoring the medial wall of the calcaneus. He believed an accurate reduction produced stability, restored length and height, and partially restored width. Burdeaux advocated a straight 8- to 10-cm incision made over the medial heel parallel to the sole, about halfway between the medial malleolus and the bottom of the foot. The fascia is divided in the line of the skin incision, and the neurovascular bundle is dissected free. The bundle is drawn aside, revealing the sustentacular fragment below. The sustentacular spike overrides the tuberosity fragment, which is displaced laterally, forward, and upward. A blunt elevator is used between the spike and the tuberosity fragment and passed to the lateral side. The joint depression type or tongue type fragment is elevated, and the posterior facet is reduced indirectly. The tuberosity fragment is reduced to the sustentacular fragment. If the fragments are not reduced fully from the medial side, a lateral incision can be made. The reduction is maintained by the use of a staple or a Steinmann pin or screw drilled through the tuberosity fragment, then into the thickest part of the sustentacular fragment. If the pin or screw is used alone, the need for exposure of the neurovascular bundle in the medial incision is eliminated. Burdeaux [36,37] pointed out that the difficulty of reduction increased with the degree of comminution. The medial reduction technique requires a stable sustentacular fragment to which an intact tuberosity fragment is reduced. The two different approaches have advantages and disadvantages. The medial approach involves accurate reduction of the medial wall and better bone quality for fixation but blind reduction of the posterior facet joint and manual compression of the lateral wall of the calcaneus. There is a greater potential for injury to the neurovascular bundle with the medial approach than with the lateral approach. The lateral approach allows direct visualization of the lateral wall and the posterior facet joint and more room for fixation. If the primary fracture line is intra-articular, however, visualization of the medial fragment of the posterior facet joint is difficult. The possibility of residual hindfoot varus also exists because of the inability to reduce the medial wall [9,38].

X.

PREFERRED METHOD OF TREATMENT

A CT scan is obtained preoperatively and the Sanders classification is used. The patient is placed in the lateral decubitus position, with a pneumatic tourniquet placed around the thigh to allow better visualization intraoperatively. Bilateral fractures are prepared and draped in the prone position. A lateral extensile approach is used, as described earlier, along with the no-touch technique of flap retraction to protect the peroneal tendons and sural nerve. This approach usually is adequate for


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visualization of the subtalar joint, the posterior facet, and the lateral wall of the calcaneus. After exposure of the lateral wall and subtalar joint, the fracture anatomy can be determined. A small elevator can be used to explore and manipulate the fracture fragments using the CT scan as a guide. The posterior tuberosity is reduced first to reestablish heel height and varus–valgus alignment of the heel. This reduction usually is done indirectly with a large threaded pin placed transversely in the tuberosity fragment to manipulate the fragment (Figure 4.11). The reduction of this fragment is maintained temporarily with Kirschner wires. The lateral posterior facet fragment then can be reduced to the constant fragment. Intraoperative fluoroscopy to obtain a mortise view or Broden’s view is used to determine the accuracy of the reduction of the posterior facet. The anterior aspect of the calcaneus, including the calcaneocuboid joint, then should be addressed. The lateral wall can be reconstructed and fixed with a low-profile plate (see Figure 4.8). A bone graft is not used routinely unless there is a large defect and the fracture is more than 2 weeks old. An allograft is used when necessary. A drain is used beneath the flap to prevent accumulation of a hematoma. The technique of Allgower and Denotti is used to close the flap [39].

XI.

POSTOPERATIVE MANAGEMENT

Patients are placed in a splint, and range of motion is delayed until suture removal. After suture removal, the patient is placed in a fracture boot with early, aggressive range of motion of the ankle and subtalar joint. The use of nonsteroidal anti-inflammatory drugs and smoking are discouraged until the fracture has healed. Weight-bearing is delayed for 8 to 12 weeks, depending on the amount of initial comminution. Return to heavy labor and clinical improvement with respect to pain and swelling can be expected in 6 to 12 months, with maximum medical benefit at 18 months after injury or surgery.

XII.

COMPLICATIONS

Complications after calcaneus fractures can be divided into two categories — early and late. Early complications include fracture blisters and compartment syndrome. Fracture blisters should be debrided and allowed to epithelialize before surgical intervention [7,8]. Compartment syndrome or suspicion thereof should be followed with immediate fasciotomy. The clinical consequences of an untreated compartment syndrome include clawing of the lesser toes, stiffness, aching, weakness, sensory changes, atrophy, and fixed deformities of the forefoot [22]. The only reliable method of diagnosis is through clinical suspicion, but a self-contained needle manometer system (Quikstik, Stryker, Kallamazoo, MI) also is used commonly to measure compartment pressures [22,23]. Decompression of the compartments of the foot can be accomplished through incisions described by Myerson and Manoli [22]. The calcaneal compartment is released by a hindfoot incision that begins 4 cm anterior to the posterior portion of the heel and 3 cm from the plantar surface, and it is approximately 6 cm long, paralleling the sole of the foot. The incision may be extended proximally to decompress the entire tibial neurovascular bundle. The fascia overlying the abductor hallucis muscle is seen, directly in line with the incision. The medial compartment is released as the fascia is opened. The abductor hallucis muscle is stripped from its overlying fascia and retracted superiorly. This retraction reveals the dense white fascial layer of the medial intermuscular septum, which releases the calcaneal compartment when incised. Care must be taken during this incision because the lateral and medial plantar nerve and vessels lie just below the septum. Two dorsal incisions should be used to release the other compartments of the foot [22,23]. Late complications include wound dehiscence, wound infection, subtalar arthritis, lateral impingement syndrome, and sural neuritis. Wound dehiscence may occur 4 weeks postoperatively. Infections must be debrided. Smokers have a high incidence of wound complications as well as delayed union. Abidi et al. [40] looked at the risk factors for wound healing and found that there were more complications after single-layered closure, high body mass index, extended time between injury and surgery, and smoking. Other variables previously believed to affect wound healing were found to have no effect, including age, tourniquet time, type of immobilization, type of bone graft,


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Fracture pattern Calcaneus fracture pattern lateral view

Typical calcaneal fracture pattern lateral view

Impacted posterior facet

Lateral wall Sustentacular fragment (constsant fragment)

Hindfoot varus

C-arm

Kirschner traction bow Bump or

Schantz pin on T-handle with comminution of tuberosity

Figure 4.11 Authors’ preferred method. (From Foot and Ankle Disorders: Tricks of the Trade, Theim Medical and Scientific Publishers, New York 2003, pp. 120–126. With permission.)


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Surgical exposure Kirschner wire retractors

Full-thickness skin flap

Trick: Use traction to unlock varus angulation and disimpact medial and lateral wall

Kirschner traction bow

Reduction of posterior facet Trick: Elevator jacks up the posterior facet

Trick: Remove lateral wall to access posterior facet

Trick: Use traction and valgus angulation to restore hindfoot alignment

Pitfall: Failure to correct varus deformity

Figure 4.11

Continued Authors’ preferred method.


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Trick: Thumb pressure reduces lateral wall bulge

Pitfall: Residual defect is left when the impacted posterior facet is elevated to anatomic position

Provisional fixation

Posterior facet fixed to constant fragment Posterior facet fixed to body

Optional bone autograft or allograft

Posterior facet fixed to constant fragment with .045 Kirschner wires

Body to posterior facet fixed with .062 Kirschner wires

Figure 4.11



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Completed fixation

Calcaneal fracture fixed with calcaneal plate and screws

Pitfalls: Forty cancellous lag screws 1. Difficult removal due to no back cutting 2. Large threads do not grip small fragments 3. Screw failure when junction near fracture line (shear line) Cannulated screws 1. Expensive 2. Guide-system problems 3. Large screw heads 4. Reduced bite

Trick: Fully threaded smaller cortical screws provide better bite (2.7 to 3.5 mm). Must lag with glide hole

Hardware placement for primary subtalar fusion Primary subtalar fusion

Trick: 1. Use fully threaded screws to prevent collapse 2. May use one 6.5 mm and one 3.5-mm screws for smaller area

Figure 4.11



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use of a drain, and diabetes. Subtalar arthritis should be treated conservatively initially through activity change, shoe modifications, and anti-inflammatory medications. Subtalar or triple arthrodesis should be considered if these means fail. Benirschke and Kramer [42] examined the rate of infection following calcaneal fractures treated with ORIF via an extensile lateral approach. Of the 341 closed fractures, only 1.8% of the fractures experienced serious infections that required intervention beyond oral antibiotics.

XIII.

OPEN CALCANEAL FRACTURES

Open calcaneal fractures are rare. As a result, there have been few studies on the outcomes of treatment of these fractures. The few studies in the literature are retrospective and limited in the number of patients. Aldridge et al. [42] reviewed 19 consecutive open fractures. These patients were treated with intravenous antibiotics, tetanus prophylaxis, and immediate and repeat irrigation and debridement. Definitive stabilization with ORIF (17 of 19 patients) was delayed by an average of 7 days. Average follow-up was 26.2 months. Five patients required free-tissue transfer for wound coverage. For the five Gustilo type I injuries, no patients developed an infection. The complication rate for Gustilo type II and III injuries was 11%. One of the eight type II injuries and one of the six type III injuries developed osteomyelitis. The latter required a below-knee amputation. Benirschke and Kramer [42] reviewed his series of 39 open calcaneal fractures. Average follow-up was 3.1 years. The patients were treated with ORIF via an extensile lateral approach. Three of the 39 patients (7.7%) developed infections. These resolved with hardware removal and antibiotics. Heier et al. [43] reported on 43 open fractures in 42 patients. They found a significantly higher infection rate of 37%, with osteomyelitis in 19% of the fractures. The open fractures were initially treated with intravenous antibiotics and immediate and repeat irrigation and debridement. Definitive fixation for 29 fractures was delayed at an average of 7.3 days. Fourteen fractures were treated nonoperatively. The Gustilo type I injuries had no infections. Three of the eight Gustilo type II injuries developed an infection with one case of osteomyelitis. Three of the 12 Gustilo type IIIA fractures developed an infection with one case of osteomyelitis. The type IIIB injuries did most poorly. Ten of the 13 fractures developed an infection, with six cases of osteomyelitis and six patients requiring an amputation. It was found that there was no significant association between the use of internal fixation and the development of infection. However, the rates of infection do correlate with the level of soft tissue injury.

XIV.

SALVAGE PROCEDURES

For Sanders type IV and for some type III injuries, primary subtalar fusion is indicated. The indications for fusion of a type III injury depend on the appearance of the articular cartilage of the posterior facet and the judgment of the surgeon. The technique for primary subtalar fusion is identical to ORIF of the calcaneus, but the articular cartilage that remains must be denuded. The subtalar fusion/posterior facet is fixed with one or two fully threaded screws to prevent collapse. [49] The advantage of this approach is that the geometry of the foot is restored (i.e., length, width, height, and valgus alignment). This advantage precludes the need to wait 6 or 9 months to see if the patient will improve, be out of work, or be in pain with a fracture that has a high probability of future fusion. This is a judgment call — but why keep a laborer out of work when the probability is high that a fusion ultimately will be needed? Buch et al. [44] showed that primary subtalar arthrodesis in severely comminuted articular fractures yields results comparable with other methods of fixation with a good return-to-work rate. Twelve of 14 patients returned to work at an average of 8.8 months after surgery.

XV.

CONCLUSIONS

Fractures of the calcaneus are a challenging dilemma. Despite advances in diagnostic and treatment modalities, treatment outcomes have remained the same. Results have been similar to the results of


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past reports by using the Sanders classification. Type II and III injuries treated with ORIF do relatively well. Some type III and IV injuries do relatively poorly whether primary fixation or arthrodesis is used. Patients with relative contraindications for primary fixation include smokers and diabetics. Further research in these areas is required.

REFERENCES 1. Crosby, L.A. and Kamins, P., The history of the calcaneal fracture, Orthoped. Rev., 20, 501–509, 1991. 2. Pennal, G.F. and Yadav, M.P., Operative treatment of comminuted fractures of the os calcis, Orthoped. Clin. North Am., 4, 197–211, 1973. 3. Carr, J.B., Mechanism and pathoanatomy of the intraarticular calcaneal fracture, Clin. Orthopaed., 290, 36–40, 1993. 4. Sanders, R., Hansen, S.T., and McReynolds, I.S., Fractures of the calcaneus, in Disorders of the Foot, Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1991, pp. 2326–2354. 5. Benirschke, S.K. and Sangeorzan, B.J., Extensive intraarticular fractures of the foot: surgical management of calcaneal fractures, Clin. Orthopaed., 292, 128–134, 1993. 6. Harty, M., Anatomic considerations in injuries of the calcaneus, Orthoped. Clin. North Am., 4, 179–183, 1973. 7. Macey, L.R., Benirscke, S.K., Sangeorzan, B.J. et al., Acute calcaneal fractures: treatment options and results, J. Am. Acad. Orthopaed. Surg., 2, 36–43, 1994. 8. Sanders, R., Intra-articular fractures of the calcaneus: present state of the art, J. Orthopaed. Trauma, 6, 252–265, 1992. 9. Paley, D. and Hall, H., Calcaneal fracture controversies: can we put humpty dumpty together again?, Orthoped. Clin. North Am., 20, 665–677, 1989. 10. Letoumel, E., Open treatment of acute calcaneal fractures, Clin. Orthopaed., 290, 60–67, 1993. 11. Carr, J.B., Hamilton, J.J., and Bear, L.S., Experimental intraarticular calcaneal fractures: anatomic basis for a new classification, Foot Ankle, 10, 81–87, 1989. 12. Stephenson, J.R., Displaced fractures of the os calcis involving the subtalar joint: the key role of the superomedial fragment, Foot Ankle Int., 4, 91–101, 1983. 13. Soeur, R. and Remy, R., Fractures of the calcaneus with displacement of the thalamic portion, J. Bone Jt. Surg. Br., 57, 413–421, 1975. 14. Stephenson, J.R., Surgical treatment of displaced intraarticular fractures of the calcaneus, Clin. Orthopaed., 290, 68–75, 1993. 15. Stephenson, J.R., Treatment of displaced intra-articular fractures of the calcaneus using medial and lateral approaches internal fixation, and early motion, J. Bone Jt. Surg. Am., 69, 115–130, 1987. 16. Crosby, L.A. and Fitzgibbons, T., Intraarticular calcaneal fractures. Results of closed treatment, Clin. Orthopaed., 290, 47–54, 1993. 17. Sanders, R., Fortin, P., DiPasquale, T. et al., Operative treatment in 120 displaced intraarticular calcaneal fractures: results using a prognostic computed tomography scan classification, Clin. Orthopaed., 290, 87– 95, 1995. 18. Sanders, R. and Gregory, P., Operative treatment of intraarticular fractures of the calcaneus, Orthoped. Clin. North Am., 26, 203–214, 1995. 19. Richman, J.D. and Barre, P.S., The plantar ecchymosis sign in fractures of the calcaneus, Clin. Orthopaed., 207, 122–125, 1986. 20. Heckman, J.D., Fractures and dislocations of the foot, in Fractures in Adults, Rockwood, C.A., Jr., Ed., Lippincott, Philadelphia, 1991, pp. 2325–2353. 21. Cave, E.F., Fracture of the os calcis — the problem in general, Clin. Orthopaed., 30, 64–66, 1963. 22. Myerson, M. and Manoli, A., Compartment syndromes of the foot after calcaneal fractures, Clin. Orthopaed., 290, 142–150, 1993. 23. Sanders, R., Displaced intra-articular fractures of the calcaneus, J. Bone Jt. Surg. Am., 82, 225–249, 2000. 24. Thordarson, D.B. and Krieger, L.E., Operative vs. nonoperative treatment of intra-articular fractures of the calcaneus: a prospective randomized trial, Foot Ankle Int., 7, 2–9, 1996. 25. Koval, K.J. and Sanders, R., The radiologic evaluation of calcaneal fractures, Clin. Orthopaed., 290, 41– 46, 1993. 26. Segal, D., Marsh, J.L., and Leiter, B., Clinical application of computerized axial tomography (CAT) scanning of calcaneal fractures, Clin. Orthopaed., 199, 114–123, 1985. 27. Kitaoka, I.T.S., Schaap, E.J., Chao, E.Y. et al., Displaced intra-articular fractures of the calcaneus treated nonoperatively: clinical results and analysis of motion and ground-reaction and temporal forces, J. Bone Jt. Surg. Am., 76, 1531–1540, 1994. 28. Degan, T.J., Morrey, B.F., and Braun, D.P., Surgical excision for anterior-process fractures of the calcaneus, J. Bone Jt. Surg. Am., 64, 519–524, 1982. 29. Dodson, C.F., Jr., Fractures of the os calcis, J. Ark. Med. Soc., 73, 319–322, 1977.


116 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47.

Juliano and Nguyen Lowy, M. Avulsion fractures of the calcaneus, J. Bone Jt. Surg. Br., 51, 494–497, 1969. Protheme, K., Avulsion fractures of the calcaneus, J. Bone Jt. Surg. Br., 51, 118–122, 1969. Lowery, R.B., Fractures of the calcaneus, Foot Ankle Int., 17, 230–235, 1996. Kundel, K., Funk, E., Brutscher, M. et al., Calcaneal fractures: operative versus nonoperative treatment, J. Trauma, 41, 839–845, 1996. Buckley, R.E. and Meek, R.N., Comparison of open versus closed reduction of intraartlcular calcaneal fractures: a matched cohort in workmen, J. Orthopaed. Trauma, 6, 216–222, 1992. Buckley, R., Tough, S., McCormack, R. et al., Operative compared with nonoperative treatment of displaced intra-articular calcaneal fractures, J. Bone Jt. Surg., 84-A, 1733–1744, 2002. Burdeaux, B.D., Reduction of calcaneal fractures by the McReynolds medial approach technique and its experimental basis, Clin. Orthopaed., 77, 87–103, 1983. Burdeaux, B.D., The medial approach for calcaneal fractures, Clin. Orthopaed., 290, 96–107, 1993. Hammesfahr, J.F., Surgical treatment of calcaneal fractures, Orthoped. Clin. North Am., 20, 679–689, 1989. Thordarson, D.B., Calcaneal fractures, in Orthopaedic Knowledge Update: Foot and Ankle 2, Mizel, M.S., Ed., American Academy of Orthopaedic Surgeons, Springfield, IL, 1998, pp. 215–228. Abidi, N.A., Dhawan, S., Gruen, G.S. et al., Wound-healing risk factors after open reduction and internal fixation of calcaneal fractures, Foot Ankle Int., 19, 856–861, 1998. Benirschke, S.K. and Kramer, P.A., Wound healing complications in closed and open calcaneal fractures. J. Orthopaed. Trauma, 18, 1–6, 2004. Aldridge, J.M., Easley, M., and Nunley, J.A., Open calcaneal fractures — results of operative treatment, J. Orthopaed. Trauma, 18, 7–11, 2004. Heier, K.A., Infante, A.F., Walling, A.K., and Sanders, R.W., Open fractures of the calcaneus: soft-tissue injury determines outcome, J. Bone Jt. Surg., 85, 2276–2288, 2003. Buch, B.D., Myerson, M.S., and Miller, S.D., Primary subtalar arthrodesis for the treatment of comminuted calcaneal fractures, Foot Ankle Int., 17, 61–70, 1996. Burdeaux, B.D., Fractures of the calcaneus: open reduction and internal fixation from the medial side a 21year prospective study, Foot Ankle Int., 18, 685–692, 1997. Myerson, M. and Quill, G.E., Jr., Late complications of fractures of the calcaneus, J. Bone Jt. Surg. Am., 75, 331–341, 1993. Thordarson, D.B., Greene, N., Shepherd, L. et al., Facilitating edema resolution with a foot pump after calcaneus fracture, J. Orthopaed. Trauma, 13, 43–46, 1999.


5 Lisfranc Injuries and Midfoot Fractures Kent Heady and Saul G. Trevino University of Texas Medical Branch, Galveston, Texas

CONTENTS I. Tarsometatarsal (TMT) (Lisfranc) Injuries ....................................................................... 118 A. Introduction............................................................................................................... 118 B. History....................................................................................................................... 118 C. Anatomy .................................................................................................................... 118 D. Biomechanics ............................................................................................................. 121 E. Mechanism of Injury ................................................................................................. 122 F. Classification.............................................................................................................. 124 G. Diagnosis ................................................................................................................... 126 H. Treatment .................................................................................................................. 129 1. Principles ............................................................................................................. 129 2. Timing of Surgery ............................................................................................... 130 3. Closed Reduction and Casting ............................................................................ 131 4. Closed Reduction and Percutaneous Fixation .................................................... 131 5. External Fixation ................................................................................................ 132 6. Open Reduction and Internal Fixation ............................................................... 132 7. Extensile Dorsomedial Approach to the Midfoot ............................................... 132 I. Postoperative Care..................................................................................................... 135 J. Prognosis ................................................................................................................... 136 K. Midfoot Sprains in Athletes....................................................................................... 140 L. Salvage Procedures .................................................................................................... 143 M. Complications............................................................................................................ 143 1. Devascularization ................................................................................................ 143 2. Skin Compromise ................................................................................................ 145 3. Other Complications ........................................................................................... 145 II. Midfoot Fractures ............................................................................................................. 145 A. Introduction............................................................................................................... 145 B. Anatomy .................................................................................................................... 145 C. Navicular Fractures ................................................................................................... 146 1. Classification and Mechanism of Injury.............................................................. 146 2. Diagnosis............................................................................................................. 148 3. Treatment............................................................................................................ 150 III. Conclusion ........................................................................................................................ 159 References .................................................................................................................................. 159

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TARSOMETATARSAL (TMT) (LISFRANC) INJURIES Introduction

Injuries to the TMT, or Lisfranc, joint complex occur in widely varying patterns and degrees of severity. They may be widely displaced derangements of the foot or may be among the subtlest and most easily overlooked of foot injuries. Yet the critical role that stability of this complex plays in the biomechanics of the foot may cause even seemingly innocuous injuries to lead to pronounced longterm disability if not properly treated [1–4]. Treatment of these injuries has evolved significantly in recent years, with new emphasis on the importance of anatomic reduction and fixation. As late as the early 1980s, Lisfranc injuries were believed to be fairly rare [1,3]. Prior reports have stated the incidence as 1 in 55,000 persons per year, or about 0.2% of all fractures [5–8]. Several authors have reported an underdiagnosis rate of up to 20%, especially in cases of multiply injured patients [9–13]. Recent studies have reported an increase in the incidence [1–3,5,6,8,14–17]. Improvement in diagnostic evaluation, especially computed tomography (CT) and magnetic resonance imaging (MRI) scans, has contributed to an increased appreciation for the frequency with which injuries to this joint complex occur [2,8,18–24]. As with most traumatic injuries, the prevalence in males is two to four times higher than in females, mostly in young adults [1,12,25–27].

B.

History

The Lisfranc complex is named after the field surgeon to Napoleon Bonaparte, who described amputations through this articulation but not injuries to it. The first significant published work on this injury was by Quenu and Kuss [4] in 1909. They first described a classification system for the injury, which forms the foundation for most systems used today. Authors in the 1950s first highlighted the importance of prompt treatment and anatomic reduction [28–30]. However, several authors in the 1960s reported a lack of correlation between reduction and functional results, prompting a trend away from anatomic reduction, with an emphasis on arthrodesis to salvage feet with persistent pain [31,32]. Further reports in the 1970s emphasized once more that good functional outcome was dependent on achieving and maintaining anatomic reduction and fixation, and this principle was reinforced by a seminal study in 1982 by Hardcastle et al. [1,16,26,33]. Work since that time has focused predominantly on ways to achieve these goals [34].

C.

Anatomy

The TMT or Lisfranc joint is composed of the articulations among the metatarsals of the forefoot and the tarsal bones of the midfoot, the three cuneiforms, the cuboid, and the navicular. The first, second, and third metatarsals articulate with their respective cuneiforms, while the fourth and fifth metatarsals articulate with the cuboid laterally. Each metatarsal also has articulations with its neighboring metatarsals (except the first and second metatarsals, which rarely articulate), and articulations exist between each adjacent midfoot bone. This articular complex is stabilized by both bony geometry and ligamentous elements [35]. The keystone to the stability of the transverse arch is the proximal articulation of the second metatarsal [35]. Its articulation with the middle cuneiform is recessed proximally relative to the first and third metatarsocunieform joints, helping to lock the complex against medial–lateral shearing forces [36,37]. The stability of the arch in the coronal plane is enhanced by the wedged shape of the metatarsal bases, cuneiforms, and cuboid, which are wider dorsally than on their plantar aspect [34,38]. This causes them to form a Roman arch type structure when viewed in this plane (Figure 5.1). The second metatarsal base also sits at the apex of this arch, further emphasizing its importance in the stability of the complex [35]. The lateral cuneiform also projects slightly more distally than the middle cuneiform and cuboid, causing it to project between the bases of the second and fourth metatarsals. This creates a second minor mortise in the joint complex. The primary ligamentous support of the complex is composed of the Lisfranc ligament, intermetatarsal ligaments, and the intercuneiform ligaments (Figure 5.2). Secondary stabilization comes from the accessory ligaments, dorsal capsules, and intermetatarsal ligaments between the


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Figure 5.1 This image of an anatomic specimen shows the Lisfranc articulation with the dorsal structures divided, allowing the joint to hinge open on the plantar ligaments. The view is toward the articular surface of the tarsal bones. Note the recession of the second TMT articulation relative to the first and third metatarsals (arrow). Note also the Roman arch configuration of the cuneiforms and cuboid, with the middle cuneiform and second metatarsal forming the apex of the arch.

second and fifth metatarsals (Figure 5.3). It should be noted that no intermetatarsal ligament exists between the first and second metatarsal bases. Thus, the ligament between the medial cuneiform and the second metatarsal base (Lisfranc ligament) (Figure 5.4) is crucial to maintaining the anatomic relationship between the first two rays. This ligament, an average of 5 mm in thickness and 10 mm in height, is the key structure maintaining the anatomic relationship between the medial and middle columns (see below) [35]. This strong ligament often avulses a fragment from the second metatarsal base before rupturing. The ligaments supporting the complex may be divided into dorsal, interosseous, and plantar components. It should be noted that the plantar ligamentous structures are much stronger than the

Figure 5.2 Anatomic depiction of the plantar ligaments supporting the Lisfranc complex. These ligaments are the main supporting structures for the complex, and are far stronger than the dorsal ligaments. Note the lack of a direct ligamentous connection between the first and second metatarsal bases. The important Lisfranc ligament is labeled 2 in this figure. (From DePalma et al., Foot Ankle Int., 18, 363, 1997. With permission.)


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Figure 5.3 Anatomic depiction of the dorsal ligaments of the TMT complex, which are essentially condensations within the joint capsules. Note that there is a weak direct interconnection between the first and second metatarsal bases. (From DePalma et al., Foot Ankle Int., 18, 363, 1997.)

dorsal ligaments, which contributes to the common patterns of injury seen here. The plantar location of these primary ligaments makes them largely inaccessible from the standard dorsal approaches to this area. This is especially true of the Lisfranc ligament, which is virtually impossible to repair directly from a dorsal incision. Thus, indirect repair of these ligaments by screw fixation between the bones is the best technique for stabilization of these injuries [39–41]. The articular facet between the lateral aspect of the medial cuneiform and the base of the second metatarsal is a small arc on the dorsal lateral surface of the cuneiform [2,35,40] (Figure 5.5). Thus, fixation screws for the Lisfranc ligament may be placed through the inferior portion of this bone without damaging this articular surface. Further reinforcement of the TMT complex is derived from the insertions of the posterior tibial and peroneus longus tendons on the plantar aspect, which provide dynamic as well as static support

Figure 5.4 From the same anatomic specimen as Figure 5.1. The arrow points to Lisfranc’s ligament between the second metatarsal base and the medial cuneiform.



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Figure 5.5 From the same anatomic specimen as Figure 5.1 and Figure 5.4. Note the dorsal location of the articular facet between the medial cuneiform and the base of the second metatarsal, outlined in black. Screws across this articulation should be placed through the plantar half of the cuneiform to avoid this articular surface.

[24,35,39]. The anterior tibialis tendon reinforces the dorsal aspect of the first metatarsal base and the medial cuneiform. These tendinous insertions help stabilize the first ray relative to the other metatarsals. The anterior tibialis insertion into the first ray often is a separate slip that can become interposed between the first ray and the middle cuneiform. Interposition of this lateral band in the first TMT joint may produce dorsiflexion of this ray, the ‘‘toe-up’’ sign [2,34,42] (Figure 5.6). For diagnostic and treatment purposes, the TMT complex may be analyzed by dividing it into three columns: the medial column consisting of the first metatarsal and the medial cuneiform; the middle column consisting of the second and third metatarsals and the middle and lateral cuneiforms; and the lateral column consisting of the fourth and fifth metatarsals and the cuboid [2,24,34,39]. The capsular compartments around the TMT articulations also reflect this compartmentalization, as a separate contiguous capsule surrounds each column’s articulations [34,43]. Injury patterns often fall along these lines of segmentation. Consideration of reduction of these columns to one another can also aid in surgical planning. While the TMT joints of the medial and middle columns are fairly restricted in motion, the lateral column articulations with the cuboid tend to be more mobile. Approximately 10 mm of sagittal motion occurs through these joints [2,35]. The motion of the fifth metatarsal–cuboid articulation in particular should be preserved for normal foot function in accommodating irregular surfaces. Several important neurovascular structures lie in close proximity to the Lisfranc complex, especially the second metatarsal base area. The medial dorsal cutaneous branch of the superficial peroneal nerve and the deep peroneal nerve both lie near this articulation, as do the deep plantar branch of the dorsalis pedis artery, the plantar arterial arch, and the arcuate artery [35] (Figure 5.7). These structures may become interposed in the injury, placing them at risk for injury during reduction, and must be protected during surgical repair of these injuries [34]. The terminal branches of the sural and saphenous nerves may also be injured during lateral and medial screw placement, respectively.

D.

Biomechanics

Normal gait biomechanics require the midfoot to form a rigid lever at the end of the stance phase to facilitate push-off. The inherent stability of the medial and middle columns is crucial in allowing this function, and is lost with disruption of the Lisfranc complex [2,12]. Even minor diastasis between the medial and middle columns may result in loss of stability of the medial longitudinal


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Figure 5.6 Diagrammatic representation of interposition of the lateral slip of the tibialis anterior insertion into the first TMT articulation, causing an irreducible dislocation (‘‘toe-up sign’’). (From DeBenedetti, M.J., Evanski, P.M., and Waugh, T.R., Clin. Orthoped., 136, 239, 1978. With permission.)

arch. This can lead to forefoot abduction, loss of push-off strength, planus foot deformity, and progressive posterior tibial tendon dysfunction [2,12,14,18–20,26,44–47]. Delayed diagnosis of these injuries may necessitate reconstructive salvage procedures rather than simple initial repair [2,3,25,39,48,49].

E.

Mechanism of Injury

The anatomic complexity of Lisfranc’s articulation and the wide variety of forces that may act upon it make it very difficult to identify the exact mechanism of injury in most cases [8]. Injuries may be grossly divided into those from direct and indirect mechanisms [4,5,7,50–53].



Lateral branch of deep peroneal nerve Lateral tarsal artery

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Dorsalis pedis artery Medical branch of deep peroneal nerve

Arcuate artery

Figure 5.7 Neurovascular anatomy surrounding the first and second intermetatarsal base articulation. Note the proximity of the dorsalis pedis artery, its arcuate branch, and the deep peroneal nerve to this articulation. This proximity places these structures at risk for damage either during the injury or during surgical repair. (From Kelikian, Operative Treatment of the Foot and the Ankle, A.S., Ed., Appleton and Lange, Stanford, CT, 1999, Figure 25.3. With permission.)

Direct injuries are those resulting from a crushing force acting on the foot. These injuries are often accompanied by severe soft tissue damage and may produce dorsal or plantar dislocations depending on the point of impact of the force relative to the joint line [8,9,34,54,55] (Figure 5.8). Plantar dislocations are usually the result of direct-force injury [34]. Indirect injuries are more common but are harder to characterize. These are most often the result of a longitudinal force acting upon the foot, usually with a combined element of rotation, forcing the foot into plantar hyperflexion [8,9,34] (Figure 5.9). The resulting cavus deformation ruptures the weaker dorsal ligamentous structures first [8]. Twisting forces usually cause abduction of the forefoot, creating fractures of the second metatarsal base and often crush fractures of the cuboid. Indirect-force injuries more commonly produce the classic displacement patterns described by classification systems [34]. Motor vehicle accidents and falls usually produce this mechanism. Displaced Lisfranc injuries are almost uniformly due to high-energy trauma. The most frequent causes of Lisfranc injuries, in descending order, are motor vehicle accidents, crush injuries, falls from ground level with or without twisting injury to the foot, and falls from a height [1,15,25,27,34,51,53]. Sports injuries are also common causes. Up to 81% of Lisfranc injuries occur in multiple-trauma patients [12,34]. Neuropathic injuries to this complex must also not be forgotten, as this is a common site for Charcot type destruction to occur [2,41,56].


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Direct force

57%

A

B or

C

D

43%

Figure 5.8 The direction of displacement and the pattern of injury produced by a direct-force injury to the TMT articular complex depends in part on the location in which the force is applied relative to the articulation. Forces acting distally to the articulation are the most common mechanism by which plantar dislocations occur. (From Myerson, M.S., Fisher, R.T., Burgess, A.R., and Kenzora, J.E., Foot Ankle, 6, 226, 1986.)

A

B C

Figure 5.9 Indirect-force mechanism of Lisfranc injury. Longitudinal loading of the foot either from body weight or from the application of an external force to the posterior heel causes plantar hyperflexion of the forefoot, causing the weaker dorsal ligaments to rupture first. This results predominantly in dorsal dislocation of the metatarsals at the TMT. (From Arntz, C.T. and Hansen, S.T.J., Orthoped. Clin. North Am., 18, 108, 1987.)

F.

Classification

The numerous patterns of injury caused by varying degrees of trauma from both direct and indirect forces make it very difficult to devise a comprehensive classification scheme for Lisfranc injuries. Several schemes have been proposed with various attempts to improve their utility, but no significant data have been produced to support the superiority of any one system for predicting



125

clinical outcome [1–4,12,14,47,49,57]. Quenu and Kuss [4] in early 1909 provided the foundation for the present classification system by dividing these injuries into three types: homolateral dislocations, partial dislocations, and divergent dislocations. Their classification focused on displacement in the coronal plane. Hardcastle et al. [1] revised and expanded this classification in 1982, noting that dislocation could occur in any plane. The modification of Hardcastle’s classification by Myerson et al. [12] in 1986 is currently the most widely used. This divides Lisfranc disruptions into type A, or totally incongruent injuries, type B, or partially incongruent injuries, and type C, or divergent injuries (Figure 5.10). Type A injuries are those in which all five TMT articulations are disrupted and all five metatarsals displaced as a unit in the same direction. These may be subdivided into primarily lateral or primarily medial dislocations, with dorsolateral dislocations by far the more common. Type B injuries are those in which one or more columns remain nondisplaced. These are subdivided into medial dislocations (medial homolateral, type B1), where the medial column has displaced, and lateral dislocations (lateral homolateral, type B2), where the middle or lateral columns, or both, have displaced. Type C injuries are those in which the medial column displaces in a separate direction from the lateral columns. These are subdivided into totally displaced (type C2), where all columns are dislocated, or partially displaced (type C1), where some of the lateral TMT joints remain intact [8,34,58]. Most classification schemes, including Hardcastle’s, do not incorporate injury to adjacent structures. As high as 95% of Lisfranc injuries are associated with metatarsal fractures, most often of the proximal second metatarsal due to its inherent bony stability that must be disrupted [2]. Up to 39% of Lisfranc injuries are associated with tarsal bone fractures [58].

Type A Total incongruity 1. Medial 2. Lateral

1

2

Type B Partial incongruity 1. Medial 2. Lateral

1

2

Type C 1. Diastasis A. Acute B. Subacute C. Chronic 2. Total 3. Partial

1A

B

C

2

3

Figure 5.10 Classification of Lisfranc injuries. Based on Myerson’s modification of the original classification of Quenu and Kuss, with additional modification to include diastasis from acute sprain injuries or chronic neuropathic injury. (From Kelikian, Operative Treatment of the Foot and the Ankle, A.S., Ed., Appleton and Lange, Stanford, CT, 1999. Figure 25.4. With permission.)


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The joint disruptions often extend into the intercuneiform area as well. Divergent injuries often exit through fractures created in the navicular [2]. Lateral homolateral injuries often fracture the cuboid [2]. Lisfranc injuries may result from mechanisms other than acute trauma, such as midfoot sprains in the athlete or chronic ligament insufficiency in neuropathic feet. These classification systems do not apply well to these mechanisms as they do not incorporate simple diastasis without dislocation. Even minor-appearing diastasis of the Lisfranc complex can lead to serious disability, as has recently been emphasized in athletic injuries [18–20,39,40,44,59]. Chronic insufficiency can lead to the same pattern of midfoot instability, forefoot abduction, push-off weakness, and progressive posterior tibial dysfunction as is seen in neglected acute injuries [2]. This sequence can be particularly disastrous in the neuropathic foot [41,56]. Figure 5.10 depicts a classification system that includes such injuries [2].

G.

Diagnosis

Various authors have reported a rate of up to 20% missed diagnosis on initial evaluations of Lisfranc injuries [9–13]. This delay in treatment often results in diminished treatment outcome. Factors contributing to this error rate include the often subtle radiographic findings of the injury compounded with the more obvious other injuries to the foot or extremity that distract the diagnostician. Most but not all Lisfranc disruptions occur from high-energy injuries, as considerable force is required to disrupt this joint complex [60]. A high index of suspicion should therefore be maintained in any foot injury, especially those that present with swelling of the midfoot or forefoot, tenderness to palpation along the TMT joints, or midfoot or forefoot fractures. This is especially true in the multiply injured patient who may have distracting injuries or altered mental status. Plantar ecchymosis in the midfoot is frequently associated with disruption of the Lisfranc ligament [2,34,61]. Exaggerated swelling or focal tenderness along the TMT joints indicates at least a probable sprain of the midfoot and warrants aggressive investigation for more serious disruptions [2]. A stress test can be performed by grasping the first and second metatarsals and moving them in dorsiflexion and plantar flexion relative to one another. Passive pronation and abduction of the midfoot and forefoot may also produce pain in these injuries. Pain associated with minimal stress from these maneuvers should be considered a positive stress test [2,39,40,59,62,63]. Routine radiographic evaluation should include weight-bearing anteroposterior (AP), lateral, and 308 oblique views of the foot. It is critically important that the physician be familiar with the normal radiographic relationships between these joints (Figure 5.11). The medial and lateral borders of the first metatarsal should align with borders of the medial cuneiform on both AP and oblique views. The width of the first and second intermetatarsal spaces at their bases should equal that of the first and second intercuneiform space on both the AP and the oblique. The medial border of the second metatarsal base should precisely align with the medial border of the middle cuneiform on the AP view. The lateral border of the third metatarsal should align with the lateral border of the lateral cuneiform on the oblique view, as should the medial border of the fourth metatarsal with the medial border of the cuboid. Any dorsal displacement of a metatarsal base relative to the dorsal aspect of the corresponding tarsal bone on the lateral view is abnormal, but plantar displacement of up to 1 mm may be normal [17,21,31,34,64]. Subtle injuries may only be seen on weight-bearing views. Bilateral AP views on the same cassette with the patient holding both feet in the same position and placing as much weight as possible on the injured foot can be extremely valuable [2,14,17,24,39,65]. This allows side-to-side comparison of the joints to reveal subtle diastasis (Figure 5.12). Weight-bearing lateral films may show flattening of the longitudinal arch, with reduction of the distance between the fifth metatarsal base and the base of the medial cuneiform, or dorsal subluxation of the metatarsal bases [58]. A stress abduction–pronation view may also be revealing. An ankle block can be administered for pain control if necessary to allow the patient to more fully cooperate with these views. The studies can also be repeated at 1 to 2 weeks post injury after the pain has improved; in subtle injuries this delay is unlikely to compromise the final outcome [2]. Late separation can also occur and may be detected up to 6 weeks post injury after previously normal films [2]. A persistently painful midfoot should therefore be reexamined radiographically. Even with such diligence, the diagnosis may still



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Figure 5.11 Normal (A) AP; (B) oblique; and (C) lateral radiographs of the foot demonstrating the normal relationship between the metatarsal and tarsal bones.


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Figure 5.12 Comparison AP radiographs with both feet standing on the same plate. This allows direct comparison of the two sides to help detect subtle diastasis between the first and second metatarsals. The patient has a type B2 lateral partially incongruent injury.

be missed. Vuori and Aro [15] reported a series of 59 patients with Lisfranc injuries, in which the diagnosis was initially missed in 39% of cases, resulting in inadequate treatment. The remaining foot should always be carefully evaluated in suspected TMT injuries for associated fractures or other injuries. Up to 95% of Lisfranc injuries have associated metatarsal fractures, usually of the second metatarsal base [58]. Associated injuries to the hindfoot or midfoot bones, such as subtle compression fractures to the cuboid or cuneiforms, are common, occurring in up to 39% of cases [58]. These fractures may distract the diagnosing physician from the more subtle Lisfranc dislocation. Other fractures have a frequent association with Lisfranc injuries and should prompt the physician to look carefully at the Lisfranc complex. These include avulsion fractures of the first or second metatarsal base (‘‘fleck sign’’) (Figure 5.13) [12] or the medial pole of the navicular, crush fractures of the cuboid or cuneiform, and anterior process calcaneus fractures [3,12,21,31,40,41,46,49,60,66]. The interosseous muscles originate on the shafts of the metatarsals and insert on the proximal phalanx of the toe on an adjacent ray. This can result in a ‘‘linked toe’’ dislocation of the MTP joint, which should be a hint to look for dislocation of the metatarsal [6,34,67,68] (Figure 5.14). Soft tissue injuries such as posterior tibial tendon disruptions and spring ligament ruptures may also occur. The diagnosis of compartment syndrome should always be considered in the severely injured foot and pressure measurements should be made in equivocal clinical presentations [2,60]. CT can also be cost effective [8] for the evaluation of highly suspicious injuries [69,70]. Cuneiform and cuboid fractures can usually be seen in detail with 3-mm sliced axial CT scans [2]. Cadaveric studies have shown that up to 67% of subtle dorsolateral subluxations displaced 2 mm or less are not visible on routine radiographs, yet these occult injuries can still produce disability. CT scans can help visualize such subtle injuries [18] (Figure 5.15). MRI scans using T1-weighted spinecho (oblique, axial) and three-dimensional spoiled gradient-recalled acquisition in steady-state sequences have demonstrated the ability to visualize the Lisfranc ligament [2,19,20]. However, the greatest limitation of CT and MRI studies is that it is not possible to obtain stress views. Plain stress images therefore still play an important role in diagnosis [34].



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Figure 5.13 ‘‘Fleck’’ sign created by avulsion of a bony fragment from the second metatarsal base by the Lisfranc ligament (arrow). This foot also has obvious fractures to the second and third metatarsal bases.

H. 1.

Treatment Principles

The goal of treatment is restoration of a stable, plantigrade, pain-free foot. In the past two decades there has been an increasing emphasis on the importance of obtaining and maintaining anatomic reduction of the TMT joint complex to achieve this goal [9,12,14,39,40,49,63]. Direct repair of the injured ligaments is seldom if ever possible. The goal is therefore to restore anatomic relations between the bones as soon as possible and maintain this relationship long enough to allow the ligaments to heal at their proper length. Snug reduction without diastasis between the lateral edge of the medial cuneiform and the medial base of the second metatarsal is especially important to allow restoration of the key Lisfranc ligament. Compromise of these goals by inadequate reduction, fixation, or postoperative immobilization frequently leads to poor results. Several treatment options have been proposed and attempted. These include closed reduction and casting, closed reduction and percutaneous fixation, open reduction and internal fixation, external fixation, and primary arthrodesis [3,19,40,44,46,48,59,64]. Fixation has varied from smooth or threaded Kirschner wires to cannulated screws or lagged AO screws [8,25,40,60]. There remains some controversy regarding the best choice for fixation of Lisfranc disruptions. Most authors currently favor rigid screw fixation over percutaneous pins. Pins are more easily placed, but do not provide rigid fixation, may break with early weight-bearing, and may present a risk for infection and migration, necessitating early removal, especially if left protruding from the skin. Using a low-speed drill to avoid osteolysis along the pin tract and bending the wires outside the skin and incorporating them in a plaster cast can decrease these complications [8,27]. Fixation hardware should be left in place for at least 16 weeks to allow adequate ligamentous healing; it is very difficult to maintain pins in place for this length of time [2,56,60]. Cannulated screws have largely obviated the need for percutaneous pinning alone [2,14,39,60]. If closed reduction is achieved, 4- or 4.5-mm cannulated screws may easily be placed through stab incisions over wires. In diabetic patients, who are usually slower to heal, a 6.5-mm cannulated screw may be used for additional stability [41]. These larger screws should not be used between metatarsals, however, as the risk of fracture after hardware removal is unacceptably high [2]. Bioabsorbable screws may


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Figure 5.14 ‘‘Linked toe’’ dislocation of the third MTP joint with displaced dislocation of the fourth metatarsal. This dislocation was caused by the pull of the interosseous muscles that arise on the medial side of the fourth metatarsal and insert on the extensor hood of the third toe. (From English, T.A., J. Bone Jt. Surg., 46B, 703, 1964. With permission.)

soon prove to be a better choice for fixation and would eliminate the need for hardware removal if suitable [34]. There has also been concern that compression of joint surfaces by partially threaded cancellous or lagged screws may be detrimental. To our knowledge, no study has so far found a correlation between compression and arthrosis. While late degenerative change in the TMT joints is common after fixation, this is most likely related to the damage from the initial injury [2,12,45,60,63,65,71]. Mild compression of the joints may also help maintain joint congruency [34]. Fully threaded cancellous screws without compression are an option in cases of special concern. 2.

Timing of Surgery

Several authors have recommended that severe traumatic Lisfranc injuries should be treated within the first 24 h after the injury [25,39,40,48]. Reduction of the fractures within this critical period



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Figure 5.15 CT scan through Lisfranc joint showing fracture of the second, third, and fourth metatarsal bases.

stabilizes the soft tissue envelope, lessens the incidence of skin breakdown and vascular compromise, and makes anatomic reduction simpler [2,8,19,25,27]. Delayed primary closure at 5 to 7 days can be performed if severe postoperative swelling occurs. Certainly, preliminary reduction and even temporary fixation of badly displaced injuries should be performed as soon as possible to reduce soft tissue complications. However, it may be prudent to delay definitive reduction and fixation for 7 to 14 days to allow swelling to resolve. This increases the chances for primary wound closure without tension and skin flap necrosis and does not seem to compromise the long-term results of care [2,8]. Good results may be obtained up to 6 weeks after injury [2,14,39,48]. Surgical results later than this are compromised by extensive soft tissue dissection, destruction of articular surfaces from prolonged malposition, and remodeling of the ruptured ligaments inhibiting proper healing [2]. 3.

Closed Reduction and Casting

Attempts to hold Lisfranc disruptions in reduction by cast immobilization alone have invariably lead to an unacceptably high rate of treatment failures [2,25,40,60]. Even when anatomic closed reduction can be achieved, it is impossible to maintain with plaster fixation alone as the fixation is lost when the initial swelling resolves [8,54]. Such treatment would only be indicated in cases that are otherwise unacceptably poor surgical risks, or in late presentations where salvage procedures are considered inevitable. 4.

Closed Reduction and Percutaneous Fixation

Less severely disrupted injuries may occasionally be successfully reduced without direct exposure. This should always be attempted before open reduction in such cases [2,7,8,14]. However, small articular fragments are almost always produced in these injuries and usually are interposed in the articulations, blocking closed reduction [12,25,27,34,48,63,67,72]. Findings associated with a poorer chance of successful closed reduction include severe comminution, soft tissue interposition of any kind, and diastasis between the medial and middle cuneiform indicating possible interposition of the anterior tibialis tendon [7,13].


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Sterile finger traps may be applied to the great toe and adjacent one or two toes depending on the injury pattern. Then 5- to 10-lb weights are suspended from the ankle to provide longitudinal traction for 5 min or more before attempting reduction with passive inversion or eversion. The reduction is seldom palpable or audible. Fluoroscopy may be used for initial assessment of reduction, but permanent radiographic films should be obtained to judge the adequacy of reduction before accepting it, as fluoroscopic images are seldom of sufficient quality [2]. Even permanent films may not be able to visualize 1-mm residual displacements [18]. Any residual diastasis may be held using a reduction clamp placed percutaneously across the base of the second metatarsal and medial cuneiform. Kirschner wires or cannulated screw guide pins may be used to hold the preliminary reduction [2,39]. Myerson et al. [12] and Myerson and Burgess [60] list as criteria for adequate reduction a gap of less than 2 mm between the bases of the first and second metatarsals and the medial and middle cuneiforms, a talometatarsal angle of less than 158, and no displacement of the metatarsals in the dorsoplantar plane. More stringent criteria are needed in athletes, and anatomic reduction should always be sought [2,18,44,59]. Once adequate reduction is verified, 4- or 4.5-mm cannulated screws may be placed percutaneously over the pins for permanent fixation. Alternatively, 3.5-mm lagged cortical screws may also be used. 5.

External Fixation

Use of external fixation is primarily limited to severe open fractures or cases in which soft tissue coverage of the injury is compromised [60]. External fixators may be used for early stabilization while wound care or compartment pressure measurements are performed. A half-pin frame may be used to stabilize the medial or lateral columns (Figure 5.16). A cross bar may be used to stabilize the transverse arch [2]. A lateral fixator may be especially useful in cases involving a crush injury to the cuboid to reestablish the length of the lateral column [34] (Figure 5.17). It is seldom possible, however, to achieve and maintain anatomic reduction of the TMT joints using external fixation alone, and such cases should be revised or augmented with internal fixation as soon as the soft tissue envelope allows. 6.

Open Reduction and Internal Fixation

Open reduction is indicated in almost every case in which closed manipulation cannot achieve anatomic reduction. Open reduction may be contraindicated in patients with severe peripheral vascular disease or neuropathy [41,45]. Most cases of neuropathic Lisfranc injury are seen too late for acute reduction and fixation, either open or closed, and are better treated with primary arthrodesis [39,41]. Open reduction may be performed up to 3 months after injury in dislocations without fracture. Beyond this time, open reduction and realignment arthrodesis is preferable (see ‘‘Salvage Procedures’’ section below). Most authors describe a surgical approach to the Lisfranc complex via two or three longitudinal incisions over the midfoot. The first is over the medial border of the foot centered at the base of the first ray, the second is between the first and second metatarsal bases, and the third over the fourth metatarsal base [2,3,12,14,25,34,41,48,73]. The skin bridges between these incisions are usually narrow, and the incisions must be kept short to avoid vascular compromise. This can result in poor visualization of the joints and excessive retraction leading to neuromas and skin necrosis. An extensile dorsomedial approach to the midfoot with an optional lateral incision is therefore preferred [2,14,39,40]. This approach allows better exposure of the medial two columns, avoids the dorsal prominence, and allows direct visualization and protection of the neurovascular structures in the region including the deep and superficial peroneal nerves and the dorsalis pedis artery. 7.

Extensile Dorsomedial Approach to the Midfoot

The variation in injury pattern makes it impossible to describe a single technique for operative fixation that will apply to all cases. What follows is an example of treatment of a hypothetical type C–divergent totally displaced injury with instability of the medial naviculocuneiform joint. Injuries



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Figure 5.16 (A) AP; (B) lateral; (C) radiographic; and (D) photographic views of a small external fixator used to support the medial column in a crushed foot with a TMT disruption combined with a type III navicular fracture. The proximal half-pin was placed in the talar neck; the distal half-pin was placed in the proximal second metatarsal.

to other bones such as the metatarsal shafts or tarsal bones may also require fixation in the same setting [8]. The treating physician must always adjust the treatment to fit the constellation of injuries present. A curvilinear incision is made starting at the midportion of the navicular and extending over the medial aspect of the third metatarsal base, then to the distal third of the second metatarsal (Figure 5.18). The branches of the superficial peroneal nerve that are located subcutaneously and retracted. The superficial fascia is divided lateral to the extensor hallucis longus tendon, and the tendon is retracted medially. The neurovascular bundle is located inferior to the musculotendinous junction of the extensor hallucis brevis [35]. The bundle is mobilized by subperiosteal dissection


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Figure 5.17 AP view of a combined Lisfranc fracture-dislocation and a compression fracture of the cuboid in which a small external fixator is used to hold the lateral column out to length, removing the compressive forces across the grafted cuboid.

from the middle cuneiform and base of the second metatarsal and protected (Figure 5.19). The perforating artery is identified between the bases of the first and second metatarsals. This artery is preserved using Homan retractors if possible but may require ligation. The medial three TMT articulations are now well visualized and can be reduced anatomically. A small lamina spreader may be used to spread the medial–middle cuneiform interval, testing its stability and exposing the remnants of the Lisfranc ligament. This allows debridement of hematoma, osteochondral fragments, and interposed soft tissue from the interval, but does not afford repair of the ligament (Figure 5.20). The TMT and intercuneiform articulations are systematically stressed to test for occult instability. The joints are debrided as necessary. The exposure may be easily extended proximally to the naviculocuneiform junction if needed. If exposure of the fourth or fifth metatarsals is required, a second longitudinal incision must be made in the interval between them. Reconstruction usually progresses from medial to lateral (Figure 5.21). Both the metatarsocuneiform and naviculocuneiform articulations of the first ray must be stabilized if injured. The first TMT joint is debrided and reduced, then provisionally stabilized using a guidewire placed dorsally 1.5 cm distal to the articulation and directed plantarly and proximally. If the medial naviculocuneiform joint is unstable, it is fixed concurrently with stabilization of the second ray. The Lisfranc ligament complex is stabilized next. The articulations between the medial and middle cuneiforms and the base of the second metatarsal are thoroughly debrided. A reduction clamp is then placed between the medial cuneiform and the base of the second metatarsal for initial reduction. The lateral metatarsals often will also be reduced by this reduction of the second



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Figure 5.18 Skin markings for the surgical incision for the extensile dorsal approach. (From Kelikian, Operative Treatment of the Foot and the Ankle, A.S., Ed., Appleton and Lange, Stanford, CT, 1999. Figure 25.11. Obtain permission to reuse and have clinical photography reproduce better or produce a new clinical photograph.)

metatarsal base. A guidewire is then placed across the medial cuneiform–second metatarsal interspace. As stated above, this pin should be placed through the plantar half of the medial cuneiform to avoid its articular facet with the second metatarsal. A third pin is placed from medial to lateral between the medial and middle cuneiforms if required. Plain radiographs are then obtained, and if adequate reduction is seen, 4- or 4.5-mm cannulated screws are inserted over these pins starting with the Lisfranc ligament screw. Generally, 4-mm screws for lighter patients and 4.5-mm screws for heavier patients are used. Screws placed into the metatarsal bases should be countersunk to avoid fracture into the adjacent joints. Lag screws should not be excessively tightened to avoid unnecessary compression of the joint surfaces. The third, fourth, and fifth metatarsals are stabilized by fixation from their base into the adjacent tarsal bone. The third metatarsal is fixed to the lateral cuneiform using cannulated or lagged screw fixation as before. However, mobility of the fourth and fifth rays should be preserved as much as possible, as stiffness of these rays is a debilitating condition. Therefore, these rays are usually pinned to the cuboid using 0.062-in. Kirschner wires, unless the injury is an isolated lateral column dislocation (Figure 5.22). Polylevolactide (PLLA) absorbable pins have also been proposed for fixation of these rays due to their minimal reactivity and slow resorption [74]. This avoids the need for removal of hardware and allows the fixation to be completely buried beneath the skin. This example presents the basic strategy and surgical goals of treatment for a typical injury. It must of course be modified or supplemented as needed to accommodate the actual injury pattern. Supplemental procedures may also be necessary, such as bone grafting or external fixation to address compression of the navicular or cuboid bones or fixation of distal metatarsal fractures [2].

I.

Postoperative Care

Conservative protocols call for immobilization in a cast for 8 to 12 weeks to allow for ligamentous healing. This may be advisable in unreliable patients. However, the trend is now toward earlier mobilization with restricted weight-bearing in a bivalve cast as early as 2 weeks postoperatively. This improves final range of motion and reduces swelling and tissue fibrosis, and may help promote


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Inferior extensor retinaculum Inferior extensor retinaculum

Base of second metatarsal

Lisfranc ligament (torn) Base of second metatarsal

Lateral cuneiform Base of third metatarsal

Extensor hallucis brevis

Medial cuneiform Extensor hallucis longus

Dorsalis pedis artery

Base of first metatarsal

Dorsalis pedis artery

Extensor digitorum longus

Extensor hallucis brevis

B

A

Figure 5.19 (A) Dorsomedial extensile approach to the first and second metatarsal base interspace. The branches of the superficial peroneal nerve have been retracted laterally, the superficial fascia has been divided and the extensor hallucis longus retracted medially, and the dorsalis pedis artery and deep peroneal nerve have been mobilized and retracted laterally along with the extensor hallucis brevis. The region of Lisfranc’s ligament is exposed, but the ligament itself is still not accessible for repair. (B) Exposure of the second and third metatarsal interspace. The neurovascular bundle and extensor hallucis brevis are retracted medially. (From Kellikian, Operative Treatment of the Foot and the Ankle, A.S., Ed., Appleton and Lange, Stanford, CT, 1999. Figure 25.12A and Figure 25.12B.)

healing [8,25]. With stable fixation, partial weight-bearing may begin at 4 weeks, progressing to weight-bearing as tolerated at 6 weeks depending on the radiographic appearance. Kirschner wires placed for fixation should be removed at 6 to 8 weeks to avoid breakage. A removable walking boot is used initially after cast removal to allow range of motion with protected ambulation. When immobilization is discontinued, we recommend placing the patient into a total-contact orthosis and a shoe modified with an extended steel shank for the first year. Others have recommended only a padded arch support for 3 months [8]. Screw removal should be delayed until at least 3 to 4 months after surgery to prevent recurrent diastasis [2]. The screws may also be left in place permanently unless they cause discomfort or break [75].

J.

Prognosis

Treatment outcomes for Lisfranc injuries have improved markedly with recent emphasis on anatomic reduction. However, the results of treatment are still uncertain [71]. Arntz et al. [25]



Figure 5.20 Surgical photographs of the extensile dorsomedial approach to the midfoot.

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Figure 5.20

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Continued Surgical photographs of the extensile dorsomedial approach to the midfoot.



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reported on 34 patients in whom AO screws were used for fixation. Thirty of these patients were deemed anatomically reduced, and of these 30, 28 (93%) had good or excellent results. Five of the remaining six with fair or poor outcomes had grade II or III open injuries. The authors concluded that posttraumatic arthrosis was related to the degree of damage at the time of injury or to nonanatomic reduction. With anatomic reduction, most series have reported 50 to 95% good or excellent outcomes. By contrast, most reports list a good to excellent outcome rate of only 17 to 30% when anatomic reduction is not achieved [12,25,27,30,34,63,67]. There appears to be a higher correlation between anatomic reduction and outcome than between the degree or pattern of displacement, except in cases of severe associated soft tissue injury [1,5,12,16,34,53,72]. Another study reporting gait analysis in 11 patients previously treated for displaced Lisfranc injuries showed that none had normal gaits [58,76]. All displayed antalgia with a shortened period of midfoot weight transfer and increased hindfoot phase, with the least gait disturbance occurring in those who had anatomic reduction. Arthrodesis by open reduction as a salvage method produced good to excellent results in 69% patients in one small series [49,58].

Torn Lisfranc⬘s ligament

A

B

Figure 5.21 Example of stabilization of a divergent Lisfranc injury. (A) Totally divergent injury pattern is demonstrated, with medial displacement of the medial column through the first naviculocuneiform joint, disruption of Lisfranc’s ligament, and lateral displacement of the second through fifth TMT joints. (B) Fixation begins with fixation of the medial to the middle column. Guidewires are placed across the first TMT joint, between the medial and middle cuneiforms, and between the medial cuneiform and second metatarsal paralleling Lisfranc’s ligament. Cannulated screws are placed over these guidewires once reduction is confirmed, as has been done with the intercuneiform guidewire here.


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Figure 5.21 Continued Example of stabilization of a divergent Lisfranc injury. (C) The lateral metatarsals are next fixed provisionally with a guidewire across the third TMT joint and Kirschner wire fixation of the fourth and fifth metatarsals. (D) The wire across the third ray is replaced with a cannulated screw. The Kirschner wires are left as final fixation of the fourth and fifth metatarsals.

K.

Midfoot Sprains in Athletes

Lisfranc injuries with or without diastasis may occur as so-called midfoot sprains, typically seen in athletes [2,44,59]. The athletes present with mild to moderate swelling over the midfoot and inability to bear weight. Injury may occur to either the lateral or the medial side of the complex, with pain localized to the area of injury. Most injuries are grade I or II sprains of the TMT ligaments, with severity usually determined by the energy of the initial injury. If no diastasis (representing a grade III injury) is seen on weight-bearing films, the patient may be treated with cast immobilization and no weight-bearing until asymptomatic. Persistent symptoms should prompt further investigation for more severe occult injuries. Weight-bearing radiographs should be repeated on the contralateral side for comparison. MRI scans, as stated above, may be used to evaluate the Lisfranc ligament or to look for other subtle joint injury. Once symptoms have resolved and cast immobilization is discontinued, the foot should be protected with a total-contact orthosis and a shoe with extended steel shank or an articulated ankle–foot orthosis for up to 1 year. Medial injuries generally have a longer recovery period than lateral injuries [44]. The recovery period for these sprains is prolonged, which may be frustrating for the avid athlete. However, morbidity is common unless the correct treatment protocol is followed [2,44,59].



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Figure 5.22 A clinical example of fixation of a type B2 injury with lateral dislocation of the second through fourth TMT joints and a Jones type fracture of the proximal fifth metatarsal. (A) Oblique; (B) AP; and (C) lateral radiographs of the initial injury.


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Figure 5.22 Continued (D to F) Radiographs of the injury after fixation. The second ray has been stabilized by placement of a cannulated screw parallel to Lisfranc’s ligament and a second screw between the first and second metatarsal bases. The third TMT joint has been fixed with an additional cannulated screw. The fourth TMT joint is stabilized by a Kirschner wire. The fifth metatarsal fracture has been fixed with a cannulated screw; the articulation was not disrupted.



L.

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Salvage Procedures

Patients frequently develop posttraumatic arthritis despite adequate reduction and fixation due to the damage to the joint at the time of injury. However, the presence of arthritis does not correlate strongly with poor results [2,12,25,34,45,48,49,63,77]. Minor arthritis of these articulations is well tolerated if the midfoot is stable at toe-off of gait. Salvage procedures should generally be delayed for at least 1 year after injury while the foot is supported with insoles and an extended steel shank shoe [2,12,34,45,49,62,71,73]. Aching midfoot pain aggravated by activity is the most common symptom of posttraumatic arthritis [34]. In persistently symptomatic patients or those in whom treatment was unacceptably delayed, salvage via a reconstructive procedure may be necessary. Reduction of deformity followed by arthrodesis is the usual treatment, although arthrodesis may be performed in situ if little deformity is present [2,12,39,49,60,65,74]. Gross deformity of the foot such as pes planus or forefoot abduction should be addressed at the time of fusion, as should posterior tibial tendon insufficiency, if present [2]. Fusion of the fourth and fifth TMT articulations should be avoided due to their critical role in adaptation of the forefoot to the ground [41,49,73]. External or pin fixation should be used for reduction of complete subluxation of these rays. An ‘‘anchovy procedure’’ in which an extensor tendon is used as an interpositional arthroplasty graft has been suggested as an alternative to fusion of these rays, but there are no published series reporting results with this technique [2]. Various methods of fusion may be used. Johnson popularized a technique of in situ fusion using a bony dowel, which is simple to perform in cases not requiring open reduction [49,73]. In severe cases, reduction may be more easily performed after resection of the joint surfaces. This exposes large cancellous surfaces, which facilitates fusion, but is a more technically demanding procedure and introduces the possibility of malalignment resulting in metatarsalgia [49]. Most cases may be treated with a lesser resection of the joint in which an exostectomy is followed by capsular release and removal of the articular cartilage and subchondral bone using osteotomes and curettes. Multiple holes are then drilled in the surface using a 1.5-mm bit followed by cross-hatching of the holes with a small osteotome. Cancellous bone from the local area, the calcaneus, the proximal tibia, or the iliac crest may be used to augment the fusion. Fixation is performed using 4- or 4.5-mm cannulated screws. Threaded pins may be used if necessary to augment fixation but can usually be avoided. This surface preparation may be tedious, but it allows for easy determination of the alignment in both the transverse and the sagittal planes. The union rate for this procedure is nearly 95% in our experience (Figure 5.23). The patient is immobilized in a cast without weight-bearing for the first 6 weeks, followed by weight-bearing in a short leg cast for an additional 6 weeks. Molded insole and steel-shank shoe support may be used until full recovery, which usually requires 9 to 12 months [2]. Salvage procedures are successful in restoring a pain-free, plantigrade foot in only about two thirds of patients, and there is a significant complication rate [12,49,73,77]. This emphasizes once more the importance of early diagnosis and proper treatment of these injuries [34].

M.

Complications

1.

Devascularization

As stated above, several important neurovascular structures lie in intimate relationship to the Lisfranc joint complex [35]. As early as 1951, Gissane [28] reported three cases of forefoot amputation due to vascular compromise from delayed treatment. The deep peroneal nerve and a communicating branch of the dorsalis pedis artery pass through between the first and second metatarsal bases. Injuries to this joint complex can easily damage these structures, resulting in nerve entrapment, denervation, and devascularization. Vascular compromise of the foot usually requires concomitant injury to the posterior tibial artery or lateral plantar artery [28,29,34,53]. Literature documents approximately a 2% occurrence of injury to the perforating branch of the dorsalis pedis combined with damage to the posterior tibial artery, resulting in an ischemic foot [2]. Ischemia or other evidence of vascular injury should be considered an indication for open reduction and exploration of the involved vessels. In rare cases, amputation may even result. Most of these cases are due to compartment syndrome in addition to the arterial insult [34,55,78,79]. Vascular


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Figure 5.23 (A and B) Postoperative radiographs showing internal fixation of a type B1 medial diastasis injury with a horizontal fracture of the medial cuneiform. (C) Despite adequate healing of the cuneiform fracture, the patient developed symptomatic arthrosis of the first and second metatarsal interspace. (D) The patient was treated with arthrodesis between the first and second metatarsal bases and the medial and middle cuneiforms. Symptoms have improved significantly but the patient still has pain with prolonged ambulation.

injury and compartment syndrome are the most important early complications of treatment. If release of compartments is required, this can usually be performed through the same incisions required for treatment of the joint disruption by extension of the incisions distally [34,75].



2.

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Skin Compromise

Skin necrosis can result from the initial trauma of the injury, swelling, tenting of the skin by nonreduced dislocations, or compromise of skin circulation from surgical incisions. The injured foot should be closely watched for evidence of soft tissue compromise in the initial injury period and early postoperative course. Additional soft tissue procedures such as skin grafting or muscle or skin flap coverage may be necessary if skin slough occurs [2]. 3.

Other Complications

Other complications that may occur include redislocation in the early period, reflex sympathetic dystrophy, nonunion of fractures, painful bony exostosis, persistently abnormal gait, degenerative arthritis, and chronic pain. Posttraumatic arthrosis is the most prevalent complication overall [8,12,34,49,51,71,73]. Planovalgus deformity of the foot with collapse of the longitudinal arch is the most common long-term outcome of untreated instability of the Lisfranc complex [34,49,71,80]. Bohay et al. [80] have also reported a series of hallux valgus deformities resulting from persistent instability of the first TMT, resulting in widening of the first intermetatarsal angle. Successful treatment of this deformity requires stabilization of the TMT articulation as well as distal soft tissue realignment. Avascular necrosis of the second metatarsal head has also been reported, probably secondary to disruption of the dorsalis pedis artery [16,34,81].

II.

MIDFOOT FRACTURES

A.

Introduction

Fractures of the midfoot have often been considered minor injuries and neglected relative to the care of long bone injuries. However, a large percentage of multitrauma patients with lowerextremity injuries have injuries to the foot, and these foot injuries can lead to significantly poorer treatment outcomes, especially if the injuries are missed or neglected. While the joints among the bones of the midfoot have little motion and are of limited importance in the function of the foot, these bones do form critical articulations with the bones of the hindfoot and forefoot. Maintenance of the overall structural integrity of the midfoot is critical to the function of the foot as a whole [82].

B.

Anatomy

The midfoot comprises the navicular, the three cuneiforms that compose the medial column, and the cuboid that forms the lateral column [35]. The medial column is held together by dense ligamentous attachments between the navicular and cuneiform bones. These ligaments limit the motion across the naviculocuneiform and intercuneiform joints, such that the medial column essentially moves as a unit. The medial three metatarsals are also tightly connected to the cuneiforms at the Lisfranc articulation, making motion at these joints also relatively unimportant to the normal overall function of the foot. The articulations between the lateral two metatarsals and the cuboid have greater mobility and contribute significantly to the ability of the foot to accommodate to uneven surfaces. Maintaining the function of these joints is therefore a key goal in the treatment of injuries to the lateral column [82]. Most of the motion of the midfoot occurs at the talonavicular and calcaneocuboid joints, which together form the transverse tarsal or Chopart’s joint. These joints contribute significantly to pronation and supination of the foot. Function of the talonavicular joint is especially critical in the overall biomechanics of the foot during gait, as motion through this joint allows the foot to transition from a flexible structure in early stance that is capable of accommodating uneven surfaces to a rigid structure in late stance that is able to bear the forces required to propel the body forward at push-off [82]. Loss of motion at this joint has been observed to severely restrict subtalar motion, resulting in difficulty in accommodating to uneven surfaces and possibly resulting in arthrosis of the surrounding articulations [83,84]. This makes the talonavicular joint the most


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critical articulation involving the midfoot, and thus the navicular the most important bone in this complex. Its structural integrity must be maintained or restored for normal function of the foot [75]. Motion through the calcaneocuboid joint is much more limited, and loss of motion here is much more readily tolerated. Strong but relatively loose ligaments connect the navicular to the talus and the surrounding bones. Several of these structures, including the calcaneonavicular (spring) ligaments, the talonavicular ligament, and the deltoid, contribute to the acetabulum pedis [35,85]. This is the complex of structures surrounding the spherical head of the talus like a socket, allowing a swiveling motion to occur there. The tibionavicular ligament, a slip of the superficial deltoid ligament, also attaches to the medial navicular [86–88]. The posterior tibial tendon is the only tendon inserting on the midfoot. Its primary attachment is to the plantar aspect of the medial pole of the navicular. This tendon also has a broad, fanlike insertion that extends to the plantar aspects of the cuneiforms, the medial metatarsals, and even the cuboid. This broad insertion helps reinforce the rigid interconnections between the midfoot bones. The strong attachment to the navicular tuberosity can create avulsion fractures of this structure [35,75,86,89]. The blood flow to the navicular enters primarily through its dorsal and plantar surfaces. The dorsalis pedis artery sends a branch to the dorsal aspect of the bone, and the medial plantar branch of the posterior tibial artery largely supplies the plantar aspect [35,88]. The medial and lateral thirds of the navicular have a relatively rich blood supply compared with the central third, making avascular necrosis and nonunion of fractures much more likely in the central region [90] (Figure 5.24).

C.

Navicular Fractures

1.

Classification and Mechanism of Injury

There are four basic types of navicular fractures: dorsal avulsion, tuberosity avulsion, body, and stress. Of these, dorsal avulsion fractures are the most common and least serious, accounting for approximately 47% of all navicular fractures [86]. These are usually avulsions from the dorsal lip of

Figure 5.24 Blood supply to the navicular in a 4-year-old girl. Note the primary contribution to the blood supply to the central third from an unnamed branch of the dorsalis pedis (1) and the anastamotic web of peripheral blood flow from the posterior tibial artery (2). (From Sarrafian, S.K., Anatomy of the Foot and Ankle, Lippincott, Philadelphia, 1983. With permission.)



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the talonavicular joint due to pull by the capsule and ligaments due to twisting and inversion motions of the foot [82,88]. Tuberosity avulsion fractures primarily occur from overpull by the posterior tibial tendon, usually with the hindfoot everted. Tension in the spring ligament may also contribute to the avulsion force [66,75,82,88]. The mechanism is similar to that for dorsal avulsion fractures but usually involves more force. The size of the avulsed fragment varies considerably. The remaining attachments of this tendon as well as the talonavicular joint capsule and tibionavicular ligament usually serve to limit the displacement of these fractures. Since this fracture usually occurs from a forcible abduction of the forefoot, fractures of the cuboid are often associated with it and should be carefully sought. This fracture may be mistaken for an os naviculare and vice versa. This is an accessory navicular bone that occurs in up to 12% of the normal population and is bilateral in 64% of cases [82]. An os naviculare can usually be distinguished on the basis of radiographic appearance, having a smoothly contoured, well-corticated margin. Navicular body fractures are the most serious type but are fortunately uncommon. These fractures involve the critical talonavicular joint and jeopardize the structural integrity of the navicular itself. These injuries therefore carry the potential for significant disability. The medial column of the foot is frequently shortened and dorsal extrusion of portions of the navicular may occur [66]. They usually result from axial loading and forced plantar flexion combined with abduction or adduction of the forefoot [75], the same mechanism that produces most Lisfranc disruptions, which are not infrequently associated. These forces serve to drive the talar head into the navicular like a wedge, with the spring ligament and the posterior tibial tendon stabilizing or retracting the medial tuberosity [91]. The dorsal fragments hinge on the talonavicular ligaments, accounting for the dorsal extrusion of fragments. Falls from heights are the classical history. The classification system of these fractures by Sangeorzan et al.[85] has been widely adopted for these injuries. This system divides the fractures into types I, II, and III [75,82,88] (Figure 5.25). In type I fractures the fracture line occurs in the coronal plane transverse to the long axis of the navicular and there is no angulation of the forefoot. Less than half of the body is involved in the fracture. These usually result from axial loading and plantar flexion without either abduction or adduction [75,85]. As such, the dorsal talonavicular ligaments are usually disrupted. In type II fractures, the primary fracture line is in an oblique plane from dorsolateral to plantarmedial, with the major fracture fragment displaced medially along with the forefoot [75,85]. Usually the dorsomedial fragment is the major fragment and the smaller plantarlateral fragment is comminuted. These usually result from axial loading and plantar flexion with an adduction component [75]. As such, there are no compressive forces acting on the lateral column, and injury to the cuboid is seldom present. Type III fractures are fractures in the sagittal plane of the navicular with comminution of the central or lateral portion and lateral displacement of the forefoot [85]. The largest fragment is again medial, but the degree of comminution of the plantar and lateral portions is more severe than in the previous types. These usually occur from axial loading and plantar flexion with forceful abduction of the forefoot [75]. Injuries to the lateral column of the foot are common due to the compressive forces generated, such as fractures of the cuboid or anterior process of the calcaneus or subluxation of the calcaneocuboid joint. Disruption of the naviculocuneiform ligaments usually occurs [75]. With severe fragmentation of the lateral body, the talar head may displace into the gap created, displacing the midfoot medially. The result is a varus shift of the hindfoot, seen both clinically and radiographically [88,92]. As with all such injuries, stress fractures of the navicular are the result of chronic repetitive injuries that overwhelm the bone’s ability to repair itself. They occur almost exclusively in highperformance athletes engaging in endurance type activities such as long-distance running or other intense training programs. The first reported case in the literature was in 1970 [93], but by the mid1990s it was recognized that these were not uncommon injuries in athletes [88,90,94,95]. These injuries undoubtedly occur more often than they are diagnosed. The average time to diagnosis when this is made is 4 months [82]. Unfortunately, failure to diagnose a stress fracture early may lead to chronic disabling pain or even a complete displaced fracture. This can lead to talonavicular arthrosis or nonunion. Not surprisingly, these fractures most often occur in the less vascular central third of the body, usually in the sagittal plane (Figure 5.26).


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Figure 5.25 Classification of navicular body fractures according to Sangeorzan et al. (A) Type I fracture. (B) Type II fracture. (C) Type III fracture. See text for detailed description of fractures. (From Hansen, S.T., Jr. and Swiontkowski, M.F., Orthopaedic Trauma Protocols, Raven, New York, 1993. With permission.)

2.

Diagnosis

Because the midfoot is such a stable structure, a high-energy injury is usually required to disrupt it. Midfoot fractures are therefore rarely isolated injuries. As is the case for Lisfranc injuries, they may be radiographically subtle and easily overlooked in the face of more obvious foot or lowerextremity injuries. Dorsal avulsion fractures usually present with swelling, pain, and tenderness localized over the fracture fragment, usually along the dorsomedial talonavicular joint. They are frequently associated with lateral ankle sprains [89]. Tuberosity avulsion fractures will present with a history of eversion of the foot and pain over the medial tuberosity that is worsened by weightbearing and resisted eversion of the foot, which places tension on the posterior tibial tendon. Navicular body fractures will present with marked midfoot pain and pain with motion of the forefoot or the midfoot. The medial navicular will usually be tender to palpation. The dorsally extruded fracture fragments may be palpable if the swelling is not too severe. Swelling, ecchymosis, or persistent pain in the foot or a mechanism of injury consistent with foot injury should always prompt the physician to obtain standard AP, lateral, and oblique series of the foot, preferably standing or at least simulated weight-bearing if possible. These films should be



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Figure 5.26 (A) AP and (B) lateral radiographs of a nearly completed stress fracture of the navicular. Note the location in the less vascular central third of the body.

checked for subtle fractures and for normal anatomic relationships among the bony elements. The navicular should overlap the three cuneiforms equally on the AP view and the dorsal aspects of the navicular and cuneiforms should align on the lateral view [96]. Avulsion fractures from the dorsal cortex will be most clearly visible on the lateral view. Tuberosity avulsion fractures will be most visible on the oblique and AP views. These may be mistaken for an os naviculare on initial assessment. However, closer evaluation should easily distinguish between these two entities. The os naviculare will have a smooth, rounded, and sclerotic margin in contrast to the sharp, jagged line of an acute fracture. A contralateral foot film may also be helpful, as os navicularae are bilateral in 64% of cases [82,97]. The picture may become more confused by the fact that a disruption of the synchondrosis between an os naviculare and the navicular tuberosity may cause this accessory bone to become painful. Despite careful evaluation of plain radiographs, navicular fractures may be missed in up to a third of all cases [98]. If a high index of suspicion remains despite negative plain radiographs, a bone scan should be obtained to rule out subtle injury. A CT scan may also be helpful in revealing nondisplaced fractures, as well as in assessing the extent of involvement in comminuted fractures. This can play a key role in planning the surgical treatment of the fracture (Figure 5.27). Stress fractures of the navicular should be suspected in an athlete who presents with an insidious onset of cramping pain and tenderness in the dorsomedial aspect of the midfoot [75,88,90,93–95]. The presenting symptoms are often confused with anterior tibial tendonitis, which they closely resemble [75]. The pain is worsened by toe standing [94]. These vague and often misdiagnosed symptoms may leave the athlete reluctant to curtail his or her training activities, leading to displacement and long-term disability. It is therefore critically important to evaluate suspicious cases radiographically. Plain films may reveal a fracture line in advanced cases, usually a vertical line through the central third of the bone [93]. Coned-down views centered on the navicular may be helpful [90]. A bone scan should be ordered when no fracture is visible on plain films. Tomograms or a CT scan will best visualize an incomplete fracture, which usually starts at the dorsal cortex and is propagated plantarly along the talonavicular articular surface [75,93,95,99]. The margins of the fracture line will be sclerotic to varying degrees depending on the age of the


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Figure 5.27 CT scan of navicular fracture showing a type III fracture with lateral comminution.

fracture [75]. The radiographic picture may be further complicated by confusion of a stress fracture with a bipartite navicular in which the ossification centers fail to completely fuse at the end of growth [90,93,94]. This can be distinguished from a fatigue fracture by the orientation of the fracture line. A bipartite navicular plane will run obliquely from proximal plantar to dorsal distal, separating a dorsal triangular ossicle from the rest of the navicular body [100]. This is clearly distinguished from the sagittal orientation of a stress fracture line. Furthermore, a bipartite navicular will show no increased uptake on bone scan [75,88]. 3.

Treatment

Dorsal avulsion fractures. Most dorsal avulsion fractures are structurally insignificant and can be managed symptomatically. This may range from a simple compression wrap such as an Ace bandage to a short 3- to 4-week course of immobilization in a short leg walking cast [82,89,101]. If symptoms persist despite immobilization, a small fragment may be excised with or without ligamentous reattachment after the soft tissue injury subsides [89,101]. However, the persistently painful patient must be carefully evaluated for the presence of a midtarsal subluxation. If this is present a longer course of cast immobilization for 6 weeks or greater followed by the use of a molded medial arch support may be necessary [102]. Larger avulsion fragments are more likely to lead to subluxation or arthrosis and several authors recommend internal fixation of such fragments with a compression screw [75,88]. Tuberosity avulsion fractures. As described above, the extensive soft tissue attachments to the medial tuberosity usually prevent significant displacement of these fractures. Most can therefore be managed conservatively. A compressive dressing may be sufficient for small fractures in inactive patients, but usually a splint followed by a short leg walking cast for 4 to 6 weeks is utilized. The cast should be applied with mild supination of the foot to reduce tension on the posterior tibial tendon and molding of the medial arch to support the fragment [82,88,89,103,104]. Even in cases where a nonunion or fibrous union occurs, these are rarely symptomatic. If a symptomatic nonunion does occur, it can be treated in a manner similar to the treatment for a painful accessory navicular, with excision of the nonunited fragment and reattachment of the posterior tibial tendon to the roughened bed via a bony tunnel or suture anchor. Advancement or tensioning of the tendon is not usually necessary if the remaining insertion is not disrupted. A short leg cast without weight-bearing is used for 4 weeks postoperatively, followed by progressive weight-bearing. A larger fragment or separation of the fracture line by more than 5 mm may be considered an indication for internal fixation, as such fractures are more likely to produce a symptomatic nonunion [88]. Open anatomic reduction and lag screw fixation may be used in such cases, or in symptomatic nonunions with large fragments (Figure 5.28). Hansen [75] advocates extending the lag screw through the naviculocunei-



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Figure 5.28 (A) Avulsion fracture of the navicular tuberosity. (B) Due to the large size of the fragment and the degree of displacement, the fracture was treated by lag screw fixation.

form or intercuneiform joints for better fixation. This is followed by 6 to 8 weeks of cast immobilization without weight-bearing. Navicular body fractures. Conservative treatment of navicular body fractures almost invariably produces a poor result. Closed manipulation of these fractures is almost never successful and leads to nonunion, avascular necrosis, and collapse of the medial column, necessitating fusion of the talonavicular joint to relieve pain and restore stability [85,91,92,98,105,106] (Figure 5.29). Anatomic reduction of this joint surface with less than 1 mm of articular step-off and rigid internal fixation should be the goal for treatment of these fractures. Closed treatment should be considered only for the most minimally displaced navicular body fractures, which are rare. If the talonavicular joint surface cannot be restored, primary or delayed arthrodesis may become necessary [84,88,107,108]. Even the relatively stable naviculocuneiform joints may be disrupted in these fractures and may need to be stabilized with internal fixation or arthrodesis. The length and alignment of the medial column must be restored to prevent forefoot malalignment and collapse of the medial longitudinal arch. In cases of severe crushing injury, this may require external fixation to relieve tension on the internal fixation construct or even an interpositional structural bone graft [75,82,88] (Figure 5.16). If nondisplaced fractures are treated conservatively, they should be immobilized in a short leg cast without weight-bearing until radiographic healing is seen, which usually requires at least 8 weeks. The fracture should be carefully monitored during immobilization for any sign of displacement or resorption along the fracture line, and there should be a low threshold for operative intervention if these are seen [88]. The surgical approach for fixation of these fractures is usually dorsal between the anterior and posterior tibial tendons, preserving the dorsal neurovascular structures. The exact plane of dissection should be as close to the plane of the fracture as possible to minimize the dissection required to approach the fracture [75]. Arthrotomies of the talonavicular joint when necessary should be minimized and stripping of the capsule from the navicular fragments should be avoided to prevent


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Figure 5.29 Talonavicular arthrosis resulting from failed conservative management of a type I navicular body fracture. This painful arthrosis required talonavicular fusion for symptom relief. Preoperative (A) AP; (B) oblique; and (C) lateral views of the foot. Postoperative (D) AP; (E) oblique; and (F) lateral views showing fixation of the fused joint. Note the extension of the screw fixation across the naviculocuneiform joints to improve bony purchase.

further compromise of the circulation to these fragments. When possible, exposure of the fracture should be performed from the less critical naviculocuneiform side. External distraction of the medial side can be invaluable both to unload the tension across the fixation construct and to harness the power of ligamentotaxis for indirect reduction. This may be accomplished with an external distractor or with a small external fixator, which can be left in place during fracture healing. The proximal pin can be placed in the talar neck or medial malleolus, and the distal pin in the medial cuneiform or first metatarsal base [75,88]. Gross reduction of the major fragments is usually then obtained via large Weber reduction forceps placed percutaneously through a medial stab wound and directly on the exposed bone laterally. Small Kirschner wires may be placed in small articular fragments for use as reduction joysticks. Definitive fixation of major fragments is usually with lagged screws. There is some debate regarding the most appropriate choice for screw fixation. Hansen [75] states that either 3.5-mm cortical or 4.0-mm partially threaded cancellous screws may be used, but cautions that the threads of the cancellous screws should cross the fracture by at least 5 mm to avoid fatigue failure of the screw. Sanders [88] likewise prefers 3.5-mm cortical screws over cannulated screws due to their larger core diameter and thus greater strength. He cautions against the use of cannulated screws due to their insufficient strength and purchase. Hansen [75] has also popularized the technique of extending these lag screws across the nonessential



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naviculocuneiform joints to allow more solid fixation in the subchondral bone (Figure 5.29). Small, 1.5- to 3.2-mm bioabsorbable pins may be used to fix small articular fragments [88]. If necessary for stabilization of talonavicular dislocations or fixation of small articular fragments, 1.6-mm smooth Kirschner wires may be placed across the talonavicular joint and into the head and neck of the talus, to be removed at 6 weeks or when fracture healing allows. Cancellous bone grafting may be necessary to fill voids in the navicular after reduction or to support articular fragments. In cases of severe lateral or plantar comminution, structural bone grafts may be necessary to replace the unreconstructable fragments [75,88]. Type I body fractures usually involve minimal comminution, simplifying their reduction and fixation. Reduction can usually be easily achieved using the techniques described above. A small talonavicular capsulotomy usually suffices for visualizing reduction of this joint. The medial point of the Weber forceps is placed just below the tubercle to reduce the coronal fracture. Manual traction may suffice without external fixation or distraction. If more aggressive direct reduction is needed, the fracture can be approached from the naviculocuneiform side, but this is seldom necessary. Two screws placed from dorsal to plantar through the navicular alone usually suffice for rigid fixation [75,85,88] (Figure 5.30). Type II fractures pose a more problematic reduction due to the usual comminution of the plantarlateral fragment and dorsal dislocation of the dorsomedial fragment. External distraction will usually be necessary for reduction of these fractures after exposure and debridement of the talonavicular joint via a minimal capsulotomy. Since most of the comminution is usually on the plantar aspect, the Weber clamp should be placed across the superior aspect of the navicular, followed by reduction of the talonavicular fragments under direct visualization. A bone graft will usually be required, and may be taken from the lateral calcaneus or the proximal tibia. If possible, direct lag fixation from the medial to the lateral fragment is still preferable, but often the lateral fragment is too comminuted for firm fixation. In this case, the screws may be aimed obliquely through the medial fragment into the medial or middle cuneiforms. The lateral fragment may be fixed to the lateral cuneiform or the cuboid. Small lateral fragments may need to be pinned to the talar head. Kirschner wire fixation from the first cuneiform into the talar head and neck may also be needed to stabilize the dorsal dislocation if the talonavicular ligament is disrupted, as it commonly is [75,85,88] (Figure 5.31). Type III fractures usually involve extensive comminution of the plantar and lateral fragments. Since these fractures usually occur from a forefoot abduction mechanism, they frequently involve fractures of the lateral column of the foot and residual lateral displacement of the forefoot. Lateral distraction with an external fixator placed between the calcaneal tuberosity and the base of the fifth metatarsal is often necessary for reduction of these fractures. A medially placed external fixator may also be necessary but can usually be removed after definitive fracture fixation. The

Figure 5.30 (A) AP and (B) lateral views of internal fixation of a minimally displaced type I navicular body fracture. The fracture was reduced with a Weber clamp placed percutaneously, and two 4-mm titanium cancellous screws were percutaneously placed across the fracture.


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Figure 5.31 (A) AP; (B) oblique; and (C) lateral views of the fixation of the injury shown in Figure 5.27. A lag screw has been placed from the lateral to the medial fragment. An additional screw has been placed between the medial fragment and the lateral cuneiform. A Kirschner wire has been used to hold the comminuted lateral fragments reduced against the talar articular surface while the fracture heals.



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calcaneocuboid injury is addressed as described under ‘‘Cuboid Fractures’’ section. An attempt is made to reduce the major navicular fragments with the Weber forceps as before, but fixation almost always requires extending the screws across the naviculocuneiform joints from both the medial and lateral fragments. This stabilizes both the fracture fragments and the naviculocuneiform disruption usually associated. The naviculocuneiform joints may be sufficiently damaged to require fusion, and this may be done without significant loss of function. Every attempt should be made, however, to reconstruct and preserve the critical talonavicular articulation. This is not always possible, in which case a structural bone graft, usually from the iliac crest, should be used to preserve the length of the medial column, followed by isolated fusion of the talonavicular joint [75,85,88]. There remains some controversy regarding whether primary triple arthrodesis should be performed in such cases, but most authors agree that the subtalar joint should be preserved unless it subsequently becomes a source of pain [86,88,91,98,104]. Prolonged immobilization without weight-bearing is usually required postoperatively. A short leg cast is left in place for 10 to 12 weeks as serial radiographs are obtained. Weight-bearing and motion are not started until radiographic evidence of union is seen. Pins placed across the talonavicular joint are usually removed at 6 weeks [88]. Screws placed across the naviculocuneiform joints may be left in place, although Sanders [88] recommends removal at 6 months to prevent breakage. The results of operative treatment vary depending on both the severity of the injury and the quality of reduction obtained and maintained during healing. Two large series have been reported in the literature. Main and Jowett [98] in 1975 published a series of 29 navicular body fractures, 5 of which were nondisplaced. All 5 of these fractures had good or excellent outcomes. Of the 24 remaining fractures treated with open reduction, only 6 patients had good or excellent results. Sangeorzan et al. [85] reported 21 navicular body fractures in their landmark paper in 1989. They considered satisfactory reduction to be restoration of more than 60% of the talonavicular joint surface in both the AP and lateral planes. This was achieved in all of their type I fractures, 67% of their type II fractures, and 50% of their type III fractures. They reported radiographic union at an average of 8.5 weeks. Overall, they reported 67% good results, 19% fair results, and 14% poor results. Of the 15 satisfactorily reduced fractures, 14 (93%) had good results and 1 had a fair result. They concluded that both the type of fracture and the accuracy of reduction directly correlated with the final clinical outcome. Even with rigorous surgical treatment, late complications are common with these fractures. Posttraumatic arthrosis is frequent due to the severity of articular damage at the time of injury even with optimal fixation [105]. This is best addressed by isolated talonavicular arthrodesis. Sangeorzan et al. [85] reported complete avascular necrosis in two patients in their case series, and partial necrosis in four. Avascular necrosis, loss of fixation, or failure to reconstruct the length of the medial column may lead to late collapse of the navicular, particularly the lateral portion. This can lead to subsidence of the talar head into the void created, to the point that the head may begin articulating with the lateral cuneiform. This shifts the forefoot medially and the hindfoot into varus deformity, as described by Sanders [88] and Sanders and Hansen [92]. Correction of this deformity requires a structural graft to reconstitute the medial column followed by triple arthrodesis. Stress fractures. Stress fractures diagnosed before completion and displacement can be treated conservatively. This requires immobilization in a short leg cast with complete non-weightbearing for at least 6 weeks for reliably successful treatment [75,88,90,95,109]. The patient should be evaluated carefully for any underlying anatomic abnormality that predisposed to the stress fracture, such as a calcaneonavicular coalition, cavovarus foot, or osteopenia [75,88,94]. If adequate healing and symptom relief is achieved at 6 weeks, the patient may gradually begin weightbearing and return to training activities over an additional 6-week course. If the fracture is already complete at the time of diagnosis or if it fails to heal with the above regimen, surgical fixation with lag screws and bone graft should be performed [88,90]. The margins are often sclerotic and healing may be improved by drilling across this sclerotic area with multiple passes with a 2.7-mm drill, followed by curetting of the sclerotic bone and fibrous tissue from the fracture site [75,110]. Care must be taken not to further displace the fracture or disrupt the vascularity during this process. Weber forceps may be useful to prevent this. Postoperative management is similar to that for conservative treatment. Custom orthosis may be advisable if the athlete returns to competitive training [75].


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Untreated stress fractures may progress to completion and displacement, with complications and sequelae similar to that for acute traumatic injuries. Management in these cases is similar to that described above for navicular body fractures. Cuneiform fractures. Isolated cuneiform fractures are exceptionally rare, and almost always occur with Lisfranc injuries or navicular fractures [75,88,89,111,112]. Isolated fractures are almost always the result of direct-blow trauma. They are rarely displaced due to the extensive strong ligamentous connections to the cuneiforms. Displaced cuneiform fractures should be presumed to be a Lisfranc injury until proven otherwise [88,106]. The standard AP, lateral, and oblique views of the foot are usually sufficient to evaluate nondisplaced chip fractures. Bipartite cuneiforms and osteochondritis dissecans of the navicular have been reported [113], but can usually be distinguished from fractures on the basis of their radiographic appearance. Acute fractures will be accompanied by localized pain and tenderness to palpation over the fracture fragment. Nondisplaced avulsion or direct-blow fractures may be treated conservatively with either a short leg walking cast or a removable walking boot. Displaced fractures should be treated surgically. When part of a Lisfranc injury, they should be treated in conjunction with the overall injury. Fixation of the cuneiform fracture will usually help stabilize the TMT complex [88]. All of the articulations surrounding the cuneiforms are relatively immobile, including the three medial TMT joints. As such, fixation across these joints and even, when necessary, fusion of them is well tolerated. Lag screw fixation of fragments to the body of the cuneiform may be performed when possible. Unstable joints should be reduced anatomically and fixed with 3.5-mm cortical lag screws as close to perpendicular to the joint surface as possible [75]. Postoperative management is usually dictated by the associated injury, but a minimum of 6 to 8 weeks of non-weightbearing immobilization followed by gradual resumption of weight-bearing and range-of-motion exercises in a removable boot for an additional month is required. Cuboid fractures. Like cuneiform fractures, isolated cuboid fractures are rare. Isolated injuries are usually associated with direct blows to the bone. Avulsion fractures may occur with twisting injuries to the foot and are often confused with lateral ankle sprains, with which they are usually associated [88,111,114]. These are the most common fractures of the cuboid. Compression fractures are less common but usually far more serious. These usually occur with axial loading injuries of the foot, with forefoot abduction. They have been referred to as ‘‘nutcracker fractures’’ due to the lateral metatarsals and anterior process of the calcaneus compressing the cuboid in a viselike fashion [115]. These same injury mechanisms can produce Lisfranc injuries, navicular fractures, and metatarsal fractures, and these fractures may distract the physician from diagnosis and treatment of the cuboid injury. Cuboid compression fractures also usually result in injury and subluxation of the calcaneocuboid joint, as well as loss of the length of the lateral column of the foot. This lateral column shortening can lead to forefoot abduction and loss of supination during push-off, impairing gait [75]. Displacement of the cuboid is constrained by the surrounding anatomy. The very shape of the calcaneocuboid joint prevents dorsal or lateral subluxation. Thus, displacement almost invariably occurs in the plantarmedial direction. The patient will usually present with a history of either a direct blow to the area or a twisting and loading injury to the foot, in which the foot was forced into plantar hyperflexion and abduction [88,89,115–117]. Compression fractures, like navicular fractures and Lisfranc injuries, usually require a high-energy injury. The patient will be focally tender over the cuboid injury and lateral border of the foot. If the patient is tender over the medial midfoot, more serious injury such as subluxation of Chopart’s joint should be suspected. Three standard views of the foot should be obtained for evaluation, preferably in the standing position. The oblique view of the foot may be especially valuable in visualizing the injury to the cuboid and surrounding bones. Complicated fractures and subluxations may benefit from evaluation with CT. Once associated injuries have been ruled out, avulsion fractures of the cuboid can usually be treated conservatively with cast immobilization or a removable boot if they are small and minimally displaced. The patient may usually bear weight on the injured foot as tolerated in the immobilization device. Immobilization should continue for 4 to 8 weeks or until radiographic healing is seen and pain with ambulation subsides [88,89,104,112,118,119]. Large or displaced fragments should be very carefully evaluated, as they are almost certainly associated with further injuries. These may benefit from internal fixation.



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Compression fractures of the cuboid almost always require operative management. The main goals of treatment should be restoration of the length of the lateral column, reduction of any subluxation of the cuboid, and restoration of the articular surfaces of the lateral TMT and calcaneocuboid joints, in that order of importance. The fracture can be approached from a dorsolateral incision parallel to the plantar aspect of the foot overlying the calcaneocuboid joint. Care must be taken to avoid damage to the sural nerve and peroneal tendons. Distraction of some form will be required to restore the length of the cuboid and lateral column. In cases where there is minimal joint damage or subluxation and solid end plates are still present, it may be possible to restore length with a lamina spreader placed within the body of the cuboid. More often, however, external distraction with a fixator placed between the calcaneus and the fifth metatarsal base will be necessary (Figure 5.32). This fixator may be left in place as a neutralization device during healing. Alternatively, it may be replaced at the end of the procedure with a long plate between the anterior process of the calcaneus and the cuboid body or metatarsal bases, an ‘‘internal external fixator’’ (Figure 5.32). Once the lateral column has been restored to length, the joint surface should be

Figure 5.32 Direct-force injury to the right foot resulting in a compression fracture of the cuboid and fractures of the second through fifth metatarsals. An external fixator was placed between the calcaneus and the fifth metatarsal base to support the lateral column at length, followed by elevation and bone grafting of the joint surface of the cuboid. (A) AP; (B) oblique; (C) axial CT; and (D) lateral views of the injury showing the compression fracture of the cuboid.


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Figure 5.32 Continued Postoperative (E) AP; (F) oblique; and (G) lateral standing views after fixation of the fracture.

carefully disimpacted, avoiding stripping of the blood supply to the fragments. A small arthrotomy may be required to visualize the joint surface reduction. The remaining defect in the cuboid body will need to be filled with bone graft. If the defect is small and the end plates are solid, the defect may be filled with cancellous graft from the proximal tibia, lateral calcaneus, or iliac crest. Larger defects with compromised end plates may need structural support from the bone graft, in which case a tricortical graft from the iliac crest should be used. The graft should be retained in place and the reduction held by a lateral plate either on the cuboid or spanning the calcaneocuboid joint. An Hshaped plate is especially useful for this purpose. Careful assessment must be made regarding the quality of the joint surface after reduction. If severe articular damage is present, fusion of the calcaneocuboid joint should be considered. This fusion is generally well tolerated with minimal compromise of foot function. All effort should be made, however, to preserve the function of the fourth and fifth TMT joints, as motion through these joints is critical to the accommodative



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function of the forefoot during the weight acceptance portion of the stance phase of gait, and fusion of these joints is almost always debilitating [75,88]. Fusion of the calcaneocuboid joint may be achieved by denuding the articular cartilage, drilling the subchondral bone, fish-scaling the surface of the joint. A tricortical graft is then placed in the cuboid side to ensure restoration of lateral column length. In almost all cases, it is better to restore the TMT joints as well as possible, leave a lateral column distractor in place, and allow the joint surfaces to mold to one another and heal. Interpositional arthroplasty or fusion may be attempted later if this leaves the joints unacceptably painful. If the joints were initially dislocated, pinning of the joints as discussed under ‘‘Lisfranc Injuries’’ may be necessary [75,82,88,111,117]. Postoperatively, the foot is immobilized without weight-bearing until radiographic healing is seen, followed by gradual resumption of weightbearing over several weeks.

III.

CONCLUSION

The multiple articulations and strong ligamentous attachments in the midfoot and its junction with forefoot provide structural integrity to the foot. The foot can be a strong lever for propulsion and can also be flexible for adaptation to the ground. A wide spectrum of injuries occur in the Lisfranc and midfoot area, ranging from subtle injury to the Lisfranc ligament to fractures and fracture dislocations involving the TMT complex and the midfoot. In the presence of significant swelling and bruising in the midfoot region following trauma, a high index of suspicion and special imaging techniques are necessary to diagnose the pure ligamentous or capsuloligamentous injuries, which if left untreated can cause long-term disability. Such injuries are missed, especially when there are other distracting injuries and also in patients with peripheral neuropathy, such as with diabetes mellitus. Anatomic reduction of joint surfaces and restoration of column length and ligament integrity are important factors in order to achieve the best functional outcome following severe fracture dislocations in the region of Lisfranc joint complex and midfoot. After stable fixation, prolonged immobilization in a cast and further protection in an orthosis is necessary. Despite appropriate treatment, there is potential for poor outcome following these injuries and the patients must be counseled in this regard. In the future, use of bioabsorbable material for internal fixation instead of metal will obviate the need for further surgery to remove the hardware.

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6 Fractures of the Metatarsals and Phalanges of the Foot Bryan J. Hawkins Central States Orthopaedic Specialists, Tulsa, Oklahoma

CONTENTS I. Introduction ................................................................................................................... 165 II. Anatomy......................................................................................................................... 166 III. Mechanism of Injury ...................................................................................................... 166 IV. Radiographic Evaluation................................................................................................ 166 V. Fractures of the First Metatarsal.................................................................................... 167 VI. Fractures of the Lesser Metatarsals................................................................................ 167 A. Shaft Fractures........................................................................................................ 167 B. Fractures of the Proximal Aspect of the Fifth Metatarsal ...................................... 172 VII. Phalangeal Fractures ...................................................................................................... 175 A. Hallucal Fractures................................................................................................... 175 B. Lesser Toe Fractures............................................................................................... 176 VIII. Conclusion...................................................................................................................... 177 References .................................................................................................................................. 177

I.

INTRODUCTION

The metatarsals and phalanges are important structural members of the foot. They form what is termed the forefoot and are responsible for the transmission of load and for shock absorption. Injuries to these bones may potentially result in the disruption of these functions, which, in turn, can cause disability if the alterations in the weight-bearing characteristics cause pain. The principles of treatment of fractures to the metatarsals and phalanges center around the concept of restoring the anatomy to normal, or as close to normal as possible, thus minimizing the potential for problems. Fractures of the metatarsals are often straightforward. The first and the fifth metatarsals can, however, pose some unique and challenging problems based upon their individual weight-bearing functions, their location, and the anatomy of the blood flow to these areas. Fractures of the phalanges are generally easy to treat because the bones are small and residual displacement is not often associated with significant clinical problems. The proximal and distal phalanges of the great toe are an exception. This is directly related to the size of these bones, the area of articular surface, and the greater loads borne by the great toe. The following discussion addresses the biomechanical and anatomic issues related to the weight-bearing function of the metatarsals and phalanges and outlines treatment methods of fractures in this area of the foot.

165


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II.

Hawkins

ANATOMY

The five metatarsals connect the midfoot with the toes and constitute the distal aspect of the plantar arch. The metatarsals project downward toward the floor at an angle of inclination that decreases from the first to the fifth metatarsal. Sarafian [1] describes the proximal aspects of the metatarsals as constituting a transverse arch, which is higher medially and lower laterally. When the metatarsal heads are viewed in the frontal plane they form a straight line by virtue of the variable slope. It becomes intuitive that weight is therefore transferred through the metatarsals via contact at the metatarsal head region. There are numerous descriptions of variations in lengths of the metatarsals ranging from the first through the fifth. In general, the second metatarsal is the longest followed by the third, then the first, then the fourth and fifth. However, this relationship is highly variable. The first metatarsal carries the greatest load of force transmission by virtue of its inclination and its position during load transfer in the gait cycle. It bears twice the load as each of the lesser metatarsals, which bear identical loads [2]. The treatment of fractures of the metatarsals is predicated on restoration of the anatomy and, thus, the weight-bearing characteristics of the bones. Displacement of metatarsal fractures will cause an alteration in the load distribution as the metatarsal heads encounter the floor. Plantar displacement of the distal aspect of the metatarsal causes increased load, whereas dorsal displacement causes decreased load, with load transfer to adjacent metatarsals [3]. Fractures at the proximal or distal ends of the metatarsals can involve the articular surfaces at either of these joints. This can lead to stiffness, altering the biomechanics and load transfer through the metatarsal, resulting in painful arthrosis of these joints. The treatment of metatarsal fractures, as with any fracture, is based on the restoration of appropriate bony anatomy and restoration of the relationship of the metatarsals to adjacent tarsal and metatarsal bones. Accomplishing this will restore the structural and biomechanical foot function to normal or as near to normal as possible. The toes consist of three bones each with the exception of the great toe, which consists of two. The lesser toes, in general, have a proximal, middle, and distal phalanx while the great toe consists of only a proximal and distal phalanx. The proximal phalanx articulates with the head of the corresponding metatarsal. The toes contact the ground during approximately 75% of the stance phase of the walking cycle [1]. The metatarsal phalangeal joints require approximately 50 to 608 of dorsiflexion to maintain normal gait. This becomes the goal of functional restoration after injury to this area.

III.

MECHANISM OF INJURY

In general, trauma to the forefoot results from either direct or indirect forces. Direct forces include crushing injuries to the foot where the force is applied directly to the metatarsal or when the foot is loaded axially and the force is transmitted through to the metatarsals. Indirect forces usually result from twisting injuries to the foot. Torque applied to a fixed foot may cause injury to the metatarsal and particularly to the fifth metatarsal [4]. The metatarsals are also subject to repetitive minor forces, which can result in stress fractures. The second metatarsal is commonly involved [5]. Fractures of the phalanges are most commonly the result of direct trauma to the specific bone and are the most common fractures encountered in the forefoot [6,7]. A common pattern of fracture of the lesser toes involves a proximal phalangeal fracture, which occurs when the toe is forcefully abducted when it hits an immobile structure such as a piece of furniture, the so-called ‘‘night walker fracture’’ [8].

IV.

RADIOGRAPHIC EVALUATION

Fractures of the metatarsals are usually readily assessed with the standard three views of the foot: anteroposterior (AP), lateral, and oblique. The lateral view is most important for assessing displacement, especially in the plantar and dorsal direction.


Fractures of the Metatarsals and Phalanges of the Foot

167

Evaluation of AP, lateral, and oblique radiographs of individual toes is helpful for assessing displacement and location of phalangeal fractures. With respect to the lesser toes, the oblique radiograph is often helpful because of the overlapping nature of the toes on the true lateral view. Separation of the toes by retraction of the noninvolved toes is sometimes possible for providing greater detail of a specific toe and the nature of a specific fracture. This can be especially helpful when the fracture involves the great toe.

V.

FRACTURES OF THE FIRST METATARSAL

The first metatarsal is considered separately from the lesser ones because of its size and load-bearing importance. Fractures of the first metatarsal are therefore treated based upon the deviation from normal anatomy. Sanders [9] advocates aggressive treatment of fractures of the first metatarsal because any displacement is poorly tolerated from a functional standpoint. Nondisplaced, stable fractures can be treated with closed immobilization. Delee [10] advocates weight-bearing within 7 to 10 days in this situation. The method of treatment for a displaced fracture of the first metatarsal should be tailored to the degree and amount of displacement as well as to the configuration of the fracture. Fractures with displacement or with an unstable configuration can often be treated successfully with closed reduction and Kirschner wire fixation. The first metatarsal shaft is large enough to accommodate plate and screw fixation as well if deemed appropriate (Figure 6.1). If the first metatarsal is severely comminuted, metatarsal length can be maintained with the use of small external fixators or spanning plates, which may, if necessary, cross onto the medial cuneiform. Fractures of the proximal or distal end of the first metatarsal should address the degree of involvement of the joint. The size of the bone permits stabilization of the bone with internal fixation. Joint involvement should be managed with the same principles that guide treatment of any joint fracture. Anatomic restoration is the goal, using any of the internal fixation methods available. Small screws or perhaps plate fixation can be used to treat fractures of the metatarsal head and neck. Large articular fractures should be reduced and stabilized with screws or Kirschner wire fixation as dictated by the fracture configuration.

VI. A.

FRACTURES OF THE LESSER METATARSALS Shaft Fractures

Fractures of the lesser metatarsal shafts can be considered in two categories with respect to treatment alternatives. Fractures can be nondisplaced or displaced and each of these two categories can occur singly or in multiple metatarsals. The metatarsals are tethered to each other by strong interosseous ligaments [1]. Lindholm [11] theorized that displacement of simple metatarsal fractures is usually minimal as a result of the tethering structures. These observations can be used in determining the optimum treatment, especially in single or multiple nondisplaced metatarsal fractures. Nondisplaced fractures are easily treated. Numerous modalities have been suggested including casting, taping, or the use of firm-soled shoes. The functional requirements of the patient, including the ability to control pain, are the best guides in determining which particular method suits a given patient. Closed treatment where weight-bearing is permitted should be followed closely in the early weeks of treatment to ensure that displacement does not occur. Multiple metatarsal fractures may involve a greater degree of soft tissue damage, which may alter the inherent stability of the adjacent metatarsal shaft. The particular treatment of multiple metatarsal fractures must be guided once again by displacement. The degree of acceptable displacement is not altogether clear. Hansen [12] states that anatomic reduction ‘‘must be achieved’’ and that as little as 2 to 4 mm of displacement can lead to a painful metatarsalgia. This sentiment is echoed by Sanders [9], who considered any sagittal plane displacement as a ‘‘cause for concern.’’ Shereff [3], however, suggests that displacement of 3 to 4 mm with an angulation of up to 108 is acceptable. It would seem intuitive that one must consider the degree of displacement and the


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Figure 6.1 (A to C) AP, oblique, and lateral radiographs of a displaced fracture of the first metatarsal. Note the anatomic reduction on the AP view, but obvious displacement on the lateral and oblique views. A nondisplaced fracture of the second metatarsal is also noted.



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Figure 6.1 Continued (D to F) Postoperative view of the same fracture. Anatomic restoration was achieved with a small plate and screw fixation. No operative treatment done on the second metatarsal fracture. Early healing is noted.


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functional requirements and medical condition of the patient to determine the degree of acceptable displacement. It stands to reason that the best method to achieve normal function is to achieve anatomic or as near anatomic restoration of the fractures as possible. The treatment of displaced metatarsal shaft fractures can be accomplished via closed reduction with cast immobilization. This is done with direct manipulation while applying the cast. Sanders [9] suggests that closed methods will often fail. Open stabilization can be carried out in a number of ways including Kirschner wire fixation, interfragmentary screw fixation, and plate and screw fixation [12]. The method described by Heim [13] can be utilized. This method uses first antegrade and then retrograde intramedullary pinning of the metatarsal shaft and is very well suited for fractures involving multiple metatarsals (Figure 6.2). Adjacent metatarsals can be treated through a single incision. The pins will exit out of the plantar surface of the foot through the distal aspect of the metatarsal and they are left this way (Figure 6.3). Sanders [9], who advocates this method as well, suggests that weight-bearing should not be permitted until the pins are removed at 4 to 6 weeks. Distally occurring fractures, including fractures in the neck of the metatarsal, tend to be unstable. The antegrade — retrograde pinning technique is again a reasonable way to treat these fractures. In this particular instance care must be taken to ensure the pin exits in the center of the metatarsal head so that it will align anatomically. Shortening of the fracture can occur if the neck is comminuted. Pin position is an important consideration, as a dorsal-exiting position will generate a plantar-flexed fracture. Metatarsal base fractures are frequently nondisplaced. The concern with any injury to the base of the metatarsal should be directed toward assessment of associated ligamentous injuries suggesting a Lisfranc dislocation. If the injury is in fact a true fracture at the base of the metatarsal, immobilization with limited weight-bearing is usually satisfactory for treatment. If there is displacement, these fractures are amenable to closed reduction and percutaneous pin fixation into the cuneiforms.

Figure 6.2 Sequential pinning technique for metatarsal shaft fractures. (From Heim, U. and Pfeiffer, K.M., Internal Fixation of Small Fractures: Techniques Recommended by the AO Group, Springer-Verlag, Berlin, 1987. With permission.)



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Figure 6.3 (A) Multiple metatarsal shaft fractures with shortening and displacement. (B and C) AP and lateral views of foot after antegrade–retrograde pinning as described by Heim and Pfeiffer. (D) Final radiograph after healing of the metatarsal shaft fractures.


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Fractures of the Proximal Aspect of the Fifth Metatarsal

Historically, fractures of the proximal aspect of the fifth metatarsal have been referred to as Jones fractures because of the original description by Sir Robert Jones, when he described an injury that he sustained while dancing. Jones [14] originally published his work in the Annals of Surgery in 1902, where he described six similar cases. Any fracture in the region of the proximal portion of the fifth metatarsal is often referred to as a Jones fracture. This has caused confusion when discussing these injuries. Fractures in this region fall into distinct patterns and not all fractures here are ‘‘Jones fractures.’’ Treatment of these fractures depends upon which pattern exists. Dameron [15] has classified proximal fifth metatarsal fractures as occurring in three zones. Zone 1 involves the tuberosity of the fifth metatarsal in its most proximal aspect and includes the insertion of the peroneus brevis tendon and the articulation with the cuboid. Zone 2 is distal to zone 1 and includes the articulation with the fourth metatarsal, while zone 3 begins just distal to the intermetatarsal ligaments between the fourth and fifth metatarsals and extends distally for approximately 1.5 cm (Figure 6.4A). A distinct transition or border does not exist between these zones. The blood supply to the fifth metatarsal, however, does have implications on the behavior of fractures in each of these specific regions. The vascular anatomy of the fifth metatarsal has been described in detail by Smith [16]. In this study, the metaphyseal portions of the fifth metatarsal proximally and distally demonstrated extensive perfusion through very small metaphyseal vessels. The main nutrient artery to the fifth metatarsal was noted to enter the medial portion of the middle third of the bone and its branches would course both proximally and distally. The proximal branch was noted to be relatively short, leaving an area relatively devoid of collateral circulation in the proximal portion of the bone

Figure 6.4 (A) Three anatomic zones of the proximal aspect of the fifth metatarsal. Zone 1 includes the articular surface of the fifth metatarsocuboid joint; zone 2 encompasses the articulation of the proximal fourth and fifth metatarsals; zone 3 extends 1.5 cm distal to zone 2. (B) The intramedullary vessel enters the medial aspect of the fifth metatarsal in its middle third. It divides into shorter proximal and longer distal branches. There are multiple minute vessels in both the proximal and the distal metaphyses. Little collateral circulation exists to the nutrient vessel between the metaphysis and diaphysis proximally. (From Dameron, T.B., J. Am. Acad. Orthopaed. Surg., 3, 110–114, 1995. With permission.)



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(Figure 6.4B). These findings correlate with clinical experience related to the occasional difficulty with healing in zones 2 and 3 of the proximal fifth metatarsal. Zone 1 fractures are generally considered to be avulsion injuries resulting from traction of the peroneus brevis tendon, although controversy exists over the actual mechanism of the injury [17]. Nondisplaced fractures are easily treated with supportive shoe wear, walking casts, or protected weight-bearing. Fractures can be expected to heal within a 6- to 8-week period. Displaced zone 1 fractures that involve more than 30% of the articular surface, or a step-off of greater than 2 mm, are amenable to open reduction and internal fixation, usually with Kirschner wires or small compressive screws [9] (Figure 6.5). Dameron [15] suggests that 3 mm of displacement is acceptable, but states that significant rotatory displacement requires internal fixation. Painful nonunions are treated with surgical stabilization. In the situation where the nonunited fracture fragment is small, excision of the fragment is recommended. Zone 2 fractures can be more problematic. The literature supports the fact that acute fractures in zone 2 can be successfully treated with casting, but controversy does exist regarding this particular situation [18–20]. The fractures are described as healing radiographically from the medial aspect of the proximal metatarsal cortex to the lateral and that clinical healing precedes radiographic healing [6]. Quill [17] has suggested, based on his review of the literature, that approximately one third of these injuries refractured if follow-up was long enough and suggests that more aggressive treatment may be indicated with these fractures. In summary, it is clear that zone 2 fractures will heal with closed treatment in limited or nonweight-bearing situations, usually within 6 to 8 weeks. These fractures can in fact go on to delayed union or nonunion, probably as a consequence of the unique vascular anatomy in this region. In this situation, more aggressive surgical intervention may be required. There is support for recommending surgery in patients who either do not have the desire to wait the expected period of time in a non-weight-bearing fashion, or are highly active athletic individuals who desire to return to the

Figure 6.5 (A) Zone 1 fracture of the proximal fifth metatarsal with significant displacement. (B) Same fracture after fixation with a 4-mm cannulated screw with anatomic reduction.


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activity at an earlier time. The specific treatment for any individual patient should be tailored to his or her activity level and personal desires. Full explanation of the risks and benefits of any treatment should be made before the institution of the ultimate treatment modality. Surgical treatment always carries the potential for complications, including failure of the intramedullary fixation, delayed union, and refracture [21]. Sanders and Heim suggests that fractures that are initially displaced should be treated with open reduction and internal fixation [9,13]. No specifics are outlined with regard to the degree of displacement that is acceptable. Zone 3 fractures are usually stress fractures [15]. There is often a prodrome of pain in the region of the fracture that exists for several days or even weeks before the appearance of the actual fracture line on the radiograph. These fractures are common in athletic individuals, often seen in football and basketball players, and can heal very slowly [9,15,22,23]. If suspected, these fractures can be treated with non-weight-bearing or activity limitation. Technetium bone scans can be used to identify a fracture that is otherwise not evident on plain radiographs. The recommended surgical treatment of zone 2 and 3 fractures is similar. The literature supports the use of intramedullary screw fixation placed through the tip of the tuberosity of the metatarsal. Dameron [15] suggests the use of a 4.5-mm malleolar screw as the recommended method of intramedullary fixation (Figure 6.6). The principles of fixation are to place an intramedullary screw with cortical fixation of the threads well beyond the fracture. Glasgow [21], in a small series of failed surgical cases, noted fewer failures when the 4.5-mm ASIF malleolar screw was used when compared with other fixation methods. The use of intramedullary screws must once again be tailored to the patient, considering the size of the bone and the ability to obtain purchase within the intramedullary canal of the fifth metatarsal. Screw breakage can occur and can be a very difficult complication when the fractured screw is seated well within the intramedullary canal of the bone.

Figure 6.6 (A) Immediate postoperative fracture in zone 2 of the fifth metatarsal in a 285-lb high-school football player. Operative treatment with a 4.5-mm malleolar screw. (B) Ten-week postoperative view of the same fracture. Solid healing is noted. Weight-bearing was begun at 3 weeks after surgery and the patient resumed full activity at 7 weeks.



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Sanders [9] suggests the use of 6.5- to 8-mm cannulated cancellous screws depending on bone dimensions when treating fractures in zone 2. He further states that he has never had to treat a fracture in zone 3 surgically. If the decision is made to treat these fractures surgically, the smallest screw that provides appropriate fixation should be used. This leaves the option of using progressively larger screws to gain fixation in the event that the fracture fails to heal. Zone 3 fractures associated with cortical sclerosis may require predrilling in order to stimulate endosteal bleeding and to facilitate screw placement. The literature clearly shows that intramedullary fixation of fractures of the proximal fifth metatarsal is an appropriate method for treating patients deemed to be surgical candidates. Other modalities are available and can be considered in special circumstances. Holmes [24] used pulsed electromagnetic fields (PEMFs) to treat nine delayed unions or nonunions of the proximal fifth metatarsal. All fractures healed in an average of 4 months. The fractures treated with non-weightbearing in association with PEMF healed in 3 months. The use of PEMF was considered a reasonable modality when taking into account risks and morbidity associated with surgical treatment and when considering that the time to healing was comparable with other treatment methods. Bone grafting has also been used in the treatment of these fractures. Described techniques include rectangular corticocancellous inlay grafts, sliding local grafting, and reversed trapezoid grafting [23,25,26]. These series report acceptable time to healing. Dameron [15], however, reports that bone grafting is not necessary, as fractures healed more quickly with intramedullary screw fixation. In general, surgical treatment of these fractures is rare. Dameron [15] reports that surgical treatment was necessary in only four patients out of a total of 237 fractures in all three zones over a period of 5 years. If surgical treatment is warranted, intramedullary screw fixation is the recommended approach. Ebraheim et al. [27] studied the anatomy of the fifth metatarsal, noting that decreased bone stock and bowing of the canal can lead to complications when intramedullary fixation is used. Adjunctive modalities such as bone grafting and PEMFs are supported as methods of fracture treatment as well. The approach to any fracture must be tailored to the needs of the individual patient.

VII.

PHALANGEAL FRACTURES

Phalangeal fractures are divided into two categories: hallucal fractures and fractures of the lesser toes. The great toe consists of two phalanges, proximal and distal. Significant loads are borne through the metatarsophalangeal (MTP) joint of the great toe. This must be kept in mind when treating fractures of the hallux.

A.

Hallucal Fractures

Fractures of the proximal phalanx of the hallux are usually either transverse or oblique with intraarticular extension [28]. Hansen [12] states that the transverse fracture is particularly unstable because of the imbalance in pull of the flexor and extensor mechanism. Displacement can lead to aberrant loading and painful keratosis formation. Therefore, he recommends aggressive treatment of this injury, with consideration of open reduction and internal fixation (Figure 6.7). Nondisplaced fractures, if considered stable, can be treated with casting or firm-soled shoes. Fractures of the proximal phalanx of the hallux can extend into the MTP joint or into the interphalangeal (IP) joint. MTP joint motion varies up to 1008 passively, with ranges during normal function of 508, whereas the IP joint functions with a much smaller range of motion [29]. Hansen [12] states that loss of IP joint motion is better tolerated than loss of MTP motion. Therefore, fractures with MTP joint involvement should be treated aggressively with open reduction and stable fixation to minimize the potential for stiffness and arthrosis. This can be accomplished with Kirchner wire fixation or screws. Sanders [9] addresses the timing of open treatment. He notes that the significant swelling that occurs with these injuries may cause problems with wound healing if the surgery is not done immediately. If swelling is too severe, surgery may need to be delayed by 7 to 10 days. In the event of involvement of both the MTP and the IP joints, aggressive treatment of both


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Figure 6.7 (A and B) Transverse fracture of the proximal phalanx of the great toe. Clinically, the patient had rotatory displacement of the fracture, causing an unacceptable pronation deformity of the hallux. Fracture successfully treated with closed reduction and percutaneous pinning.

joints should be considered because of the disability when both joints have significant loss of motion. Fractures of the distal phalanx of the hallux are invariably due to a direct blow such as when a heavy object is dropped on the toe. These fractures often involve comminution. These injuries can be adequately treated with buddy taping and protected weight-bearing, as dictated by comfort, in a firm-soled shoe, a cast with a toe plate, or in a walking boot. Subungual hematomas should be drained appropriately and the nail should be preserved if possible to function as a splint for the fracture [30].

B.

Lesser Toe Fractures

Fractures of the phalanges of the lesser toes are very common. The proximal phalanx is most commonly involved, certainly in part to its length compared with the other bones in the toe. Fractures of the phalanges are commonly due to direct-blow injuries, either from dropping a weight on the toe or by ‘‘stubbing’’ the toe, often on furniture. Discussions on the subject of phalangeal fractures of the lesser toes unanimously place emphasis on the fact that these injuries rarely cause significant problems. Giannestras and Sammarco [8] suggest that as long as the clinical alignment of the toe is satisfactory, the outcome will be satisfactory, irrespective of the reduction of the fracture. Sanders [9] reports that moderate displacement of the phalanges of the lateral four toes is usually of no consequence. Treatment of these fractures is not controversial. Fracture displacement is treated with digital block and attempted reduction, if appropriate, due to clinical malalignment. The fracture is then immobilized with wadding in between the involved toe and an adjacent toe, to which the fractured



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toe is taped, so-called ‘‘buddy taping’’. Open reduction of displaced fractures is rarely necessary. When considering this as a possible treatment, one should always remember that very little morbidity is generally associated with the treatment of these fractures. Long-term complications from these fractures, if they occur, are due to malunion. These most commonly occur in the proximal phalanx of the second, third, or fourth toe. They are due to an angular malunion, which causes a plantar prominence [6]. In the rare instance that this does occur, it can usually be treated with exostectomy or correction of the angular malunion.

VIII.

CONCLUSION

Alterations in the ability of the forefoot to bear weight can result in clinical disability for patients. Restoration of the anatomy to normal is the goal with any fracture. The nature of a specific fracture will often dictate whether or not this is even feasible. If the fracture pattern dictates that anatomic restoration is not possible, due perhaps to fracture location or comminution, then an understanding of the implications on the weight-bearing function is vital so that alterations in weight-bearing characteristics can be minimized.

REFERENCES 1. Sarafian, S.K., Anatomy of the Foot and Ankle: Descriptive, Topographic, and Functional, Lippincott, Philadelphia, 1983. 2. Sammarco, G.J., Biomechanics of the foot, in Basic Biomechanics of the Skeletal System, Frankel, V. and Noroin, M., Eds., Lea & Febiger, Philadelphia, 1980, pp. 193–220. 3. Shereff, M.J., Fractures of the forefoot, Instr. Course Lect., 39, 133–140, 1990. 4. Sammarco, G.J., The Jones fracture, Instr. Course Lect., 42, 201–205, 1993. 5. Harrington, T. and Crichton, K.J., Overuse ballet injury of the second metatarsal: a diagnostic problem, Am. J. Sports Med., 21, 591–598, 1993. 6. Myerson, M.S., Injuries of the forefoot and toes, in Disorders of the Foot, Jahss, M., Ed., W.B. Saunders, Philadelphia, 1991, pp. 2233–2273. 7. Morrison, G.M., Fractures of the bones of the foot, Am. J. Surg., 38, 721–726, 1937. 8. Giannestras, N.J. and Sammarco, J., Fractures and dislocations in the foot, in Fractures, Rockwood, C.A., Jr. and Green, D.P., Eds., Lippincott, Philadelphia, 1975, pp. 1400–1489. 9. Sanders, R.T., Fractures of the hindfoot and forefoot, in Surgery of the Foot and Ankle, 7th ed., Coughlin, M.J. and Mann, R.A., Eds., Mosby, St. Louis, MO, 1999, pp. 1574–1605. 10. Delee, J.C., Fractures and dislocations of the foot, in Surgery of the Foot and Ankle, 6th ed., Coughlin, M. and Mann, R., Eds., Mosby, St. Louis, MO, 1993, pp. 1465–1703. 11. Lindholm, R., Operative treatment of dislocated simple fracture of the neck of the metatarsal bone, Ann. Chir. Gynaecol. Tenn., 50, 328–331, 1961. 12. Hansen, S., Foot injuries, in Skeletal Trauma, Browner, B.D., Jupiter, J.B., Levine, A.M., and Trafton, P.G., Eds., W.B. Saunders, Philadelphia, 1992, pp. 1959–1991. 13. Heim, U., Internal Fixation of Small Fractures: Techniques Recommended by the AO Group, SpringerVerlag, Berlin, 1987. 14. Jones, R., Fractures of the base of the fifth metatarsal bone by indirect violence, Ann. Surg., 35, 697–700, 1902. 15. Dameron, T., Fractures of the proximal fifth metatarsal: selecting the best treatment option, J. Am. Acad. Orthopaed. Surg., 3, 110–114, 1995. 16. Smith, J., The intraosseous blood supply of the fifth metatarsal: implications for proximal fracture healing, Foot Ankle, 13, 143–152, 1992. 17. Quill, G., Fractures of the proximal fifth metatarsal, Orthoped. Clin. North Am., 26, 353–361, 1995. 18. Lehman, R.C., Fracture of the base of the fifth metatarsal distal to the tuberosity, Foot Ankle, 7, 245–252, 1987. 19. Josefsson, P.O., Closed treatment of Jones fracture: good results in 40 cases after 11–26 years, Acta Orthopaed. Scand., 65, 545–547, 1994. 20. Clapper, M., Fractures of the fifth metatarsal: analysis of a fracture registry, Clin. Orthopaed., 315, 238–241, 1995. 21. Glasgow, M.T., Analysis of failed surgical management of fractures of the base of the fifth metatarsal distal to the tuberosity: the Jones fracture, Foot Ankle, 17, 449–457, 1996. 22. Lawrence, S.T., Jones fractures and related fractures of the proximal fifth metatarsal, Foot Ankle, 14, 358–365, 1993.


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23. Dameron, T., Fractures and anatomical variations of the proximal portion of the fifth metatarsal, J. Bone Jt. Surg., 57A, 788–792, 1975. 24. Holmes, G.B., Treatment of delayed unions and nonunions of the proximal fifth metatarsal with pulsed electromagnetic fields, Foot Ankle Int., 15, 552–556, 1994. 25. Torg, J., Fractures of the base of the fifth metatarsal distal to the tuberosity: classification and guidelines for non-surgical and surgical management, J. Bone Jt. Surg., 66A, 209–214, 1984. 26. Hens, J., Surgical treatment of Jones fractures, Arch. Orthopaed. Trauma Surg., 109, 277–279, 1990. 27. Ebraheim, N.A., Haman, S.P., Lu, J., Padanilam, T.G., and Yeasting, R.A., Anatomical and radiological considerations of the fifth metatarsal bone, Foot Ankle Int., 21, 212–215, 2000. 28. Holmes, G., Forefoot fractures, in The Traumatized Foot, Sangeorzan, B., Ed., American Academy of Orthopaedic Surgeons, Rosemont, IL, 2001, pp. 55–75. 29. Joseph, J., Range of motion of the great toe in men, J. Bone Jt. Surg., 36B, 450, 1954. 30. Taylor, G., Treatment of the fractured great toe, Br. Med. J., 1, 724–725, 1943.


7 Foot and Ankle Fractures in Diabetic Patients Michael S. Pinzur Loyola University Medical School, Maywood, Illinois

CONTENTS I. Introduction ................................................................................................................... 179 II. Wound Healing in the Diabetic Patient.......................................................................... 179 III. Fracture Susceptibility in the Diabetic Patient ............................................................... 180 IV. Undisplaced Fractures.................................................................................................... 180 V. Displaced or Unstable Fractures .................................................................................... 182 VI. Charcot Foot .................................................................................................................. 185 VII. Fractures of the Calcaneus ............................................................................................. 185 VIII. Fractures of the Hindfoot............................................................................................... 185 IX. Fractures of the Midfoot (Tarsometatarsal) ................................................................... 188 X. Fractures of the Forefoot ............................................................................................... 188 XI. Summary ........................................................................................................................ 190 References .................................................................................................................................. 191

I.

INTRODUCTION

The U.S. Centers for Disease Control and Prevention estimates that there are more than 16 million Americans afflicted with diabetes. These individuals consume more than $44 billion in direct medical costs. Death rates from heart disease and the risk of stroke are two to four times that of adults without diabetes. Diabetic retinopathy causes 12,000 to 24,000 new cases of blindness yearly. Diabetes accounts for 40% of new cases of renal failure and multiple other organ system morbidities [1]. There are greater than 50,000 lower-extremity amputations yearly in the U.S. alone, with 85% being preceded by foot ulcers or foot infections [2,3]. A simple, undisplaced fracture in the foot or ankle of a diabetic patient may be the first step in the downward spiral leading to foot deformity, tissue breakdown, infection, and eventual lower-extremity amputation and premature death. When one considers the impact that foot and ankle fracture imparts to the diabetic population, one must appreciate diabetes as a complex metabolic disease that affects the woundhealing process, the peripheral vascular and nervous systems, and virtually every organ system in the body.

II.

WOUND HEALING IN THE DIABETIC PATIENT

In individuals afflicted with diabetes, the basic ability to repair damaged tissue is adversely affected by several mechanisms. Prolonged periods of hyperglycemia affect circulating structural and

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functional proteins, leading to changes in the basement membranes of the peripheral arterial system and alterations in nerve conduction in the peripheral nervous system. At the same time, this altered metabolic environment appears to impair the initiation of the inflammatory (and wound-healing) response and the function of white blood cells involved in wound healing and the native response to infection. This combination of vascular and nerve conduction disease, combined with an impaired immune response, appears to be the primary disease process responsible for the impact diabetes has on virtually every organ system in the body [4]. Basic granulocyte function is impaired in diabetic patients, limiting the body’s attempt to initiate a healing response. The protein loss from associated renal disease and the local hypoxia associated with hyperglycemia creates an environment with limited healing potential and with increased susceptibility to infection. Ischemic peripheral vascular disease is an obvious risk factor that impacts the cascade of wound healing. Autonomic vasomotor neuropathy adversely affects vascular tone, leading to increased acute and chronic swelling from outflow obstruction. The venous effects of vascular disease impact the healing process, and vasomotor and motor neuropathy may be as important as loss of protective sensation [5–8]. When preparing a treatment plan for the diabetic patient with a fracture of the foot or ankle, one must appreciate the impaired native wound-healing environment. One must accommodate for a host with impaired sensation when contemplating closed treatment or immobilization following surgery. If surgery is considered, the diabetic patient’s impaired wound-healing potential and an increased susceptibility to infection must also be considered. The issue of whether the fracture is simply a fracture in a high-risk patient population or the initial presentation of a neuropathic (Charcot) foot deformity must also be addressed.

III.

FRACTURE SUSCEPTIBILITY IN THE DIABETIC PATIENT

When the epidemiology of fracture in the diabetic population is examined, it becomes clear that the diabetic population is more prone to fracture [9–13]. Metabolism-associated forms of osteoporosis are likely responsible [14,15]. These may be related to secondary hyperparathyroidism or simply due to the bone loss from decreased levels of 1-25 hydrocholecalciferol secondary to the associated renal disease. It may be related to the multiple associated hormone abnormalities [16]. Combined with the structurally weakened bone is absence of protective sensation. Approximately one in four diabetics has evidence of peripheral neuropathy, as measured by insensitivity to the Semmes– Weinstein 5.07 (10 g) monofilament (Figure 7.1) [5–10,17]. This risk factor of peripheral neuropathy and loss of protective sensation increases in incidence with duration of disease [18–22]. Peripheral neuropathy is also associated with impaired balance. As in so many features of this disease process, the additive combination of impaired balance, decreased protective sensation, and biomechanically weak bone creates an environment prone to fracture.

IV.

UNDISPLACED FRACTURES

Low-energy undisplaced fractures, or supposed repetitive ‘‘stress’’ fractures, of the foot and ankle in diabetic patients with a loss of protective sensation are an unlikely occurrence. This specific clinical scenario presents a difficult diagnostic dilemma. It can often be difficult to clinically distinguish an acute low-energy fracture from the acute presentation of a Charcot foot arthropathy. The presence of a diabetic foot abscess must be identified. In all three conditions, patients are able to bear weight and may have little, if any, pain. The first step is to eliminate the diagnosis of deep infection, as a delay in diagnosis of foot abscess or osteomyelitis may lead to sepsis, lower-extremity amputation, and death. Patients with infection generally feel ‘‘sick.’’ Careful examination will almost always reveal an entry point for the infection. The entry portal may be as simple as an infected ingrown toenail or a crack in the dry skin between the toes. Hematogenous seeding of the foot is very unusual. White blood cell counts may be only slightly elevated due to the defects in the immune response, as discussed earlier. The subtlest sign of developing infection in the diabetic patient is a slow elevation in blood sugar or insulin


Foot and Ankle Fractures in Diabetic Patients

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Figure 7.1 Semmes–Weinstein 5.07 (10 g) monofilament. This nylon filament is one of a series of variable-thickness filaments that can impart specific amounts of pressure to skin, depending on the thickness or stiffness. Ten grams of pressure applied to skin appears to be the threshold for detecting loss of protective sensation in individuals with peripheral neuropathy [20].

requirement in the days preceding presentation. The patient with foot fracture or acute Charcot foot arthropathy is in the normal state of health, while the foot infection patient generally feels ill and has some form of purulent drainage. Once infection is eliminated from the differential diagnosis, one must attempt to distinguish between acute fracture and Charcot foot arthropathy. While the patient with Charcot arthropathy is almost always insensate to the Semmes–Weinstein 5.07 (10 g) monofilament, it must be remembered that the insensate patient may also sustain a relatively low energy fracture. Initially, it may be impossible to distinguish acute fracture from acute Charcot arthropathy, making the initial therapy confusing. While the literature is consistent that the treatment for either should be immobilization and non-weight-bearing, this approach is based on anecdotal information [23,24]. When experts in the treatment of acute Charcot foot arthropathy were surveyed, most agreed on nonsurgical treatment, but half allowed weight-bearing with immobilization in a total-contact cast (Figure 7.2) [25]. These patients should be followed closely. The recent trend in the literature suggests early surgical stabilization, yet this recommendation is also based on anecdotal experience [26–28]. Therefore, it seems reasonable to initiate treatment for either an undisplaced fracture in a diabetic with loss of protective sensation or an acute Charcot arthropathy with immobilization in a well-padded total-contact cast. Weight-bearing status is controversial. Non-weight-bearing decreases the risk for displacement of the fracture at the cost of disuse osteopenia, which may lead to mechanical deformity. Because the literature gives no insight on the relative risks of weightbearing, this decision should be left to the treating physician (Figure 7.3). In either case, patients should be followed closely with frequent cast changes, skin examination, and follow-up radiographs.


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Figure 7.2 (A) The total-contact cast is a well-contoured, well-padded cast that is classically fabricated with plaster, but can be made with fiberglass. (B) Gauze is generally placed between the toes, and they are usually covered with cast padding and enclosed within the cast [24]. (C) This commercially available pneumatic walking boot has plantar cushioning with a replaceable pressure-dissipating microfoam material. It allows similar immobilization and protection, while also allowing inspection, dressing changes, and topical wound management (Aircasty Diabetic Walker, Aircast, Summit, NJ).

V.

DISPLACED OR UNSTABLE FRACTURES

Displaced fracture of the foot or ankle can lead to catastrophic results (Figure 7.4) [29]. Undisplaced, or ‘‘stress,’’ fractures are unusual in this patient population. The so-called ‘‘stress fracture’’ is more likely to be an acute presentation of Charcot foot arthropathy. Patients should be examined with the Semmes–Weinstein 5.07 (10 g) monofilament to determine if they have lost protective sensation due to peripheral neuropathy. It may be virtually impossible to distinguish the two diagnoses in the emergency department. Many patients presenting with an apparently lowenergy Lisfranc fracture-dislocation of the tarsometatarsal joint are actually presenting with an acute Charcot foot arthropathy. At least half of patients eventually diagnosed with Charcot arthropathy can remember a specific episode of trauma at about the time of the initiation of the process [30]. When the diagnosis is clearly a fracture, one should proceed with treatment, understanding the unique risks in this patient population. Patients should be examined for pulses. Patients with acute Charcot arthropathy have increased vascular inflow and arterio–venous shunting due to their vasomotor autonomic neuropathy. Patients with apparently decreased vascular inflow, as



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Figure 7.3 (A) A 64-year-old insulin-requiring, long-standing diabetic patient sustained this simple undisplaced ankle fracture. (B) Open reduction and non-weight-bearing for 8 weeks following surgery. Anteroposterior (AP) radiograph at (C) 6 weeks, and, at (D) 12 weeks following surgery.


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Figure 7.3 Continued (E and F) Ankle fusion to provide a stable, plantargrade foot.

Figure 7.4 (A and B) Attempted open reduction of an unstable ‘‘stress fracture’’ in an insulin-requiring neuropathic patient. He eventually progressed to bony union. He refused to use therapeutic footwear, developing an infection that required ankle disarticulation amputation.



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evidenced by decreased pedal pulses, should have noninvasive vascular testing to determine vascular status of the limb. Both ischemic and neuropathic patients are more prone to develop pressure ulcers from immobilization in a plaster or fiberglass cast [31]. The ischemic patient is more prone to develop wound failure and wound infection when treated with surgery. Even with adequate vascular inflow, the long-standing diabetic patient is more prone to infection due to leukocyte dysfunction and immune deficiency. When compared with nondiabetic patient populations, these individuals take longer to heal fractures, have a higher incidence of nonunion, and have more morbidity, whether treated with open or closed methods [29,32,33].

VI.

CHARCOT FOOT

There are two currently held theories for the development of Charcot arthropathy. Both theories are predicated on the presence of a long-standing peripheral neuropathy. The neurovascular theory suggests that vasomotor neuropathy creates an arterio–venous shunt that creates a localized osteopenia. The loss of protective sensation allows a low level of trauma to produce a fracture. Since the patient has no protective sensation, he or she continues walking, creating a hypertrophic attempt at a healing response. The neurotraumatic theory opines that an injury in an individual with a loss of protective sensation initiates an exaggerated healing response. When viewed with this perspective, it is easy to accept contributions from both theories. Most published series indicate that the prototype patient is one who is significantly overweight, has had both diabetes and peripheral neuropathy for a long period of time, and likely has an episode of trauma, sometimes at a trivial level [30]. The fact that many of the individuals are morbidly obese gives credence to a mechanical contribution to the development of the process. The literature is clear that the initial treatment of Charcot foot should be non-weight-bearing immobilization with a well-padded total-contact cast. However, when experts were surveyed, half allowed weight-bearing and many advised early surgical stabilization [25–28]. While treatment of acute Charcot arthropathy is controversial, it behooves the judicious orthopedic surgeon to recognize the susceptibility of this patient population to develop this potentially limb- or lifethreatening process.

VII.

FRACTURES OF THE CALCANEUS

In the best of circumstances, the treatment of fractures of the calcaneus is controversial. Due to a combination of osteopenia and loss of protective sensation in long-standing diabetic individuals, the calcaneus is mechanically weak and prone to ‘‘stress fracture’’ or simple mechanical failure. These individuals rarely develop arthritic pain following fracture, so the goal of treatment is preservation of a plantargrade foot capable of walking with therapeutic or protective footwear and accommodative foot orthoses. Surgery should be avoided due to the difficulty of mechanically maintaining reduction following surgery in severely osteopenic bone and the high risk of wound infection in this complex patient population (Figure 7.5). Should a deformity develop that precludes the use of standard therapeutic footwear, corrective osteotomy vs. custom accommodative orthotic treatment are the available options.

VIII.

FRACTURES OF THE HINDFOOT

Acute low-energy fractures, fracture-dislocations, or dislocations of the hindfoot (talus, navicular) in diabetic patients are unusual. If the patient is sensate to the Semmes–Weinstein 5.07 (10 g) monofilament, standard methods of treatment are advised. When insensate to the monofilament, the loss of protective sensation should make one suspicious of an acute Charcot arthropathy. When plantargrade, treatment can be nonoperative with a carefully applied total-contact cast. Varus deformity that leads to lateral weight-bearing, or acute dorsolateral peritalar subluxation with weight-bearing under a depressed talar head, should be treated with surgical stabilization. The surgery should be combined with percutaneous Achilles tendon lengthening as a method of


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Figure 7.5 (A and B) Weight-bearing AP and lateral radiographs of an insensate diabetic 8 weeks following non-weight-bearing closed treatment of a neuropathic fracture-dislocated at the transverse tarsal joint.



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Figure 7.5 Continued (C and D) Radiographs following tendon achilles lengthening and midfoot stabilization


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Figure 7.5 Continued (E, F and G) Photo and radiographs following removal of the hardware. The foot was stable and could be managed long term with a custom accomodative foot orthoses and depth inlay shoes.

balancing the motor imbalance caused by the motor peripheral neuropathy. Rigid internal fixation is required to avoid late deformity (Figure 7.6).

IX.

FRACTURES OF THE MIDFOOT (TARSOMETATARSAL)

In the emergency department, one should be suspicious when a patient presents with an acute lowenergy fracture dislocation at the midfoot (tarsometatarsal) level. Sensate patients require rigid internal fixation. While controversial, most experienced foot and ankle surgeons would treat this injury with rigid internal fixation [34]. Due to the high risk of late displacement, methods of rigid internal fixation should be employed. The author’s preferred method is oblique large fragment screw fixation, or stabilization with a dorsally applied small fragment dynamic compression plate combined with large fragment screws. Weight-bearing before bony healing is controversial, but can be considered with the use of a total-contact cast (Figure 7.5).

X.

FRACTURES OF THE FOREFOOT

Acute forefoot swelling in the diabetic with peripheral neuropathy is likely to be a forefoot presentation of a Charcot foot arthropathy. These fractures can almost always be treated with a carefully applied total-contact cast (Figure 7.7).



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Figure 7.6 (A and B) Plantar ulcer under an unstable Charcot midfoot deformity in a type II diabetic woman. She underwent percutaneous Achilles lengthening to correct the motor imbalance, combined with midfoot stabilization with rigid internal fixation. She was allowed to bear weight in a total-contact cast until bony healing.


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Figure 7.6 Continued (C and D) At 1 year, the foot is stable and ulcer-free.

XI.

SUMMARY

Individuals with diabetes are more likely to sustain a fracture of the spine or extremities. When they sustain a fracture, they are less likely to heal and more likely to develop fracture-associated morbidities. When they have surgery, they are more likely to develop a postoperative infection. The development of Charcot foot osteoarthropathy is presently generally confined to long-standing diabetic patients with loss of protective sensation, as measured by insensitivity to the Semmes– Weinstein 5.07 (10 g) monofilament.



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Figure 7.7 Forefoot fractures can almost always be treated with total-contact casts. (A) The patient was seen several weeks after developing forefoot swelling with minimal pain. A weight-bearing total-contact cast was used for 6 weeks. (B) Radiograph taken at 3 months; the patient was allowed to return to his therapeutic footwear.

When diabetic patients, especially those with peripheral neuropathy, present with low-energy fractures, one must determine if the fracture is simply an injury in a high-risk patient population, or the presentation of a Charcot foot. The goal of treatment is the preservation of a plantargrade foot, capable of being managed long-term in commercially available depth-inlay shoes and custom accommodative foot orthoses. When this cannot be accomplished by nonoperative methods, surgical stabilization is often indicated. When surgery is advised, rigid methods of internal fixation, careful postoperative monitoring, and prolonged periods of weight-bearing protection are essential components of the treatment plan. These patients are at lifelong risk for foot ulcer or infection that can lead to lower-extremity amputation and premature death. They require thorough foot-specific patient education, protective or therapeutic footwear, and careful ongoing lifelong monitoring.

REFERENCES 1. National Diabetes Fact Sheet, United States Department of Health and Human Services, Washington, D.C., Nov. 1, 1998. 2. American Diabetes Association, Technical Review: Foot Care in Patients with Diabetes Mellitus, 1994.


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3. Reiber, G.E., Lipsky, B.A., and Gibbons, G.W., The burden of diabetic foot ulcers, Am. J. Surg., 176 (Suppl. 2A), 5S–10S, 1998. 4. Cotran, R.S., Kumar, V., and Robbins, S.L., Eds., The pancreas, in Robbins Pathologic Basis of Disease, 4th ed., Robbins, Ed., W.B. Saunders, Philadelphia, 1990, pp. 981–1010. 5. Bagdale, J.D., Root, R.K., and Bulger, R.J., Impaired leukocyte function in patients with poorly controlled diabetes, Diabetes, 23, 9–15, 1974. 6. Hunt, T.K. and Pai, M.P., The effect of ambient oxygen tensions on wound metabolism and collagen synthesis, Surg. Gynecol. Obstet., 135, 561–567, 1972. 7. Nolan, C.M., Beaty, H.N., and Bagdale, J.D., Further characterization of the impaired bactericidal function of granulocytes in patients with poorly controlled diabetes, Diabetes, 27, 889–894, 1978. 8. Stadelmann, W.K., Digenis, A.G., and Tobin, G.R., Impediments to wound healing, Am. J. Surg., 176 (Suppl. 2A), 39S–47S, 1998. 9. Nicodemus, K.K. and Folsom, A.R., Type 1 and type 2 diabetes and incident hip fractures in postmenopausal women, Diabetes Care, 24, 1192–1197, 2001. 10. Melchior, T.M., Sorensen, H., and Torp-Pedersen, C., Hip and distal arm fracture rates in peri- and postmenopausal insulin treated diabetic females, J. Intern. Med., 236, 203–208, 1994. 11. Forsen, L., Meyer, H.E., Midthjell, K., and Edna, T.H., Diabetes mellitus and then incidence of hip fracture: results from the Nord-Trondelag Health Survey, Diabetologia, 42, 920–925, 1999. 12. Heath, H., Melton, L.J., and Chu, C.P., Diabetes mellitus and risk of skeletal fracture N. Engl. J. Med., 303, 567–570, 1980. 13. Schwartz, A.V., Sellmeyer, D.E., Ensrud, K.E., Cauley, J.A., Tabor, H.K., Schreiner, P.J., Jamal, S.A., Black, D.M., and Cummings, S.R., Older women with diabetes have an increased risk of fracture: a prospective study, J. Clin. Endocrinol. Metab., 86, 32–38, 2001. 14. Kayath, M.J., Tavares, E.F., Dib, S.A., and Vieria, J.G.H., Prospective bone mineral density evaluation in patients with independent diabetes mellitus, J. Diabetes Complications, 12, 133–139, 1998. 15. Piepkorn, B., Kann, P., Forst, T., Andreas, J., Pfutzner, A., and Beyer, J., Bone mineral density and bone metabolism in diabetes mellitus, Horm. Metab. Res., 29, 584–591, 1997. 16. Bouillon, R., Diabetic bone disease, Calcif. Tissue Int., 48, 155–160, 1991. 17. Pinzur, M.S., Anderson, R., Cantrell, R., and Lamborn, K., The American Orthopaedic Foot and Ankle Society diabetes 2000 foot screen, Foot Ankle Int., in Press. 18. Apelqvist, J. and Agardh, C.D., The association between clinical risk factors and outcome of diabetic foot ulcers, Diabetes Res. Clin. Pract., 18, 43–53, 1992. 19. McNeeley, M.J., Boyko, E.J., Ahroni, J.H., Stensel, V.L., Reiber, G.E., Smith, D.G., and Pecoraro, R.F., The independent contributions of diabetic neuropathy and vasculopathy in foot ulceration, Diabetes Care, 18, 216–219, 1995. 20. Olmos, P.R., Cataland, S., O’Dorisio, T.M., Casey, C.A., Smead, W.L., and Simon, S.R., The Semmes– Weinstein monofilament as a potential predictor of foot ulceration in patients with non-insulin-dependent diabetes, Am. J. Med. Sci., 309, 76–82, 1995. 21. Rith-Najarian, S.J., Stolusky, T., and Gohdes, D.M., Identifying diabetic patients at high risk for lower extremity amputation in a primary health care setting: a prospective evaluation of simple screening criteria, Diabetes Care, 15, 1386–1389, 1992. 22. Veves, A., Uccioli, L., Manes, C., Van Acker, K., Komninou, H., Philippides, P., and Katsilambros, N., Comparison of risk factors for foot problems in diabetic patients attending teaching hospital outpatient clinics in four different European states, Diabetes Med., 11, 709–713, 1994. 23. Pinzur, M.S., Benchmark analysis of diabetic patients with neuropathic (Charcot) foot deformity, Foot Ankle Int., 20, 564–567, 1999. 24. Myerson, M., Papa, J., Eaton, K., and Wilson, K., The total-contact cast for management of neuropathic plantar ulceration of the foot, J. Bone Jt. Surg., 74A, 261–269, 1992. 25. Pinzur, M.S., Shields, N., Trepman, E., Dawson, P., and Evans, A., Current practice patterns in the treatment of Charcot foot, Foot Ankle Int., 21, 916–920, 2000. 26. Early, J.S. and Hansen, S.T., Surgical reconstruction of the diabetic foot, Foot Ankle Int., 17, 325–330, 1996. 27. Myerson, M.S., Henderson, M.R., Saxby, T., and Wilson Short, K., Management of midfoot diabetic neuroarthropathy, Foot Ankle Int., 15, 233–241, 1994. 28. Simon, S.R., Tejwani, S.G., Wilson, D.L., Santner, T.J., and Denniston, N.L., Arthrodesis as an early alternative to nonoperative management of Charcot arthropathy of the diabetic foot, J. Bone Jt. Surg., 82A, 939–950, 2000. 29. Connolly, J.F. and Csencsitz, T.A., Limb threatening neuropathic complications from ankle fractures in patients with diabetes, Clin. Orthopaed., 348, 212–219, 1998. 30. Pinzur, M.S., Sage, R., Stuck, R., Kaminsky, S., and Zmuda, A., A treatment algorithm for neuropathic (Charcot) midfoot deformity, Foot Ankle Int., 14, 189–197, 1993. 31. Flynn, J.M., Rodrigues-del Rio, F., and Piza, P.A., Closed ankle fractures in the diabetic patient, Foot Ankle Int., 21, 311–319, 2000.



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32. Bibbo, C., Lin, S.S., Beam, H.A., and Behrens, F.F., Complications of ankle fractures in diabetic patients, Orthoped. Clin. North Am., 32, 113–133, 2001. 33. Blotter, R.H., Connolly, E., Wasan, A., and Chapman, M.W., Acute complications in the operative treatment of isolated ankle fractures in patients with diabetes mellitus, Foot Ankle Int., 20, 687–694, 1999. 34. Pinzur, M.S., Trepman, E., Shields, N., Dawson, P., and Evans, A., Current practice patterns in the treatment of Charcot foot, Foot Ankle Int., 21, 916–920, 2000.



8 Dislocations of the Ankle, Subtalar, and Great Toe Metatarsal–Phalangeal Joints David A. Porter and Todd Arnold Thomas A. Brady Clinic, Methodist Sports Medicine Center, Indianapolis, Indiana

CONTENTS I. Introduction ...................................................................................................................... 196 II. Ankle Dislocation.............................................................................................................. 196 A. Historical Review....................................................................................................... 196 B. Epidemiology and Anatomy ...................................................................................... 197 C. Pathogenesis and History .......................................................................................... 197 D. Clinical Findings........................................................................................................ 197 E. Radiographic Findings .............................................................................................. 198 F. Treatment Options..................................................................................................... 199 G. Prognosis and Long-Term Follow-Up....................................................................... 199 III. Subtalar Joint Dislocation................................................................................................. 199 A. Historical Review....................................................................................................... 199 B. Epidemiology and Anatomy ...................................................................................... 200 C. Pathogenesis and History .......................................................................................... 200 D. Clinical Findings........................................................................................................ 200 E. Radiographic Findings .............................................................................................. 200 F. Treatment Options..................................................................................................... 201 G. Long-Term Results and Prognosis............................................................................. 203 IV. Great Toe MTP Dislocation ............................................................................................. 203 A. Historical Review....................................................................................................... 203 B. Epidemiology and Anatomy ...................................................................................... 203 C. Pathogenesis and History .......................................................................................... 203 D. Clinical Findings........................................................................................................ 204 E. Radiographic Findings .............................................................................................. 205 F. Treatment Options..................................................................................................... 205 G. Prognosis and Long-Term Outcome.......................................................................... 207 V. Conclusion ........................................................................................................................ 207 References .................................................................................................................................. 208

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INTRODUCTION

Dislocations of the ankle, subtalar, and great toe metatarsal–phalangeal (MTP) joints are not common but can result in significant long-term disability if not recognized and reduced expediently and treated properly. Dislocation of these joints involves forceful energy and results in severe soft tissue injury. Open dislocation can occur at all three of these joints and must be treated on an emergency basis with surgical lavage and repeated debridements as indicated. Closed dislocations also require emergency reduction, but can often be accomplished in an outpatient setting such as an emergency room. Stiffness, joint debri (Figure 8.1), and resultant arthrosis can all accompany ankle and subtalar dislocations. Stiffness can also accompany MTP dislocations of the great toe, but disruption of the plantar plate, retraction of the sesamoid complex, and chronic pain are the most common sequelae. In this chapter, dislocation of the ankle, subtalar, and great toe MTP joints will be presented in separate subsections, with a brief historical review, description of the epidemiology and anatomy, pathogenesis or history, clinical and radiographic findings, treatment options, and prognosis with long-term follow-up.

II.

ANKLE DISLOCATION

A.

Historical Review

The orthopedic literature regarding pure ankle dislocations is replete with isolated case presentations and small series [1–12]. There are no articles on randomized treatment protocols or prospective analysis. Thus, most of our experience from the literature is anecdotal, retrospective, and

Figure 8.1 CAT scan of an athlete after closed reduction of subtalar dislocation. Note the small amount of joint debri in the sinus tarsi. Operative removal of the joint debri was not undertaken. A repeat CAT scan 8 months later revealed resorption of the debri.


Ankle, Subtalar, and Great Toe Metatarsal–Phalangeal Joints

197

involves case-series or case studies. This is due to the relatively rare nature of ankle dislocations without fracture.

B.

Epidemiology and Anatomy

Ligamentous injuries of the ankle are the most common lower-extremity injuries suffered in sports and work. Pure or isolated ankle dislocation is uncommon [1–13]. Dislocation of the ankle is typically associated with fractures of the ankle (medial or posterior malleoli of the tibia or fibula fracture — Weber B or C (see Chapter 1). Lateral ankle ligamentous injuries comprise 80 to 90% of all ligament injuries of the ankle. However, isolated ankle dislocations without fracture comprise less than 1% of all ligament injuries evaluated at Methodist Sports Medicine Center between 1987 and 2001. It has been proposed that preexisting ligamentous laxity [1,6,11–13] and hypoplasia of the malleoli [1,6,13] can contribute to pure ankle dislocations. Classification [2] of pure ankle dislocations from most common to least common is listed as posteromedial [3], anterolateral, rotatory (within the ankle mortise) [11], and superior (within the tibiotalar syndesmosis). The bony anatomy of the ankle provides inherent stability to the talocrural joint. The tibial plafond provides the weight-bearing surface, which is mildly convex with a small central sulcus. Medially, the extension of the distal tibia creates the medial malleolus. The stout deep, superficial, and anterior deltoid ligaments originate off this distal extension. Laterally, the distal fibula is attached to the lateral tibia via the interosseus, or syndesmosis, ligament, which has anterior and posterior extensions to form the anteroinferior tibiofibular ligament (AITFL) and the posterior inferior tibiofibular ligament (PITFL), respectively. The tibial and fibular orientation provides a constrained ‘‘box-like’’ receptacle for the relatively square, or rhomboid, talus. This creates a very stable ‘‘box within a box’’ alignment as the ankle is weight-bearing and in neutral dorsiflexion. However, because the talus is more narrow posteriorly than anteriorly, as the ankle rotates into more plantar flexion the bony stability is less constraining and the talus translates slightly anterior, unlocking the talus from the tibial–fibular mortise constraint. Thus, with the foot in neutral dorsiflexion, ankle dislocation is extremely rare, but, with progressive plantar flexion or extreme dorsiflexion, dislocation can occur. Ankle dislocations without fracture occur with the foot in maximal dorsiflexion (anterolateral) or maximal plantar flexion (posteromedial). Anterolateral ankle dislocation without fracture inherently requires rupture of the deltoid ligament and posteromedial capsule, while posteromedial dislocations require disruption of all the lateral ligaments: the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PFL). Syndesmosis rupture is uncommon in pure ankle dislocations (except with the rare superior dislocation).

C.

Pathogenesis and History

The two most common activities resulting in pure ankle dislocations are motor-vehicle trauma and sports. Motor-vehicle trauma involves a severe axial load with the foot and ankle in a maximal plantar-flexed and inverted position (posteromedial dislocation) or an axial load with the foot and ankle slightly externally rotated and in maximal dorsiflexion (anterolateral dislocation). Similarly, with sports, the mechanism is an axial load landing from a jump, with the foot typically in a plantarflexed and inverted position (posteromedial dislocation). Anterolateral dislocation is unusual in the sports population. Approximately one half of ankle dislocations are open injuries. Open injuries are more common in patients that suffer an ankle dislocation with motor vehicle trauma. Open injuries are especially common in motorcycle injuries. The patients are acutely aware of a severe injury and complain of immediate painful deformities, which require emergency medical treatment.

D.

Clinical Findings

The most striking clinical feature is the gross deformity of the lower extremity. This deformity is accompanied by pain and often by fear. Posteromedial dislocations (Figure 8.2) present with the foot plantar flexed, supinated, and positioned medially and slightly posterior to the lower leg.


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Figure 8.2 Posteromedial ankle dislocation in an 18-year-old high-school basketball player. The injury was closed, it was reduced under sedation, and the athlete returned to recreational basketball 2 months after injury.

Anterolateral dislocations present with the foot in a position that is neutral, slightly everted, and anterior and lateral to the lower leg. A careful neurovascular examination must be undertaken because neuropraxia or frank nerve rupture or laceration can be present. Closed dislocations will often demonstrate stretched skin tented over the prominent malleoli (distal fibula with medial dislocations and medial malleoli with lateral dislocations). The skin lacerations related to open dislocations are lateral with medial dislocations and medial with lateral dislocations. Arterial injuries are less common, but do occur. Posterior tibial artery lacerations or rupture occur with anterolateral dislocations. It is important to reexamine the foot and assess the neurovascualar status as well as the skin after definitive reduction.

E.

Radiographic Findings

Standard radiographs of the dislocated ankle should be obtained (Figure 8.2), when possible, before definitive reduction is initiated. Routine anteroposterior (AP), oblique, and lateral views typically suffice in the prereduction examination. Postreduction views are also necessary to document concentric reduction and to assess for occult fractures. Magnetic resonance imaging (MRI) and computed axial tomography (CAT) scans are less commonly obtained. MRI is helpful to assess for late causes of pain, such as bone contusions of the tibia or talus, osteochondral lesions of the talus, occult tendon injuries, or avascular necrosis (AVN) of the distal tibia or talus. CAT scan evaluation is helpful to assess for occult avulsion fractures (not seen well on MRI), lateral process fractures, anterior process fractures of the calcaneus, and os trigonum injuries. Vascular studies are needed for the dysvascular foot in the acute setting.



F.

199

Treatment Options

Treatment centers around concentric reduction of the ankle joint, surgical management of open wounds, and repair of injured tendons, nerves, and arteries when needed. Venous injuries involve surgical ligation rather than repair. Since most wounds are lacerations, they can usually be closed loosely primarily. If a tension-free closure cannot be obtained or the wound edges have questionable viability, closure can be delayed. Definitive wound closure, either primarily or with a flap, should be obtained within the first week. Definitive treatment for the ligamentous injury requires immobilization. Primary repair of the ligaments is typically reserved for open dislocations after appropriate debridement. Closed ankle dislocations without fracture can be treated without surgical repair. Immobilization is required for 3 to 4 weeks either with cast immobilization or with a fracture walking boot. The author prefers use of an off-the-shelf Aircast walking boot (Aircast1, Summit, NJ). The boot is used during the day for activities of daily living (ADL), aerobic exercise, and at night to keep the ankle in neutral position for ligament healing. Rehabilitation is begun immediately with stationary bike aerobic exercise and ankle strengthening. Patients with posteromedial dislocations are instructed in dorsiflexion and eversion exercises with the use of elastic tubing and Achilles stretching to encourage both protected range-of-motion (ROM) and musculotendinous strengthening. Patients with anterolateral dislocations are instructed in plantar flexion and inversion ROM, as well as strengthening. During 4 weeks of immobilization, this author allows gradual full weight-bearing for his patients as they are weaning off the crutches over a 1- to 2-week period of time. The patient can be weaned out of the boot into an ankle brace after 4 weeks. At this time (after 4 weeks), the rehabilitation can be advanced to stair stepper training and then on to running and functional progression to sports or full manual labor. Return to sports takes typically 6 to 8 weeks. Return to sit-down work can begin as early as the first week after injury with a closed dislocation. Return to full heavy manual labor takes 6 to 8 weeks. Open dislocations require infection-free healing of the wound before advancing to a rehabilitation program. That is, the ankle should be immobilized until the wound is sealed and dry. After this, the rehabilitation sequence is the same as that described for closed dislocation.

G.

Prognosis and Long-Term Follow-Up

The prognosis for closed dislocations without neurovascular injury or fracture is good. Stiffness is the most common complaint. Chronic instability has also been reported, but probably less than 10% of patients complain of instability. The recovery after a closed dislocation without neurovascular injury or fracture is similar to a grade III lateral ankle sprain. Associated intraarticular fractures can lead to a higher risk for long-term arthrosis. Open dislocations carry a more guarded prognosis. Chronic osteomyelitis, the need for rotational or free-tissue transfer grafts, and nerve and tendinous injuries are all possible. Common complications are more prevalent after open injuries than after closed injuries. In the absence of these devastating complications, open dislocations can have a prognosis similar to closed dislocations. AVN is a rare complication of pure ankle dislocations [8]. Chronic nerve pain is rare even after nerve laceration or rupture, but small areas of numbness can occur even after skillful repair. Also, some element of cold sensitivity can occur after nerve injury. In rare instances, total talar dislocation without fracture can occur and typically results in AVN and infection [14]. Stabilization of the wound and early tibiocalcaneal fusion is recommended [14]. There has been one case of a lateral total talar dislocation without fracture that was closed and treated with surgical reduction and pinning. The technique had a good long-term result [15]. Closed posterior total talar dislocations have also been reported with similar results [16].

III. A.

SUBTALAR JOINT DISLOCATION Historical Review

Subtalar joint dislocation is an uncommon injury with few reports in the literature with more than five cases [17–27]. It does appear to be more frequently reported in the last 65 years compared with


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the previous 130 years [17]. The dislocation can occur in all directions: anterior, posterior [16], medial, and lateral [24]. The most common direction for closed dislocation is medial, followed by lateral [27]. Open dislocations are more common to the lateral side [21]. Subtalar dislocation involves simultaneous injury of both the talocalcaneal and the talonavicular joints. Subtalar subluxations have also been reported [28]. These subluxations have been observed in dancers and are treated with reduction by manipulation and taping [28]. No further discussion of these subluxation injuries will be undertaken in this chapter.

B.


The lateral subtalar ligaments, CFL, spring ligaments, and medial subtalar ligaments are probable sites of injury associated with a subtalar joint dislocation. Medial dislocations are more common than lateral dislocations. Dislocations are more common in males than in females [19]. The lateral subtalar ligaments include the ATFL, the cervical ligament, and the lateral talocalcaneal ligament. The medial subtalar joint is stabilized by the distal deltoid ligaments and the medial talocalcaneal ligament.

C.


Subtalar joint dislocation is most frequently seen as the result of a fall from heights, the result of a motor vehicle accident, or a twisting injury, such as landing from a jump in basketball [27]. Medial dislocations of the subtalar joint are created by forced inversion of the ankle, adduction, and supination of the foot. The sustentacular tali acts as a fulcrum for the posteromedial talar body, resulting in adduction and internal rotation of the hindfoot (calcaneus, navicular, and remaining midfoot–forefoot complex). The laterally directed forces on the talus cause disruption of the calcaneal fibular ligament and lateral subtalar ligamentous complex. Also, these forces disrupt the lateral talonavicular capsule, allowing medial displacement of the navicular and calcaneus. The talus remains locked in the ankle mortise. Lateral subtalar dislocations result from a forceful eversion and abduction of the foot through the subtalar joint while the ankle mortise remains stable. The anterior process of the calcaneus acts as a fulcrum on the anterolateral corner of the talus (lateral process) disrupting the medial subtalar and talonavicular ligaments. These medially directed forces on the talus result in the calcaneus and navicular displacing laterally. Concommitant lateral talar head fractures or impaction injuries can occur. It is inherently obvious in both medial and lateral dislocations that the interosseus ligament of the subtalar joint must be (and always is) disrupted. However, the spring ligament is spared from injury, thus allowing the navicular to remain with the calcaneus during subtalar joint dislocation.

D.

Clinical Findings

A severely deformed foot displaced in the direction of the dislocation is the hallmark of the traumatic subtalar joint dislocation injury (Figure 8.3). The medial dislocation appears like that of an acquired clubfoot deformity (Figure 8.3). Anatomically, the foot and heel are displaced medially and the head of the talus tents the lateral skin (Figure 8.3). The talar head is often located between the extensor hallucis brevis and the long toe extensors [22]. The lateral subtalar dislocation has the appearance of an acquired flatfoot. The foot and heel are lateral to the ankle and the head of the talus is prominent over the medial aspect of the foot. Skin ischemia will often be noted overlying the talar head. The blanching of ischemia is noted medially with lateral dislocation and laterally with medial dislocations. Open wounds, when present, are in similar locations.

E.


Standard radiographic views initially involve AP and lateral views of the foot and ankle. More involved radiographic evaluations, such as a CAT scan or MRI, are reserved for postreduction workup. Ankle radiographs of the medial dislocation reveal the talus normally aligned in the



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Figure 8.3 Clinical photograph of a patient with a closed medial subtalar dislocation. Note blanching of skin over the lateral hindfoot and medial displacement of the foot. Note the obvious deformity of the hindfoot. The patient underwent closed reduction with sedation in the emergency department.

mortise, with the remaining hindfoot medially displaced. The lateral view again demonstrates the normal talocrural alignment, with the inability to visualize the subtalar joint because of concomitant overlap of the medially displaced foot. Medial dislocation will also demonstrate dislocation of the talonavicular joint (Figure 8.4). It has been reported that there are associated fractures in up to 50% of medial dislocations [17]. Similarly, lateral dislocations present with the hindfoot displaced laterally on the AP with a normal ankle mortise. Again, the lateral dislocation will demonstrate the calcaneus lateral to the talus on the AP radiograph of the ankle and the subtalar joint poorly visualized on the lateral radiograph. CAT scan evaluation after reduction can be helpful in assessing joint debri or occult fractures (Figure 8.1).

F.

Treatment Options

The majority of these dislocations can be treated with closed reduction under intravenous sedation either in the emergency department or in the operating suite. Infrequently, soft tissue or fractures may make closed reduction difficult. Medial dislocations are reduced with the knee in a flexed position to reduce the deforming force of the gastrocnemius [18]. The foot is firmly grasped while an assistant applies counterpressure to the thigh. The calcaneus, talus, and foot are disengaged with traction through the heel, with the foot in plantar flexion. Gentle pressure over the talonavicular joint will reduce the talonavicular and subtalar joints. The foot should then be held in neutral or slight dorsiflexion position and slightly everted if casted. Typically, the hindfoot is very stable after


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Figure 8.4 Radiograph demonstrating a medial subtalar dislocation in a professional football player. Note the dislocation of the talonavicular joint and subluxation of the subtalar joint. The joint was reduced under sedation. The athlete was able to return to football after 6 weeks and played 4 more years before retiring.

reduction. Careful documentation of neurovascular status and radiographic evaluation should follow reduction. Postreduction radiographs are particularly helpful to evaluate for subtle fractures. Computed tomography (CT) scan is recommended for traumatic subtalar dislocation, as there is a high incidence of occult fractures. Nine cases were reported. All had occult injuries. Fortyfour percent changed treatment as a result of the CT scan [29]. Lateral dislocations are reduced in a similar fashion with the knee flexed. After reduction, the foot is held in a slightly inverted position in combination with the dorsiflexion or neutral alignment at the ankle if casted. Lateral dislocations occasionally cannot be treated by closed reduction because of entrapment of the talar head by the posterior tibial tendon [10,18,25,26]. The lower leg is then placed into a walking boot with cold compression. Weight-bearing is allowed if there is no fracture. Open reduction with internal fixation (ORIF) of a lateral process fracture will require 4 to 6 weeks of crutch use and nonweight-bearing. If no fracture is noted the boot is worn for 4 weeks. Concomitant ORIF will require boot immobilization for 6 to 8 weeks or until healing is documented radiographically. After the required period of immobilization, the patient is weaned out of the boot into an ankle brace. The brace is worn for 3 to 4 months (one competitive season for athletes). Return to sports or heavy manual labor can be as early as 6 to 8 weeks in the uncomplicated case or as long as 3 to 4 months if concomitant fractures have occurred. Open dislocations require emergency surgical debridement, concentric joint reduction, and repeat lavage to obtain a culture-free wound. Skin grafting and rotational or free-tissue flaps can be required to obtain closure.



G.

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Long-Term Results and Prognosis

The greatest long-term problems may be more related to the associated injuries. The literature has mixed results regarding whether medial or lateral dislocations have a worse prognosis. Zimmer and Johnson [27] noted instability was a significant complaint in 1 of 12 patients while 4 others subjectively had mild hindfoot instability. These findings were secondary to shorter periods of immobilization and younger patient age [27]. Each of the four patients with normal examinations, but mild instability complaints, had reduction in symptoms with footwear modification. Heppenstall et al. [23] found overall good results after subtalar joint dislocation, but noted that stiffness of the joint was the limiting factor. This stiffness was attributed to long-term immobilization [19,23]. Recurrent dislocations are rare [20]. Special consideration is made for open subtalar dislocations. These occur less frequently than closed dislocations and are more common laterally. Overall, these have a fair to poor prognosis. This less-than-favorable outcome is attributed to the higher energy required to create the open dislocation, the associated injuries, and, potentially, osteomyelitis [21].

IV. A.

GREAT TOE MTP DISLOCATION Historical Review

Few articles have been written regarding first MTP dislocations. To date, there are fewer than 40 dislocations reported in the literature [30–35]. Brunet [30] reported the largest series, which included 11 complex (type I) dislocations [30]. Most reports are isolated case reports.

B.


MTP dislocations of the great toe are considered rare. An MTP dislocation can be a result of either high-energy trauma (motor-vehicle accident) or lower-energy trauma (sports, fall from heights, etc.). High-energy trauma often results in an MTP dislocation in conjunction with multiple injuries to the foot (such as metatarsal [MT] fractures or Lisfranc dislocations). Lower-energy trauma often results in an isolated MTP dislocation. There is a high predilection for this injury in males. Lowenergy dislocations are commonly seen in tackling sports such as football and rugby.

C.


Since there is a paucity of literature regarding first MTP dislocation, there is no well-defined mechanism of injury. However, the dislocation is thought to be associated with hyperextension of the MTP joint. Commonly, the foot is in equinus, and there is an extension moment through the MTP joint. This foot position results in the body weight forces projecting through the MT head plantarly and the contact surface transferring this force in a dorsal direction through the proximal phalanx. Further hyperextension results in tearing of the plantar structures (plantar plate, sesamoids, or a combination of these structures). MTP dislocations are well described and classified by Jahss [33]. It is important to understand that hyperextension injuries of the great toe also occur without dislocations. These have traditionally been associated with tackling sports, especially football on artificial turf. Hyperextension ‘‘turf toe’’ injuries have also been classified by Clanton and Ford [36]. It is important to understand that grade III ‘‘turf toe’’ injuries, as described by Clanton and Ford [36], are most likely MTP dislocations that have reduced spontaneously. The grade III ‘‘turf toe’’ involves disruption of the plantar plate and dorsal dislocation of the proximal phalanx (Figure 8.5A and Figure 8.5B). We will focus primarily on the Jahss [33] classification for this discussion. Jahss [33] described the type I dislocation as being an irreducible MTP dislocation without interruption of the intersesamoid ligament or evidence of fracture. Type IIA dislocations were described as a rupture of the intersesamoid ligament and widening of the sesamoid complex, and type IIB dislocations were classified by the evidence of transverse fracture of one or both sesamoids with a concomitant dislocation. Copeland and Kanat [31] have added a type IIC dislocation, which is a combination of types IIA and IIB.


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Figure 8.5 (A) Lateral and (B) AP radiographs demonstrating a grade III turf toe injury with MTP joint dislocation. Note the sesamoids proximal to the MTP joint and the proximal phalanx dorsal to the MT head.

D.

Clinical Findings

The most striking clinical findings are severe pain at the MTP joint, the hyperextension posture of the joint, and the significant swelling with plantar ecchymosis. The head of the first MTP is found to be prominent on the plantar surface of the foot. A dimple in the skin over the dorsomedial aspect of



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the joint is also commonly present. Blanching on the plantar surface of the great toe can be noted as the skin is stretched over the MT head. Type I dislocations are irreducible, by definition, via closed means and ultimately require open reduction. The first MT head buttonholes through the weaker soft tissues, which are proximal to the plantar plate–sesamoid complex. The head of the first MT is located plantar to the proximal phalanx with this dorsal dislocation. The sesamoids and plantar plate remain with the proximal phalanx and lie dorsal to the MT head. Attempts at reduction with traction, given this dislocated anatomy, result in a noose-like effect, tightening the medial and lateral structures around the MT preventing reduction of the proximal phalanx to the MT head. Type II injuries are typically reducible by closed techniques and are subdivided into types IIA, IIB, and IIC. Type IIA dislocations involve a dislocation of the MT head between the sesamoids, resulting in a disruption of the intersesamoid ligament. The fibular sesamoid is lateral to the MT head and the tibial sesamoid is medial. Type IIB dislocation involves fracture of one (usually tibial) or both sesamoids. Type IIC dislocations involve a combination of the IIA and IIB patterns, with fracture of one sesamoid and disruption of the intersesamoid ligament. Occasionally, the forces of dislocation result in a more valgus or varus stress with the dislocation. This can result in a dorsolateral (valgus stress) or dorsomedial (varus stress) dislocation. Careful assessment should be made of the neurovascular structures, extensor hallucis longus (EHL) and flexor hallucis longus (FHL) tendons, and medial and lateral collateral ligaments of the MTP joint.

E.


Radiographic evaluation is imperative for all hyperextension injuries of the great toe. Prereduction (Figure 8.5A and Figure 8.5B) and postreduction (Figures 8.6A and 8.6B) radiographs are necessary to evaluate the dislocated toe. Radiographs help to assess the type of dislocation and help to evaluate associated injuries including medial and lateral MT head avulsion fractures, sesamoid fractures, MT head impaction fractures, MT fractures, as well as position of the sesamoids. Radiographs reveal dislocation of the first MTP joint with the proximal phalanx of the great toe dorsal to the head and neck of the first MT (Figure 8.5A and Figure 8.5B). In type I dislocations the sesamoids are also dorsal to the first MT and there is no evidence of fracture or widening of the intersesamoid anatomy. Type IIA dislocations have the same appearance regarding the position of the proximal phalanx, but there is evidence of a widening of the sesamoid complex, suggestive of disruption of the intersesamoid ligament. Radiographs of type IIB injuries reveal a fractured sesamoid without widening of the intersesamoid interval. Type IIC dislocations present with both fracture of the sesamoid and widening of the intersesamoid interval. Given the high energy required for a first MTP dislocation, other injuries are common. Radiographs may reveal dislocations at other MTP joints and fractures of phalanges, MTs, or midfoot tarsal bones. Dislocations may also be present in the midfoot (Lisfranc). Stress radiographs are not commonly used in the presence of a clinical dislocation except to determine postreduction stability. Standard AP, lateral, and oblique views are obtained for prereduction and postreduction evaluation. A sesamoid tangential view can be helpful in the postreduction evaluation to assess for sesamoid MT head congruity. A comparison AP standing view of the foot is helpful in assessing position of the sesamoids, specifically the presence or absence of retraction. This can be particularly critical in following a grade III turf toe injury to assess for proximal migration of the sesamoids. Since much of the injury is soft tissue related, MRI is often the preferred ancillary radiograph. With MRIs, the radiologist and the surgeon can assess plantar plate integrity, occult dorsal impaction fractures, and related soft tissue structures (such as FHL and EHL injuries).

F.

Treatment Options

Type I dislocations require surgical intervention to reduce the dislocation successfully. There are some reports of reducible type I dislocations with ipsilateral injuries that allowed closed reduction [30]. However, by definition, these injuries require open reduction. A dorsal approach has been recommended [32,35,37] secondary to good visualization of restraining tissue and history of problems with a plantar approach. Plantar incision problems can include potential injury to the medial plantar hallucal nerve and postoperative scar pain. The lateral structures are taken down to


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Figure 8.6 (A) Lateral and (B) AP postreduction radiographs of the same foot demonstrating concentric reduction of the MTP joint. Note the proximal phalanx now reduced to the MT head and the sesamoids reduced. The athlete required operative repair of the plantar plate.

facilitate reduction. In their procedure, Lewis and DeLee [34] describe first tagging and then dividing the adductor hallucis. They found reduction was still limited. They then proceeded to divide the deep transverse MT ligament. This division was performed slightly plantar and distal to the conjoined tendon where it joined the volar plate. This allowed reduction of the proximal phalanx and the sesamoids [34]. Intraoperative radiographs should be obtained to insure concentric reduction.



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Type IIA, IIB, and IIC dislocations are treated by closed reduction under local digital block anesthesia, conscious sedation, or general anesthesia, if necessary. Surgical repair is typically not required for the type IIA dislocation. Type IIB and IIC dislocations have a concomitant sesamoid fracture. If postreduction radiographs demonstrate anatomic alignment of the fractured sesamoid, the authors prefer nonoperative treatment and follow healing radiographically. If widening greater than 2 mm exists after reduction, ORIF may be required. Soft tissue interposition can be the cause of nonanatomic reduction. An inferior medial approach is undertaken to expose, reduce, and fixate the tibial sesamoid. Suture fixation or, if the bone is not comminuted, a small headless bone screw is recommended. Postoperative or postreduction care is similar for all dislocations. Immobilization is required above the ankle because both the EHL and the FHL cross this joint. Immobilization can involve either cast immobilization with a toe-plate extension or, as the author prefers, boot immobilization. The MTP joint must be kept at neutral or at slight plantar flexion to allow appropriate healing of the plantar soft tissues (type IIA, IIB, or IIC injuries) and the tibial sesamoid (type IIB or IIC injuries). Immobilization with a walking removable boot allows early passive and active flexion. The patient must not walk without immobilization or extension past neutral before 4 to 6 weeks after reduction. Pool therapy, gentle active assisted ROM, and aerobic bike therapy with the boot can be initiated at the 4- to 6-week time period, depending on the degree of healing. After 6 full weeks of immobilization, patients are weaned out of the boot into a custom orthosis with a great toe rigid extension (Morton’s extension) or an extended steel shank over a 2-week period of time. Return to sports or heavy manual labor requires 3 to 4 months for healing after injury.

G.

Prognosis and Long-Term Outcome

Brunet [30] has data collected to a mean follow-up of 7 years for ten complex (type I) dislocations. Nine out of ten patients had reduced MTP motion, but not to the extent that it limited their endurance while walking or exercising. All but one returned to the same or modified work. The one patient unable to return to preinjury work experienced multiple traumas and was severely disabled. One-half of these patients (five of the ten) reported tenderness in one or both sesamoids. One patient complained of decreased sensation secondary to an injury to the medial plantar digital nerve. Four patients reported that orthotics were essential in order to limit symptoms. Plantar scar sensitivity was common in those patients who had a plantar approach or had acquired lacerations on the plantar surface during injury. Also, the overall outcome was significantly affected by the presence of concomitant injuries as noted by a patient with multiple traumas. Predicting long-term outcome and prognosis of type II injuries is difficult because of the low number of injuries reported in the literature. Stiffness associated with pain is the most common sequelae. Hallux rigidus can result from any type of first toe MTP dislocation. AVN can also accompany long-term findings. AVN is more likely to follow type IIB or type IIC dislocations, but can be seen with each type. Occasionally, gross instability of the MTP joint can occur after a type II dislocation. Surgical reconstruction of the plantar plate is advocated with an abductor hallucis tendon transfer and sesamoidectomy [37].

V.

CONCLUSION

Joint dislocations are one of the injuries that constitute an orthopedic emergency. Joint dislocations of the foot and ankle are rare. Ankle, subtalar, and MTP joints are the most common in the pedal region. There is a paucity of literature regarding the diagnosis, management, and prognosis for these potentially devastating injuries. Joint dislocations require significant energy and trauma. Dislocations result in severe soft tissue disruption and often have associated bone injury such as fracture, bone contusion, and cartilage damage. Associated neurovascular injury can also occur and must be recognized and treated appropriately. Subtalar dislocations are the most common joint disruption in the foot and ankle. Ankle and first MTP dislocations are more rare. Open injuries or dislocations are not infrequent, require appropriate lavage and protection from infection, and can occur at all three joints. Closed ankle


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dislocations have the best prognosis. Stiffness can be associated with long-term pain at each joint. Recent advancements in immobilization apparatuses have allowed more protected motion and hopefully a better long-term result.

REFERENCES 1. Colville, M.R., Colville, J.M., and Manoli, A., II, Posteromedial dislocation of the ankle without fracture, J. Bone Jt. Surg., 69A, 706–710, 1987. 2. Fahey, J.J. and Murphy, J.L., Talotibial dislocation of the ankle without fracture, Surg. Clin. North Am., 45, 80–101, 1965. 3. Krishnamurthy, S. and Schultz, R.J., Pure posteromedial dislocation of the ankle joint, Clin. Orthopaed., 201, 68–70, 1985. 4. Larsen, J., Burzotta, J., and Brunetti, V., Ankle dislocation without fracture in a young athlete, J. Foot Ankle Surg., 37, 334–338, 1998. 5. Moehring, H.D., Tan, R.T., Marder, R.A., and Lian, G., Ankle dislocation, J. Orthopaed. Trauma, 8, 167– 172, 1994. 6. Rivera, F., Bertone, C., De Martino, M., Pietrobono, D., and Ghisellini, F., Pure dislocation of the ankle, Clin. Orthopaed., 382, 179–184, 2001. 7. Segal, L.S., Lynch, C.J., and Stauffer, E.S., Anterior ankle dislocation with associated trigonal process fracture, Clin. Orthopaed., 278, 171–176, 1992. 8. Sloane, D. and Coutts, M.B., Traumatic dislocation of the ankle without fracture. A case report, J. Bone Jt. Surg., 19, 1110–1112, 1937. 9. Toohey, J.S. and Worsing, R.A., A long-term follow-up study of tibiotalar dislocations without associated fractures, Clin. Orthopaed., 239, 207–210, 1989. 10. Wehner, J. and Lorenz, M., A case report and review of the literature. Lateral ankle dislocation without fracture, J. Orthopaed. Trauma, 4, 362–365, 1990. 11. Wilson, A.B. and Toriello, E.A., Case report. Lateral rotatory dislocation of the ankle without fracture, J. Orthopaed. Trauma, 5, 93–95, 1991. 12. Wilson, M., Michele, A., and Jacobson, E., Ankle dislocation without fracture, J. Bone Jt. Surg., 21A, 198–204, 1939. 13. Fernandes, T.J., The mechanism of talo-tibial dislocation without fracture, J. Bone Jt. Surg., 58B, 364– 365, 1976. 14. Jaffe, K.A., Conlan, T.K., Sardis, L., and Meyer, R.D., Traumatic talectomy without fracture: four case reports and review of the literature, Foot Ankle Int., 16, 583–587, 1995. 15. Korovessis, P., Spastris, P., Sidiropoulos, P., Katsardis, T., and Spyropoulos, P., Case report and review of the literature. Complete lateral dislocation of the talus without fracture, J. Orthopaed. Trauma, 6, 125–128, 1992. 16. Katz, B.E. and Yang, E., Case report. Complete closed posterior talus dislocation without fracture, Orthopaedics, 23, 846–848, 2000. 17. Bohay, D.R. and Manoli, A., II, Foot fellow’s review. Subtalar joint dislocations, Foot Ankle Int., 16, 803– 808, 1995. 18. Buckingham, W.W., Jr., Subtalar dislocation of the foot, J. Trauma, 13, 753–765, 1973. 19. Christensen, S.B., Lorentzen, J.E., Krogsøe, O., and Sneppen, O., Subtalar dislocation, Acta Orthopaed. Scand., 48, 707–711, 1977. 20. Dendrinos, G., Zisis, G., and Terzopoulos, H., Recurrence of subtalar dislocation in a basketball player, Am. J. Sports Med., 22, 143–145, 1994. 21. Goldner, J.L., Poletti, S.C., Gates, H.S., III, and Richardson, W.J., Severe open subtalar dislocations, J. Bone Jt. Surg., 77A, 1075–1079, 1995. 22. Heck, B.E., Ebraheim, N.A., and Jackson, W.T., Anatomical considerations of irreducible medial subtalar dislocation, Foot Ankle Int., 17, 103–106, 1996. 23. Heppenstall, R.B., Farahvar, H., Balderston, R., and Lotke, P., Evaluation and management of subtalar dislocations, J. Trauma, 20, 494–497, 1980. 24. Tucker, D.J., Burian, G., and Boylan, J.P., Lateral subtalar dislocation: review of the literature and case presentation, J. Foot Ankle Surg., 37, 239–246, 1998. 25. Waldrop, J., Ebraheim, N.A., Shapiro, P., and Jackson, W.T., Anatomical considerations of posterior tibialis tendon entrapment in irreducible lateral subtalar dislocation, Foot Ankle Int., 13, 458–461, 1992. 26. Woodruff, M.J., Brown, J.N., and Mountney, J., A mechanism for entrapment of the tibialis posterior tendon in lateral subtalar dislocation, Injury, 27, 193–194, 1996. 27. Zimmer, T.J. and Johnson, K.A., Subtalar dislocations, Clin. Orthopaed., 238, 190–194, 1989. 28. Me´ne´trey, J. and Fitschy, D., Subtalar subluxation in ballet dancers, Am. J. Sports Med., 27, 143–149, 1999.



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29. Bibbo, C. et al., Missed and associated injuries after subtalar joint dislocation. The role of CT, Foot Ankle Int., 22, 324–328, 2001. 30. Brunet, J.A., Pathomechanics of complex dislocations of the first metatarsophalangeal joint, Clin. Orthopaed., 332, 126–131, 1996. 31. Copeland, C.L. and Kanat, I.O., A new classification for traumatic dislocations of the first metatarsophalangeal joint: type IIC, J. Foot Surg., 30, 234–237, 1991. 32. Hussain, A., Dislocation of the first metatarsophalangeal joint with fracture of fibular sesamoid. A case report, Clin. Orthopaed., 359, 209–212, 1999. 33. Jahss, M.H., Traumatic dislocation of the first metatarsophalangeal joint, Foot Ankle, 1, 15–21, 1980. 34. Lewis, A.G. and DeLee, J.C., Type-I complex dislocation of the first metatarsophalangeal joint — open reduction through a dorsal approach. A case report, J. Bone Jt. Surg., 66A, 1120–1123, 1984. 35. Yu, E.C. and Garfin, S.R., Closed dorsal dislocation of the metatarsophalangeal joint of the great toe. A surgical approach and case report, Clin. Orthopaed., 185, 237–240, 1984. 36. Clanton, T.O. and Ford, J.J., Turf toe injury, Foot Ankle Int., 13, 731–741, 1994. 37. Watson, T., Anderson, R., and Davis, W.H., Periarticular injuries to the hallux metatarsophalangeal joint in athletes, Foot Ankle Int., 5, 687–713, 2000.



9 Pediatric Foot and Ankle Fractures Kelly D. Carmichael Department of Orthopaedics and Rehabilitation, University of Texas Medical Branch, Galveston, Texas

CONTENTS I. Introduction ...................................................................................................................... 212 II. Ankle Fractures................................................................................................................. 212 A. Anatomy of the Distal Tibia and Fibula Region ....................................................... 212 B. Etiology, Prevalence, Diagnosis, and Natural History of Fractures about the Ankle Region............................................................................................................. 213 C. Classification Systems ................................................................................................ 214 D. Treatments................................................................................................................. 215 1. Distal Tibia Metaphyseal Fractures .................................................................... 215 2. Salter–Harris Type I Fractures............................................................................ 215 3. Salter–Harris Type II Fractures .......................................................................... 215 4. Salter–Harris Type III and IV Fractures............................................................. 222 5. Salter–Harris Type V Fractures .......................................................................... 228 6. Isolated Fibula Growth Plate Injuries and Fibula Fractures .............................. 229 E. Transitional Fractures ............................................................................................... 229 1. Juvenile Tillaux Fractures ................................................................................... 229 2. Triplane Fractures............................................................................................... 236 3. Adolescent Pilon Fractures ................................................................................. 243 F. Complications of Ankle Fractures............................................................................. 246 III. Pediatric Foot Fractures ................................................................................................... 247 A. Anatomy .................................................................................................................... 247 B. Talus Fractures .......................................................................................................... 247 1. General Features ................................................................................................. 247 2. Talar Neck Fractures .......................................................................................... 248 3. Body Fractures and Other Injuries of the Talus.................................................. 251 C. Calcaneus Fractures................................................................................................... 252 D. Lesser Tarsal Fractures and Tarsometatarsal Injuries ............................................... 253 E. Metatarsal Fractures.................................................................................................. 254 F. Phalanx Fractures...................................................................................................... 257 IV. Summary ........................................................................................................................... 257 References .................................................................................................................................. 257

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212

I.

Carmichael

INTRODUCTION

Children’s bones in general have a lower modulus of elasticity, more blood, and less mineral content than those of adults [1]. This makes children’s bones more porous than those of adults. The periosteum of children is much thicker and more vascular than that of adults [2]. Periosteum often remains at least partially attached even in displaced fractures, leading to less fracture displacement and more rapid healing times. The osteogenic inner layer of periosteum that is closest to the bone will often stay intact, leading to the rapid healing times noted in children [2]. In addition, children usually have a thicker cartilage [3]. The immature osteochondral bone absorbs and dissipates energy more evenly than adults, leading to far fewer displaced intra-articular or comminuted fractures in children [4]. In late adolescence, as body weight increases and bone is more osseous, the adult-type fracture patterns start to become more common. Because children have lower body weight and more elastic bones with thick periosteum, most of the fractures they sustain will have relatively less displacement and comminution than those of adults. The management of children’s fractures is aided by these anatomic differences, and most fractures in children can be treated nonoperatively [5,6]. This chapter discusses fractures about the ankle and foot region. These fractures are frequently amenable to nonsurgical management. However, surgical options are available for treatment of some fractures. Displaced intra-articular fractures and those with growth plate displacement may benefit from surgical intervention. These types of fractures are more common in the older adolescent population. If surgery is considered about the ankle or foot region the surgeon must be aware of growth plate anatomy and the implications of future growth disturbances. Fixation devices that are used in adults may not be applicable in children with significant growth remaining. Threaded fixation devices such as screws are usually inserted entirely within the epiphysis or the metaphysis so as not to cross the growth plate. Smooth pins that cross the growth plate are occasionally required. As children get older and future growth is minimal, fixation devices with more adult-type options are applicable [7].

II.

ANKLE FRACTURES

A.

Anatomy of the Distal Tibia and Fibula Region

Epiphyseal ossification centers appear around the ankle at 6 months to 2 years of age [4,8]. The medial malleolus appears as an elongation of the ossific nucleus of the tibia around 7 to 8 years of age and is complete by around age 10 [4]. About 20% of the time a separate ossification center termed the os subtibiale appears and can be confused with a fracture [9]. The distal tibia growth plate fuses by about age 15 in girls and age 17 in boys [10]. Closure of this plate takes place over a period of about 18 months [10]. Closure occurs first anterocentrally and proceeds medially and posteriorly, leaving the anterolateral segment as the last to close. This pattern of closure makes the adolescent ankle susceptible to the transitional fractures discussed below [4,10]. The distal fibula ossification center appears at around 9 to 24 months and fuses 1 to 2 years after the distal tibia [10]. The distal tibial physis grows about 3 to 4 mm per year, contributing about 15 to 20% of the lowerextremity length [8]. The anatomy of the ankle is discussed more thoroughly in other chapters, but some pediatric concerns are discussed here. Ligaments are attached to the epiphyseal region of both the tibia and the fibula distal to the growth plate [11]. The ligaments are usually stronger than the growth plate and so failure is more likely to occur through the growth plate than through the ligaments [10,12,13]. Therefore, it is more common for children to have growth plate injuries than adultlike ligament injuries [8,14,15]. Sprains become more of a concern in the 12- to 18-year-old patient. Before that age, fractures are the dominant injury pattern [16]. The rate of distal tibiofibular diastasis is also lower in children for this reason. With displaced tibia fractures, children are more likely to have a fibular fracture than a true syndesmosis injury. Lower-extremity malalignment is also common in children and may influence injury patterns. Excessive femoral anteversion, genu valgus, genu varus, and metatarsus adductus often spontaneously correct, but may influence injury patterns while present [17].


Pediatric Foot and Ankle Fractures

B.

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Etiology, Prevalence, Diagnosis, and Natural History of Fractures about the Ankle Region

Most fractures about the ankle have a benign course in children. They occur through a mechanism that is similar to that of adults. Some injuries, especially supination injuries that would produce ligament sprains in adults, may produce growth plate injuries in children [10]. As discussed above, the growth plate is weaker than the ligaments and is more likely to fail. The statement that ‘‘children don’t get sprains’’ may not be entirely true, but is useful to remember when dealing with young children and ankle injuries [18]. Another unique feature of children is the buckle or greenstick fracture pattern. Bone can fail in tension with a high loading rate and produce a complete fracture [1]. Occasionally, the bone will deform but not have a true cortical fracture, producing the bent bone type fracture, or it will fail only on the tension side producing a greenstick fracture [1,4]. Both greenstick (bent bones) and complete transverse fractures are more likely to occur in the fibula. Transverse fibula fractures are often associated with complete fractures of the tibia. A child’s bone may also fail on the compression side, producing a buckle fracture. This is most common in the distal tibial metaphyseal region of young children [19]. Further mechanisms of injury are discussed in the ‘‘Classification Systems’’ section. The ankle is a common location for physeal injuries [20]. This region accounts for 25 to 38% of all physeal injuries, making it second only to the distal radius in terms of growth plate injuries [21]. The incidence of injuries to the distal tibial physis is about 63 and 53 per 10,000 for boys and girls, respectively [22]. Because the ligaments are stronger than the physeal cartilage, growth plate injuries are more common than ligament injuries. Also, some of the inversion injuries of the ankle may produce foot fractures, such as fifth metatarsal base or Lisfranc midfoot injuries [18]. The diagnosis of fracture is obvious when it is displaced, but some pediatric fractures may be difficult to appreciate. In an effort to reduce radiographic exposure, some guidelines are useful in deciding whether to take radiographs of a child’s injured ankle. Pain around the malleoli (growth plates), inability to bear weight, and any obvious deformity should prompt radiographic investigation [23,24]. Usually anterior to posterior (AP), mortise, and lateral views are obtained [18]; the AP should be omitted if only two views are sought. Stress views may be needed in older children if ligamentous instability is suspected or to differentiate acute fractures from accessory ossicles [8,10]. The interpretation of ankle films is frequently aided by comparison views [18,25]. Some Salter– Harris type I fractures may appear as only slight physeal widening on the injured side compared with the uninjured side (for a complete description of the Salter–Harris system refer to ‘‘Classification Systems’’ section). Variations in ossification centers can make radiographic interpretation difficult, so any radiographic findings must be coupled with physical examination [8]. The tibia– fibula overlap is different from that of adults on AP and mortise views. Overlap appears around the age of 5 years on AP views, while on the mortise view it may not occur until the age of 10 years in girls and the age of 16 years in boys. Clear space measurements range from 2 to 8 mm and nearly one fourth of children have clear spaces above 6 mm, which would be considered abnormal in adults [26]. Examination of the proximal fibula and radiographs of the entire leg are required if Maisonneuve injuries are suspected [27]. Additional studies are useful in selected situations. Computed tomography (CT) scans can be used in intra-articular fractures, especially the epiphyseal fracture patterns of adolescence. Plane films may underrepresent the amount of displacement in transitional fractures and a CT scan is recommended if nonoperative management is considered [28–30]. The CT scan can also be used to plan reductions, for preoperative assessment of fracture fragments, and for assessment of the adequacy of reductions. Magnetic resonance imaging (MRI) has limited application in acute fractures, but can be used to evaluate osteochondral injuries and suspected crush injuries to growth plates, and in mapping of physeal bars that may develop after acute injuries [31,32]. Most injuries are relatively nondisplaced and do not involve the articular surface. Children have a low rate of nonunions compared with adults. Growth disturbance after growth plate injuries is often the most difficult problem encountered while dealing with ankle fractures. Salter– Harris type I and II injuries do not involve the articular surface and have a low rate of growth disturbances. The intra-articular Salter–Harris type III and IV injuries as well as the crush Salter–Harris type V injuries do have significant rates of growth problems and should be followed


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closely [33]. ‘‘Treatment’’ section of this text will discuss how best to minimize these growth disturbances.

C.

Classification Systems

At least three different types of classification systems are available for ankle fractures in children. Classification can be based on mechanism of injury, anatomy, or outcomes and risk of growth disturbance. A complete discussion of each system is beyond the scope of this text, but each shall be described briefly below. All classification systems have strengths and weaknesses, which shall be discussed, but the reader is advised to use the system that best suits his or her needs. The mechanistic classification system of Dias–Tachdjian [34] is similar to the adult system of Lauge-Hansen. Fractures are described based on mechanism of injury in terms of foot position and deforming forces, respectively. A brief description of this system is outlined in Figure 9.1, but the reader is referred to the original work for a more complete description. Supination–inversion (SI) injuries are divided into two types. Type I SI involves an avulsion of the distal fibula epiphysis (Salter–Harris type I or II) or ligamentous injury. Type II SI produces a tibia fracture, usually a Salter–Harris type III or IV, but occasionally a type I, type II, or a medial malleolar fracture below the level of the growth plate. Supination–plantar flexion (SPF) produces a Salter–Harris type I or II fracture of the tibia that is displaced posteriorly. Supination–external rotation (SER) injuries are divided into two groups: type I is a Salter–Harris type II of the tibia displaced posteriorly with the fracture line extending proximally and medially, and type II produces the type I pattern in addition to a spiral fibula fracture. Pronation–eversion–external rotation (PEER) produces a Salter–Harris type I or II of the tibia with a transverse fracture of the fibula, or occasionally in older children a diastasis of the ankle joint. Axial compression injuries produce a growth plate crush (Salter–Harris type V), which becomes evident only at follow-up [7]. The Tillaux and triplane fractures are considered separate and will be discussed later. The mechanism of injury classification has some advantages and some disadvantages. The system is useful in describing the deforming forces sustained at the time of injury and thus aids in the reduction of fractures. However, it is a cumbersome system that can be difficult to remember. Interobserver reliability is low with this system [8]. Also, this system does not address prognosis, and the true mechanism of injury may not be discernable by radiographs. When the physical appearance of an injured extremity is combined with radiographs, the deforming forces should be identifiable, thereby making reliance on a complicated system unnecessary. The anatomic classification of Salter–Harris is well known, with good intraobserver and interobserver reliability [8,18]. Fractures are classified according to growth plate, epiphyseal, and metaphyseal involvement [35]. The Salter–Harris system also aids with prognosis. Figure 9.2 illustrates the Salter–Harris system of growth plate injuries. Type I and II fractures have a good prognosis and type III, IV, and V fractures have a poorer prognosis [13]. The anatomic system does not address mechanism of injury and is therefore not as useful in guiding reduction maneuvers. A simple system was designed by Vahvanen and Aalto [33]. They divided these fractures into two groups: low risk and high risk based on outcomes and prognosis. Low-risk fractures, likely to

I

Supination− invertion(I)

Supination− Supination− Supination− invertion(II) plantar plantar flexion flexion (AP view) (lateral view)

Supination− external rotation

II

Pronation eversion extermal rotation

Figure 9.1 Simplified diagram of the mechanistic Dias–Tachdjian classification system of pediatric ankle fractures.



I

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II

III

IV

V

Figure 9.2 Salter–Harris classification system of pediatric growth plate injuries.

do well with low risk of growth sequelae, are avulsion fractures and include Salter–Harris type I and II fractures. High-risk fractures with increased potential for growth disturbances are Salter–Harris type III, IV, and V fractures and transitional fractures. Spiegel et al. [36] have a similar system, but transitional fractures are considered a separate category. The author prefers the Salter–Harris system for several reasons. First, the system is simple and universal [18]. When a fracture is described by this system almost any audience, from medical students to attending surgeons, can understand. Second, a clinician should be able to examine an extremity and ascertain the deforming forces, thereby making the mechanistic classification unnecessary. Third, the prognostic system may not provide enough description and it seems obvious that displaced intra-articular fractures will not fair as well as extra-articular fractures. Finally, the anatomic system provides a reasonable description of the fracture and insight into prognosis; the mechanism of injury can be obtained by examining the patient.

D.

Treatments

Descriptions of how adult foot and ankle fractures are treated are found elsewhere in this book. If a particular pediatric fracture is treated similarly to the corresponding adult fracture, the reader will be referred to that chapter. 1.

Distal Tibia Metaphyseal Fractures

Complete fractures of the tibia metaphysis can occur when the bone fails in tension. This pattern is more common in the adolescent and adult population than it is in children. Buckle fractures occur in younger children when the metaphyseal bone fails in compression (Figure 9.3). The buckle type fracture can usually be treated with a non-weight-bearing long leg cast for 3 to 4 weeks followed by an additional 3 to 4 weeks of a weight-bearing short leg cast. These fractures should be closereduced if more than 158 of angulation exists and then they are treated as above [19]. 2.

Salter–Harris Type I Fractures

These fractures often offer more of a diagnostic dilemma than a challenge to treat. These fractures are frequently nondisplaced and may require a radiograph of the uninjured side to make the diagnosis [25]. A subtle Salter–Harris type I fracture will show growth plate widening on the injured side (Figure 9.4). Most Salter–Harris type I fractures involve only the fibula and are produced by inversion stresses [18]. Salter–Harris type I fractures of the tibia are considered to be less common by some authors [18] and more common by others [36]. Tibia Salter–Harris type I fractures occur by any mechanism in younger children [34]; the average age is around 10.5 years, and these injuries may account for up to 15% of pediatric ankle fractures [11,36]. The treatment of both Salter–Harris type I and II fractures is similar and will be discussed below. 3.

Salter–Harris Type II Fractures

Salter–Harris type II fractures are the most common type of growth plate fracture about the ankle. Type II fractures may account for 40 to 45% of growth plate fractures [36–38]. The fracture line


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Figure 9.3 Ankle radiographs of a distal tibial metaphyseal fracture in a 4-year-old girl. (A) From left to right: AP, oblique, and lateral views of the acute injury showing some angulation, which was thought to be within acceptable limits. (B) Radiographs at 6-week follow-up after casting showing lateral (left) and AP (right) views of the tibia and fibula. Note the excellent healing and remodeling after only 6 weeks.

involves the physis, with extension into the metaphysis. The metaphyseal fragment is often triangular and is sometimes termed the Thurston–Holland fragment [8]. Displaced fractures may produce a periosteal tear that becomes interposed in the Thurston–Holland fragment [8]. A transverse fibula fracture may also result with displaced fractures [18]. Fractures with minimal displacement can be treated in either a short leg or a long leg cast (Figure 9.5). There are advocates of both weight-bearing casts and non-weight-bearing casts. The most common recommendation is 3 to 4 weeks of non-weight-bearing and an additional 3 to 4 weeks in a weight-bearing cast [10]. Treatment of displaced fractures may require reduction before casting.



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Figure 9.4 Radiographs of a Salter–Harris type I distal tibia fracture in a 9-year-old boy. Oblique views of the ankles showing (A) the injured left side. Note the widening of the growth plate on the injured side (arrows) and (B) comparison view of the right ankle.

Opinions vary as to what constitutes an acceptable reduction. Some authors have recommended anatomic reduction of these fractures [36], while others have noted good remodeling potential with fractures angulated over 108 [39]. There are no firmly established standards defining an acceptable amount of angulation. The amount of growth remaining, the initial displacement, and the acuity of the fracture must all be considered in the treatment of these fractures. Fracture reduction should be attempted in the acute fracture if significant angulation (more than 10 to 158) is present. The most important point to remember is that the reduction should be attempted under adequate sedation to allow reduction on the first attempt [8,10]. If the reduction is attempted in the emergency room under conscious sedation, then only one reduction attempt should be performed. Repeated forceful attempts are to be avoided. Fractures that continue to show angulation or physeal widening without much angulation may have soft tissue interposition [4,8,10]. Unsatisfactory reductions should be taken to the operating room so that open reduction is possible and iatrogenic growth plate injury is minimized. Open reduction will be needed if neurovascular structures are interposed in the fracture fragments [40]. Some authors have also advocated open reduction to extract the periosteum in fractures that have physeal widening without angulation, but studies demonstrating that this is absolutely necessary are lacking [10,41]. Once these fractures are reduced, they can be treated with casting as described for nondisplaced fractures if they are stable [8]. Unstable Salter–Harris type II fractures can be held with percutaneous screws in the metaphyseal fragment staying proximal to the growth plate. The screw can be cannulated and is inserted AP in some fractures (Figure 9.6). Other fractures may require medially or laterally placed screws, depending on the fracture displacement (Figure 9.7). If the metaphyseal fragment is small, smooth Kirschner wires can be inserted across the growth plate to hold the reduction (Figure 9.8). Smooth-wire fixation is also indicated in the rare displaced Salter–Harris type I fracture since there is no metaphyseal fragment to hold a screw. Kirschner wires are left protruding through the skin and are removed at 3 to 4 weeks after surgery. Casting and weight-bearing continues as described above.


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Figure 9.5 Radiographs of a relatively nondisplaced Salter–Harris type II distal tibia fracture that was treated conservatively in a 9.5-year-old girl. (A) AP and (B) lateral views of the ankle showing the acute injury in a bivalved long leg cast. At 6-week follow-up (C) AP view and (D) lateral view demonstrate the fracture is healing well.

Fractures that present late are unfortunately fairly common. The treatment of these fractures takes an individualized approach. A fracture is considered to be a late presentation at 3 days by some authors and 7 to 10 days by others [10]. If angulation is not severe it is best to cast these fractures without reduction, especially if they have already had reduction attempts. Several



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Figure 9.6 Ankle radiographs of a displaced Salter–Harris type II distal tibia fracture in a 14-year-old male. (A) AP view, (B) oblique view, and (C) lateral view of the acute injury. The extent of the metaphyseal fragment is best appreciated on the lateral view. This fracture was close-reduced in the operating room. Once reduced the fracture is held with two percutaneously placed lag screws from AP. Postoperative radiographs: (D) AP.


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Figure 9.6 Continued (E) oblique, and (F) lateral views demonstrating good reduction of the metaphysis and the physis.

reduction attempts spaced days or even weeks apart may cause iatrogenic damage to the growth plate. The ankle region is capable of substantial remodeling. If the growth plate is horizontal, the metaphyseal region will remodel in most cases. If the growth plate is injured during a reduction attempt of a fracture that is several days old, this remodeling may not occur. Therefore, delayed reductions are to be done with caution, if at all. Fractures that present late with residual displacement can be allowed to heal and then are treated with osteotomies if persistent deformity exists [10]. Having said that, there are fractures that present late that are clearly unacceptable. Remodeling has its limits, and treatment of unacceptably angulated fractures with reduction in the operating room may be necessary. The author’s approach to grossly angulated fractures is as follows: Children under 10 years of age with fractures angulated more than 258 who are less than 2 weeks from injury are offered surgical intervention with an explanation that the intervention may lead to growth arrest. Parents are also given the option of closed management and informed that a future osteotomy may be needed to correct any residual deformity. Children aged 10 and older are offered intervention for fractures angulated more than 158 and less than 2 weeks from injury. Injuries more than 2 weeks old are treated with casting and late osteotomies for any residual deformities. In the older child, with only a few months of growth remaining, injury to the growth plate becomes less of a concern, and late fracture reduction can be done. One attempt is made to reduce them closed and, if unsuccessful, they are opened, reduced, and usually fixated with a screw or Kirschner wire. There are no extensive studies to confirm that delayed reduction of grossly angulated growth plate fractures improves outcomes, so universal recommendation of this practice is not possible.



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Figure 9.7 Ankle radiographs of a displaced Salter–Harris type II distal tibia fracture in a 9-year-old boy. (A) AP, (B) oblique, and (C) lateral views of the ankle demonstrating the acute injury. The metaphyseal fragment is located more medially than the injury depicted in Figure 9.6. After closed reduction in the operating room the fracture is held with lag screws that are placed from medial to lateral. Postoperative views of (D) AP.


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Figure 9.7 reduced.

4.

Continued (E) oblique, and (F) lateral projections show the metaphyseal spike is well

Salter–Harris Type III and IV Fractures

The Salter–Harris type III and IV fractures are both intra-articular fractures that share many treatment options, so they are discussed together. Each type may account for 20 to 25% of distal tibia fractures [11,37,38]. Treatment of these fractures will involve restoration of growth plate anatomy and the articular surface. The articular surface of these fractures should be anatomically reduced, as remodeling will not correct any articular incongruity [42–44]. Salter–Harris type III fractures are most commonly Tillaux type fractures, which are discussed below in the ‘‘Transitional Fractures’’ section. Inversion stresses may produce a Salter–Harris type III of the medial malleolus with accompanying type I or type II fibula fracture [18]. The Salter–Harris type IV fractures located medially are the result of inversion and shear; the lateral types are often triplane variants, which will be discussed below [18]. The fibular fractures associated with these tibia fractures are usually Salter– Harris type I or type II fractures or are transverse and often reduce when the tibia is reduced [8]. Nondisplaced fractures can be treated with long leg casting (Figure 9.9). If a decision to treat these fractures nonoperatively is made, a CT scan is recommended to insure reduction is anatomic because radiographs may underestimate the articular displacement [28]. If the CT scan confirms anatomic reduction, nonoperative management may be undertaken. Follow-ups at frequent intervals are necessary to monitor for loss of reduction in the cast. Many of these fractures are displaced and will need reduction. Preoperative CT scans are used to plan exposure and fixation, especially in Salter–Harris type IV fractures. Closed reduction may be possible with some minimally displaced fractures, but is difficult with displaced fractures [4,10]. Once reduced, the fractures are held with casting or percutaneous screws or wires. If closed reduction is used, a postoperative CT scan is recommended to insure the adequacy of the reduction. If the articular surface reduction is uncertain or inadequate, an open reduction should be performed [45,46]. The exposure should allow direct visualization of the joint surface so that it can be anatomically reduced. The exposure is generally an anterolateral or anteromedial arthrotomy, depending on the position of the fracture fragments. Fixation of fractures reduced by either closed or open methods can be by means of screws or Kirschner wires. Screws can be inserted



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Figure 9.8 Salter–Harris type II distal tibia fracture and distal fibula fracture in a 13-year-old male. Preoperative (A) AP and (B) lateral radiographs of the ankle. The fibula is somewhat comminuted and the tibial metaphyseal spike is small. The tibia was treated with a closed reduction and held with smooth Kirschner wires inserted through the medial malleolus. The fibula did not reduce with the tibial reduction and was treated with ORIF using a 1/3 tubular plate and screws. Postoperative radiographs of (C) AP and (D) lateral ankle. The small free fragment of fibula was not incorporated into the plate, but the fibula went on to heal well. Note the fibula plate is placed proximal to the distal fibular growth plate.


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Figure 9.9 Ankle radiographs of a Salter–Harris type III medial malleolar fracture in a 14-year-old male. Acute injury radiographs (A) from left to right: AP, oblique, and lateral views showing a minimally displaced fracture. It was elected to treat this injury conservatively. At 2-month follow-up radiographs of (B) AP and mortise view show excellent healing.

into Salter–Harris type III fractures that are completely intraepiphyseal [8]. Usually, a cannulated screw is used, and the guidewire is inserted parallel to the joint surface and the growth plate, taking care that neither will be violated by the screw threads [45] (Figure 9.10). Every effort should be made to avoid crossing the growth plate with fixation devices, but reducing the articular surface is the main priority [4]. Salter–Harris type IV fractures can be fixed with an additional screw that captures the metaphyseal fragment but not the growth plate (Figure 9.11). When these fractures occur near skeletal maturity, hardware can be placed perpendicular to the fracture fragments and across the growth plate [4]. Figure 9.12 shows fixation across the growth plate in an open fracture that could not be adequately held without crossing the plate. Another option for fixation is the absorbable pin [47–49]. The advantage of the absorbable pin is that hardware removal is not needed. At this time, not enough is known about absorbable pins for fracture fixation, so universal recommendation of these pins is not possible.



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Figure 9.10 Intraoperative radiographs of a Salter–Harris type III medial malleolar fracture in an 11-year-old male. (A) AP and mortise views and (B) lateral view demonstrating screw placement. Percutaneous cannulated screws are placed from medial to lateral and stay completely within the epiphysis.


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Figure 9.11 Salter–Harris type IV distal tibia fracture in a 14-year-old male. Radiographs of the ankle: (A) AP and (B) lateral view demonstrate the preoperative injury pattern. The metaphyseal fragment was large enough to accept fixation. Postoperative radiographs (C) AP and (D) lateral view demonstrating the screw placement. Both screws are parallel to the physis, but do not violate either the physis or the joint surface.



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Figure 9.12 Salter–Harris type IV distal tibia fracture in a 14-year-old male. This was an open injury with some loss of bone, growth plate, and soft tissue from the medial ankle. Radiographs of (A) AP, (B) mortise, and (C) lateral views of the injured right ankle demonstrating the tibia fracture as well as a Salter–Harris type I fracture of the distal fibula. The (D) left ankle mortise view is included to show that the medial side of the distal tibia growth plate was beginning to fuse. After irrigation and debridement, the fracture was fixed with two screws. An intraepiphyseal screw did not provide enough stability and so a cross-physeal screw was placed from the medial malleolus.


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Figure 9.12 Continued Postoperative (E) AP and mortise, and (F) lateral views demonstrating screw placement. The screws were placed in such a way that they could be covered with soft tissue. A small open area that healed by secondary intention remained. Growth disturbance is likely after this injury, but the patient has not returned for follow-up after soft tissue healing.

The author’s preferred approach to these fractures is as follows. In rare cases, a fracture seems so minimally displaced that nonsurgical management is considered. In these cases, a CT scan is obtained after casting to be sure the fracture is displaced 1 mm or less. Displaced fractures are treated operatively. Preoperative CT scans are obtained only when fracture fragments and displacement cannot be ascertained by plane films. In the operating room, attempts are made to reduce the fracture with manipulation and percutaneous bone clamps. If an anatomic reduction is uncertain, an open reduction is preformed. The fragments are fixated with cannulated screws that do not cross the growth plate, or, occasionally, smooth Kirschner wires that can cross the plate. Adequate reduction should be obtained in the operating room; these fractures should be reduced and held under one general anesthetic. Reliance on postoperative CT scans for fractures that are close-reduced and casted may mean an additional trip to the operating room, and the risks of a second general anesthetic, if they are not anatomically reduced. In addition, the intra-articular fracture gap is closed more securely with fixation, so that synovial fluid is not interposed in the fracture gap, potentially causing delayed healing. 5.

Salter–Harris Type V Fractures

True crush injuries to the ankle growth plates are rare, accounting for less than 1% of fractures [8]. Some authors have classified comminuted, otherwise nonclassifiable, fractures as Salter–Harris type V injuries [36], but that is not the true crush injury as discussed below. The magnitude of the injury will usually not be evident in the acute setting and initial radiographs may be negative [18]. Growth disturbance is often the first sign of a crush injury. The growth disturbance will often be angular as it is unlikely that the entire growth plate will be crushed. Both CT scans and MRIs have been used to evaluate the amount of growth plate involvement. When less than 50% of the growth plate is involved and the patient is young, consideration of physeal bar resection and interposition of fat or cranioplast should be considered [8]. Older patients and those with more than 50% growth plate arrest will require reconstructive efforts. Arthroscopically assisted physeal bar resection has also been described [18,50]. The injured ankle may require late osteotomies, lengthening procedures, or completion of the epiphyseodesis on the injured side [8]. Depending on growth remaining, consideration may also be given to well-ankle epiphyseodesis. The entire spectrum of treatment options for complete and partial growth arrests is beyond the scope of this text. Since this type of injury is so



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rare, no large studies exist to make universal treatment recommendations. Treatment is directed toward minimizing growth disturbances when possible and then treating them when necessary. 6.

Isolated Fibula Growth Plate Injuries and Fibula Fractures

The most common injury encountered is a Salter–Harris type I fracture. Together, the Salter– Harris type I and II injuries account for 90% of isolated fibula fractures in children [8]. The diagnosis is made by tenderness over the lateral malleolus and a widening of the growth plate seen on radiographs. A comparison view of the uninjured side can help to make this diagnosis [25]. Salter–Harris type II fractures of the fibula usually produce a small metaphyseal fragment and are treated similar to type I fractures. The treatment is usually with a short leg cast for 3 to 6 weeks [10]. Weight-bearing is controversial; there are proponents of both non-weight-bearing and weightbearing as tolerated. In compliant patients and families, an air-stirrup or other off-the-shelf brace can be substituted for cast immobilization, as these are usually stable fractures. Salter–Harris type III and IV fibula fractures are very rare and must be distinguished from the more common accessory ossification center [8]. A fibula fracture is often associated with a tibia fracture. The fibula will often reduce when the tibia is reduced (Figure 9.13). Sometimes, a separate reduction or even open reduction and internal fixation (ORIF) will be required [8]. If ORIF is performed, it is best to stop fixation proximal to the growth plate if possible (Figure 9.8 and Figure 9.14). In long spiral fibula fractures, lag screws without plate fixation may suffice (Figure 9.15).

E.

Transitional Fractures

Transitional fractures are so named because they occur during a time of transition from open growth plates to skeletal maturity. These fractures occur in children in the 11- to 15-year-old age range. The two main types are the juvenile Tillaux fracture and the triplane fracture. Growth plate closure of the distal tibia physis helps explain these two fracture patterns. Closure first occurs anterocentrally and proceeds medially and then posteriorly. This leaves the anterolateral aspect of the distal tibia as the last area to fuse. Once begun, the closure of the distal tibia growth plate takes about 18 months [4,10]. The distal fibular growth plate closes about 1 to 2 years after the tibia [4,10]. The mechanism of injury is primarily external rotation for both types of fractures [4,10,51]. Some variants of the triplane fracture involve different mechanisms of injury. Additional forces and the stage of growth plate closure helps explain the variety of fracture patterns that are seen [51]. The foot position at the time of injury may also vary and influence fracture patterns [52–54]. Some consider the triplane fracture to be a more severe form of the Tillaux fracture, occurring through similar mechanisms [52], while others consider the amount of physeal closure to be the primary determinant of fracture type [55]. 1.

Juvenile Tillaux Fractures

The ligaments of the skeletally immature ankle are generally stronger than the growth plate. Because of this, the forces that might lead to ligament failure in adults will produce the unique fracture pattern of the partially closed physis. The Tillaux fracture produces an anterolateral epiphyseal fragment produced by the pull of the anteroinferior tibiofibular ligament during SER injuries [8,10]. A Salter–Harris type III fracture results as the anterolateral open physis fails. External rotation of the fibula and foot coupled with an intact anteroinferior tibiofibular ligament avulses a piece of the epiphysis, displacing it laterally and anteriorly. These injuries account for 3 to 5% of pediatric ankle fractures [8,36]. Diagnosis of a Tillaux fracture is made by physical examination, radiographs, and, frequently, CT scans. There is little displacement or obvious clinical deformity in most patients because the fibula is intact. Swelling may also be minimal. Pain will be present along the anterolateral joint line with more pain over the bone than over the ligament. Plane radiographs demonstrate the anterolateral fragment. The AP and mortise views often show minimal displacement. The lateral view is helpful because the fragment is often displaced anteriorly. In fractures that show little displacement


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Figure 9.13 Salter–Harris type IV distal tibia and Salter–Harris type II distal fibula fracture in an 11-year-old male. Ankle radiographs (A) AP and (B) mortise views show the acute injury to both the tibia and the fibula. The fracture was reduced by closed means and with the aide of Kirschner wire to joystick the medial malleolar fragment. The tibia fracture was held with a single medial-to-lateral screw and the fibula reduced well with reduction of the tibia. Postoperative radiographs (C) AP and mortise.



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Figure 9.13 Continued (D) lateral views demonstrate the screw placement and reduction of the fibula. The fibula remained reduced by postoperative splinting and then casting.

on plane films, a CT scan is recommended because articular incongruity and displacement may be underestimated, especially in fractures displaced over 2 mm [28,56]. Treatment is directed at restoration of the articular surface. Most of these fractures occur at a time when there is little growth remaining in the distal tibia and efforts to preserve the growth plate are secondary to articular congruity. If the fracture displacement is less than 2 mm, nonoperative management with a long leg cast for at least 4 weeks can be considered [8]. CT scans are recommended if nonoperative management is chosen to make sure the displacement is acceptable. Displaced fractures require reduction and every effort should be made to insure anatomic reduction of the joint surface. Closed reduction is done with internal rotation followed by a long leg cast. If an adequate reduction cannot be obtained by closed reduction then operative intervention should occur. Percutaneously placed reduction clamps can aid in the reduction. The clamp is inserted under fluoroscopic control into the anterolateral fragment, with the other end gaining purchase in the medial malleolar region. Closed reduction maneuvers are repeated as the clamp is tightened. Direct manual pressure over the fragment may also be used to obtain reduction. Another technique is to use a Kirschner wire to joystick the fragment into place; the Kirschner wire can then be advanced to hold the reduction with the addition of a supplemental wire, or the wire can be replaced with a screw [10,57]. If these maneuvers fail to produce an anatomic reduction, then an open approach through an anterolateral arthrotomy will be needed. A case report exists of a fracture fragment that was trapped between the distal tibia and fibula, appearing like a syndesmosis disruption radiographically [58]. After extraction of the fragment and ORIF, the tibia–fibula diastasis reduced spontaneously. If the fracture is reduced in the operating room by any of the above means, it should be held with some form of fixation. Fixation is accomplished with Kirschner wires [57] or an intraepiphyseal


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Figure 9.14 Salter–Harris type II distal tibia fracture and displaced fibula fracture in a 12.5-year-old male. Preoperative radiographs of the ankle: (A) AP, (B) mortise, and (C) lateral views demonstrating the large tibial metaphyseal fragment and the displaced fibula fracture. The tibia was close-reduced and fixed with two AP lag screws. The fibula remained displaced after reduction of the tibia and was open reduced and internally fixated with a 1/3 tubular plate and screws. Postoperative radiographs of the ankle in.



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Figure 9.14 Continued (D) AP and mortise and (E) lateral projections demonstrating the hardware placement. The fibular plate is placed so as to stay proximal to the distal fibular growth plate.


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Figure 9.15 Ankle fracture in a 15-year-old male. Radiographs of the ankle: (A) AP, (B) mortise, and (C) lateral views of the acute injury. These films demonstrate a Salter–Harris type II tibia fracture and a spiral fibula fracture. Also note the nondisplaced epiphyseal fracture. The fragment extends to the nonweight-bearing zone of the distal tibia, making this an intramalleolar triplane variant. The tibia fracture was close-reduced and fixed with a single AP screw. Postoperative radiographs: (D) AP and mortise, and (E) lateral views showing the fixation. The fibula was a long spiral fracture and was open reduced and held with two lag screws. The epiphyseal fragment remained nondisplaced throughout and was not internally fixated.



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screw. A single 4-mm cannulated screw is usually adequate. The guide pin for the cannulated screw is inserted parallel to the joint surface and the physis. The pin is inserted laterally just anterior to the fibula after the fracture has been reduced (Figure 9.16). Care is taken to insure that the screw stays within the epiphysis and does not violate either the joint surface or the growth plate [59]. Near

Figure 9.16 Tillaux fracture in a 14.5-year-old male. Preoperative radiographs: (A) AP, (B) mortise, and (C) lateral views of the ankle. Note the anterior displacement of the anterolateral epiphyseal fracture on the lateral view. (D) Axial CT scan shows the displacement of the fragment in an anterolateral direction. The fracture was reduced by both closed means and a percutaneously placed bone-reduction clamp.


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Figure 9.16 Continued (E and F) Postoperative mortise and lateral radiographs, respectively. The cannulated screw is inserted percutaneously just anterior to the fibula. The screw is completely within the epiphysis so that neither the joint surface nor the physis is violated.

skeletal maturity the fixation devices may cross the growth plate if this is required for secure fixation [8]. However, it is best not to cross the growth plate if this can be avoided [28]. Postoperatively, the use of a short leg cast with the foot held slightly internally rotated is preferred. However, some authors prefer a long leg cast with the knee extended or in 308 of flexion. The patient is kept nonweight-bearing for a period of at least 3 weeks followed by another 3 weeks of weight-bearing immobilization. In some cases, the patient is treated the entire 6 weeks with non-weight-bearing followed by protection in a walking boot. Fractures that present late should also be reduced and fixed if they are displaced. A case report of a fracture that was treated operatively at 5 weeks after injury still had a good result [60]. Fractures of the ipsilateral tibia shaft have been reported with Tillaux fractures, so an inspection of the entire leg is warranted when this fracture is encountered [61]. 2.

Triplane Fractures

The triplane fracture is a fairly common fracture of adolescence. About 20% of growth plate fractures of the ankle are triplanes [28]. In girls, this injury represents 6 to 7% of all ankle fractures from age 0 to 18 years. In boys, this may be 11 to 15% of all ankle fractures [28]. The mean age of occurrence is 12.8 years in girls and 14.8 years in boys. In one study, no patient was under 10 and no patient was over 16.7 years [28]. The typical triplane fracture occurs with external rotation forces similar to those of a Tillaux fracture. This may represent a more severe form of the Tillaux fracture [22,62]. Variants of the triplane fracture have been described with fracture patterns and mechanisms that differ from that of the classic triplane fracture. These variants should be considered a separate entity and not a continuum of the triplane fracture [28]. The diagnosis of a triplane fracture is usually more obvious than that of a Tillaux fracture. Swelling can be marked and deformity frequently accompanies these



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fractures; the fibula is fractured much more often with triplane fractures. Physical examination must carefully document neurovascular status and other areas of tenderness. Occasionally, soft tissues may be incarcerated in the fragments [28,63]. Ipsilateral tibia fractures, proximal fibular tenderness, or other signs of syndesmotic disruption should be sought. Plane radiographs including AP, mortise, and lateral views are essential. The amount of displacement is sometimes underestimated by the AP and mortise views. Lateral views show the metaphyseal fragment and any anterior displacement of the anterolateral epiphyseal fragment. CT scans are used frequently to discern displacement and the number of fracture fragments. Triplane fractures were first described in the late 1950s. In 1957, Johnson and Fahl [64] described the injury, as did Bartl [65] in the same year. The fracture was created and studied experimentally by Gerner-Smidt [66] in 1963. Lynn [67] coined the term triplane in 1972. The classic description of these fractures consisted of three main parts: an anterolateral fragment (Tillaux equivalent), medial and posterior epiphysis attached to a metaphyseal spike, and the remaining distal tibial metaphysis [67]. This fracture configuration was later confirmed by a CT scan in 1981 [68]. It is felt by some that most of these fractures consist of only two parts; the anterolateral epiphyseal fragment is connected to the posterior metaphyseal spike, creating only two fragments [59]. Classification or description of the fractures is based on number of fragments or anatomically. CT scans are required to accurately classify these variations [28]. Classifications based on number of fragments divide these into two-, three-, and sometimes four-part fractures (Figure 9.17). Several authors describe only two- and three-part fractures [4,51]. The two-part fracture involves a single fracture line through the epiphysis on CT scan. The anterolateral epiphyseal fragment is attached to the metaphyseal spike in two-part fractures. A three-part fracture involves three radiating fracture lines seen on CT, creating the ‘‘Mercedes’’ sign [4]. The three-part fracture occurs when the anterolateral epiphyseal fragment is separated from the metaphyseal spike fragment. Others have identified two- and three-part fractures with a medial type as a variant [69]. Karrholm et al. [68] describe two-, three-, and four-part fractures. Two-part fractures consist of the anterolateral epiphyseal fragment connected to the metaphyseal spike fragment. Three-part fractures consist of the anterolateral epiphyseal fragment being separate and the metaphyseal spike being attached to the posterior epiphysis, with the shaft creating the third piece. The four-part fractures consist of the anterolateral epiphysis, the medial malleolus, the posterior epiphyseal or metaphyseal spike, and the shaft, creating the four pieces. Using CT scans, Karrholm et al. [70] were able to identify these various fracture patterns. Anatomically, VonLaer [71] has divided these fractures into two types. A type I fracture involves a metaphyseal fracture that extends to, but is not across, the physis. In type IA fractures, the sagittal fracture line is located in the central or lateral epiphysis and creates the anterolateal epiphyseal fragment. In type IB fractures, the sagittal fracture line extends through the medial malleolus without reaching the articular surface, creating the intramalleolar variant. The type II fracture occurs with extension of the metaphyseal fracture into the joint. The type II fractures are three-part fractures, and all are intra-articular, as the frontal plane fracture is a Salter–Harris type IV fracture. The sagittal fracture line can run central, lateral, or intramalleolarly through the epiphysis [71,72]. An extra-articular or intramalleolar variant, produced by the same SER mechanism as most triplanes, occurs when the fracture line exits through the medial malleolus instead of through the anterolateral joint line [28,70,71,73]. Shin et al. [74] have further divided these intramalleolar variants into three types based on the fracture patterns of five patients. In type I fractures, the fracture line exits the malleolus in the weight-bearing zone; in type II, the fracture exits outside the weight-bearing zone; and type III fractures are completely extra-articular. Thus, in the Shin system, only type III fractures are truly extra-articular intramalleolar variants (Figure 9.18). Medial triplane fractures have also been described. Denton and Fisher [75] and Marmor [76] have both described a medial triplane fracture. These rare fractures occur through mechanisms that differ from the classic triplane and have also been described by others [77,78]. The Denton–Fisher type medial triplane fracture produces a medial and anteriorly displaced fragment (Figure 9.19). The Marmor type fracture occurs when there is an anterolateral fragment and the posteromedial metaphyseal spike and medial malleolus are displaced medially [28,76] or when the anterolateral epiphysis stays attached to the metaphysis while the medial malleolus and posteromedial metaphyseal spike are displaced medially (Figure 9.20) [28]. Another variant has been described in which the


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A

L

Metaphyseal fracture Physeal fracture Epiphyseal fracture

A A

L

Metaphyseal fracture Physeal fracture Epiphyseal fracture B A

L

Metaphyseal fracture Physeal fracture Epiphyseal fracture

C

Figure 9.17 Diagram of two-, three-, and four-part triplane fractures. (A) Two-part triplane fracture. (B) Three-part triplane fracture. (C) Four-part triplane fracture. (From Karrholm, J., J. Pediatr. Orthoped. B, 6, 91–102, 1997. With permission.)



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Figure 9.18 Intramalleolar types of triplane fractures diagram. (A) Type I, (B) type II, and (C) type III. (From Shin, A.Y., Moran, M.E., and Wenger, D.R., J. Pediatr. Orthoped., 17, 352–355, 1997. With permission.)

anteromedial epiphysis and medial malleolus create one fragment and the anterolateral epiphysis is attached to the posterior metaphyseal spike [78]. The exact mechanism of injury and anatomy of these medial triplane variants has shown some variation in subsequent interpretations. This fracture occurs through adduction and vertical loading [75], supination, and adduction [28,79] or plantar flexion and inversion [80]. It seems evident that variation and controversy exist about the exact anatomy and mechanism of injury of medial triplane fractures. What is important to

Figure 9.19 Diagram of medial triplane fracture Denton–Fisher type. (From Karrholm, J., J. Pediatr. Orthoped. B, 6, 91–102, 1997. With permission.)


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Figure 9.20 Diagram of medial triplane fracture (Marmor type). (From Karrholm, J., J. Pediatr. Orthoped. B, 6, 91–102, 1997. With permission.)

remember is the fracture displacement of a medial triplane fracture occurs medially, the mechanisms differ from that of a classic triplane, and the reduction will therefore be different from that of the more classic triplane fractures. No universal system exists to classify these fractures. The various systems described above are included as a reminder that variation exists. Most fractures will consist of lateral fractures, usually in two or three parts, produced by supination and eversion or external rotation [28]. Reduction will include the anterolateral epiphysis and the metaphyseal spike. The fragments may reduce together in two-part fractures or require separate reductions in the three-part fractures. Comminution may exist as well as rare medial and intramalleolar variants. A quadriplane fracture has even been described in which there are the classic three-part patterns and an additional metaphyseal spike [69]. Since the medial triplanes occur by different mechanisms and their anatomy is controversial, some have rejected their classification as triplanes [28]. Injuries occurring in association with the triplane fracture are common. The fibula is fractured nearly 50% of the time and the ipsilateral tibia shaft 8.5% of the time [81]. The fibula fracture can consist of a growth plate fracture or a transverse fracture above the growth plate. Since these fractures occur near skeletal maturity, a syndesmotic injury or proximal fibula fracture should be considered [27]. Treatment of triplane fractures depends on displacement and number of fragments as well as surgeon preference. About 35% of these fractures are treated without a reduction, 30% with a closed reduction, and 35% with an open reduction [28]. Since these injuries occur near skeletal maturity, the main indication for operative intervention is articular incongruity. Some children with this injury will have growth potential, and physeal sparing procedures are indicated in these patients. The lateral type of triplane fracture will be discussed first. Fractures with 2 mm or less displacement can be treated nonoperatively. A long leg cast is applied with some internal rotation to the foot and knee flexion of 30 to 408. CT scans are required after casting to insure adequate reduction, as plane radiographs frequently do not adequately demonstrate displacement. The majority (65%) of lateral triplane fractures will be displaced more than 2 mm at presentation; therefore, some type of reduction will be indicated [28]. Articular displacement of more than 2 mm is poorly tolerated [63]. Although the upper limit of what constitutes an acceptable reduction is not universally known, a fracture that has 2 mm or more of displacement should be reduced [28]. Fractures with more than 3 mm of displacement are often difficult to close-reduce because of soft tissue interposition [28,63]. Closed reduction of external rotation injuries is done by internal rotation, distraction, and direct pressure over the anteriorly displaced fragments. The reduction needs to be done with adequate sedation and relaxation. If done in the emergency room, multiple



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attempts are to be avoided. Reduction in the operating room is preferred, as fixation of the reduced fragments is then possible. Fractures that are reduced by close means can be casted as described above for nondisplaced fractures, but will require a CT scan to insure the adequacy of the reduction. When closed reduction is done in the operating room, percutaneous bone reduction clamps can be used to help reduce both the anterolateral epiphyseal fragment (see ‘‘Juvenile Tillaux Fractures’’ section) and the metaphyseal fragment. A clamp placed AP can be used to close the metaphysis to the epiphysis, incorporating the metaphyseal spike. The clamp should be placed into small incisions in order to capture the fragments, but avoid tendons or neurovascular structures. If closed reduction fails or the reduction is uncertain then open reduction will be required [28]. Forceful closed reductions are to be avoided as further comminution may develop [62]. Figure 9.21 shows a two-part fracture that was reduced by closed means with the aid of a bone clamp and then fixed with percutaneous internal fixation. Figure 9.15 shows a two-part fracture with fixation of only the metaphysis and fibula; the anterolateral epiphyseal fragment was a type II intramalleolar variant and remained nondisplaced. Incisions for open reductions must be individualized to approach fragments that continue to be displaced. Several approaches have been recommended [14,52,54,82]. The order in which fragments are reduced is probably not important and left to personal preference. An anterolateral arthrotomy is often the most useful for two-part lateral fractures. This allows reduction of the anterolateral epiphyseal fragment under direct visualization [28]. Further anterior to medial dissection will allow interposed structures to be extracted. Anterior periosteum and sometimes tendons can block reduction of the anterior metaphysis onto the epiphysis, necessitating a medial approach [28]. Once soft tissue structures are extracted, dorsally directed pressure or a bone reduction clamp can be used to reduce the metaphysis. Some three-part fractures require an additional posteromedial incision [8]. When reduction has been obtained, threaded screws are used to hold the fragments. Even though future growth may be limited, it is best to avoid fixation across the physis if possible [28,43]. The screw in the anterolateral fragment is inserted in the same fashion as for a Tillaux fracture. Another screw can be used to hold the metaphyseal spike (Figure 9.22). Generally, these are inserted from AP. If the metaphyseal spike is small, then Kirschner wires can be used. Smooth wires can be inserted from the epiphysis into the metaphysis across the growth plate. If little growth remains in the physis and the fracture pattern dictates, then threaded wires or even screws can be placed across the growth plate [8]. Two-part lateral fractures may also be amendable to arthroscope-assisted reductions. In this technique, an anterolateral ankle portal is used to debride the fracture site and visualize joint reduction. Steinman pins or Kirschner wires are used to joystick the reduction and can then be advanced to hold the reduction with a supplemental pin [83]. Comminuted fibula fractures and those that do not reduce with the tibia may need ORIF. Plates that stop short of the distal fibular growth plate are preferred [8]. The fibular growth plate closes about 18 months after the tibia so it may have significant growth potential at the time of a triplane injury. Postoperatively, a cast can be used in the position that best held the reduction. Usually for the lateral fractures this involves slight internal rotation. If stable internal fixation has been accomplished, a short leg cast is adequate with non-weight-bearing for 4 to 6 weeks. A removable walking boot provides additional weeks of protection while allowing range of motion exercises to begin. Fractures that are close-reduced or treated nonoperatively are best treated with a long leg cast for the first 4 weeks. The prognosis for triplane fractures is generally good. Since they occur near skeletal maturity, significant limb length discrepancy is unusual. Most of these patients exhibit premature growth plate closure, but this is rarely of clinical significance. There is little chance of remodeling of inadequately reduced fractures, so any deformity noted should be corrected at the time of initial treatment [28]. In a meta-analysis by Karrholm [28] approximately 80% of patients had good or excellent results, 16% had minor symptoms, and approximately 4% had significant degenerative joint disease or deformity. There does seem to be a slight deterioration of good results with the passage of time; results at 3- to 13-year follow-up are worse than at 1- to 3-year follow-up [63]. The poor results were noted in fractures that had inadequate reductions, with more than 2 mm of residual displacement [28,63,79,81,84].


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Figure 9.21 Two-part lateral triplane fracture in a 13-year-old female. Preoperative radiographs of the ankle in (A) AP and (B) lateral projections. The epiphyseal displacement is best seen on AP view, while the lateral view shows the metaphyseal displacement. (C) Coronal CT scan shows the epiphyseal fragment. (D) Axial CT scan demonstrates the metaphyseal spike.



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Figure 9.21 Continued (E) Lateral reconstruction tomogram demonstrates the metaphyseal fragment. The tibia fracture was close-reduced and fixation achieved with two AP screws. The anterolateral epiphyseal fragment is fixed with a medial to lateral screw. Postoperative radiographs: (F) AP and (G) lateral. The epiphyseal screw appears to go through the physis. Although the CT scan indicates her medial distal tibia growth plate is nearly closed, it is best to avoid the physis with fixation devices.

3.

Adolescent Pilon Fractures

These are rare injuries sustained by older children near skeletal maturity. The average age of injury is nearly 16 years, with a range of 13 years and 6 months to 17 years and 7 months. A classification system has been proposed by Letts et al. [85] for these injuries. All fractures have more than 5-mm joint displacement in order to be included as a pilon fracture in this system. Type I injuries have no physeal displacement or comminution. Type II injuries have less than 5 mm physeal displacement and little comminution. Type III injuries have more than 5 mm physeal displacement, comminution, and may have other associated injuries like ankle dislocation or ipsilateral tibial shaft fracture. Only eight fractures were described, and all were treated with ORIF. There were 63% excellent results with two cases of degenerative joint disease and one case of residual deformity.


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Figure 9.22 Three-part lateral triplane fracture in a 13-year-old male. Preoperative ankle radiographs: (A) AP and mortise views demonstrate the anterolateral epiphyseal fragment, and (B) lateral views show the metaphyseal displacement. The anterolateral epiphyseal fragment reduced well with the aide of a percutaneous bone reduction clamp. The metaphyseal fragment could not be close-reduced and required an anterolateral exposure to extract the periosteum and an extensor tendon.



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Figure 9.22 Continued Postoperative radiographs: (C) AP and mortise, and (D) lateral views demonstrate the fixation. The distal screw is completely intraepiphyseal. The metaphyseal screws are directed AP with a proximal-to-distal-slope to capture the metaphyseal spike and avoid the physis.


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Complications of Ankle Fractures

Pediatric ankle fractures give rise to the same types of complications as those of adults. Nonunion, delayed union, malunion, and arthritis do occur in children, but are less prevalent than in adults. In addition, pediatric fractures have the added risk of growth arrests and growth deformities. Nonunions and delayed unions are rare in pediatric fractures [10]. Fractures treated operatively are the most likely to present with nonunions. Treatment for this is repeat open reduction with possible bone grafting [10,54]. Malunions are usually the result of incomplete reductions. Growth disturbances from asymmetric growth plate closure will be considered a separate category of complication. Rotational malunions are the most common type encountered around the ankle. Many of the growth plate fractures involve some degree of external rotational deformity that may not be appreciated by radiographs alone. The true incidence of rotational deformity is not known because many of these patients are asymptomatic and do not seek follow-up [86]. Sagittal plane malunions can occur if the anterior fracture gap between the metaphysis and epiphysis is not closed during reduction. This type of deformity is in the ankle plane of motion and seems to remodel well, making an equinus malunion very rare. The initial treatment of these malunions should be observation. Some of the deformity will remodel with growth [10,54], but some may not [36]. Progressive deformities are the result of growth arrests and will be discussed below. If a symptomatic deformity exists at skeletal maturity, a supramalleolar osteotomy can be used. An opening wedge osteotomy can often assist with any limb length discrepancy that may have developed [87,88]. Growth arrests can produce a progressive malunion. About 3 to 4 mm of growth per year is present in the distal tibial physis [8]. Many of the severe growth plate injuries occur near skeletal maturity. Limb-length discrepancy is therefore significant only in children with 3 or more years of growth remaining. The amount of discrepancy that develops from growth plate injuries is usually about 1 to 2 cm [43,89]. Growth arrests range from complete closure to partial closures. In complete closures, the uninjured bone of the ipsilateral ankle will have relative overgrowth. Complete growth arrest is very rare and is best treated with epiphyseodesis of the uninvolved bone and consideration of contralateral ankle epiphyseodesis depending on how much growth remains [8]. When considerable growth remains and less then 50% of the growth plate is involved, consideration of physeal bar resection and interposition should be given [8]. Partial growth arrests are far more common, producing both angular and rotational deformities. The amount of growth plate involvement needs to be determined before treatment decisions can be made. Both CT scan and MRI have been used to determine the percentage of growth plate involvement and the area involved. In very young children, physeal bar resection may be considered for injuries that involve up to 50% of the growth plate area. As the child matures, bar resections are attempted for up to 25% involvement [8]. If bar resection and interposition of fat or cranioplast is attempted, the child should be followed to skeletal maturity. The growth plates of children who have had physeal bar resections fuse on average 1 to 2 years earlier than the contralateral extremity. Large areas of bar formation and those that have already produced significant deformity are best treated with reconstructive procedures. Older children with little growth remaining are also better served with these reconstructions. Reconstructive procedures are similar to those used in adults. Osteotomies can be opening or closing types that acutely correct the deformity and are internally fixated. Gradual correction with Ilizarov type fixators is another option. Surgeries should include a completion of the growth plate closure of both the tibia and the fibula on the involved limb. Contralateral limb epiphyseodesis is considered if significant limb length discrepancy might result. Posttraumatic arthritis can occur after pediatric ankle fractures. This is unusual after extraarticular fractures, but does occur with intra-articular fractures. Up to 30% of patients with intraarticular fractures may develop arthritis at long-term follow-up [89]. Careful reduction of the articular surface is essential and helpful in preventing this complication [63]. Symptoms may not develop for several years and often occur after skeletal maturity. Patients with early adult onset arthritis may present to adult orthopedic surgeons. The pediatric orthopedic surgeon must be aware of this possible sequelae. Patients with 2 mm or more of articular incongruity may do well as children, but with time results deteriorate [63]. The articular surface does not remodel well and care should be taken to get accurate reductions during the initial treatment.



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Reflex sympathetic dystrophy (RSD) can develop in children after ankle injuries. The findings of RSD are similar in adults and children. Symptoms include pain out of proportion, skin changes, and other dystrophic features. The diagnosis is frequently delayed for up to 1 year in children and up to 84% of the patients are girls [90]. The management of RSD in children is similar to that of adults, including physical therapy, various drugs, psychiatric care, and sympathetic nerve blocks. The treatment may be prolonged in children because of the frequent delay in diagnosis [90].

III.

PEDIATRIC FOOT FRACTURES

Fractures of the foot are relatively less common in children than in adults. Fractures of the metatarsals and phalanges account for 7 to 9% of all pediatric fractures [5,6,38]. Fractures of the tarsal bones account for less than 1% of all children’s fractures [7]. Occult fractures of the tarsals may, however, be the cause of limping in the toddler [91–93]. Children have a lower body weight, and their bones have a higher percentage of cartilage. The combination of lower mass and higher elasticity of the bones produces fewer fractures in the child’s foot. When fractures do occur in the child’s foot they are usually minimally displaced for the same reasons discussed in ‘‘Ankle Fractures’’ section. Many, if not most, of the foot fractures sustained by preadolescent children are treatable by conservative means. Adolescent patients and those near skeletal maturity are susceptible to displaced and intra-articular fractures. The treatment of these displaced or intra-articular fractures follow guidelines similar to that of adult fracture management. For a particular fracture that is treated in a manner similar to the corresponding adult fracture, the reader should refer to the appropriate chapter in this book.

A.

Anatomy

A complete review of foot anatomy is beyond the scope of this chapter. What follows are some of the important differences between the pediatric and adult foot. The ossification pattern of children’s feet has a great deal of variation. This variation makes identification of fractures more difficult. Normal variations of ossification are sometimes confused with fractures. Radiographs of an uninjured foot can help, as can an understanding of the normal ossification pattern [4]. Figure 9.23 shows the ossification patterns of the pediatric foot [10,94]. The first bone to ossify is usually the calcaneus, followed by the talus [10]. Accessory bones are also common in the young foot [4,10]. The ossific nucleus that is visible on radiographs usually does not represent the actual shape of the chondro-osseus bone [14]. Fracture identification in the young foot can be challenging because of the immature skeleton and its variety.

B.

Talus Fractures

1.

General Features

Fractures of the talus are rare in children [10,95]. The talus is composed of three main parts: the body, neck, and head. The body has a large articulation with the tibia that is referred to as the dome. A narrow area between the body and the head is the talar neck. The head of the talus articulates with the navicular. To understand the treatment options and prognosis of talus fractures knowledge of its blood supply is essential [96]. Blood supply to the talus comes from two principal sources: An anastomotic loop of arteries enters the neck from within the tarsal canal and a deltoid branch enters through the deltoid ligament. The anastomotic loop of arteries is formed from the artery of the tarsal canal, the artery of the tarsal sinus, perforating peroneals, and lateral tarsal branches. The deltoid branch is formed from an anastomosis of the dorsalis pedis artery and the artery of the tarsal canal. The tarsal canal is an area between the sulcus of the talus and the sulcus of the calcaneus. The principal blood supply to the talus enters through the tarsal canal at the base of the neck. The deltoid branch supplies the medial quarter of the talus. Displaced fractures of the neck may compromise this tenuous blood supply, leading to avascular necrosis (AVN) [95,97].


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Figure 9.23 Ossification patterns of the human foot. Both the time of appearance and the fusion of the ossification centers are included (y ¼ years, m.i.u. ¼ months in utero, y and m.i.u. indicate time of fusion of the ossification centers). (From San Giovanni, T.P. and Gross, R.H., Fractures and dislocations of the foot, in Rockwood and Wilkins’ Fractures in Children, 5th ed., Beaty, J.H. and Kasser, J.R., Eds., Lippincott, Williams & Wilkins, Philadelphia, 2001, p. 1170. With permission.)

2.

Talar Neck Fractures

Talar neck fractures are the most common talus fracture in children. Forced dorsiflexion is thought to be the mechanism of most talar neck fractures [98,99]. The medial malleolus is also fractured in 25 to 30% of talar neck fractures, suggesting that supination accompanies some of these fractures [100]. Diagnosis requires a high index of suspicion because many of these fractures are nondisplaced [101]. Radiographs of the foot should include the AP, lateral, and oblique views. The Canale and Kelly view can also be helpful; this is obtained with the ankle plantar flexed and the foot internally rotated 158. The x-ray beam is then angled 758 cephalad from the table [102]. Classification of these fractures is similar to that of adults. The familiar Hawkins classification (Figure 9.24) is also used in children [97,102]. Letts and Gibeault [101] described four types of pediatric talus fractures. Type I fractures are minimally displaced fractures of the neck. Type II fractures are minimally displaced fractures of the proximal neck or body. Osteonecrosis rates are low for type I and II fractures. Type III injuries are displaced talar neck or body fractures in which osteonecrosis is more likely. Type IV injuries are talar neck fractures with body dislocations; osteonecrosis is expected. Osteonecrosis rates are related to fracture displacement in both classification systems.



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Figure 9.24 Diagram of Hawkins classification of talar neck fractures. (From Sangeorzan, B.J., Ankle and Foot: Trauma in Orthopaedic Knowledge, Update 4, Frymoyer, J.W., Ed., American academy of orthopaedic surgeon rosement, IL, 1993, 639. With permission.)

Treatment of pediatric talar neck fractures is similar to that of adults. Some controversy exists as to what constitutes acceptable displacement. Fractures should have less than 58 of angulation to be treated closed [102,103]. The amount of acceptable displacement varies from 2 mm [102] to 3 to 5 mm [10,103]. Hawkins type I fractures are treated closed with casting and nonweight-bearing for 6 to 8 weeks. Type II fractures may require a reduction to obtain acceptable alignment [10]. Once reduced, casting is continued as in type I injuries. Casting in plantar flexion may be needed for some type II fractures if attempts at dorsiflexion cause displacement. Any future attempts to bring the ankle out of plantar flexion at follow-up must be carefully monitored to make sure displacement is not occurring. If reduction cannot be obtained closed then open reduction will be indicated. Displaced fractures (types III and IV) usually require ORIF. The approach used is like that for adults. An anteromedial approach should stay medial to the extensor hallucis longus tendon to avoid anterior tibial vessels. Anterolateral approaches are sometimes needed to obtain reduction (Figure 9.25). Kirschner wires placed AP are used to hold the provisional fixation. Posterior to anterior screws are used to hold the final reduction. A posterolateral cannulated screw is inserted from just lateral to the Achilles tendon and is used for definitive fixation of most displaced fractures [10] (Figure 9.25). In some fractures, an AP screw position is employed (Figure 9.26). Consideration of Kirschner wire fixation alone is given for very young children, but most fractures are treated with compression screw fixation because of superior biomechanical fixation compared with wires alone [100,104]. AVN occurs after talar neck fractures because of the tenuous blood supply. Rates of AVN are usually related to initial fracture displacement. Even nondisplaced type I fractures may experience AVN, with rates ranging from 0% [100] to 25% [101] in the literature. The average rate based on available literature is 16%, which is slightly higher than that of adults. More than half of the cases of AVN were noted in children with a delay in diagnosis of their injury [95]. Displaced fractures have even higher rates of AVN. Differences exist between adults and children with regard to AVN. During fracture healing a subchondral lucency (Hawkins sign) indicates vascularity to the body in adults. Children may not develop this lucency even if vascularity is still intact. So the lack of a


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Figure 9.25 Diagram of (A) anterior exposures for reduction of talar neck fractures, and (B) posterior exposures and fixation with posterior to anterior screw. (From Adelaar, R.S., Complex fractures of the talus, in Instructional Course Lectures, Vol. 46, Springfield, D.S., Ed., American Academy of Orthopaedic Surgeons, Rosemont, IL, 1997, pp. 323–338. With permission.)

Hawkins sign in children is not necessarily a poor prognostic indicator as it is in adults [10,102]. The subchondral region in children is more cartilaginous, making radiographic visualization of a Hawkins sign unreliable, and so MRI may be needed to diagnose AVN [14]. The prognosis for AVN in children is better than that in adults. Some children who develop AVN will still have good results. Prolonged non-weight-bearing status during the healing stages of AVN is controversial. Some studies have shown better remodeling after prolonged non-weightbearing [101,102]. Protection from weight-bearing may allow revascularization and reconstitution of bone, but it may take 6 months or more [97]. Even though healing and remodeling may occur, some flattening of the talus and decreased ankle range of motion is to be expected after AVN [101]. Other authors have questioned the utility of prolonged non-weight-bearing, stating that it may be detrimental to the child’s overall development and produce shortening of the limb from nonuse [95,97]. The ability of non-weight-bearing to affect remodeling has not been clearly established [97]. The deformity and the healing may be more a function of the natural history of AVN than of weight-bearing status [10]. Malunions are another complication of talus fractures. Varus malalignment produces a varus hindfoot and a supinated forefoot [105–107]. Conservative measures should be tried if malalignment develops, as children are capable of remodeling some deformity [10]. Late osteotomies or talectomies are used as salvage procedures.



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Figure 9.26 Diagram showing AP screw fixation for talar neck fractures. (From Adelaar, R.S., Complex fractures of the talus, in Instructional Course Lectures, Vol. 46, Springfield, D.S., Ed., American Academy of Orthopaedic Surgeons, Rosemont, IL, 1997, pp. 323–338. With permission.)

3.

Body Fractures and Other Injuries of the Talus

The large cartilage component of the talus coupled with lower body weight makes fractures of the body very unusual. Because body fractures are so rare there exists no large series from which treatment options can be obtained. If a body fracture is present it is likely to be minimally displaced and is treated nonoperatively [108]. No convincing evidence exists that early anatomic reduction of these fractures will reduce the rates of AVN. Some authors have recommended that displaced fractures undergo anatomic reductions [109]. Displaced body fractures will be seen around the time of skeletal maturity and are treated like those of an adult. Osteochondral fractures of the dome of the talus occur in older children. These injuries can be difficult to diagnose and may present with ankle sprain type symptoms. If the symptoms of an ankle sprain do not resolve quickly, an osteochondral injury should be considered. Diagnosis may be difficult from plane radiographs and bone scans or MRI may be needed [110]. MRI is probably superior to bone scan because it shows the anatomy of the injured area more clearly [10]. The area of the dome that is injured is related to the mechanism of injury. Posteromedial lesions occur with foot plantar flexion or inversion with external rotation of the tibia. Anterolateral lesions of produced by inversion and dorsiflexion [111]. The medial-based lesions may not always be traumatic in origin [112]. Treatment of these lesions is similar to that for adults and may range from casting or non-weight-bearing, subchondral drilling, and abrasion arthroplasty or microfracture to internal fixation. Lateral process fractures occur by dorsiflexion with hindfoot inversion. This may occur by transmission of the force through the calcaneus or by ligamentous avulsions [113]. Snowboarding is a common cause, and these fractures are sometimes referred to as ‘‘snowboarder’s fracture.’’ Frequently, lateral process fractures are misdiagnosed as ankle sprains, as the pain of a fracture is in a similar location to that of a lateral ankle sprain [113]. The mechanism of injury is also similar to a sprain and many minimally displaced fractures may be missed. Minimally displaced fractures that are extra-articular can be treated with casting and protection from weight-bearing until symptoms subside [113]. Fractures treated with casting may occasionally require late excision of painful, nonunited fragments. If the fragment is 1 cm or larger and displaced more than 2 mm; internal fixation may be useful [113]. Intra-articular fractures that are not diagnosed or treated appropriately may lead to subtalar arthrosis [114]. Posterior process fractures must be differentiated from an os


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trigonum because the treatment is different. The secondary ossification center that creates the os trigonum appears around 8 to 10 years of age in girls and 11 to 13 years in boys [115]. Acute fractures of the posterior process will have sharp margins on radiographs to help differentiate them from the smooth contours of an os trigonum. Treatment of acute fractures is usually conservative, consisting of short leg casting. The cast can be placed in 10 to 158 of equinus and weight-bearing allowed. If the fragment does not unite and remains symptomatic after casting then excision of the fragment may be required. Subtalar dislocations are extremely rare in children and are treated as in adults. Subtalar dislocations occur by forced plantar flexion mechanisms [116–118]. Dislocations recognized acutely are close-reduced and immobilized. Delayed diagnosis is common. Dislocations that are recognized late, and those with soft tissue interposition may require open reduction and temporary cross-joint Kirschner wire fixation [10].

C.

Calcaneus Fractures

Fractures of the calcaneus are rare in children because of their low body weight and higher percentage of cartilage. They account for 0.0005% of all pediatric fractures [119]. Anatomic differences between adults also help explain the rarity of these fractures in children. The lateral process of the talus is smaller and immature in children, so the wedging on impact is less than that of adults. The posterior facet is more parallel to the ground (less inclined) and is covered by thicker cartilage, so forces are dissipated over a larger area [10]. Radiographically, this results in a smaller Bohler’s angle in children [10]. The Bohler’s angle is the angle formed by two lines. The superior point of the anterior facet and the posterior facet forms one line. The other line is formed by the superior tip of the posterior facet and the tuberosity. This angle is normally about 25 to 408 in adults, but is less in children [120,121]. When a fracture is suspected, radiographs of the foot should include AP, lateral, oblique, and axial views. If a fracture is identified, some authors recommend lateral x-rays of the spine because of the axial loading mechanism of injury [10,122]. Most calcaneus fractures are minimally displaced [93] and about 75% are extra-articular in young children [4]. Intra-articular displaced fractures are more common near skeletal maturity. A delayed diagnosis is noted 30 to 50% of the time as nondisplaced fractures may take up to 2 weeks to become visible on radiographs [122–124]. Some authors recommend CT scans if the diagnosis is uncertain from plane radiographs alone. Another approach is to splint, make the patient nonweight-bearing, and repeat a radiograph in 2 weeks when the fracture should become visible on plane radiographs [4]. Schmidt and Weiner [122] classified pediatric calcaneal fractures into four anatomic groups: extra-articular, intra-articular, those with loss of Achilles insertion, and those with significant soft tissue injury. Treatment of calcaneal fractures in children is usually nonoperative, and the prognosis is good [91,122,125–127]. Extra-articular fractures are treated with short leg casting; weight-bearing is individualized. Intra-articular fractures in young children are also treated with casting, but they should be non-weight-bearing. Intra-articular fractures will usually do well as children have tremendous remodeling potential and most fractures are relatively nondisplaced. With intraarticular fractures the fracture line often passes behind the posterior facet and the facet may be depressed but the joint surface is intact, helping to explain the generally good outcomes [119]. ORIF has been described for intra-articular calcaneal fractures, but these are generally case report type occurrences [113,128,129]. Not enough evidence exists in the literature to recommend routine ORIF for displaced intra-articular calcaneal fractures in children [119,125]. Reductions are indicated in tongue fracture patterns and those with loss of Achilles insertion. The Essex–Lopresti reduction maneuver described for adults may be used in tongue fractures, which can then be stabilized by percutaneous Kirschner wires [10,125,130]. Tuberosity fractures involving the Achilles tendon insertion can often be close-reduced by flexing the knee and plantar flexing the ankle [4]. Direct pressure over the fragment may aid the reduction. Kirschner wires may be used to hold the tuberosity fragment if it is not stable. ORIF will be required if the Achilles insertion cannot be close-reduced. Adolescents near skeletal maturity may sustain displaced intra-articular fractures like those of adults [125]. Treatment of these older patients follows that of adults.



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The prognosis for pediatric calcaneal fractures is better than that for adults. Short-term prognosis has been excellent in several studies [91,122,126]. Even at long-term follow-up of about 17 years the results continue to be good for both intra-articular and extra-articular fractures [125].

D.

Lesser Tarsal Fractures and Tarsometatarsal Injuries

The lesser tarsal bones consist of the navicular, the cuboid, and the three cuneiforms. Isolated fractures of these bones are extremely rare. If a fracture of one of these bones is noted other injuries should be sought. Lisfranc injuries may produce lateral column compression and cuboid nutcracker type fractures. Isolated cuboid fractures are rare. If a cuboid fracture is identified then investigation into tarsometatarsal injuries should occur [131]. The nutcracker fracture of the cuboid is produced as the cuboid is compressed between the fourth and fifth metatarsal and the anterior process of the calcaneus [132,133]. Falls from heights with a plantar-flexed foot can also produce lateral column compression fractures or cuboid fractures and are sometimes referred to as a ‘‘bunk bed injury’’ [134–136]. Children with nondisplaced cuboid fractures are treated with short leg casting and nonweight-bearing until symptoms resolve. Good results have also been noted in fractures that were diagnosed late and had no treatment [137]. Displaced intra-articular cuboid fractures are rare case report type injuries [133]. Medial column loading may produce navicular fractures or Lisfranc injuries with cuneiform fractures. Displaced intra-articular fractures of the lesser tarsals are sustained at or near skeletal maturity and are treated like those of adults, with ORIF or medial/ lateral column external fixation. Injuries of the tarsometatarsal region do occur in children, but are much more likely near skeletal maturity. Descriptions of children under 10 years old sustaining Lisfranc injuries are rare. Direct injuries occur from an object falling on the foot. The more common mechanism is an indirect injury [10,131,132]. Forced plantar flexion with or without abduction or rotation can produce indirect Lisfranc injuries. The injury pattern and classification of Hardcastle et al. [138] is like that of adults. Subtle injuries may require weight-bearing radiographs. In young children, radiographic findings suggestive of Lisfranc injuries include metatarsal base fractures of the first or second metatarsal or injuries to two to four metatarsal bases [139,140]. Findings suggestive of a Lisfranc injury in the more skeletally mature patient are first and second metatarsal interspace widening, second metatarsal base shifting in the mortise, and avulsion fractures of the basilar second metatarsal [10]. Lateral shifting of metatarsals two to five may cause nutcracker cuboid fractures. The medial base of the fourth metatarsal should also align with the medial edge of the cuboid on oblique radiographs. On lateral weight-bearing radiographs if the medial cuneiform is plantar to the fifth metatarsal this is also suggestive of a Lisfranc injury [141]. Treatment decisions depend upon the age of the patient. In young children these injuries can usually be treated nonoperatively with short leg casting with good short-term results [131,140]. Longer follow-ups showed that degenerative joint disease did develop after only 3 years in one out of eight patients [139]. The treatment of patients who are near skeletal maturity is similar to that of adults. In adolescents, it is often possible to close-reduce these injuries and perform percutaneous fixation. If anatomic reduction is not possible, then ORIF will be required. The prognosis for patients near skeletal maturity is similar to that for adults. In general, however, the prognosis for pediatric Lisfranc injuries is better than that for adults. In the Wiley series [131] patients ranged from 6 to 16 years and were treated conservatively. At 3- to 8-month follow-up, 14 of 16 patients were asymptomatic, suggesting a more benign course in children. The ‘‘bunk bed’’ fracture can also refer to a variant of the Lisfranc injury or to the cuboid fracture as previously described. These injuries are produced as the foot is axially loaded in a plantar-flexed position as would occur when a child steps out of a top bunk [140]. Injuries can occur to both medial and lateral columns. Lateral column loading cuboid fracture ‘‘bunk bed’’ injuries have already been described [136]. The first metatarsal or the medial or lateral cuneiform may be compacted when a fall from a bunk bed occurs. The epiphysis of the first metatarsal or the medial cuneiform may be wedged into the first interspace in these injuries [140]. Treatment is individualized. In young children, these can often be managed conservatively but in older children it involves accurate articular reduction and may require ORIF.


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Metatarsal Fractures

Fractures to the metatarsals are fairly common, accounting for 5 to 7% of children’s fractures [5,6]. The mechanism is usually direct force as an object falls on the foot [4]. Most shaft fractures are treated conservatively with a short leg walking cast for 4 to 6 weeks [4]. Metatarsal neck fractures occur when torque is applied to the forefoot with an axial load. The most common fracture is to the fifth metatarsal followed by the first metatarsal [142]. Children under 5 years sustain first metatarsal fractures most commonly from falls; the fifth metatarsal fractures are produced by inversion injuries [142]. In very young children metatarsal fractures and hand fractures should raise the suspicion of abuse [143]. Treatment of metatarsal neck fractures is usually nonoperative, as the dorsal angulation and lateral displacement will remodel [142]. Widely displaced fractures, multiple metatarsal neck fractures, displaced intra-articular fractures, and fractures occurring near skeletal maturity can be reduced and pinned with Kirschner wires (Figure 9.27). The Kirschner wire is inserted from the plantar surface through the head in a retrograde fashion up the shaft [10]. Crossing the metatarsophalangeal joint can aid in holding reduction and preventing the fracture from healing in an extended position [4]. The wires are left protruding through the plantar skin and are removed at 3 to 4 weeks postoperatively. Fractures at the base of the fifth metatarsal require special consideration. The apophysis of the fifth metatarsal is parallel to the shaft and this, as well as normal variant accessory ossification centers (os vesalianum), must be distinguished from avulsion fractures [144]. The apophysis of the fifth metatarsal is present after 8 years of age and fuses by about age 12 years in girls and 15 years in boys [145]. Comparison views may be helpful. Avulsion fractures are usually noted plantarly and are oblique to the shaft. Fractures may be intra-articular; the apophysis does not extend into the joint. Avulsion fractures probably occur from plantar aponeurosis [146] (abductor digiti quinti) avulsions and not the peroneus brevis [10]. The peroneus brevis inserts dorsally and distally to most avulsion fractures. Avulsion fractures of the base of the fifth metatarsal are usually treated

Figure 9.27 Multiple metatarsal neck fractures in a 16-year-old male. Preoperative (A) AP and oblique radiographs of the foot demonstrate metatarsal neck fractures 2 to 5. Displacement is noted on metatarsals 3 to 5. The fractures were reduced by open means as he presented nearly 3 weeks after injury and closed reduction was unsuccessful. A 2-cm incision centered over the fourth metatarsal allowed a freer elevator to be placed. The elevator is used to remove the fracture debris and then to hold the reduction. The fractures are fixed using retrograde Kirschner wires placed from the plantar surface of the metatarsal heads. Postoperative radiographs.



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Figure 9.27 Continued (B) AP and oblique, and (C) lateral showing the reduction. The second metatarsal remained reduced and was therefore not fixated.

nonoperatively with a weight-bearing short leg cast for 3 to 6 weeks [10,145]. Large fragments displaced more than 3 mm may require ORIF [145]. Fractures around the metaphyseal–diaphyseal junction may be problematic. This area is prone to stress fractures as well as acute fractures. Acute fractures in areas of chronic stress fractures also occur [147–149]. Surgical intervention is considered for acute Jones type fractures in athletes and consists of an intramedullary screw inserted from proximal to distal [150–152]. Fracture fixation may speed up healing and hasten return to play. Fractures that show sclerotic edges are likely to be acute on chronic stress fractures and the prognosis for healing with only cast immobilization is not good [153]. Consideration should be given to operative intervention with an intramedullary screw


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and possible bone grafting in patients with sclerotic fracture edges [152]. Figure 9.28 shows intramedullary screw for a Jones fracture in an athlete. Stress fractures can occur in the tarsals and metatarsals in school-aged athletes. Sudden increases in activity level can cause bone absorption due to increased metabolic demands. If the

Figure 9.28 Basilar fifth metatarsal fracture in a 16-year-old male. This fracture is in the metaphyseal– diaphyseal junction, making it a Jones type fracture. The patient was an avid basketball player who complained of a several-month history of activity-related pain before an acute injury. Because of the sclerotic fracture edges and his history of several months of activity-related pain this was deemed an acute fracture through a stress fracture. It was elected to treat this with ORIF. Supplemental bone graft was also used. Postoperative radiographs: (A) oblique and AP, and (B) lateral views show the partially threaded cannulated 6.5-mm screw.



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bone absorption exceeds the new bone formation then the bone will have increased susceptibility to stress fractures [153]. Second and third metatarsal stress fractures commonly occur in female runners [10]. Treatment of these stress fractures is by activity modification and possibly casting if symptoms warrant [153].

F.

Phalanx Fractures

Fractures to the phalanges are usually the result of objects falling onto the foot. Intra-articular growth plate injuries to the great toe proximal phalanx may occasionally need operative intervention [154] (Figure 9.29). Most phalanx fractures are treated nonoperatively by buddy taping and hard-soled shoes [10]. Dislocations of the metatarsophalangeal–interphalangeal joint are rare, but can usually be treated by closed reduction followed by buddy taping to adjacent toes. Irreducible dislocations can occur in the great toe and require operative extraction of trapped sesamoids, or tendons, or both [10].

G.

Other Injuries

Compartment syndrome of the foot can occur in children. Crush injury with or without underlying fractures is the most common etiology of foot compartment syndrome (155). The diagnosis and treatment is like that of adults. The foot is composed of nine compartments (four interosseous, three central, one lateral, and one medial) and all must be released (155). Incisions can vary depending on author and surgeon preference. Extensive medial incisions from malleolus to first metatarsal head can be used with retraction to release all compartments. Additional dorsal incisions are used to release the interossei. Combinations of medial and dorsal incisions are also used. Delayed skin closure is often possible in children during the first five days, alleviating the need for skin grafting (155). Open fractures, lawnmower injuries, and injuries with severe soft tissue disruption are treated with adult principals. Lawnmower injuries are devastating open injuries that commonly affect the foot and ankle. Almost 20% of all lawnmower injuries involve children (156). Mayer (156) describes interventions that are useful to avoid these injuries. Ride on mowers produce some of the most devastating injuries and are the most frequent source of lawnmower injuries; 20 out of 32 injuries in one study were from ride on mowers (157). Restriction of children on riding lawnmowers is advised (157). Adequate debridement is the first consideration. Intra-articular fracture fixation is important, but is secondary to wound debridement in importance. Growth plates and cartilaginous surfaces should be covered with grafts as soon as possible. Care should be taken to insure the growth plates do not dry out after the initial debridement. Every effort is made to preserve the foot in children, but amputations may occasionally be required. Split thickness skin grafts may be used in most areas of the child’s foot (157). Puncture wounds to the foot are treated with puncture tract debridement alone. If pain persists beyond two or three days, the wound should be explored and debrided again (158,159). Antipseudomonal coverage is suggested after debridement. Pseudomonal infections are more common if the wound occurred through tennis shoes. Both bone and soft tissue infections are possible after puncture wounds. Infections with Staphylococcus spp. usually become evident in the first few days. Pseudomonal infections may take several days to weeks to become evident (160).

IV.

SUMMARY

Fractures about the foot and ankle are common in children. Knowledge of the anatomy, ossification patterns, and patterns of growth plate closure is helpful when dealing with these injuries. Some fractures are subtle and must be differentiated from normal variant ossification patterns; comparison radiographs of the uninjured extremity can be helpful. Ligaments are generally stronger than the growth plate; therefore, growth plate injuries must be suspected when a child presents with foot or ankle trauma. The majority of fractures about the ankle can be treated conservatively. Children have a much thicker periosteum than adults, and most fractures will heal; adultlike nonunions are rare.


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Figure 9.29 Intra-articular fracture of the hallux proximal phalanx in a 16-year-old male. (A) Preoperative radiographs show AP and oblique projections of the displaced and rotated fragment. (B) The fracture was open reduced and held with two Kirschner wires.

However, not all pediatric ankle fractures are benign. Injuries to growth plates are a special concern unique to children. Intra-articular fractures and those with wide growth plate displacement often require operative intervention in an effort to minimize future growth disturbances. Patients who sustain displaced fractures must be followed until skeletal maturity to monitor for growth arrests and angular deformities. Transitional fractures of the ankle (Tillaux and triplane fractures) are another exception to the usual conservative approach. These fractures are unique to the closing adolescent growth plate and frequently require operative intervention. CT scans are often used to make treatment decisions and to assess reductions in the transitional fractures.



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The lower body weight and higher percentage of cartilage make displaced fractures of the foot relatively rare in children. Like ankle fractures, the vast majority of foot fractures can be treated conservatively in young children. However, the rare displaced talar neck fracture-dislocation is one exception. During adolescence displaced intra-articular foot fractures can occur and are treated with adultlike principles. Ossification patterns about the foot can be variable. Comparison radiographs are often helpful in differentiating subtle fractures from variant ossification patterns; differentiating a basilar fifth metatarsal avulsion from an apophyseal growth plate is a good example. Complications of pediatric foot and ankle fractures are rare, but they do occur. The preceding chapter was devoted mainly to the acute management of ankle and foot fractures designed to minimize complications. Angular deformities and growth arrests may require late reconstructive procedures. If possible, these reconstructive procedures are best done at or near skeletal maturity. Complete descriptions of reconstructive procedures can be found in the sections of this book dealing with fractures in adults.

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10 Soft Tissue Coverage of the Foot and Ankle R. Michael Johnson and Steven Schmidt Division of Plastic Surgery, Department of Surgery, Miami Valley Hospital, Wright State University, Dayton, Ohio

CONTENTS I. Introduction ................................................................................................................... 266 II. Wound Evaluation ......................................................................................................... 266 III. Patient Evaluation .......................................................................................................... 266 IV. Mechanism ..................................................................................................................... 267 V. Wound Management Principles...................................................................................... 267 VI. Reconstruction ............................................................................................................... 267 VII. Nonoperative Treatment ................................................................................................ 267 VIII. Nonoperative Coverage of Foot and Ankle Wounds ..................................................... 268 A. Platelet-Derived Growth Factor (PDGF) ............................................................... 268 B. Topical Negative Pressure....................................................................................... 268 C. Hyperbaric Oxygen (HBO) ..................................................................................... 268 IX. Operative Treatment....................................................................................................... 268 A. Primary Closure ...................................................................................................... 269 B. Skin Grafts.............................................................................................................. 269 C. Local (Pedicle) Flaps............................................................................................... 269 1. Lateral Calcaneal Artery Flap.......................................................................... 269 2. Medial Plantar Flaps ........................................................................................ 271 3. Sural Fasciocutaneous Flap.............................................................................. 271 4. Flexor Digitorum Brevis................................................................................... 271 5. Extensor Digitorum Brevis ............................................................................... 271 6. Dorsalis Pedis ................................................................................................... 273 D. Free-Flap Reconstruction ....................................................................................... 273 1. Vascular Disease and Free-Tissue Transfer ...................................................... 274 2. Diabetes and Free-Tissue Transfer ................................................................... 274 3. Sensitivity and Foot and Ankle Reconstruction............................................... 274 4. Free Flaps and the Elderly ............................................................................... 275 5. Long-term Results of Free-Flap Foot Reconstruction ..................................... 275 6. Failures and Revisions...................................................................................... 275 7. Gait .................................................................................................................. 275 E. Specific Free Flaps .................................................................................................. 276 1. Radial Forearm Flap........................................................................................ 276 2. Rectus Abdominus ........................................................................................... 277

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3. Latissimus Dorsi (LD)...................................................................................... 278 4. Parascapular ..................................................................................................... 279 5. Serratus Anterior.............................................................................................. 279 6. Gracilis ............................................................................................................. 279 7. Lateral Arm Flap ............................................................................................. 280 F. Other Flaps ............................................................................................................. 280 X. Conclusion...................................................................................................................... 282 Acknowledgment........................................................................................................................ 282 References .................................................................................................................................. 283

I.

INTRODUCTION

Soft tissue coverage of foot and ankle wounds remains a challenging problem. The goal of soft tissue reconstruction is to achieve a stable, healed wound that is free of chronic infection and pain. Protective sensation and independent ambulation are also important outcome measures. Reconstructive surgery of the distal lower extremity is a complex undertaking. Many factors must be considered before determination of safe and effective treatment. These factors are either patient related, mechanism related, or wound related (Table 10.1).

II.

WOUND EVALUATION

The location of foot and ankle wounds can be divided into five functional zones: the posterior weight-bearing heel, anterior plantar foot, non-weight-bearing posterior heel, malleoli and Achilles tendon, and dorsum [1]. The depth of the wound is probably the most important factor in determining therapy. If adequate soft tissue is present, wounds can be grafted regardless of location. The differences between the fibrous attachments of the plantar skin and the thin pliable skin on the dorsum are dramatic. The main concerns with plantar wounds are sensitivity and stable weightbearing, while dorsally the main concerns are thin coverage of tendons and prevention of toe deformity and contracture. Exposure of bone and tendons are important findings and dramatically complicate reconstruction and recovery.

III.

PATIENT EVALUATION

A detailed physical examination should be performed. The presence or absence of pulses from the femoral level down to the dorsalis pedis should be noted. Noninvasive lower-extremity vascular studies are easily performed in the vascular laboratory. Ankle-brachial indices can be performed at

Table 10.1

Factors Requiring Consideration in Soft Tissue Coverage

Patient related

Wound related

Other issues

Age Comorbid illness Diabetes Heart disease Obstructive Peripheral Vascular disease Venous disease Smoking history

Size Depth Location Weight-bearing Non-weight-bearing Mechanism Ischemic Diabetic Traumatic

Foot sensation Timing of surgery


Soft Tissue Coverage of the Foot and Ankle

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the bedside or in the office [2]. Noninvasive vascular studies can be helpful indicators of vascularity. However, diabetic patients may have incompressible arterial walls caused by calcification that may falsely elevate indices. Usually, diabetic patients should have angiography to evaluate distal runoff if major reconstruction is planned. Doppler studies are helpful in delineating arterial waveforms. Monophasic waveforms of the posterior tibial artery usually require revascularization before flap reconstruction [3]. Palpable pedal pulses are generally recommended before free-flap reconstruction. Transcutaneous oxygen is an excellent means of assessing tissue perfusion [4]. Molecular oxygen is required for collagen synthesis. Angiography is indicated if vascular reconstruction is required before flap transfer.

IV.

MECHANISM

The mechanism of injury is an important consideration. Severe crush injuries may lead to a zone of injury that will require a more proximal dissection for suitable microvascular anastomosis [5]. This concept has been challenged by Isenberg and Sherman [6], who found excellent results by placing free-flap anastomosis within 5 cm of the proximal osteotomy without using vein grafts. It is also possible that the microanastomosis can be placed distal to the zone of injury although this may lead to a slightly higher failure rate [7]. To prevent infection, necrotic tissue should always be removed. The effect of surgical debridement on wound healing is dramatic. Steed et al. [8] demonstrated that wounds debrided routinely heal faster than wounds debrided sporadically.

V.

WOUND MANAGEMENT PRINCIPLES

General principles of wound management are: 1. 2. 3. 4. 5. 6.

VI.

Elevation of the extremity Reduction of edema using compression in patients with stasis ulcers Mechanical or enzymatic debridement of all devitalized tissue Control and treatment of any infection with appropriate antibiotic therapy Presence or reestablishment of adequate arterial inflow Control of medical illnesses such as diabetes mellitus and hypertension

RECONSTRUCTION

Reconstructive options are determined only after careful patient evaluation has been performed. Treatment may be operative or nonoperative, depending on the results of the evaluation. Nonoperative therapy might be considered for patients with small wounds or small areas of tendon exposure. Operative indications include coverage of fracture sites, large areas of exposed tendons, prevention of deformity, and reduction of cost and recovery time.

VII.

NONOPERATIVE TREATMENT

The goal of many of the nonoperative therapies is to promote angiogenesis. Three innovative techniques have emerged as major promoters of angiogenesis. These are: (1) cytokines, clinically available as recombinant platelet-derived growth factor (PDGF) (Regranex1), (2) topical negative pressure (VAC1), and (3) hyperbaric oxygen (HBO). The healing of full-thickness wounds consists of two distinct processes. First, the wound must undergo angiogenesis, which provides the granulation tissue associated with a healthy wound. Angiogenesis does not occur without good arterial flow and nutrition. In diabetic patients, granulation tissue does not always develop despite good nutrition and vascular supply. When granulation tissue does form it is usually much slower than in nondiabetics. The second process is reepithelialization. This is achieved by keratinocyte migration. Keratinocytes migrate faster in a wet environment [9]. Large wounds require split thickness to allow reepithelialization.


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Good local wound care and debridement provide the standard by which other wound care must be compared. Local wound care usually consists of saline gauze dressings. This provides a nontoxic, moist environment for keratinocyte migration if frequent dressing changes are performed; otherwise occlusive dressings are needed to maintain the moist environment.

VIII. NONOPERATIVE COVERAGE OF FOOT AND ANKLE WOUNDS A.

Platelet-Derived Growth Factor (PDGF)

PDGF (Regranex) is the only cytokine available for commercial use. Randomized, prospective, multicenter trials have shown improved healing rates in diabetic foot ulcers [10,11]. However, the expectation of complete healing with PDGF is not realistic in every patient. The 20-week healing rate with PDGF is approximately 50% vs. 39% for placebo. This represents a 40% increase in complete healing [12]. Recombinant PDGF is very expensive, costing between $400 and $600 per 15-g tube. However, it is only used as a thin layer once daily and higher concentrations are not more effective. While the initial cost of treatment with PDGF is high, when the costs of amputation and standard wound care are considered, there appears to be a cost benefit to the use of PDGF [13,14]. A useful application of PDGF in the treatment of traumatic injuries to the foot is promotion of granulation tissue over small areas of tendon exposure either dorsally or in the Achilles tendon region. Wound closure may then be achieved with a skin graft instead of a free flap.

B.

Topical Negative Pressure

An innovative approach to promote granulation tissue is the use of topical negative pressure. Clinically known as vacuum-assisted closure, this technique involves placement of a sponge on the wound, which is then covered with an occlusive dressing; the suction tubing attaches to a machine that applies subatmospheric pressure either intermittently or continuously. Most of the available data on topical negative pressure are small case series and pilot studies [15–17]. Joseph et al. [18] reported a randomized prospective trial in chronic wounds that improved ulcer reduction to 78% compared with 30% using saline gauze. Again, complete healing was not the final end point.

C.

Hyperbaric Oxygen (HBO)

HBO is a highly controversial therapeutic modality in the care of foot and ankle wounds. Small prospective trials have suggested improved healing rates [19–21]. A retrospective study by Ciaravino et al. [22] showed only 11% of patients had slight improvement and none achieved complete healing with HBO. The cost of HBO is approximately $14,000 per 30 treatments. The role of HBO in the treatment of chronic foot and ankle wounds is yet to be determined. Although the role of HBO remains controversial, a selective approach using transcutaneous oxygen measurements is reasonable. A diabetic patient with palpable pedal pulses and low transcutaneous pO2 that is improved with a trial HBO treatment is a good candidate for HBO therapy.

IX.

OPERATIVE TREATMENT

Injuries around the foot and ankle are very challenging. The area is limited in the amount of useful local tissue available for wound coverage. The skin around the foot, by necessity, is thin and has limited elasticity. Full-thickness skin defects may easily lead to joint contractures of the toes and ankles, with decreased range of motion. The reconstructive ladder concept remains useful as a guide to surgical treatment of the foot (Table 10.2). Simple procedures are begun first in this concept. However, there are certain situations in which the best procedure may be a more complicated reconstruction, such as a free-tissue transfer. This is the reconstructive elevator concept.



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Table 10.2 Treatment Options

A.

Nonoperative

Operative

Dressing changes Enzymatic debridement + topical antibiotic PDGF Topical negative pressure HBO

18 closure Skin grafts Pedicle flaps Free flaps

Primary Closure

Primary closure of foot and ankle wounds is possible in minor injuries only if the wound is small. The sole of the foot is glabrous skin. Closure without tension is possible. Many of the ulcers on the plantar surface are due to diabetes and up to 85% of these will have underlying osteomyelitis. Some authors advocate resection of the metatarsal heads and either primary closure or healing by secondary intention. Although there is some concern regarding metatarsal resection, off-loading and the transfer of pressure loads to adjacent metatarsals is possible. Primary closure may be possible in small dorsal foot wounds. However, consideration must be given to the position of the toes and excessively tight skin closure may lead to contracture or rotation of the toes. This is especially true for wounds of more than 2 to 3 cm on the dorsum.

B.

Skin Grafts

Much of the available information regarding the use of skin grafts in foot wound coverage is related to burn wounds, and is covered in Chapter 11. Two key points worth reinforcing are: the importance of the plantar fascia and whether or not adequate soft tissue is available for splitand full-thickness skin grafts to provide adequate stable wound coverage to weight-bearing surfaces. Sommerlad and McGrowther [23] showed that significant changes in gait occur in patients who have the plantar foot resurfaced. Significant differences were not found in outcome between splitand full-thickness grafts and flaps in that study. Split grafts may provide stable wound coverage in plantar burns [24].

C.

Local (Pedicle) Flaps

Since the advent of microsurgical free-tissue transfer, the popularity of local flaps in the foot and ankle has declined. However, many patients are either not candidates for free-tissue transfer or a pedicle skin or muscle flap is available that can provide a useful alternative. Specific areas where local flaps are particularly useful are in small defects of the posterior heel that are less than 3 cm in diameter and in small defects of the lateral malleoli and Achilles tendon. Stark [25] first described the use of pedicle muscle flaps in World War II. In the l960s, Ger [26] refined their use in stasis ulcers and traumatic wounds. He first described the use of soleus, tibialis anterior, peroneus brevis, and tertius flaps. He later described intrinsic muscle flaps such as the abductor hallucis brevis, the abductor digiti minimi, and the flexor digitorum. 1.

Lateral Calcaneal Artery Flap

This is a very reliable flap that can be used as a transposition flap to cover small defects of the Achilles tendon area or the lateral malleolus (Figure 10.1A and Figure 10.1B). The pedicle is the lateral calcaneal artery, which is a branch of the anterior tibial artery. It forms a lateral arch with the lateral tarsal artery, which is a branch of the dorsalis pedis artery [27]. This lateral arch allows the flap to be done as a distally based flap [28]. Several case series document the safety and efficacy of this flap [29–33]. Anatomic studies show the flap has reliable blood flow in


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Figure 10.1 (A) Preoperative lateral calcaneal flap. Patient has exposed hardware. (B) Postoperative view.



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92% of patients with peripheral vascular disease [34]. The disadvantage of the flap is limitation to small defects and requirements of skin grafting of the donor site. 2.

Medial Plantar Flaps

Medial plantar flaps are usually used to cover defects of the posterior plantar aspect of the foot. Great consideration should be given to the risks and benefits of this procedure. It is quite possible to take a 1- or 2-cm wound and turn it into a 4- or 5-cm open wound if the flap fails. The pedicle of the flap is the medial plantar artery. The medial plantar artery flap is located in the instep of the foot. The medial plantar artery is located between the abductor hallucis and the flexor digitorum brevis muscles. The flap is very useful for the small posterior heel and when raised can reach the posterior heel. Small case series data show reliable soft tissue coverage [35,36]. Inclusion of the medial plantar nerve in the flap can provide protective sensation, but sacrifices sensation in the toes. The medial plantar flap can also be used as a free flap for finger reconstruction [37] (Figure 10.2A to Figure 10.2C). 3.

Sural Fasciocutaneous Flap

The reverse sural artery flap may be used for ankle and heel defects. The blood supply is based on the peroneal circulation, which is often spared in diabetics. The flap is supplied by distally based peroneal artery perforator flow around the sural nerve. The incision is made in the posterior midline. The sural artery penetrates the deep fascia 5 cm above the lateral malleolus [38]. The flap is dissected from proximal to distal. Proximal extent of dissection is usually at the junction of the upper one third and lower two thirds of the leg. The proximal sural neurovascular bundle is ligated. The dissection proceeds with a 3-cm wide span of fascia preserved and centered on the sural nerve and vessels. The pivot point is where the vessels penetrate deep fascia 5 cm above the malleolus. Several case series reports show the safety of the reversed sural artery flap [39,40] (Figure 10.3A and Figure 10.3B). The use of this flap is increasing in popularity and may be used either proximally based to cover proximal tibia or knee wounds or distally based for distal tibia or heel defects. It is also more reliable if a delay procedure is performed first. 4.

Flexor Digitorum Brevis

Flexor digitorum brevis may be used as a turnover flap for calcaneal defects. A neurovascular island flap also can be created based on the lateral plantar artery branches. A midline incision is used for muscle flap elevation. The plantar aponeurosis is reflected with the skin flaps. The flexor digitorum brevis tendons are divided distally and reflected toward the origin from the calcaneus [41]. The flexor digitorum brevis may be used as a turnover flap in conjunction with a split-thickness skin graft (STSG). There is limited support in the literature for this technique [42]. There is some evidence that there are long-term complications with this flap in ambulatory patients [43]. 5.

Extensor Digitorum Brevis

The extensor digitorum brevis muscles’ main blood supply arises from the lateral tarsal artery. It can be harvested based on this vessel, but with limited reach. If the dorsalis pedis artery is divided distal to the origin of the lateral tarsal vessels, the arc of rotation is markedly improved, allowing the flap to reach either malleolus. Exposure can be obtained by a dorsolateral incision. Long extensors are dissected off the short muscle slips and retracted. The extensor digitorum brevis muscle tendons are cut distally and tacked together to prevent splitting. The dorsalis pedis artery and venae comitantes are divided distal to the extensor digitorum brevis. Medial tarsal branches are ligated as dissection proceeds. The four slips of muscle are placed in the defect and covered with a skin graft. The donor site can usually be closed primarily [44]. Two small case series totaling 26 patients showed healing of all patients, with only one flap failure [45,46].


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Figure 10.2 (A) Exposed nonhealing posterior heel ulcer in a preoperative patient. (B) Intraoperative view of elevated medial plantar flap. (C) Early postoperative medial plantar flap.



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Figure 10.3 (A) An open ankle fracture in a 77-year-old male who fell from a ladder. (B) One-week postoperative stage II sural flap.

6.

Dorsalis Pedis

The dorsalis pedis artery flap is another option in the coverage of the ankle region. The flap has been criticized for its donor site deformity, with donor site complications occurring in all patients in one series [47]. However, Zuker and Manktelow [48] reported minimal donor complications in 45 patients.

D.

Free-Flap Reconstruction

Due to the limited arc of rotation and size of local tissue available for transfer, free flaps have emerged as a first choice for many foot and ankle wounds. While the initial flap loss rate was quite


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high, as experience has been gained the overall success rate has climbed to approximately 90%. Before free-tissue transfer, a large wound of the lower extremity required either amputation or complicated multistaged reconstructions, such as walking tube flaps or cross leg flaps. The high success rate of microsurgery has allowed the use of free-tissue transfer even in patients with vascular disease and diabetes. The use and published outcomes of these comorbidities are discussed below. However, it is important to consider the risk to the patient and extensive microsurgical procedures on patients with comorbidities should not be taken lightly. There is probably an element of negative publication bias in the microsurgery literature because surgeons with less than a 90% success rate with microsurgery are unlikely to submit their experience for publication. 1.

Vascular Disease and Free-Tissue Transfer

Obstructive peripheral vascular disease is a frequent cause of foot and ankle wounds. Small wounds will heal when arterial inflow is reestablished. However, large wounds with exposed bone or tendon are considered nonsalvageable before free-tissue transfer. A study from the University of California, Los Angeles (UCLA), demonstrated the 3-year limb salvage rate to be 72% in a small series of 15 patients treated with simultaneous peripheral vascular bypass and free-tissue transfer [49]. Serletti et al. [50] showed a similar success rate of 73% limb salvage at 22-month mean follow-up. All patients in their series with successful free flaps were independent ambulators. Only one of eight patients whose free flap failed ever regained independent ambulation. A longer-term follow-up study from the Rochester group showed the 5-year limb salvage rate for bypass and free-tissue transfer to be 60%. This is equivalent to arterial bypass alone [51]. The microarterial anastomosis may be performed to the native artery distal to the bypass, or to the bypass graft directly. Two case reports utilized a polytetrafluoroethylene graft as the arterial inflow for the free flap [52,53]. The microvenous anastomosis is usually performed to the vena comitantes end to end. 2.

Diabetes and Free-Tissue Transfer

Diabetes is a significant comorbidity as well as an etiologic factor in foot wounds. Small wounds may be treated with local tissue transfer or with cytokine therapy. Larger wounds frequently lead to proximal amputation. However, free-tissue transfer has become a reasonable alternative to amputation. Extremely small, calcified vessels can be reliably reconstructed with microsurgery in the diabetic foot [54–56]. It is difficult to separate the effect of peripheral vascular disease from diabetes in the clinical setting. Cooley et al. [57] demonstrated similar flap survival rates in diabetic and nondiabetic rats. Reendothelialization of the arterial anastomosis was slower in diabetic rats. Diabetes can also cause nephropathy, which further complicates reconstructive microsurgery. A series of patients from the University of Rochester demonstrated the high risk of limb loss in patients with diabetes and dialysis-dependent renal failure [58]. This combination may be considered a contraindication to free-tissue transfer. However, Armstrong et al. [59] reported three cases of successful free-tissue transfer and independent ambulation in diabetic renal transplant recipients. The mechanism for the dismal outcome of microsurgery in dialysis-dependent patients is unknown at this time. It appears the results can be improved with renal transplant. 3.

Sensitivity and Foot and Ankle Reconstruction

An insensate foot has generally been considered an indication for amputation in lower-extremity trauma. In the setting of severe tibial fractures with soft tissue loss and neurovascular damage, it is difficult to argue against amputation. However, there are several areas where sensitivity is not an absolute requirement for amputation. Diabetic neuropathy frequently leads to decreased or absent sensation. Full-thickness plantar burns and isolated avulsion injuries are likely to have reasonable outcomes with skin grafts to reconstruct the plantar surface [60].



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There is still a significant debate in the literature over whether a neurosensory (innervated) free flap is better than a free-muscle flap with a split graft for coverage of the weight-bearing surface. A smaller series indicated that sensate fascial flaps were less prone to breakdown than innervated flaps [61]. However, this is disputed by Potparik and Rajacic [62] who found no significant difference between reinnervated and noninnervated flaps. The advantages of the increased sensation of the neurosensory fasciocutaneous flaps are balanced against increased mobility of the skin after swelling decreases in the subcutaneous tissue. A comparison by Sinha et al. [63] showed equivalent complication rates in free-muscle flaps and STSG and innervated fascial flaps. Another study by Buncke [64] found that it is possible to innervate a muscle by anastomosis, joining a motor nerve stump to a sensory nerve. 4.

Free Flaps and the Elderly

Chronologic age does not always determine the patient’s suitability for a free flap. Many microsurgery studies have elderly patients in the cohort or case series reports. Two studies demonstrate the safety and efficacy of microsurgery in the elderly [65,66]. The research by Serletti found the use of the anesthesiology (ASA) classification correlated with medical complications postoperatively. Surgical complications correlated more with operative time. Overall reconstructive success exceeded 90% [66,67]. 5.

Long-term Results of Free-Flap Foot Reconstruction

The first step in achieving a successful reconstruction is free-flap survival. The overall flap survival in large microsurgical centers is 95%. The results in community or county hospitals are slightly lower at 85 to 90% depending upon the experience of the microsurgical team. The main reason for the improved results at large centers appears to be the ability to salvage thrombosed flaps [68,69]. Several case series have demonstrated the effectiveness of free-muscle flaps and STSGs [70–72]. Ranier et al. [73] demonstrated that approximately one third of patients with free-muscle flaps to the plantar surface developed trophic ulcers. In all cases, recurrent ulcerations were due to underlying untreated osseous pathology. 6.

Failures and Revisions

Fortunately, free-flap failures are not a common occurrence. However, since so many free-tissue transfers are now being performed, most microsurgical centers have several patients with flap failures. A failing free flap is generally reoperated as soon as possible to reestablish blood flow. Leech therapy may be useful to relieve venous obstruction at the expense of large blood loss with subsequent transfusions. A failed free flap does not always lead to amputation; Weinzweig and Gonzales [74] reported a series of ten patients who underwent serial debridement and skin grafting and all patients achieved a successful outcome. Yakuboff et al. [75] found the converse is not always true. Patients with a successful free flap do not always have functional success. Up to one third of patients were found to be late functional failures. Debulking procedures may be required to prevent trophic ulcerations in free-tissue transfers. Goldberg et al. [76] demonstrated debulking procedures in 22 of 46 flaps for microvascular foot reconstruction. Careful attention to closure is important to reduce the need for debulking. Freemuscle flaps that are not innervated generally do not require debulking if given several months to atrophy. Composite fasciocutaneous fascial flaps can be debulked with liposuction if excessive subcutaneous tissue is present [77]. 7.

Gait

Severe injuries of the foot and ankle lead to gait abnormalities. The most common change in gait is shortening of the stance phase on the affected limb [78]. A study by Perttunen et al. [79] found that


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only one of seven patients treated with a free flap to the sole of the foot walked normally. This finding demonstrates two things: (1) the importance of continued monitoring of the flap for pressure necrosis and (2) the need for good foot orthotics postoperatively.

E.

Specific Free Flaps

1.

Radial Forearm Flap

The radial forearm flap is a workhorse flap in the lower extremity. Survival rates are generally over 90% [80–82]. The pedicle length allows proximal inflow vessels to be used in crush injuries with an extensive zone of injury. The flap may be innervated and provides a thin durable coverage. The palmaris longus may also be included as a vascularized tendon transfer if tendon reconstruction is required. Since donor-site morbidity is the main disadvantage of the radial forearm flap in up to one third of the cases and an unsightly scar is the most common problem, careful attention to donor-site closure by imbricating muscle over the flexor carpi radialis tendon will limit tendon exposure. Ninety-five percent of patients experience no functional deficit in the donor limb [83]. The donor site is then covered with an STSG. A sheet graft provides a better cosmetic result than a meshed graft (Figure 10.4A and Figure 10.4B).

Figure 10.4 (A) Lawn mower injury to the right foot in a 16-year-old male. (B) Three-month postoperative radial forearm free flap.



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The radial forearm may be used as a proximally based anterograde flap or a distal reverse flow flap. This concept may allow simultaneous bilateral foot reconstruction with a single radial forearm flap [84,85]. 2.

Rectus Abdominus

Another commonly used flap in foot and ankle reconstruction is the rectus abdominus. The inferior epigastric pedicle is a very consistent vessel. The dissection of the flap is very straightforward. The main complication is the abdominal bulging (pseudohernia or transverse rectus abdominis myocutaneous [TRAM] hernia), which is due to the separation of internal and external oblique layers and failure of both layers to remain secure together. True hernias do occur, but are rare. The rectus abdominus can be used to cover long, but fairly narrow, defects. The flap may be used in segments to cover smaller defects [86]. Initial muscle edema is dramatic, but the denervated flap shrinks over time (Figure 10.5A and Figure 10.5B). A case series by Musharafieh et al. [87] demonstrated a 92.5% flap survival rate.

Figure 10.5 (A) An open ankle fracture due to a motorcycle accident in a 47-year-old male. (B) Sevenmonth postoperative rectus free flap.


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Latissimus Dorsi (LD)

Another workhorse flap is the LD muscle. Originally, this was the most common flap used in freetissue transfer for lower-extremity reconstruction. The LD flap remains useful when very large areas require soft tissue coverage. When the muscle alone is required, a significant portion of the muscle may be harvested endoscopically or through a limited incision. Although the donor deformity is mild, Russell et al. [88] showed the decrease in muscle strength to be approximately 15% after LD harvest. The pedicle is the thoracodorsal artery. Up to 10 to 12 cm of skin may be removed and still allow primary closure of the donor site. A pinch test to assess laxity of the skin on the back will help determine the amount of skin that can be removed. In female patients, the incision may be placed transversely just below the tip of the scapula. In this manner the scar may be hidden in the bra line. If the recipient artery is the posterior tibial artery, the patient may be positioned laterally and simultaneous dissection of the opposite LD muscle and the recipient vessel may take place. This dramatically reduces operative time (Figure 10.6A to Figure 10.6C).

Figure 10.6 (A) Shotgun blast through the foot in a 23-year-old male. (B) Free latissimus dorse flap and STSG. The second, third, and fourth toes all survived as random tissue. Both dorsum and plantar surfaces were grafted.



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Figure 10.6 Continued (C) Plantar view of LD flap — good contour. The patient was ambulatory 4 months postoperatively.

4.

Parascapular

Based on the descending branch of the circumflex scapular artery, the parascapular flap is a fasciocutaneous flap. When only thin coverage is required, it can be used as a fascial flap with an STSG. This flap provides excellent coverage for the dorsum of the foot and the posterior nonweight-bearing heel and Achilles tendon [89,90]. The pedicle lies within the triangular space of the teres major, minor, and the long head of the triceps. The arterial diameter may be small but the anatomy is quite consistent. The donor site has minimal deformity, but the scar does tend to spread over time. If a large skin paddle is needed, donor site closure can be difficult. Generally, a 6-cm wide skin paddle is the maximum that can be closed primarily. The flap is harvested with the patient in lateral position, and the donor site can be rotated anteriorly as far as the intramammary fold [91] (Figure 10.7A and Figure 10.7B). 5.

Serratus Anterior

The serratus anterior is a relatively thin muscle with minimal to mild donor site deformity. A winged scapula deformity occurs in approximately one third of patients, but is usually asymptomatic [92]. The pedicle is the serratus branch of the thoracodorsal artery. By dividing the thoracodorsal artery as it enters the latissimus, the pedicle can be traced from the serratus anterior muscle and dissected all the way to the axillary artery if a long pedicle is required. Along with the serratus muscle, additional flaps may be used, such as the LD muscle to form a combined ‘‘sandwich’’ [93]. This can be useful to cover anterior and posterior wounds or exposed tendons. The serratus anterior is generally associated with high success rates in microvascular centers [94] (Figure 10.8A and Figure 10.8B). 6.

Gracilis

The gracilis muscle is a commonly used flap in some microsurgical centers [95–97]. The advantage of the gracilis is minimal donor deformity and thin coverage. However, it is a small thin muscle that cannot cover large areas. The cutaneous portion of the flap is unreliable. Muscle transplants used for coverage are covered with STSGs. Occasionally, the gracilis is used for functioning muscle transfers.


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Figure 10.7 (A) Open ankle fracture due to a motorcycle accident in a 30-year-old male. (B) Healed parascapular free flap.

An area of particular benefit may be in a patient who is not a candidate for general anesthesia. The entire dissection of donor and recipient sites can be done with epidural anesthesia. 7.

Lateral Arm Flap

The lateral arm flap is a useful fasciocutaneous flap based on the posterior radial collateral artery. It can be used for small wounds and may be harvested with a portion of the humerus as an osteocutaneous flap. However, the donor site may occasionally cause elbow pain and numbness. The pedicle also comes from the midportion of the flap and is short limiting the arc of rotation [98] (Figure 10.9A and Figure 10.9B).

F.

Other Flaps

Many other flaps can be used for lower-extremity reconstruction; some of the choices include the temporal parietal fascia [99], the rectus femoris [100], the tensor fascia lata [101], and the scapular



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B

Figure 10.8 (A) Severe frostbite injury with loss of plantar surface of the foot and all toes in a 15-yearold female. She was treated initially with STSGs. An unstable heel wound required a free serratus flap. (B) Four-months postoperatively healed — good contour after muscle atrophy.

Figure 10.9 (A) Avulsion injury and open fracture of the left great toe in a 22-year-old male. (B) A 6-month postoperative view after a lateral arm free flap.


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Heel Weight-bearing Metatarsal

Plantar

Small defect - 2 intent PDGF - Medial plantar flap Large defect − exposed bone → free flap

Non-weight-bearing (instep)

Large defect − adequate soft tissue plantar fascia intact → STSG

2 intent PDGF STSG

Exposed tendon

Large area free flap Small area

Plantar No tendon exposed

STSG

If no granulation VAC PDGF

Free flap

Good granulation

STSG

Lateral ankle − exposed bone → small area → lateral calcaneal artery flap Large area → free flap

Posterior ankle Achilles tendon

Small area or poor surgical candidate − VAC PDGF

Granulation No granulation

Sural artery flap Large area

STSG Free flap (if reasonable surgical candidate)

Free flap

Figure 10.10

Algorithm guideline based on location.

flaps [102]. The use of these flaps offers some advantages and their use is dependent upon the surgeon’s level of comfort with the donor harvest.

X.

CONCLUSION

Recent advances in soft tissue reconstruction and orthopedic techniques have made functional restoration of the foot and ankle possible. A basic clinical algorithm is included in Figure 10.10. The question has become not, ‘‘what can we do?’’ but ‘‘what should we do?’’ Is all the work worth the effort to the patient? Occasionally it is not; however, a study by Dagum et al. [103] demonstrated very good late functional results and high patient satisfaction with limb salvage. The decision remains a complex combination of factors. The doctor and patient ultimately must decide on the best course of action for the individual patient and wound.

ACKNOWLEDGMENT We gratefully acknowledge the assistance of Jaime Garza, M.D., D.D.S., senior attending physician on two of the cases mentioned in this chapter.



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Quinones-Baldrich, W.J., Kashyap, V.S., Taw, M.B., Markowitz, B.L., Watson, J.P., Reil, T.D., and Shaw, W.W., Combined revascularization and microvascular free tissue transfer for limb salvage: a sixyear experience, Ann. Vasc. Surg., 14, 99–104, 2000. 50. Serletti, J.M., Deuber, M.A., Guidera, P.M., Herrera, H.R., Reading, G., Hurwitz, S.R., Jones, J.A., Ouriel, K., and Green, R.M., Atherosclerosis of the lower extremity and free tissue reconstruction for limb salvage, Plast. Reconstr. Surg., 96, 1136–1144, 1995. 51. Illig, K.A., Moran, S., Serletti, J., Ouriel, K., Orlando, G., Smith, A., Shortell, C.K., and Green, R.M., Combined free tissue transfer and infrainguinal bypass graft: an alternative to major amputation in selected patients, Vasc. Surg., 33, 17–33, 2001. 52. Bergman, B.A., Zamboni, W.A., and Brown, R.E., Microvascular anastomosis of a rectus abdominis free flap into a prosthetic vascular bypass graft, J. Reconstr. Microsurg., 8, 9–12, 1992. 53. 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Microsurg., 13, 1–5, 1997. 60. Jeng, S.F. and Wei, F.C., Classification and reconstructive options in foot plantar skin avulsion injuries, Plast. Reconstr. Surg., 99, 1695–1703, 1997. 61. Chang, K.N., DeArmond, S.J., and Buncke, H.J., Sensory reinnervation in microsurgical reconstruction of the heel, Plast. Reconstr. Surg., 78, 652–664, 1986. 62. Potparic, Z. and Rajacic, N., Long-term results of weight-bearing foot reconstruction with noninnervated and reinnervated free flaps, Br. J. Plast. Surg., 50, 176–181, 1997. 63. Sinha, A.K., Wood, M.B., and Irons, G.B., Free tissue transfer for reconstruction of the weight-bearing portion of the foot, Clin. Orthopaed., 242, 269–271, 1989. 64. Joldberg, J.A., Trabulsy, P., Lineaweaver, W.C., and Buncke, H.J., Sensory reinnervation of muscle free flaps for foot reconstruction, J. Reconstr. Microsurg., 10, 7–9, 1994. 65. 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11 Burns to the Feet Sidney F. Miller and Matthew R. Talarczyk Department of Surgery, Miami Valley Hospital, Wright State University, Dayton, Ohio

CONTENTS I. Introduction ................................................................................................................... 288 II. Development of Modern Burn Care and the Burn Team Concept................................. 288 III. Initial Evaluation............................................................................................................ 289 A. Inhalation Injury and Associated Injuries............................................................... 289 B. Pathophysiology of the Burn Injury........................................................................ 289 C. Evaluation of the Burn Wound............................................................................... 289 1. Assessing the Extent and Depth of the Burn Wound ....................................... 289 IV. Treatment ....................................................................................................................... 291 A. Resuscitation........................................................................................................... 291 B. Escharotomy ........................................................................................................... 292 C. Initial Wound Care ................................................................................................. 292 D. Definitive Wound Coverage.................................................................................... 294 E. Hyperbaric Oxygen ................................................................................................. 296 V. Reconstruction and Rehabilitation, Hypertrophic Scars, and Contractures .................. 297 A. Classification of Contractures ................................................................................. 299 B. Treatment................................................................................................................ 300 1. External Fixators.............................................................................................. 300 2. Limb Suspension .............................................................................................. 301 3. Garments .......................................................................................................... 301 4. Orthotics........................................................................................................... 302 VI. Special Orthopedic Issues ............................................................................................... 302 A. Bone and Achilles Tendon Exposure ...................................................................... 302 B. Fractures ................................................................................................................. 302 C. Involved Joints........................................................................................................ 303 VII. Complications................................................................................................................. 303 A. Dystrophic Calcification ......................................................................................... 303 B. Osteoporosis............................................................................................................ 303 C. Pigmentation ........................................................................................................... 303 D. Marjolin’s Ulcers .................................................................................................... 303 VIII. Special Types of Burns ................................................................................................... 305 A. Electrical Burns....................................................................................................... 305 B. Chemical Burns....................................................................................................... 306 IX. Prevention....................................................................................................................... 307 X. Summary ........................................................................................................................ 307 References .................................................................................................................................. 308 287


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I.

Miller and Talarczyk

INTRODUCTION

Burns to the feet are different from burns of other areas of the body. Because of dependency and the frequent occurrence of either peripheral vascular disease or diabetic neuropathy, even small foot burns may be limb or life threatening. Burns of the feet cannot be discussed outside the context of the management of the burn patient in general. Although frequently of minor proportion to the overall extent of the burn injury, foot burns are a significant concern. The major objective in the management of patients with burned feet is to return them to normal function with unimpeded ambulation and weight-bearing on pain-free feet. The American Burn Association has defined foot burns as one of the ‘‘special’’ areas of burns that need to be referred to a regional burn center [1]. Frequently first responders, primary care and emergency department physicians do not appreciate the potential magnitude and lethality of these relatively ‘‘minor’’ injuries. This chapter addresses the initial evaluation of the burn patient in general and burns of the feet specifically. The pathophysiology of the burn injury, initial wound management, definitive wound coverage, reconstruction and rehabilitation, the long-term management of complications such as scarring and contracture, and special types of burns, including electrical and chemical burns are also discussed. Wound healing is impaired by the development of wound edema and infection. An integral part of the care of the burned feet is bed rest. Particularly in the diabetic patients or patients with neuropathic feet, the lack of sensation can lead to deep burns of the feet. Diabetics have impaired wound healing because of their microvascular disease and hyperglycemia. These patients are at significant risk for major impairment and possible amputation if their wounds are cared for improperly. The majority of patients with burned feet should be evaluated and treated at a tertiary burn care facility. Early and appropriate communication with the burn team is of the essence. If early transfer is not possible, communication with the burn center can provide guidance for the early management of these wounds. Frequently, the care given to the burn wound during the first 24 to 48 hours after the burn will have a decisive effect on the ultimate outcome and goal of pain-free weight-bearing.

II.

DEVELOPMENT OF MODERN BURN CARE AND THE BURN TEAM CONCEPT

The seminal event in burn care was the November 28, 1942, Coconut Grove fire in Boston. This disaster led to an understanding of the diagnosis and management of burn wound shock. Fortunately, research scientists related to the Harvard Medical School were studying fluid and electrolyte balance and were able to apply these principles to the victims of this major disaster. The modern era of burn care came about during the late 1960s and early 1970s with the development of multispecialty burn care teams and dedicated burn centers. The development of these teams and units allowed for the development and concentration of experience and expertise needed for the management of these complex injuries. The realization for the necessity of early excision of burn wound eschar, essentially gangrene of the skin, was a major advancement in burn wound care [2]. Before the introduction of early wound excision, the eschar was allowed to ‘‘separate’’ naturally. This eschar separation occurs due to subeschar tissue liquefaction by bacteria. It is little wonder that many patients became septic while waiting for eschar separation. Additionally, during the late 1960s and early 1970s, effective topical antibiotics became available. These antibiotics were able to penetrate the eschar and decrease subeschar infection but delay natural eschar separation. These advancements in care created new problems and opportunities. Although early excision of smaller burn wounds was very effective and led to decreased morbidity and length of hospital stay, management of larger wounds awaited the development of advancements in alternate forms of wound coverage. These included biosynthetic wound coverings and the use of cultured epidermal autografts and other composite skin replacements [3,4]. As the complexity of the care issues related to these patients increased, the need and contribution of the interdisciplinary burn care team became of increasing importance. Additionally, dedicated facilities led to improved patient outcomes. The immediate initiation of physical and occupational therapy minimizes or eliminates the severe physical disability of burn patients seen in


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the past. Early and aggressive nutritional support prevents or limits the severe malnutrition that had once been common in the burn patient. Dedicated social, psychological, and chaplaincy services are provided not only to the patients, but also to their families.

III.

INITIAL EVALUATION

The initial management of the burn patient starts with a general evaluation and the standard ABCs (airway, breathing, circulation). Burn patients are trauma patients and frequently have associated injuries. The burn itself is an attention-grabbing injury, but these patients frequently have been involved in motor vehicle accidents or other violent forms of injury. The early mortality of burn patients is rarely due to the burn injury itself, but from associated injuries. Initial ABC control is essential.

A.

Inhalation Injury and Associated Injuries

Patients with inhalation injuries will rarely present with signs or symptoms of airway obstruction. Burn patients injured in an enclosed space or who have soot or burns on the face or in the oral pharynx should be considered to have an inhalation injury and should be evaluated by bronchoscopy. If bronchoscopy demonstrates erythema, ulceration, or sloughing of the tracheobronchial mucosa at or below the vocal chords, an endotracheal tube should be placed in order to maintain airway patency. An assessment for sites of internal or external hemorrhage must be completed. Other associated potential life- or limb-threatening injuries must be vigorously sought. These associated injuries are the causes of the majority of the early mortality in burn patients and affect the ultimate outcomes.

B.

Pathophysiology of the Burn Injury

Burn wounds are most commonly referred to as first, second, or third degree. The preferred descriptive terms, however, are partial- or full-thickness burns. The partial burn injury ‘‘recovers’’ by reepithelization from retained viable skin appendages in the partially intact dermis. Inadequate management of burn wound shock with prolonged hypovolemia or the inappropriate use of vasoconstricting agents that adversely effect the capillary blood flow to the partially damaged but viable skin appendages can lead to their destruction and the ‘‘conversion’’ of the partial-thickness wound to a full-thickness burn. In those wounds where the entire dermis is destroyed, healing of the wound can only occur by reepithelization from the wound margin or by skin grafting. As with most injuries, burn wounds are not uniform (Figure 11.1). The burn wound frequently consists of three identifiable zones of injury. The inner zone of necrosis is where there is no blood flow, with full-thickness injury to the skin and occasionally underlying tissues. This zone of necrosis is surrounded by a variable zone of stasis where blood flow is sluggish (Figure 11.2). A number of factors will influence whether continued adequate blood flow will occur in this zone. Effective resuscitation will improve the circulation in the zone of stasis. Surrounding this area is a zone of hyperemia where blood flow is increased.

C.

Evaluation of the Burn Wound

1.

Assessing the Extent and Depth of the Burn Wound

After the airway has been evaluated and stabilized, associated injuries identified, and external hemorrhage controlled, the burn wound can be evaluated. Appropriate resuscitation is predicated on the extent and depth of the burn wound. The depth of the burn wound is estimated by the appearance of the wound. Superficial partial-thickness burns are red and painful and resemble sunburn. Partial-thickness wounds generally are red and have capillary refill, blisters or a moist surface, and intact sensation because some or all of the skin appendages necessary for reepithelization


290


Figure 11.1

Burn depth of nonuniform burn.

are retained. With full-thickness burns, the entire epidermis and dermis and all of the skin appendages have been destroyed, and the wound does not have capillary refill and is usually dry and insensate. The extent of the burn wound is determined by one of a variety of methods. Many emergency departments use either the ‘‘Rule of Nines’’ (Figure 11.3) or the Lund–Browder chart (Figure 11.4) [5]. Electronic programs are now being developed to estimate the extent of the burn wound size. One such program is available online (www.sagediagram.com) and allows for printing and storage

Figure 11.2 Burn depth zones of burn.


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9% Percent of total BSA

Adult body Part Arm

9

Head

9

Neck

1 18

Anterior trunk

18

Posterior trunk

18

18%

14%

9%

Back 18%

9%

18% 18%

Leg

9%

1% Front 18%

Front 18% Back 18%

Child body Percent of total BSA Part 9%

14%

Arm

9

Head and neck

18

Leg

14

Anterior trunk

18

Posterior trunk

18

Figure 11.3 Rule of Nines.

of burn diagrams that not only estimate the burn wound extent, but also estimate fluid needs based on the Parkland formula for larger burns, generally those greater than 20% of the body surface area.

IV.

TREATMENT

A.

Resuscitation

Initial resuscitation is begun with balanced salt solution. Intravenous access must be obtained at an appropriate site even if placed through the burned wound. Resuscitation is based on the extent and depth of the burn wound. Resuscitation of the burn patient begins in the emergency department. The Parkland formula is the most commonly used estimate of the patient’s fluid requirements; however, the goal of adequate resuscitation is a patient with a stable blood pressure and pulse and a urine output of 30 to 50 cc/h in


292


Age A − ½ of head

0−1

1−4

5−9

10−14

15

9½%

8½%

6½%

5½%

4½%

B − ½ of one thigh 2¾%

3¼%

4%

4¼%

4½%

C − ½ of one leg

2½%

2¾%

3%

3¼%

2½%

A

A 3½%

3½% 1%

Adult

1% 2%

2%

2%

2% 13%

13% 1½%

1½%

1½%

1½% 2½%

1½%

1½%

1%

2½% 1½%

1½%

4¾% B

4¾% B

4¾% B

4¾% B

C 3½%

C 3½%

C 3½%

C 3½%

1¾%

1¾%

1¾% 1¾%

Figure 11.4 Lund–Browder chart.

the adult, and 1 cc/kg/h in the pediatric patient. The Parkland formula of 3 to 5 cc/kg/ % of body surface area burn is a guideline to the fluids needed. The fluid choice is generally lactated Ringer’s solution.

B.

Escharotomy

The full-thickness burn has a tough leathery feel and appearance. It loses its natural elasticity, and as the resuscitation process begins, fluid is lost to the extracellular space with the development of wound edema. With circumferential extremity burns, as this fluid accumulates under the tough leathery eschar, compartment pressures in the extremities will exceed both venous and arterial pressures, and the blood supply to the extremity will be impaired. An escharotomy through the leathery eschar into the subcutaneous tissues will immediately release this pressure on the vascular supply and reestablish good blood flow to the extremity. The absence of distal pulses or capillary refill will indicate the need for escharotomy.

C.

Initial Wound Care

Foot burns must be evaluated in the context of the whole patient. Frequently, with major burns, burns of the foot play a relatively minor role because the primary efforts must be directed at saving the patient’s life. The general approach to patients with large body surface burns is to excise the fullthickness burns — essentially dry gangrenous skin that has not become grossly infected — as early as possible, including the feet. Many patients, however, are seen with primarily foot or lower leg burns. The principles applied to these burns also apply to the patients with larger burns in which the feet are involved.


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After the initial evaluation and resuscitation of the burn patient has been accomplished, attention can be turned to the burn. The wound is initially washed with a mild cleansing agent and then soaked in either normal saline or 5% Sulfamylony solution. Drying of the wound inhibits reepithelization and contributes to wound conversion by interfering with the capillary blood flow, particularly during the first 24 hours after injury. There is much evidence that wounds heal best in a moist environment, which is why the classic wet-to-dry dressing, although helpful for debriding necrotic material, is detrimental to healing tissues [6]. Additionally, every effort should be made to diminish edema in the feet by bed rest and elevation of the feet. Topical antibiotics are frequently used in the partial-thickness wound where surgery is probably not necessary or likely. The most commonly used initial antibiotic is silver sulfadiazine cream (SSD), which is painless on application and has a good coverage for Gram-positive organisms. SSD’s major adverse effect is pancytopenia. The active antibacterial effect of SSD is from the silver ion, and recently a silver-impregnated dressing (Acticoaty, Smith & Nephew Wound Management, Largo, FL) (Figure 11.5) has come on the market, which has promise for use with partial-thickness wounds by not only ‘‘closing’’ the wound, but also supplying an antibacterial effect. Mafamide (Sulfamylon, Mylan Laboratories, Pittsburgh, PA) has better Gram-negative coverage, but is painful on application. It is a carbonic anhydrase inhibitor and can produce metabolic acidosis, usually compensated with hyperventilation. Initial wound management involves once- or twicedaily dressing changes with the use of topical antibiotics. The newer synthetic and biosynthetic agents, such as Xeroformy (Sherwood Medical, St. Louis, MO), Transcytey (Smith & Nephew Wound Management, Largo, FL), and Acticoat, used in the management of patients with partialthickness wounds, may be left in place for 7 to 10 days and markedly decrease the nursing or patient time to provide wound care. At the time of removal, the majority of these wounds will be reepithelized. Systemic antibiotics are only used when there has been some type of heavy contamination at the time of the injury. In general, the only indications for systemic antibiotics in the burn patient are positive blood cultures or systemic signs of sepsis, such as a change in mentation, unexplained ileus, or low systemic vascular resistance. As these patients are at potential risk for sepsis as long as they have either undebrided eschar or ungrafted wounds, the use of systemic broad-spectrum antibiotics will only lead to the overgrowth of resistant organisms. However, burn patients are at risk for tetanus. The guidelines of the American College of Surgeons should be followed in all burn patients. Previously immunized patients should have a tetanus booster. Unimmunized patients should have both tetanus immunoglobulin and tetanus antitoxin. It is the obligation of the individual initiating the course of immunization in the burn

Figure 11.5 Acticoat applied to partial-thickness burn.


294


patient to inform the patient or a responsible family member of the need for further required injections to complete immunizations [7]. After 24 hours, all wounds are reinspected and decisions are made regarding definitive care. Superficial partial-thickness burns should heal in 7 to 10 days. These wounds are painful, red, and moist and may be treated in a variety of ways. They traditionally have been treated with topical SSD cream. Acticoat [8] is a silver-impregnated polyester dressing that when moistened releases silver ions, which are felt to be the primary antibacterial agent of SSD. Xeroform gauze, which is applied and allowed to stay in place for 7 to 10 days until the wound has healed, is also an effective agent for partial-thickness wounds. Daily inspection should demonstrate a dry wound without drainage. Several newer topical dressings are also available. OpSitey (Smith & Nephew Wound Management, Largo, FL) and other occlusive dressings allow for collection of large amounts of transudate and frequently need to be reapplied. Superficial and deeper partial-thickness wounds that have retained sensation, capillary refill, and exudates can be treated with a number of newer biosynthetic dressings including Transcyte, xenograft, and allografts. Each of these treatments has its advocate in the literature and has been shown to effectively close partial-thickness wounds and possibly enhance reepithelization. They all achieve the same degree of pain control and markedly decrease the time spent by nurses or patients doing wound care. These newer dressings can be divided into biological and biosynthetic dressings. Frozen xenograft (pig skin) can be obtained commercially from a number of sources. It tends to ‘‘take’’ to the underlying partial thickness and can be very painful with removal. The other option is to use it as a dressing and change it daily. Cadaveric allografts are also readily available through most blood banks. Allodermy (AlloDerm Life Cell Corp., Woodlands, TX), a human fibroblast matrix, closes the wound and provides significant pain relief. When used with excised full-thickness wounds, Alloderm provides a neodermis. A number of new biosynthetic dressings are available. Although expensive, they decrease pain, appear to promote wound healing, and decrease patient or nurse time performing wound care. These products work best with clean noncontaminated wounds. When infection intervenes, the wounds should be debrided in all or in part and appropriate topical antibiotics should be started. Biobraney (Bertek Pharmaceuticals, Morgantown, WV), one of the first biosynthetic dressings, has a bilaminar construct with an outer silicone membrane and inner nylon filaments bonded to type I collagen. In the early 1980s, Hull et al. [9] first described the lack of antigenicity of crossspecies dermal fibroblast sheets. Transcyte (Smith & Nephew Wound Management, Largo, FL) is a biosynthetic dressing of cryo-preserved human fibroblast sheets covered with Biobrane and has been advocated for temporary coverage of partial-thickness burns and freshly excised wounds. Apligrafy (Organogenesis, Canton, MA) has not yet been approved for burns, but has some potential. It is a composite of cadaveric fibroblast sheets and neonatal foreskin keratinocytes. It has been shown to be an effective biological dressing for venous and diabetic ulcers, but questions remain as to the ‘‘take’’ with Apligraf. Integray (Integra Life Sciences, Plainsboro, NJ) is the highly publicized ‘‘artificial skin.’’ It is a silastic membrane overlying a fibroblast sheet, which becomes vascularized and can be left in place for long periods of time. The silastic sheet is removed and the vascularized neodermis is covered with a thin split-thickness autograft.

D.

Definitive Wound Coverage

Early primary excision of deep burns represents a major advance in burn care during the past 20 years. Full-thickness burns larger than approximately 1% of the body surface area will require skin grafting. The sooner this is performed with proper excision of the necrotic skin the less likelihood there is of the development of subeschar colonization and subsequent sepsis. Varieties of methods are now available to cover the excised area and their use depends on the available donor sites and the location of the burn. Generally, burns of the face, hand, and feet have a better cosmetic appearance with sheet grafts than with meshed grafts. Meshed split-thickness autografts from a ratio of 1:1 up to 9:1 are possible with the newer meshing devises. Full-thickness grafts, flap, cadaver skin, cultured epithelial autografts all have their role. The definitive management of foot burns must be evaluated in the overall perspective of the entire patient. Obviously, the major effort is directed toward saving the patient’s life. With large


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295

body surface burns, the goal is to excise the burn as soon as possible. If there are only limited sites for autografts, skin may be harvested for cultured keratinocytes grafts (Epicel-CEA, Genzyme Tissue Repair, Cambridge, MA). Additionally, a number of synthetic and biosynthetic agents are available, which may be used for temporary closure of the freshly excised burn wounds. When only the legs and feet are involved, the decisions are easier since there is usually an abundance of donor sites. Full-thickness burns are addressed differently if they occur on the plantar or dorsal surface of the foot. Because of the thickness of the sole of the foot, many apparent full-thickness burns of the plantar surface heal spontaneously because enough of the dermal elements needed for reepithelization of the wound survive the injury. Full-thickness burns of the sole of the foot that do not heal within 3 to 4 weeks eventually will need to be treated with a sensate skin flap (Figure 11.6 to Figure 11.9). Full-thickness burns of the dorsal aspect of the foot should be excised early and, if there are generous donor sites, covered with a split-thickness sheet graft (unmeshed). The cosmetic appearance of the unmeshed split-thickness skin graft far exceeds that of the meshed grafts. The sheet graft

Figure 11.6 Free-flap frostbite injury of the foot.

Figure 11.7 Free-flap frostbite injury of the foot.


296


Figure 11.8 Free-flap ankle reconstruction.

Figure 11.9 Foot and ankle free flap.

should be ‘‘pie-crusted’’ before application to allow any seroma to drain. Grafts may be fixed in place with staples; however, Steri-Strips and fibrin sealants are as effective and are less painful. This excision is usually carried out to the metatarsal phalangeal joints, but not onto the toes. If a tendon or bone is involved in the injury, flap closure may be necessary. Extensive burns of the last two toes frequently are best treated with amputation; however, every effort is made to preserve the function of the great toe. Pinning of the toes to maintain function is occasionally used. The immediate application of an Unna boot or Proforey (Smith & Nephew Wound Management, Largo, FL) dressing over fresh skin grafts can allow for immediate ambulation. Without either of these dressings, the patient should be at limited bed rest (bathroom privileges only).

E.

Hyperbaric Oxygen

The use of hyperbaric oxygen for medicinal purposes was first introduced in England during the 17th century. Since then, hyperbaric oxygen has been hypothesized to facilitate healing in a number


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of ailments including frostbite injury, osteomyelitis, soft tissue infections, carbon monoxide poisoning, burns, and as an adjuvant therapy in cardiac surgery. The use of hyperbaric oxygen in the management of Caisson disease (divers’ ‘‘bends’’) has been well defined and accepted in scientific literature. The physics and physiology of hyperbaric oxygen therapy can be easily simplified. The most efficient means of delivering pressurized oxygen is through one’s systemic circulation rather than by diffusion. Under normal ambient pressure (1 atm), the arterial oxygen tension (PAO2) is approximately 90 mmHg while tissue oxygen tension (PTO2) nears 55 mmHg. Less than 3 atm pressure, the PAO2 is approximately 1800 mmHg and PTO2 increases to over 500 mmHg. Once removed from the pressurized environment, depending on tissue perfusion, the PTO2 may remain elevated for hours. It has been shown that PTO2 levels greater than 40 mmHg are required for normal tissue repair. Enhanced elevation of PTO2 is proposed to stimulate angiogenesis, enhance leukocyte function, increase granulation tissue formation and collagen deposition, and reduce injured tissue edema [10]. The use of hyperbaric oxygen in the management of burns is less defined. Anecdotal reports of burn wound treatments do not support the routine use of hyperbaric oxygen. Hammarlund et al. [11] and Niezgoda et al. [12] were unable to demonstrate improved rates of epithelization of superficial wounds. However, Brannen et al. [13] performed hyperbaric oxygen treatments twice daily in a randomized prospective study of 125 burn patients and were unable to demonstrate a treatment advantage. To date, there are no prospective studies justifying the use of hyperbaric oxygen in the routine treatment of burn injuries. The patient with high carboxyhemoglobin and smaller burns can be treated initially in a hyperbaric chamber. The critically burned patient with high carboxyhemoglobin must be treated in a facility that can provide the required critical care. There are some large multiplace hyperbaric units that can dive nursing personnel and provide critical care during the dive. Survival of the patient is of primary importance and no significant benefit of the treatment of carbon monoxide poisoning with hyperbaric oxygen has been shown in a prospective manner.

V.

RECONSTRUCTION AND REHABILITATION, HYPERTROPHIC SCARS, AND CONTRACTURES

Rehabilitation of the burn patient starts at admission. Both physical and occupational therapists must see the patient shortly after admission. Range-of-motion exercises are begun even before definitive wound care has been carried out. Skin grafts applied in an appropriate fashion should be ‘‘stuck’’ by 24 hours after surgery, and at that time physical therapy is resumed. The majority of these patients had normal range of motion before their injuries and the goal of therapy must be to maintain, not recapture, lost range of motion. Hypertrophic scars and burn contractures are a major cause of morbidity in the burn patient. Partial-thickness burns are susceptible to scar hypertrophy formation for up to 18 months after the initial thermal insult. As a burn heals, myofibroblasts predominate, with ensuing vasculogenesis leading to marked collagen deposition. Early burns consist of a soft and pliable scar, with collagen fibers predominantly residing in a parallel alignment. As the scar matures, there is increased disorder of these collagen fibers, progressing to the classical ‘‘whorl-like’’ arrangement (Figure 11.10 and Figure 11.11). During the normal healing process of injured tissue, there is persistent contraction of the healing wound. These contractions may subsequently lead to significant impairment of mobility and function, as the wound will continue to contract until it meets an equal and opposing tissue force. In order to address and combat these internal forces, a number of techniques have been described to facilitate early return to functional activity. Regardless of the technique employed, the ultimate goal in minimizing contractures is to maintain the injured region in a neutral and functional position and initiate early ambulation. If a contracture develops and was not addressed early in the burn management, early implementation of corrective techniques is encouraged, as contractures are most responsive to nonoperative management during the first 3 to 6 months following healing. Whenever possible, nonoperative intervention should be used to minimize


298


Figure 11.10

Immature scar.

hypertrophic scarring, contractures, and functional impairment while maximizing range of motion with aggressive physical therapy. When nonoperative techniques are unsuccessful, contractures can be surgically treated with soft tissue releases, soft tissue flaps, osteotomies, or even amputations. Nonoperative treatments of wound contractures include range-of-motion exercises, pressure garments, silicone gel pads, continuous passive motion (CPM) machines, serial casting, and specially fabricated devices. These all require the special expertise of the personnel and resources in a tertiary care center that specializes in the management of the burn patient to ensure optimal results. Contractures involving the pediatric population are especially troublesome. The surgeon has to not only consider the potential functional impairment caused by contractures, but also the psychosocial aspect of a burn injury. Further, it is well documented that contractures, if managed incorrectly, can result in abnormal growth and development of underlying bone and tissue. Waymack et al. [14] performed a 4-year retrospective evaluation of reconstructive procedures for

Figure 11.11

Immature scar.


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the treatment of burn scar contractures in 55 children involving 90 different operations. The mean time span between burn injury and surgical correction was 4 years and involved transverse arch contracture release followed by skin grafts. The observed 15% contracture recurrence was not influenced by the use of meshed or unmeshed split-thickness vs. full-thickness grafts or the time delay from injury to the reconstructive procedure. Early release of contractures can facilitate early ambulation while minimizing potential growth abnormalities and has not resulted in increased recurrence. Postoperative immobilization played an integral role in minimizing contracture recurrence and preventing graft loss. Alison et al. [15] combined the standard transverse metatarsal contracture release with the longitudinal metatarsal contracture release and prolonged the time interval until contracture recurrence.

A.

Classification of Contractures

Leung and Cheng [16] performed a study on 85 patients, divided nearly equally between adults and children, with a variety of burn wounds to their feet. Four degrees of dorsal foot contractures and a single pure plantar type contracture were described. The four degrees of dorsal foot contractures included the mild, moderate, severe, and mutilated, each requiring different degrees of correction and intervention. The mild type presented with minimal dorsiflexion contractures secondary to hypertrophic scarring, with minimal impairment of activity. The moderate dorsal foot contractures involved fewer than three toes with dorsiflexion contractures, while the severe contractures involved three or more toes with dorsiflexion contractions. With moderate and severe contractures, the metatarsophalangeal joints were pulled into dorsiflexion while the corresponding proximal interphalangeal joints showed compensational flexion, giving the foot a ‘‘clawtoe’’ appearance. The mutilated contractures were cases in which the toes and ankle were in dorsiflexion contractures with possibly exposed tendons, bones, or joints, and as expected, are associated with the most diminished functional level (Figure 11.12 and Figure 11.13). The severity of contractures dictated the type of intervention to be employed to best attain early and functional activity. In general, Z-plasties and excision with split-thickness skin grafting are used for the mild to moderate contractures, while pedicle, free, and cross-leg flaps were used for the severe and mutilated injuries. Some authors have argued that full-thickness skin grafts should be used on the foot to minimize the development of hypertrophic margins and further contractures with an increase in the overall stability of the graft. Kirschner wire splints are used to maintain neutral position after contracture release of the moderate and severe contractures for 3 to 8 weeks.

Figure 11.12

Ankle contracture.


300


Figure 11.13

Ankle contracture.

A multitude of splinting techniques have been described in the literature including plaster and acrylic casts, silicone boots, dynamic splints, and thermoplastic splints [17,18]. Splints are often fitted before and after grafting of injured regions to maintain a neutral position and have been shown to decrease foot contracture recurrence. These must be modified and refitted as edema subsides. Nonetheless, splints are easy to fit, apply, and remove, allowing burn team members access to injured regions. This easy access facilitates debridement when necessary and early implementation of range-of-motion exercises.

B.

Treatment

1.

External Fixators

Skeletal traction using tibial and calcaneal pins is used extensively for postoperative positioning and immobilization. External fixation devices have been described to slowly correct major foot contractures not amenable to nonoperative intervention [19] (Figure 11.14). Although tendon

Figure 11.14

Release ankle contracture.


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301

release and lengthening could be implemented in a single procedure, neural and vascular structures require gradual lengthening. Erdogan et al. [20] combined soft tissue release procedures with external fixators in five burn patients and corrected the contracture deformities over a period of 30 to 40 days followed by excision and grafting of the burns with split-thickness skin grafts. Calhoun et al. [19] have described the use of an Ilizarov fixator in equinus, cavus, rocker bottom, and toe dislocation burn deformities and even in the more complex burn deformities with varus or valgus, along with bone, joint, or muscle abnormalities. After correction of the contracture deformity, the Ilizarov fixator is left in the neutral position for 4 to 6 weeks, at which time a cast or splint is applied for an additional 6-week duration. 2.

Limb Suspension

Burns on the dorsal surfaces of the arms and legs are a particular problem for the burn surgeon. Applying skin grafts to these areas is a challenge because if the patient remains in a supine position, significant pressure will be exerted on these skin grafts, which will cause them to fail. A variety of methods have been tried to relieve this pressure. This is an area in which the orthopedic surgeon can be quite helpful. As most patients cannot tolerate lying in the prone position for extended periods of time, alternate methods have been tried to avoid pressure on these grafts. Balanced traction or suspension and pins through the elbows, wrists, knees, and ankles were moderately successful, but frequent adjustments were needed to maintain appropriate limb elevation. Recently, we have had an excellent experience with the use of external fixation devices placed in the tibia or ulna in order to elevate the extremity (Figure 11.15 and Figure 11.16). By using these devices, elevation of the limb and care of the wounds are easier. 3.

Garments

External pressure garments are used to prevent hypertrophic scarring. Application of external pressure garments producing greater than 25 mmHg of skin pressure have been shown to reduce hypertrophic scarring and result in a more normal collagen pattern [21]. Normally, collagen is lined up in an orderly fashion. Early scar tissue is characterized by chaotic collagen fibers that resemble the rubber bands inside a golf ball. As the scar matures, the fibers line up in an ordered fashion. Surface pressure appears to hasten this orderly progression of the collagen. The use of pressure garments is often used with nocturnal splinting for approximately 1 year after burn injury.

Figure 11.15

ExFix for leg elevation.


302


Figure 11.16

4.

ExFix for leg elevation.

Orthotics

Burns to the dorsum of the feet are especially susceptible to contractures due to the loose connective tissue within the subdermal plane. A very simple technique, often used in management of pediatric burn injuries, is to fit the patient in a high-top shoe that is to be worn both night and day except during physical therapy exercises. Custom-made orthotics or thermoplastic boot splints have been described in the literature. Most regional burn centers work with orthotists and pedorthotists. Custom-made footwear has made a marked difference in the care of the healing and healed burned foot.

VI. A.

SPECIAL ORTHOPEDIC ISSUES Bone and Achilles Tendon Exposure

A special area of concern with foot burns is the heel. Both the Achilles tendon and the calcaneus are relatively superficial, with little overlying muscle or subcutaneous fat. Exposure of the Achilles tendon will lead to rupture. Frequently, if the lower leg and foot require early skin grafting, a portion of the eschar will be left in place on the Achilles tendon and calcaneus. This eschar serves as a protective covering over both. The amount of eschar left is relatively small, but it will keep the exposed tendon or bone from becoming exposed. An exposed Achilles tendon and calcaneus should be considered for early flap coverage. The same holds true for the shin. Here the tibia is very superficial and grafts applied to the periosteum do poorly. Also, at this location a narrow strip of eschar is left in place and allowed to separate over the next 10 to 14 days. Once this eschar has separated, a narrow strip of granulation tissue will remain, which will frequently be covered over by the surrounding skin.

B.

Fractures

Not infrequently, patients suffer fractures at the time they receive their burn injury. Motor vehicle accidents, falls, and electrical injuries with hyperflexion from violent muscle contractions can all lead to fractures at various sites in the body. Burn patients presenting with early hypotension must be thoroughly examined for the source of the hemorrhage. This must include a search for fractures. When found, they must be treated as they would if the patient were not burned. Stabilization and fixation can be accomplished through the burn wound if required. After fixation, the overlying burns can be skin grafted around whatever device is used for fixation.


Burns to the Feet

C.

303

Involved Joints

Every effort must be made to maintain the integrity of the joints. Frequently, burns about the foot and ankle will result in exposure of the involved joints. Early flap coverage may maintain joint function, while grossly infected or involved joints may need debridement with fusion or partial amputation.

VII. A.

COMPLICATIONS Dystrophic Calcification

Dystrophic calcifications are uncommon and are thought to be due to prolonged immobilization, usually in patients with prolonged intensive care stays. These calcifications most commonly occur about the elbows and knee, but can occur at the ankles. They are characterized by painful movement of the joints. X-rays show calcifications along the tendons, which frequently improve with mobilization. Occasionally, surgical excision of the calcifications is required.

B.

Osteoporosis

Prolonged immobilization, especially with the elderly, predisposes patients to osteoporosis. It is therefore very important to initiate a treatment and rehabilitation program that encourages and facilitates early ambulation. Hydrotherapy to improve mobility and range of motion has been advocated as early as 5 days after grafting.

C.

Pigmentation

Abnormal pigmentation is a common occurrence following burn injuries. While skin grafts are often hyperpigmented, burn injuries that heal primarily may be hypo- or hyperpigmented. With partial-thickness burns in African Americans, some degree of pigment change is quite common. Patients need to be informed early of this potential outcome. After complete healing has occurred, cosmetics or tattooing can be considered to assist in a better pigment match with the surrounding unburned skin. It is important for patients to be cognizant that healing wounds are very sensitive to ultraviolet radiation. Following burn injuries and reconstruction, proper precautions should be implemented including use of sunscreen and adequate clothing.

D.

Marjolin’s Ulcers

Malignant transformation of chronic burn scars is well documented in the literature. Jean-Nicholas Marjolin first described malignant transformation in a chronic wound in 1828 [22]. The majority of documented malignant changes of chronic burn ulcers involve squamous cell carcinomas, although basal cell carcinoma, malignant melanoma, liposarcoma, and even fibrosarcoma have been reported in the literature. It is hypothesized that dermal and subdermal embryonic mesodermal cells are subject to chronic desmoplastic changes and accelerated cellular regeneration. Without one’s normal protective dermal barrier, these embryonic cells undergo unmonitored cellular regeneration, predisposing themselves to mutational malignant transformation. Other proposed etiologic factors of accelerated malignant transformation include chronic mechanical or solar irritation, release of local inflammatory toxins, and poor lymphatic regeneration within scars that slows the influx of stimulated antibodies in the diseased tissue. The average time for malignant transformation is reported to be approximately 35 years. An average of 30% of Marjolin’s ulcers metastasize. In order to provide an improved barrier and prevent malignant transformation, early application of skin grafts or flaps is advocated to cover chronic burn ulcerations. Treatment of Marjolin’s ulcers includes radical excision with lymph node dissection or even amputation of the affected extremity (Figure 11.17 to Figure 11.19). Patients need to be aware of the possibility of cancer developing in the healed burn scar and that if an ulcerated lesion occurs, they should seek medical care immediately.


304


Figure 11.17

Marjolin’s ulcer.

Figure 11.18

Marjolin’s ulcer.

Figure 11.19

Marjolin’s ulcer.


Burns to the Feet

VIII. A.

305

SPECIAL TYPES OF BURNS Electrical Burns

The initial assessment of electrical injury should follow the basic concepts of the Advanced Trauma Life Support and Advanced Burn Life Support protocols, with specific attention directed at securing an adequate airway and a thorough evaluation for more immediate life-threatening injuries. Once the patient has been properly evaluated, cardiac monitoring for dysrhythmias is warranted if baseline electrocardiogram demonstrates any irregularities. The pathophysiology of electrical burn injury has been studied extensively. Life-threatening problems, including cardiac or respiratory arrest, can be caused by the effect of alternating current on the cardiac and respiratory centers, respectively. The majority of electrical injury sequelae are caused by thrombosis or coagulation of small blood vessels, with less involvement of larger vessels. Small vessel disease is a significant factor in myonecrosis and subsequent myoglobinuria-induced renal failure. Peripheral nerve injury is common and can encompass paresthesias to complete paralysis. Serious electrical burns comprise approximately 3% of burn admissions. Because of their more superficial appearance, the extent of electrical burn injuries is often underestimated. Electricity preferentially follows the path of least resistance, with the majority of current traversing blood vessels and nerves followed by muscle, skin, tendons, fat, and bone. In general, the longer one is in contact with a current, the greater the extent of injury. For example, the tetanic muscle contractures induced by alternating current prevent victims from withdrawing from the electrical source, compounding the electrical injury. The greatest tissue injury often occurs at the site of electrical entry and exit. Electrical current can produce a variety of injuries. The initial electrical current can produce muscular depolarization with violent forceful contraction. Fractures can occur from these contractions of the skeletal muscle. Depolarization of cardiac muscle can lead to arrhythmias. Cellular membranes are breached by the electrical current, with release of intracellular contents into the circulation, leading to hyperkalemia. Additionally, hemoglobin is released from lysed red cells and myoglobin from muscle cells. Both of these large molecules are filtered by the kidneys and can plug the renal tubules, leading to renal failure. Electrical current can facilitate aggregation of platelets and thrombosis of small blood vessels. Small vessel thromboses can occur in the mesentery of the small bowel, leading to perforations of the bowel. Injury to the feet is a frequent occurrence in any workplace, particularly in those with highvoltage electrical injuries (Figure 11.20). The electrical current seeks the ground, which is commonly the feet. The injuries can range from small pin-sized exit wounds to massive blowout injuries with loss of significant portions of the foot. Because of the mechanism by which the current passes through the body, even small ‘‘insignificant’’ wounds might hide significant underlying injury to muscular or bony structures. Electrical current flows through the body as a function of the resistance of the various tissues. Resistance leads to heat production. Bone has the highest resistance and therefore produces the most heat. Not infrequently, due to the passage of the current and heat production, muscle around the bone will be totally destroyed without damage to the more superficial structures. Technetium-99m (Tc-99m) pyrophosphate (PYP) scanning can detect this necrotic muscle. The Achilles tendon is occasionally ruptured due to the forceful contraction of the gastrocnemius muscles. Portions or all of the calcaneus, because of its rather superficial location, may become necrotic with immediate or later sequale of bone sequestration. Nonviable muscle must be debrided early and, at times, early amputation of obvious neurovascularly deprived tissue may be required. Frequent and wide debridement is necessary before the dead muscle becomes colonized and the patient becomes septic from the added bacterial myonecrosis (Figure 11.21). Because of the hidden tissue injury, additional fluid needs to be included in the resuscitative efforts. If the urine appears pigmented (usually a port wine–colored appearance), fluid resuscitation should be increased to maintain urine output of 100 cc/h until the urine is clear. Mannitol is given to maximize urine flow in order to flush the hemoglobin and myoglobin molecules from the renal tubules. Additionally, sodium bicarbonate may be given to alkalinize the urine to make the myoglobin and hemoglobin more soluble and enhance its removal and minimize risks of renal injury.


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Figure 11.20

B.

Electrical injury.

Chemical Burns

The risk of chemical exposure exists everywhere since chemical solutions are ubiquitous in the home and in the workplace. Chemical injuries to the feet are not uncommon. These injuries are very challenging, whether the offending chemical is stepped in or spilled into the shoe. Delay in diagnosis is frequent. Early and copious washing of the injured skin is frequently not performed because the injured person may not immediately appreciate the extent of injury. A worker will frequently wait until the next day to go to the concerned health personnel during the next working shift. By the time the magnitude of the injury is appreciated and appropriate referral is made to the tertiary care center, the damage may have extended far beyond it original limits. Hot metals are another source of injuries to the feet. These are usually poured onto the leg or down the boot. Because of the high temperature of these molten metals, an immediate full-thickness burn occurs. The worker frequently does not appreciate the extent of the injury because it is a painless full-thickness injury. Patients may not present for days or weeks and then only because

Figure 11.21 Myonecrosis from electrical injury.


Burns to the Feet

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they have a sore, infected, ulcerated lesion. The opportunity to excise and graft these injuries early is lost. The final management of the injuries will require weeks to months to achieve definitive closure as opposed to days to weeks if the wound had been excised and grafted early. This higher cost of health care to both the employer and the general community is considerable. Chemical burns are categorized into acid, alkali, and organic compound exposure. Severity and depth of the chemical burn is a direct function of the area of skin exposed, concentration and volume of the chemical agent, and the duration of contact. Initial management of any chemical injury is copious irrigation with water until the injury can be evaluated at an appropriate facility. Neutralizing agents are discouraged because they may interact with the exposing agent and have the potential to produce an exothermic reaction, promoting additional heat and further tissue damage. Exposure to acidic and alkaline agents is a common occurrence in the workplace. Acids cause cellular injury through dehydration, coagulation necrosis, and protein precipitation, while alkali agents cause cellular injury and death through liquefaction necrosis, lipid saponification, and protein denaturation. Acid injuries are generally localized with limited tissue injury. Alkali injuries, on the other hand, penetrate deeply into the tissue planes, causing extensive tissue injury. Both acid and alkali injuries require immediate and extensive irrigation of the affected limb to dilute the chemical agent, impede further tissue injury, and minimize the need for tissue debridement and skin grafting. Hydrofluoric acid burns are an uncommon, but potentially deadly, injury. The use of this acid is critical in the metal and glass etching industry as a cleansing agent. After initial exposure to hydrofluoric acid, the patient may present with early, or even delayed, intense pain of the exposed area. This significant ‘‘pain out of proportion’’ to examination typifies this type of chemical injury. Hydrofluoric acid penetrates deeply into the soft tissue and even the bones, allowing the fluoride ion to bind available calcium, resulting in hypocalcemia, impaired cellular function, and resultant cell death. Severe pain is caused by cellular death–induced hyperkalemia that irritates nerve endings. Cardiac arrhythmias and even death have been attributed to electrolyte, most notably calcium, abnormalities. In general, treatment is aimed at minimizing further tissue destruction, which concomitantly provides pain relief. Additional pain relief using narcotics is generally not advocated because the pain serves as a marker for adequate therapy of the chemical injury. Topical, local, intravenous, and intra-arterial administrations of calcium gluconate have been used in the treatment of hydrofluoric acid burns. Intravenous and intra-arterial infusion of calcium gluconate appears to provide the best treatment for the hydrofluoric acid injury. Intravenous treatment requires a Bier block to delay the systemic absorption of the calcium. Intra-arterial infusion is easier to perform. Early excision of frankly necrotic tissue with or without grafting will occasionally be required.

IX.

PREVENTION

Burns of the feet, as with most burns in general, are preventable. Prevention is the ultimate goal of the American Burn Association and the tertiary burn centers. Injuries in the home can be prevented with relatively simple measures. Most work-related feet burns also are preventable through education and implementation of safety measures. Teaching employer health departments about on-thejob burn injuries is extremely important. In the U.S., the Occupational Safety and Health Administration (OSHA) has had a significant impact on increasing safety in the workplace.

X.

SUMMARY

Injuries to the feet are a significant health care problem. Patients must be approached in the same fashion as any other injury or trauma patient. Life- and limb-saving measures take first priority. Once these issues are dealt with, attention can be turned to the feet. Most feet burns should be evaluated by a tertiary burn care facility. Care of the burned feet must take place within the overall management of the injured patient. Fixation of fractures must take place promptly in conjunction with appropriate early excision or


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debridement with skin grafting. A number of new synthetic and biosynthetic materials are helpful and will frequently decrease wound care time and costs. Ultimately, coverage of full-thickness injuries requires autografting. The ultimate goal must be to return the patients to their prior state of health. Early and aggressive physical therapy is important. The major objective in the management of patients with burned feet is to return them to normal function with unimpeded ambulation and weight-bearing on pain-free feet. Prevention of burns is possible and safety measures in the home and workplace are of the utmost importance.

REFERENCES 1. Committee on Trauma, Resources for Optimal Care of the Injured Patient, The American College of Surgeons, Philadelphia, PA, 1999. 2. Janzekovic, Z., A new concept of the early excision and immediate grafting of burns, J. Trauma, 10, 1103– 1108, 1970. 3. Mardovin, W., Miller, S.F., Eppinger, M., and Finley, R.K., Micrografts: the ‘‘super’’ expansion grafts, J. Burn Care Rehab., 13, 556–559, 1991. 4. Nelson, C., Miller, S.F., Eppinger, M., and Finley, R.K., Micrograft II: evaluation of 25:1, 50:1, and 100:1 expansion skin grafts in the porcine model, J. Burn Care Rehab., 16, 31–35, 1995. 5. Herndon, D.N., Ed., Total Burn Care, W.B. Saunders, Philadelphia, PA, 1997, pp. 35–36. 6. Demling, R.H., DeSanti, L., and Orgill, D.P., The Burn Wound, Section II: Pathogenesis of Burn Injury (Initial and Delayed), Part B: Delayed Injury Online: www.burnsurgery.org 7. The ABLS Advisory Committee, Tetanus immunization, in Advanced Burn Life Support Instructor’s Manual, The American Burn Association, Chicago, 1994, pp. 103–106. 8. Wright, J.B., Lam, K., Hansen, D., and Burrell, R.E., Efficacy of topical silver against fungal burn wound pathogens, Am. J. Infect. Control, 27, 344–350, 1999. 9. Hull, B.E., Finley, R.K., and Miller, S.F., Coverage of full-thickness burns with bilayered skin equivalents: a preliminary clinical trial, Surgery, 107, 496–502, 1990. 10. Sheridan, R.L. and Shank, E.S., Hyperbaric oxygen treatment: a brief overview of a controversial topic, J. Trauma, 47, 426–435, 1999. 11. Hammarlund, C., Svedman, C., and Svedman, P., Hyperbaric oxygen treatment of healthy volunteers with UV-irradiated blister wounds, Burns, 17, 296–301, 1991. 12. Niezgoda, J.A., Cianci, P., Folden, B.W., Ortega, R.L., Slade, J.B., and Storrow, A.B., The effect of hyperbaric oxygen therapy on a burn wound model in human volunteers, Plast. Reconstr. Surg., 99, 1620– 1625, 1997. 13. Brannen, A.L., Still, J., Haynes, M., Orlet, H., Rosenblum, F., Law, E., and Thompson, W.O., A randomized prospective trial of hyperbaric oxygen in a referral burn center population, Am. Surg., 63, 205–208, 1997. 14. Waymack, J.P., Fidler, J., and Warden, G.D., Surgical correction of burn scar contractures of the foot in children, Burns, 14, 156–160, 1988. 15. Alison, W.E., Moore, M.L., Reilly, D.A., Phillips, L.G., McCauley, R.L., and Robson, M.C., Reconstruction of foot burn contractures in children, J. Burn Care Rehab., 14, 34–38, 1993. 16. Leung, P.C. and Cheng, J.C., Burn contractures of the foot, Foot Ankle, 6, 289–294, 1986. 17. Staley, M. and Serghiou, M., Casting guidelines, tips, and techniques: proceedings from the 1997 American Burn Association PT/OT Casting Workshop, J. Burn Care Rehab., 19, 254–260, 1998. 18. Rayatt, S.S., Grew, P., and Powell, B.W.E.M., A custom-made thermoplastic boot splint for the treatment of burns contractures of the feet in children, Burns, 26, 106–108, 2000. 19. Calhoun, J.H., Burke, E.E., and Herndon, D.N., Techniques for the management of burn contractures with the Ilizarov fixator, Clin. Orthopaed., 280, 117–124, 1992. 20. Erdogan, B., Go¨rgu¨, M., Girgin, O., Ako¨z, T., and Deren, O., Application of external fixators in major foot contractures, J. Foot Ankle Surg., 35, 218–221, 1996. 21. Linares, H.A., Larson, D.L., and Willis-Galstaun, B.A., Historical notes on the use of pressure in the treatment of hypertrophic scars or keloids, Burns, 19, 17–21, 1993. 22. Konigova, R. and Rychterova, V., Marjolin’s ulcer, Acta Chir. Plast., 42, 91–94, 2000.


12 Tendon Ruptures and Lacerations Lew C. Schon and Steven A. Herbst Department of Orthopaedic Surgery, The Union Memorial Hospital, Baltimore, Maryland

CONTENTS I. Introduction ................................................................................................................... 310 II. Anterior Tibial Tendon .................................................................................................. 310 A. Etiology of Rupture ................................................................................................ 311 B. Nonoperative Treatment......................................................................................... 311 C. Operative Treatment ............................................................................................... 313 III. EHL Tendon .................................................................................................................. 313 A. Etiology of Rupture ................................................................................................ 313 B. Nonoperative Treatment......................................................................................... 313 C. Operative Treatment ............................................................................................... 316 IV. EDL Tendon .................................................................................................................. 317 A. Ruptures of the EDL .............................................................................................. 317 V. Achilles Tendon.............................................................................................................. 317 A. Prerupture Conditions and Treatment .................................................................... 318 1. Nonoperative Treatment .................................................................................. 318 2. Operative Treatment......................................................................................... 319 B. Achilles Tendon Rupture ........................................................................................ 321 1. Conservative Treatment ................................................................................... 322 2. Comparison of Operative and Nonoperative Treatment .................................. 322 3. Operative Treatment......................................................................................... 323 4. Percutaneous Repair......................................................................................... 323 C. Chronic Rupture ..................................................................................................... 323 1. Operative Treatment......................................................................................... 325 VI. Peroneals ........................................................................................................................ 328 A. Anatomy ................................................................................................................. 328 B. Peroneal Tenosynovitis, Attritional Tears, and Rupture ........................................ 328 C. Peroneus Brevis Tears ............................................................................................. 329 D. Os Perineum and Peroneus Longus Tears............................................................... 329 E. Peroneus Brevis Subluxation or Dislocation........................................................... 331 F. Chronic Repairs ...................................................................................................... 333 VII. Flexor Digitorum Longus............................................................................................... 336 VIII. Flexor Hallucis Longus .................................................................................................. 336 A. Etiology................................................................................................................... 337 B. Nonoperative Treatment......................................................................................... 337

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C. Operative Treatment ............................................................................................... 337 Posterior Tibial Tendon.................................................................................................. 338 A. Etiology................................................................................................................... 338 B. Nonoperative Treatment......................................................................................... 339 C. Operative Treatment ............................................................................................... 339 D. Dislocation of the Posterior Tibial Tendon ............................................................ 340 X. Conclusion...................................................................................................................... 341 References .................................................................................................................................. 341 IX.

I.

INTRODUCTION

Tendon ruptures and lacerations are common conditions affecting the foot and ankle. Understanding the normal function of intact tendons is helpful in appreciating the deficits of impaired tendons. Acute injuries are often responsible for the patient’s deterioration, but it is important to realize that there may be underlying preexisting tendon degeneration or abnormal mechanics that predispose the patient to acute injury. These conditions must be taken into consideration when addressing the patient surgically. In this chapter we discuss the anterior tibial tendon (ATT), extensor hallucis longus (EHL) tendon, extensor digitorum longus (EDL) tendon, Achilles tendon, peroneal tendons, flexor digitorum longus (FDL) tendon, and flexor hallucis longus (FHL) tendon, including laceration, acute rupture, degenerative rupture, and subluxation or dislocation. We present a variety of surgical techniques including debridement, repairs, reconstructions, and tendon transfers for the most common conditions encountered.

II.

ANTERIOR TIBIAL TENDON

The major dorsiflexor of the ankle originates from the anterior proximal half of the upper two thirds of the lateral border of the tibia and the anterior interosseous membrane and passes in front of the ankle joint deep to the superior extensor retinaculum. It courses beneath both limbs of the inferior retinaculum to insert on the medial aspect of the first cuneiform and the first metatarsal. It receives its innervation from the deep peroneal nerve (L4 and L5). It is active in the heel-strike phase in an eccentric mode as it allows the ankle to slowly plantar flex until the foot is flat and is again active in the swing phase in a concentric mode as it keeps the ankle dorsiflexed and keeps the forefoot from dragging. The tendon receives its blood supply from a mesotenon and vincular system located on the posterior aspect [1]. Pathology involving the tendon can include traumatic rupture, spontaneous rupture, stenosing tenosynovitis, and laceration. In the case of rupture, clinical examination will show weakness with foot dorsiflexion and foot inversion with ankle dorsiflexed, pain, and possibly a palpable defect along the course of the tendon. Chronic ruptures can manifest with a fullness or a growing nodule typically located anterior to the ankle. Dorsiflexion can often be preserved even in the case of a complete tendon rupture as a result of recruitment of other dorsiflexors of the foot (EHL and EDL). In these cases, the foot dorsiflexes and everts, and there is a visible and palpable void anterior to the ankle (Figure 12.1). A good test for this condition is to examine the ability to dorsiflex the ankle with the toes flexed at the metatarsophalangeal (MTP) joint. Spontaneous ruptures are most commonly encountered 1.5 to 3 cm proximal to the insertion site, but they have also been reported at the musculotendinous junction. The majority of tibialis anterior ruptures are spontaneous. The second most common cause is acute laceration. Lacerations have been reported in hockey players as a result of cuts from the skate blade just above the padded leather tongue of the skate [2]. These injuries are frequently treated as simple skin lacerations, which result in neglected cases. The differential diagnosis of spontaneous rupture should include peroneal nerve palsy, neoplasm, and disc herniation. Patients with pathology of the ATT may be unable to recall a specific mechanism of injury or trauma. In the older population, the presentation is usually slowly progres-


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Figure 12.1 This photograph shows front and side views of a foot with an ATT rupture. There is a nodule above the ankle within the ATT. With attempted dorsiflexion, the foot goes into eversion and also dorsiflexes less than the other side.

sive, with foot drop and swelling and pain in the anterior ankle. Magnetic resonance imaging (MRI) can be helpful in diagnosing the extent and location of the rupture (Figure 12.2). Patients with stenosing tenosynovitis complain of pain and swelling, but their muscle strength is good. Peritendinitis can present with a painful rubbing or crackling sensation over the anterior ankle. This ‘‘peritendinitis crepitans’’ occurs as an overuse injury. The sensation of crepitus is caused by fibrin exudates within the ATT sheath and can be easily palpated as the patient actively flexes the ankle.

A.

Etiology of Rupture

Forst et al. [3] note four potential mechanisms of rupture: 1. Acute laceration has been reported with sharp penetrating trauma and with tibial shaft fracture [4] 2. Acute or chronic tears (aka ‘‘spontaneous rupture’’) have been linked to inflammatory arthritis [5], impingement from osteophyte [6], steroid injection [7], and diabetes [8] 3. Acute indirect laceration (i.e., blunt injury without penetration) 4. Inner trauma (unexpected sudden force on the dorsiflexed foot)

B.

Nonoperative Treatment

Foot deformity can occur after neglected rupture. Plattner and Mann [9] have reported a progressive flatfoot deformity in adults. Equinocavus has also been reported in children due to the unopposed action of the peroneus longus and Achilles tendons [10]. However, most patients remain supple and without significant deformity or contracture. Isolated reports of nonoperative treatment are noted throughout the literature. Forst et al. [3] reviewed the literature in 1995 and noted six cases treated nonoperatively. All patients had either


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Figure 12.2 (A) Sagittal MRI demonstrating thickening and rupture of the ATT. (B) A coronal view demonstrates a rounded thickened fibrotic ATT.

good results (one) or mild residuals (five). One of largest series of ATT ruptures in the literature compares outcomes in an operative and in a nonoperative group [11]. No difference was noted between the American Orthopaedic Foot and Ankle Society (AOFAS) scores and an outcomebased foot and ankle score. However, the nonoperative treatment group was likely to be less active in general. Interestingly, these investigators noted an increased incidence of toe deformities in the nonoperative group (from recruitment of the long toe extensors), but scoring did not reveal any functional differences. The authors concluded that, although no statistical difference emerged between the groups, the younger and more active population would not likely fare as well as the older population if treated nonoperatively.



C.

313

Operative Treatment

Ouzounian and Anderson [5] state in their report on 12 ATT ruptures that the primary indication for surgery is functional and not pain related. They note that the pain involved with tendon rupture abates rather quickly after the injury. Acute injuries whether by laceration or by plantar flexion– eversion against a resistance should be treated early in young, active patients. Consideration for nonoperative treatment should be given for those with significant comorbidities. The authors prefer operative treatment in all acute cases and in most subacute cases. Direct primary repair is the recommended treatment for cases in which the tendon ends can be reapproximated. Biomechanical studies have shown the modified Krackow suture to be stronger than the Kessler–Tajima suture [12]. In the case of chronic rupture, the tendon ends cannot be reapproximated. Possibilities for reconstruction are sliding tendon graft, tendon transfer, tendon autograft interposition, tendon allograft interposition, or some combination of these. The authors prefer a sliding or turndown graft combined with EHL transfer in the chronic setting. The sliding or turndown graft can cover distances of up to 4 cm. The graft can be slid proximally or distally, depending on the location of the laceration. The authors usually augment this with an EHL transfer. The distal stump of the EHL is tenodesed to the extensor hallucis brevis (EHB). The proximal stump is woven through the reconstruction and placed into a drill hole in the medial cuneiform. The EDL slips to the second and third toes can also be considered as a transfer possibility. This procedure is accompanied by tenodesis of the distal EDL stump to the intact extensor digitorum brevis (EDB) tendon. Occasionally, substance loss from injury or infection can leave too large a gap to be covered by a sliding graft alone. In these cases, the authors recommend tendon autograft in which one-half or the entire peroneus brevis tendon is harvested, followed by proximal and distal tenodesis to the peroneus longus tendon and EHL transfer [3]. A tendon allograft using semitendinosis is also an excellent alternative (Figure 12.3).

III.

EHL TENDON

The EHL tendon lies between the ATT and the EDL at the level of the ankle joint. The EHL crosses dorsally over the anterior bundle just distal to the ankle joint. The EHL originates from the middle half of the extensor surface of the fibula and the adjacent interosseous membrane. It courses under the superior and inferior extensor retinaculum to an insertion at the base of the dorsal surface of the distal phalanx. The nerve supply is L5-S1 proximally, and the muscle belly is served by the deep peroneal nerve distally. The EHL receives its motor supply much further distally than the ATT and the EDL. The motor branch to the EHL travels close to the fibula for about 10 cm before entering the muscle belly [13].

A.

Etiology of Rupture

The EHL can be sharply lacerated anywhere along its course. Attritional rupture follows an etiology similar to that described for the ATT [14]. This usually occurs at or around the level of the ankle joint [15]. Some of the earlier foot tendon literature suggests that EHL injuries need no treatment. Griffiths [16] reports on six lacerations of the EHL: Five patients underwent primary repair, and one underwent conservative treatment. He concluded that formal repair is unnecessary. Although the patient with nonoperative treatment did well, it is difficult to draw any conclusions from a single case.

B.


Nonoperative treatment has its place if injury occurs at or distal to the level of the hallux MTP joint, when the extensor expansion prevents proximal migration of the proximal stump. Splinting the hallux in extension should allow for healing with the tendon ends in good apposition. Noonan et al. [17] presented three pediatric traumatic physeal injuries distal to the MTP joint with good conservative results.


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Figure 12.3 Surgical sequence for allograft reconstruction. (A) An incision is made over the ATT above the ankle. (B) Visualization of the ruptured tendon. (C) Allograft semitendinosis is woven through the ATT proximal to the rupture (black arrows).



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Figure 12.3 Continued (D) Bone tunnels are created in the medial cuneiform, one dorsally and one medially for the allograft (black arrow). There are wires in these tunnels (open arrows). (E) The ends of the allograft tendon are secured into the bony tunnels with soft tissue interference screws. (F) The final appearance of the reconstruction.


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Operative Treatment

Operative consideration should be given for all acute lacerations or ruptures and for symptomatic patients presenting in the chronic phase (Figure 12.4). Operative treatment involves a longitudinal incision along the course of the tendon. In the case of laceration, thorough inspection of surrounding structures including the anterior neurovascular bundle and the tibialis anterior tendon should be undertaken. Other tendon injuries and injury to the bundle itself are common after these lacerations. Outcome is dependent on the surrounding structures injured and the zone of injury [18]. Care should be taken to identify and protect the anterior tibial artery and the deep peroneal nerve. The tendon ends can usually be identified through the laceration, but occasionally the incision will have to be extended longitudinally. Painful scars are common after repair and can be minimized by meticulous soft tissue technique [19]. Direct repair should be undertaken in all cases possible. In chronic cases or in acute cases with substance loss, tendon grafting or transfer should be considered. The authors assess the amount of tendon loss by placing moderate tension on the tendon ends and placing the ankle and hallux in neutral position. If we are not able to oppose the tendon ends without excessive tension, we prefer a tendon slide for defects up to 4 to 5 cm and a tendon transfer for anything greater than 5 cm. The most common reported transfer is the peroneus tertius [20]. Also reported is the use of a split of the extensor to the second toe for use in lacerations distal to the ankle joint [21].

Figure 12.4 MRI showing laceration of the ATT, EHL, and EDL. The normal foot is on the left; the injured foot is on the right.



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Postoperative care consists of a cast with a limit to MTP flexion but with a cutout over the dorsum of the hallux to prevent opposed accidental dorsiflexion against resistance and to allow for early passive extension exercises to promote tendon glide.

IV.

EDL TENDON

The EDL tendon lies lateral to the ATT and the EHL tendon and medial to the peroneus tertius at the level of the ankle. It originates from the crest of the fibula, the interosseous membrane, and the lateral condyle of the tibia. It inserts on the dorsal aspect of the terminal phalanx of each of the four lesser toes. It divides from one common tendon to two at the level of the superior retinaculum and from two tendons to four at or distal to the level of the inferior retinaculum. The motor supply is the deep peroneal nerve, and the segmental innervation is L5-S1. The motor branch to the Achilles tendon (TA) and the EDL is more proximal than that of the EHL. The function of the EDL is to extend the MTP joint. The tendon is anchored to the dorsum of the MTP joint by the dorsal hood.

A.

Ruptures of the EDL

Attritional ruptures of the EDL are rare. Physical examination reveals a lack of active extension of the MTP joint past the neutral position. EDB substitution can make the diagnosis confusing at times. Lacerations can be approached in much the same way as EHL lacerations. Patients with extensor tendon lacerations will experience frustration putting on socks or sliding into shoes because the toe tends to curl passively underneath the foot. This also has some functional applications in activities of daily living. Wicks et al. [19] reported four pediatric cases repaired with good results. Floyd et al [22] reported seven patients with operative repair and good results. One patient without repair developed symptomatic claw toes. Griffiths [16] reported three primary repairs and one patient treated nonoperatively, who did well. Bell and Schon [23] recommend repair with 2-0 or 3-0 nonabsorbable suture and immobilization in neutral for 3 to 4 weeks and then a program of controlled passive motion followed by active motion, and finally strengthening.

V.

ACHILLES TENDON

The Achilles tendon is the strongest tendon in the human body. The gastrocnemius originates posteriorly from the medial and lateral femoral condyles. The soleus origin is the fibular head and proximal third of the shaft, the proximal tibia, and the interosseous membrane. The gastrocnemius fibers form a midline raphe and then coalesce distally into an aponeurosis. This aponeurosis joins with that of the soleus to form the Achilles tendon. The healthy tendon is composed entirely of type I collagen. The fibers rotate 908 as they descend from medial to posterolateral and from lateral to posteromedial. Anatomically this means that most of the fibers of the gastrocnemius insert laterally, and most of the soleus fibers insert medially. The Achilles tendon is enclosed by a paratenon that is not lined with synovial tissue. The paratenon allows for approximately 1.5 cm of tendon glide. The gastroc–soleus lies in the superficial posterior compartment of the leg and is supplied by the tibial nerve. Spinal cord innervation is predominantly S1. The blood supply is considered to be poor, especially in the tendon midsubstance. The tendon is encased in a paratenon, but no true synovial sheath exists. The distal 2 cm of the tendon is supplied in a retrograde fashion from the calcaneus. Proximally, the tendon receives blood supply from the musculotendinous junction. The midsubstance paratenon is supplied from a scant mesotenon, which lies ventrally [24]. Interestingly, recent studies with laser Doppler flowmetry have failed to show diminished flow in this area [25]. It is in this proposed relative zone of hypovascularity (2 to 6 cm proximal to the insertion) where most ruptures occur [26]. This is the same zone where the maximal twist of the fibers occurs. A ‘‘wringing out’’ effect has been described where the blood supply is diminished by excessive pronation in midstance [27].


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A.

Prerupture Conditions and Treatment

Spontaneous disruption of the Achilles tendon is associated with other disorders, including autoimmune disease, infectious disease, fluoroquinolone usage, previous corticosteroid use, collagen abnormalities, and neurological abnormalities. Biomechanical causes are pronation, cavovarus, and weakness and stiffness of the gastroc–soleus complex. The incidence of rupture increases with age. Diminished vascularity is thought to be associated with that observation [28]. The classification of Achilles tendon disorders has been described by many authors. This chapter is limited to the discussion of traumatic tendon injury. Traumatic tendon injury occurs most often in asymptomatic tendinosis or peritendinitis with tendinosis (Table 12.1). Less often it occurs in a healthy tendon. Tendon degeneration is thought to precede rupture in the vast majority of cases. Collagen degeneration noted by histopathological analysis at the time of acute repair has been shown in the vast majority (> 90%) of specimens of multiple studies [29,30]. However, studies have also shown that the vast majority of spontaneous ruptures are not symptomatic at the time of rupture. Kannus and Jozsa [31] reported one third of patients presenting with tendon rupture to have reported symptoms previously. Even lower numbers (< 5%) were reported by Mafulli [32]. This means that asymptomatic tendon degeneration is likely a predisposing factor to rupture. Degeneration seems to be a component of aging; Kannus and Jozsa [31] showed tendon degeneration in one third of healthy age- and sex-matched cadaver controls. They also noted the incidence of tendon degeneration to increase with age. During the physical examination it is important to determine the point of maximum tenderness. Soft tissue swelling and warmth are often observed. Nodularity and swelling of the tendon are noted (Figure 12.5). Strength is usually measured by the ability to do a single-stance heel raise. Any palpable gaps should be examined as well. If swelling is noted, the anatomic location can be determined by assessing whether the area of swelling is mobile or stationary with respect to the excursion of the tendon. If the swelling moves with the tendon, it is likely intratendinous; if it is stationary with tendon excursion, it is likely located outside of the tendon (i.e., in the paratenon) [33]. Treatment of peritendonitis with tendinosis and treatment of tendinosis is important in that it might prevent acute rupture or chronic microtearing of the tendon. Usually, these conditions can be treated nonoperatively. 1.


Initial treatment should include a range-of-motion (ROM) walker boot with a dorsiflexion stop at 108 of plantar flexion or a cast in 10 to 158 of equinus. Corrective orthotics or heel wedges should be used for the variants caused by hyperpronation or cavus conditions. Nonsteroidal anti-inflammatories and physical therapy for modalities only (ultrasound, iontophoresis, phonophoresis) may have some benefit in the early stages of treatment. Once the initial symptoms have subsided, a rehabilitation phase can be entered [34]. The patient should be weaned into a shoe with a 1/4- to 3/8in. heel lift. Physical therapy for stretching and gentle strengthening can be started at this point. Table 12.1 Type and Description of Traumatic Tendon injury Type

Description

I

SPR is still attached to periosteum on posterior aspect of fibula; however, periosteum is elevated from underlying malleolus by dissecting tendons that are displaced anteriorly. SPR is torn free from its anterior insertion on malleolus, and periosteum of tendons dissects through at this level. SPR is avulsed from insertion on malleolus with avulsion of small fragment of bone. SPR is torn from its posterior attachment as tendon dissects through, with SPR lying deep to dislocating peroneal tendon.

II III IV

Source: From Mann, R.A., Surgery of the Foot and Ankle, chap. 18, Table 18.2. With permission.



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Figure 12.5 A fullness of the Achilles tendon is noted at the site of intrasubstance rupture. Palpable and sometimes audible crepitus is occasionally noted. Decreased dorsiflexion is often present.

Should these measures fail, some advocate brisement of the tendon. This process involves the rapid injection of 5 to 10 cc of 1% lidocaine into the pseudosheath. This effectively breaks the adhesion between the mesotendon and the tendon itself. Should these measures fail, operative treatment is likely to be necessary. 2.

Operative Treatment

If one is considering operative treatment, we generally recommend MRI imaging of the tendon. MRI will help to determine the exact areas of tendon degeneration and should help prepare the surgeon and the patient if more extensive reconstructions can be anticipated. Operative options for the treatment of isolated paratendinitis are reported [35–37]. Most authors advocate debridement of constrictive areas of the pseudosheath. Schepsis and Leach [37] emphasized that the anterior soft tissue envelope of the tendon should remain intact. They reported more than 90% good and excellent results in a group that included patients with tendinosis in addition to paratendinitis. They performed excision of the pseudosheath and inspection of the tendon. Kvist and Kvist [35] report similar (96.5% good and excellent) results with incision of the crural fascia and debridement of thickened portions of the sheath. When the tendon is involved (paratendinitis with tendinosis), appropriate debridement is indicated. Most authors recommend a central tendon-splitting approach with debridement of the degenerative tissue. Interestingly, histopathology shows little signs of inflammation in these areas. Changes are limited to hypoxic degenerative tendonopathy, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, either alone or in combination [31]. Grossly, the tissues show a fusiform thickening, yellowish discoloration, and central areas of mucoid or granulomatous material. Rarely, sarcomas can mask themselves as tendinopathy. The lack of inflammatory


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changes is likely related to the relative avascularity in these zones. If excessive debridement of the tendon is needed, tendon augmentation with V-Y advancement, fascial turndown, or tendon transfer is required. It is difficult to extrapolate from the literature at what level of cross-sectional resection these procedures are required, but we generally consider augmentation when greater than one third of the cross-sectional area has been debrided. There are several considerations that one should take into account when assessing the type of reconstructive procedure for tendon gap and tendon cross-sectional loss. We believe two important patient considerations are: (1) type of substrate tissue, i.e., does the patient have other comorbidities that would render the reconstruction less able to deal with stress, such as chronic steroid use, diabetes, inflammatory arthopathy, advanced age, and (2) the patient’s physiological age, demands, and expectations. For cross-sectional loss greater than 30% and a gap of less than 2.5 cm, the authors recommend a V-Y advancement (Figure 12.6). For gaps greater than 2.5 cm, the authors generally use a

Figure 12.6 (A) After the fibrotic torn tendon is debrided, a 2-cm gap remains. (B) V is created proximally at the musculotendinous junction, which is at roughly the junction of the middle and lower third of the leg.



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Figure 12.6 Continued (C) The contralateral side is prepped so that proper tension can be reestablished by side-to-side comparison. Note the distal gap has been closed with the whip suture, and the proximal VY portion is not yet sutured.

gastrocnemius fascial turndown flap. In cases where the fascial turndown is unusually thin and the patient has extremely high demands or comorbidities that might compromise the remaining tissue, we use an FHL tendon transfer. These transfers are discussed in the treatment of chronic Achilles tendon ruptures.

B.

Achilles Tendon Rupture

The occurrence or possibly the reporting of Achilles ruptures is increasing with time. Leppilahti et al. [38] estimated that the incidence of ruptures of the Achilles tendon was approximately 18 per 100,000. The typical patient is the so-called ‘‘weekend warrior,’’ usually male in the fourth or fifth decade of life. The history is classically described as a sharp stabbing pain as though the patient had just been hit in the back of the heel. The chief complaint is generally described as calf pain with an inability to push-off. Most orthopedic surgeons can generally make the diagnosis without difficulty. However, the diagnosis is often missed in the emergency and primary care setting. Up to 20% of ruptures presenting in one series were missed initially. A palpable gap may be felt. The Thompson test is often used to test for continuity of the tendon (Figure 12.7). With the patient in the prone position, the fleshy portion of the calf is squeezed. With an intact tendon this results in plantar flexion of the ankle. The result should always be compared with the contralateral side. The resting position of the ankle with the knees flexed to 908 and the patient prone can also be helpful in determining Achilles tendon rupture. An intact leg will generally be in slight plantar flexion, whereas the leg rests in neutral or slight dorsiflexion with a rupture. Radiographs are occasionally helpful. They should be obtained for all ruptures at or near the insertion and in cases where symptoms preceded rupture. They are helpful in noting avulsion


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Figure 12.7 Squeezing the calf with no plantar flexion of the ankle. Also note the visible defect in the tendon posteriorly (arrow).

fractures of the calcaneus and areas of previous calcific tendonitis that require further debridement. Ultrasound and MRI can be helpful, but are rarely used in the acute situation unless conservative treatment is being considered. In these cases, ultrasound can help assess tendon end apposition. The three possible treatments or acute Achilles tendon rupture are closed, percutaneous, and open treatment. The surgeon and the patient must discuss the risks and benefits of each treatment to arrive at a decision. The literature suggests a higher rate of rerupture and slightly lower functional results with conservative treatment. However, some reports find nonoperative treatment to be equal to operative treatment from a functional standpoint. Results of operative treatment should be qualified by noting that this form of treatment is associated with potential wound problems. The financial, physiological, and psychological costs of a single wound dehiscence in a patient with other comorbidities is difficult to assign a score or value. 1.

Conservative Treatment

Nonoperative treatment was formerly the mainstay of acute treatment of Achilles injury. Most authors support operative repair in active individuals, but the surgeon should also be skilled in nonoperative treatment. One weakness with most of the randomized studies on this subject is the lack of a standardized postoperative protocol. Most randomized studies relegate nonoperative treatment to cast immobilization and operative treatment to functional rehabilitation. Immobilization has been shown to be detrimental to tendon healing [39]. Functional bracing has also been shown to have good results in nonoperative treatment [40]. An ideal study would have the same carefully controlled progressive functional bracing protocol for each group. Reported rerupture rates vary greatly after nonoperative treatment; ranges are from 13% [41] to as high as 35% [42]. The ideal candidate is an older individual with lower demands. If nonoperative treatment is chosen, the authors recommend a below-knee cast or fixed-hinged brace in 308 of plantar flexion, which is changed to 158 at 6 weeks and to neutral at 8 weeks. After 12 weeks, the cast or brace can be removed and progressive activities can be performed. The patient should avoid running and quick ascent or descent of stairs until the fourth month after injury. When the brace is used, patients are allowed to do gentle ROM beginning at 6 weeks. 2.

Comparison of Operative and Nonoperative Treatment

Numerous studies have compared methods of treatment. Studies by Nistor [43] and Carden et al. [44] support nonoperative management. They note minimally increased rerupture rates and the avoidance of significant postoperative complications. A functional bracing study by Thermann et al. [45] has shown similar results. A meta-analysis reviewed multiple previous studies according to rigid inclusion criteria and reported rerupture rates of 2.8 and 11.7% in operatively and nonoperatively treated patients, respectively [46].



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Conversely, Cetti and Christsen [47] (despite finding no significant difference between operative and nonoperative groups) recommend operative treatment based on a review of more than 4000 ruptures in the current literature. It is often quoted that operative patients achieve better strength than nonoperative patients. Several studies and reviews have examined this hypothesis. In a review of strength-tested outcomes, Wills et al. [48] found that operative patients tended to have better strength than nonoperative patients. He also showed a 20% complication rate in patients treated operatively. Nistor [43] found strength results equal in each extremity after both operative and nonoperative results. This study has been criticized because it lacks a more rigid functional evaluation. Haggmark and Eriksson [49] believes that strength is best assessed by evaluating muscle fatigue or work capacity rather than strength assessment over brief intervals as it was done in Nistor’s study. 3.

Operative Treatment

Acute ruptures generally occur in the region 2 to 6 cm above the insertion. Lacerations can occur anywhere along the length of the tendon. Acute ruptures can generally be repaired with nonabsorbable suture. Various techniques including end-to-end repair, Krackow, Bunnell, and Kessler style suture techniques have been advocated. The incisions recommended for repair are varied as well. Various authors have proposed central, medial, and lateral incisions. A medial incision avoids the sural nerve. All authors recommend avoidance of any subcutaneous dissection. The paratenon should be repaired as well. It is extremely important to pay close attention to tensioning of the repair. For this reason the authors recommend prone positioning of both the lower extremities. At the time of tensioning the authors flex both knees and then tie the sutures of the repair to equal the ankle position of the intact opposite extremity. 4.

Percutaneous Repair

Percutaneous repair had the initial hope of restoring appropriate musculotendinous length with minimal wound complications. However, early techniques had unacceptable rates of sural nerve entrapment [50,51] and rerupture [52,53]. However, recently, a promising new technique has been introduced through a mini-open repair. An instrument is inserted into the peritenon from a small open incision. Sutures are placed through this instrument and then pulled through the skin so that they rest entirely within the peritenon. They are then tied through the mini-open incision. Initial results from a functional and wound and nerve complication standpoint are encouraging [54]. Artificial tendon implants have been recommended in the past with materials such as carbon fiber [55], Marlex mesh [56], and a collagen tendon prosthesis [57]. The authors have no experience with these materials and see very little use for them given the success rate of acute repair and the other biological substrates that are available. Complications of operative repair are often cited as one of the prime reasons for considering nonoperative or percutaneous treatment. The poorly vascularized tissue in the posterior calf is prone to breakdown, with rates as high as 13% [29]. The authors recommend that repair generally take place as close to the time of injury as possible. Previous results have not supported this conclusion [58], and some think that some hematoma consolidation and early heeling of the tendon ends actually makes repair easier in a semi-delayed fashion. Postoperative care is extremely important. Both casting and functional bracing have been used successfully. In patients with questionable compliance, the authors initially use a splint in resting equinus followed by serial casting from plantar flexion to neutral over a 4-week period with weightbearing. In compliant, motivated patients the authors place them into a hinged boot locked in 15 degrees of plantar flexion and have them progressively bring the foot to neutral over a 4-week period. They are allowed passive plantar flexion and active dorsiflexion to whatever the boot setting is.

C.

Chronic Rupture

Delayed, missed, chronic, reruptured, and chronically painful cases of tendinosis have similar surgical treatment options. With a chronic rupture and loss of tendon continuity, patients often


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Figure 12.8 Photographs of a chronic rupture and excessive dorsiflexion and weakness of plantar flexion. A loss of the resting position of the ankle is noted with the patient lying in the prone position and the knees flexed.

complain of easy calf fatigue, prior history of injury, weakness of push-off (difficulty with walking, running, climbing stairs), sensation of falling forward, and balance difficulty. Swelling of the posterior ankle, calf, or leg may be present. With chronic intrasubstance rupture without loss of continuity, the patients complain of pain, swelling, decreased endurance, but not necessarily the extent of weakness seen in patients with loss of continuity. Physical examination in patients with chronic rupture and loss of continuity often shows increased passive dorsiflexion, calf swelling, thickening of the tendon, and weakness (Figure 12.8). A loss of the resting position of the ankle is noted with the patient lying in the prone position and the knees flexed. Sometimes tendon substitution is seen with recruitment of the FHL and FDL to assist in plantar flexion strength (Figure 12.9). In patients with chronic rupture without loss of continuity, there is tenderness, swelling, and warmth of the tendon at the rupture site. Loss of resting position and tendon substitution is generally not seen. Chronic rupture in continuity typically occurs at the insertion (Figure 12.10) or at the area about 2 cm above the calcaneus.

Figure 12.9 Photograph of patient with chronic tendon rupture using the FHL and FDL to achieve plantar flexion at the ankle.



Figure 12.10

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Sagittal MRI of the hindfoot showing a degenerative Achilles tendon insertion.

Diagnostic studies can be helpful. MRI is usually the most helpful. Bracing should be offered to those who want to avoid surgery. Usually, a solid ankle-foot orthosis (AFO) or an articulated AFO with plantar flexion assist is most helpful. 1.

Operative Treatment

Once a decision has been made to proceed with surgery one must decide on what type of reconstruction should be done. The protocol depends on whether there is loss of continuity. Insertional tendinosis or chronic degeneration higher up in the tendon without loss of continuity can be addressed with debridement of the tendon and repair of the tendon or calcaneus. When greater than 80% of the width of the tendon or more than 2 cm of the length is involved, the debridement will compromise the tendon integrity, necessitating a grafting procedure. An FHL transfer, Achilles turndown, or V-Y advancement can be useful in these conditions (see below). If there is loss of tendon continuity, there are many options available. Autologous grafting options include plantaris tendon, fascia lata, Achilles turndown, and V-Y advancement. Synthetic options include Marlex mesh, Dacron vascular graft, collagen tendon prosthesis, polyglycol threads, polymer, and carbon fiber. Autologous tendon enhancements include peroneus brevis [59,60], FHL [61–63], and FDL [64]. The authors prefer a combination of the above options, opting for fascial turndown and FHL transfer (Figure 12.11). After induction of anesthesia, the patient is placed in the prone position. A medial incision is made down to the anteromedial border of the Achilles tendon. Once the tendon is exposed, chronic tendon or fibrous tissue is excised; this typically leaves a substantial gap. The FHL tendon is identified deep to the fascia that divides the deep posterior compartment from the superficial compartment. The FHL muscle is identified by dorsiflexing the great toe and palpating and visualizing the movement. The tibial nerve, which lies just medial to the FHL tendon, must be avoided, the FHL muscle belly can extend to the level of the posterior talus, making it difficult to identify. The FHL tendon is cut at the level of the talus. If a longer FHL tendon graft is needed, the authors will approach it through the plantar aspect of the arch through an oblique incision. Although most authors advocate approaching the FHL through the medial side of the foot, the authors find it more direct to pick up the FHL through the arch of the foot. This approach also avoids the venous leash that is encountered from the medial approach.


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Figure 12.11 A 30-year-old male sustained a closed rupture to his Achilles tendon. He underwent immediate surgical repair with good initial apposition. The patient had three subsequent episodes where he misstepped and eventually completely ruptured his repair. (A) Sagittal MRI demonstrates a 5- to 6-cm zone of tendon rupture. (B) Coronal view demonstrating the torn thickened degenerative tendon. (C) Intraoperative photograph demonstrates the large gap after widely debriding the nonviable tendon. (D) FHL tendon is harvested at the ankle level. (E) The gap here measures 6 cm. (F) The graft length must account for the overlap of 1.5 cm proximally and 1 cm distally.



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Figure 12.11 Continued (G) The tendon will be delivered anteriorly by the hemostat. (H) Intermediate step as tendon is passed. (I) The passing is completed. (J) Final repair with central defect closed proximally and FHL tendon and Achilles tendon graft attached distally.

A plantar oblique incision is made in the arch of the foot along the skin line at the point at the master knot of Henry, where the FHL crosses superficial to the FDL. After the subcutaneous tissues, the plantar fascia is encountered and divided. Deep to the plantar fascia, the medial plantar nerve is identified. The FDL and FHL are found by palpating in the depths of the wound and moving the toes. The surgeon should look for crossover tendon branches, typically from the FHL into the FDL. There usually is a tendon branch that goes to the second toe. Anastomosis for tenodesis of the FDL to the FHL is performed using #1 Ethibond suture. Next, a suture is placed 1 cm proximal to the tenodesis site, and the FHL is transected distal to the suture. In the defect at the posterior ankle, the deep fascia is divided, exposing the FHL muscle belly and tendon. The tibial nerve that is posterior and slightly medial to the FHL is avoided. The FHL is delivered into the ankle wound. If the tendon does not pass, it is usually because of the crossover fibers to the second toe. The FDL tendon in the arch of the foot is observed while pulling on the FHL at the ankle to find these fibers. This portion is then transected. If it still cannot be passed (< 5% of the time), the entire course of the FHL is dissected. The proximal portion of the Achilles tendon is then mobilized by putting the tendon under traction (approximately 20 lb). The foot is held in neutral position; the gap is measured between the tendon ends to determine length of turndown. For a 6-cm gap, the proximal portion of the graft is 12 cm from the proximal end of the defect. This number is determined by sum of the following numbers: size of the gap plus the amount of overlap at the turndown site plus the amount that will overlap between the tendon graft and the distal portion of the remaining tendon. The overlap at the turndown site is usually 1 to 2 cm (Figure 12.11). At 2 cm proximal to the defect, two #1 Ethibond


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sutures anchor the corner of the turndown graft, reinforcing the high-stress junction so there is no propagation of the split between the strip and the main body of the tendon. The tendon is then passed anteriorly deep to the tendon instead of posteriorly. There is less bulk created with this method. To secure the FHL tendon distally, a 1-cm incision is made and a drill hole is created from the medial aspect of the calcaneus (halfway between dorsal and plantar cortices) through the lateral side of the calcaneus. The tendon is passed through the hole and secured to itself proximally or to surrounding periosteal tissues. Alternatively, the distal tendon can be secured to the remaining viable Achilles tendon. Tensioning the graft requires checking the ROM and the ‘‘springiness’’ of the operative side vs. the normal side. Usually, the foot should have a 15˜8 plantar flexion resting position. The graft and the turndown are held in place either by hand or by suture. Once position is established, whipstitches are used for final anastomosis. Resting tension and ‘‘springiness’’ at the end of the procedure are again checked. Postoperative care is similar to care in the treatment of acute Achilles tendon ruptures, with an initial splinting and non-weight-bearing period followed by a gradual increase in dorsiflexion. The foot is held in 208 of plantar flexion in a posterior splint. At 2 weeks, if the wound is healing well, the foot is placed in a boot brace in 208 of plantar flexion, weight-bearing in the plantar-flexed position is allowed, and ROM only to neutral is begun. At 6 weeks, the brace is adjusted to neutral, full weight-bearing is continued and ROM increased. The brace is discontinued at 12 weeks, as tolerated. Full recovery may take 6 months.

VI. A.

PERONEALS Anatomy

The peroneus longus and brevis tendons lie in the lateral compartment of the leg. They are innervated by the superficial peroneal nerve proximally. The brevis lies medial and posterior to the longus muscle, against a groove in the lateral malleolus. The tendon runs beneath the inferior tip of the malleolus and beneath the peroneal tubercle on the lateral wall of the calcaneus and inserts onto the base of the fifth metatarsal. The longus becomes tendinous slightly distal to the point where the brevis is tendinous. It takes three separate turns before inserting onto the lateral tubercle of the first metatarsal. Slips of this tendon run to the medial cuneiform and the second metatarsal. The first turn is around the lateral malleolus, the second around the trochlear process of the calcaneus, the third around the cuboid, and then obliquely travels across the plantar aspect of the foot toward its insertion. The tenosynovial sheath starts 3 to 5 cm proximal to the lateral malleolus. It extends as a single sheath to the level of the peroneal tubercle and then splits into two separate sheaths. The sheath is stabilized by the fibula anteriorly, the superior peroneal retinaculum (SPR) posterolaterally, and by the posterior talofibular ligament, the posterior inferior tibia–fibula ligament, and the calcaneal– fibular ligament medially. There is always an osseous or cartilaginous sesamoidal structure within the substance of the longus tendon [65]. It is ossified in about 20% of individuals. If present, it may have attachments to the fifth metatarsal, cuboid, peroneus brevis, and plantar fascia. The groove for the peroneals is well described. Edwards [66] described the anatomic variation of the groove in detail. He noted it to be concave in 82% of cases, flat in 11%, and convex in 7%. Additional stability comes from an osteocartilaginous rim, which adds an additional 2 to 4 mm of depth to the sulcus. Sequential sectioning studies have shown the SPR to be the primary soft tissue restraint to peroneal dislocation [67]. The retinaculum attaches to the periosteum of the fibula rather than to the cartilaginous rim. Five distinct variants of the retinaculum have been described [68]. The inferior peroneal retinaculum forms two fibrous tunnels over the peroneal tubercle and holds the tendons against the lateral wall of the calcaneus.

B.

Peroneal Tenosynovitis, Attritional Tears, and Rupture

The peroneus longus and brevis can be affected by tenosynovitis. Multiple etiologies have been described, including blunt trauma, inflammatory conditions, mechanical trauma from a stenotic retinaculum, and strain or sprain. The os peroneum plays a role in peroneus longus pathology as



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well, and there is undoubtedly some overlap between tendinosis with peritendinitis and the painful os syndrome. The diagnosis of peroneal paratendinitis is relatively easy to make. The symptoms include lateral ankle pain with activity, especially active eversion. Physical examination shows swelling and tenderness over the peroneals and pain with resisted eversion and the extremes of passive inversion. Radiographs are helpful in excluding potential etiologies such as an exostosis, osteochondroma, hypertrophic peroneal tubercle, or an acute fracture of the os peroneum. Differentiating peroneal longus and brevis tenosynovitis is helpful. Usually the brevis is affected at the level of the lateral malleolus or near its insertion into the base of the fifth metatarsal. The most common locations for irritation of the longus are at the level of the peroneal tubercle and the inferior retinaculum [69] and at the level of the cuboid tunnel [70]. The presence of an os peroneum predisposes to stenosis at the latter location. This condition usually responds to conservative measures. The authors recommend activity modification, lateral heel wedge or lateral heel wedge orthotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy. If these measures fail, a removable cast boot with a rocker bottom or a cast is usually the next step. Occasionally, a single, carefully placed steroid injection into the sheath is necessary. Should conservative measures fail, operative tenosynovectomy is indicated. Incision along the tendon sheath and inspection of the tendon is recommended. The area of maximal tenderness should give a clue to the offending anatomic structure.

C.

Peroneus Brevis Tears

Frequently, with pain and tenderness behind the lateral malleolus a tear of the brevis is noted. A tear of the brevis often indicates instability of the tendons within the retinacular groove from an incompetent SPR [71]. The retinaculum insufficiency, in turn, can be caused by incompetent lateral ligamentous structures. Peroneus brevis tears are more commonly reported than longus tears. The incidence of brevis tears in a cadaver study is 11%. Certainly, the clinical extent of this specific entity is much, much smaller than 11% of the general population. What makes a tear symptomatic is not really clear. It appears, based on the location of the tears, that the etiology is purely mechanical. Laxity of the superior retinaculum has been implicated in all cases of one author’s series [70,72]. Other potential causes are long-term tenosynovitis with tendon attritional changes and the presence of a peroneus quartus tendon, which results in overcrowding of the peroneal tendon sheath. A staging system of brevis tears has been proposed, but its use in prognosis and treatment decision making is not clear [73]. Tears are inspected and resected or repaired based on the location of the tear, length of the tear, and the health of the musculotendinous unit in general (preoperative strength testing, tendon excursion judged intraoperatively, etc.). Tears of the anterior one fourth to one third of the tendon are resected; tears more posterior than that are resected longitudinally and then repaired side to side with nonabsorbable braided suture (Figure 12.12). Large tears (> 5 cm in length) with significant tendinosis should be considered for tendon transfer. The authors’ preference is for tenodesis of the peroneus brevis to the longus proximally and distally. If the longus is degenerative as well (rare), the authors opt for an FDL transfer behind the tibia, around the lateral aspect of the fibula, and then attached to the base of the fifth metatarsal (Figure 12.13). Complete traumatic rupture of either peroneal is a relatively uncommon occurrence. A review of the existing literature in 1994 by Kilkelly and Mchale [74] revealed 13 cases of peroneus longus ruptures. One must have a high degree of suspicion for this injury. Physical examination can be nearly normal and MRI can often detect intratendinous signal but is not specific at detecting complete rupture. Traumatic rupture should be treated in the acute period for best results.

D.

Os Peroneum and Peroneus Longus Tears

There is always an osseous or cartilaginous sesamoidal structure within the substance of the longus tendon [65]. It is ossified in about 20% of individuals. If present, it may have attachments to the fifth metatarsal, cuboid, peroneus brevis, and plantar fascia. The os peroneum plays a role in several different scenarios involving chronic peroneus longus pain. Sobel [75] outlined five distinct conditions that could arise:


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Figure 12.12 A longitudinal tear of the peroneus longus and brevis are repaired. The edges of the tear are excised, and a side-to-side repair is performed with burial of the knots using a 4-0 nonabsorbable suture.

Figure 12.13 An FDL transfer is performed for a patient with chronic tendinosis and rupture of both the peroneus brevis and the peroneus longus. The patient had previously failed debridement procedures. The image shows the lateral side of the ankle with the FHL transferred from anteromedial to lateral into the peroneal tendon sheath. The suture anchor device is secured into the fifth metatarsal. Inset radiograph demonstrates placement of the suture anchor.

1. 2. 3. 4. 5.

Acute fracture of the os peroneum Chronic nonunion or fibrous union of os peroneum fracture (Figure 12.14) Attrition or partial tendon rupture proximal or distal to the os peroneum Complete rupture proximal or distal to the os peroneum Presence of a large peroneal tubercle, which entraps the longus or the os peroneum



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Figure 12.14 (Top) Radiograph shows chronic fracture of the os peroneum. (Bottom) Fragment diastasis after further twisting injury.

The recommended treatment for these conditions (six of eight surgically treated) is debridement of the os peroneum and tendon transfer of the peroneus longus to the brevis proximally. One case was treated with repair and one with tubulization of the tendon. An alternative is to perform a free graft to fill the defect between the ends of the ruptured tendon. The graft can be harvested from the proximal intact section of the peroneus longus (Figure 12.15). All had good or excellent results. There is concern in the literature over the development of a dorsal bunion from the lack of first ray plantar flexion. The authors have not seen this clinically.

E.

Peroneus Brevis Subluxation or Dislocation

Peroneus brevis subluxation or dislocation is thought to occur traumatically by a sudden forceful dorsiflexion moment on an inverted foot, with reflex firing of the peroneals [76]. However, multiple different mechanisms have been described in the literature. The peroneal tendons are most commonly injured during ankle sprains. In type I injury, the retinaculum and periosteum is stripped away from the attachment to the bone. In type II injury a cartilaginous rim is also pulled off; in type III, bone also pulls off. Type IV injury was added by Oden [77] in 1987. The patient presents with a history of a snapping sensation over the distal fibula with or without pain. Patients may also describe ankle instability and inability to balance on one leg and may complain of a locking or catching of the ankle. Physical examination demonstrates swelling and tenderness behind the lateral malleolus. Resisted dorsiflexion and eversion of a plantar-flexed and inverted foot is painful. Clockwise and counterclockwise active circumduction of the foot and ankle may elicit subluxation of the tendons. Demonstrating frank dislocation of the tendons may not be possible because of pain. Also, certain cases require a complex or particular stress to trigger a dislocation, making this injury difficult to appreciate clinically.


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Figure 12.15 Intraoperative photograph of a patient with peroneus longus tendon rupture. Upper left, rupture after debridement with exposure of proximal and distal portions of tendon. Black arrow indicates free graft harvested from proximal half of the peroneus longus tendon. The larger picture shows the final repair of the free graft interposed.

Radiographs occasionally demonstrate a rim avulsion fracture (Eckert and Davis type III injury). A stress ankle radiograph may show ankle instability. Computed tomography (CT) evaluation will help to discern the anatomy of the fibular groove (Figure 12.16) and MRI may further elucidate tendon pathology. Nonoperative treatment of acute dislocation or subluxation has a high failure rate. McLennan [78] noted conservative care to be acceptable, but with a high failure rate (44%). Immobilization probably has the best chance of success for type I and II injuries. According to the literature, operative treatment has a high degree of success in the acute period. A review of the existing literature indicates a 96% success rate [78]. The authors recommend

Figure 12.16 Computed axial tomography (CAT) scan demonstrating peroneal dislocation shows tendon lateral to fibula.



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direct repair with drill holes through the osseous ridge. If significant pathology of the lateral ligaments or a convex fibular groove is present, repair of this is also recommended.

F.

Chronic Repairs

There are many surgical options for treatment of chronic peroneal subluxation or dislocation, including direct reattachment of the retinaculum, reconstruction with transferred tissue, bone block procedures, groove-deepening procedures, and tendon rerouting procedures. The authors recommend a technique that deepens the groove, advances the SPR, and reinforces the SPR with fibular periosteum (Figure 12.17). The patient is placed in a lateral decubitus position, and a 3- to 5-cm incision is made along the posterior border of the fibula. The SPR is divided 1 mm posterior to the border of the fibula exposing the tendons. Anteriorly, the remaining SPR is raised in a flap with the fibular periosteum. This flap of tissue should be 1 to 2 cm wide. The tendons are debrided and repaired using sutures with buried knots. Along the posterior border of the fibula 1 or 2 mm medial to the lateral border of the fibula, a chisel is used to create an osteotomy extending 3 to 5 mm. The chisel is then manipulated progressively to raise a bone or fibrocartilaginous posterior flap from the posterior aspect of the fibula. The osteotomy should be completed through to the medial cortex of the fibula. Two Hohmann retractors are inserted between the flap and the fibula protecting the peroneal tendons. A 5-mm burr is used to create a deepened groove by removing 4 to 5 mm of posterior fibular width. The flap is then maneuvered back into place against the posterior aspect of the fibula and contoured with the gentle use of a bone tamp. Using 0.045-in. Kirschner wires, drill holes are created in the posterior aspect of the fibula. Beginning 3 to 4 mm anterior to the posterior edge, the Kirschner wire is directed into the groove just below the cortical surface (not deep within the groove). The wires once placed are then cut short and left in the hole. Thus, the SPR is lying on the interior or medial surface of the lateral fibular cortex. The periosteal flap that was raised earlier is then closed over the junction and onto the SPR with 2-0 absorbable suture. Postoperatively, a patient is placed in a well-padded, non-weight-bearing neutral splint for 10 to 14 days. Afterwards, the patient is placed in a weight-bearing boot brace for 2 to 6 weeks. An Aircast stirrup brace is worn for 6 to 12 weeks. ROM exercises are begun at 2 weeks, avoiding plantar flexion and eversion beyond 158. Circumduction of the foot should be avoided for 3 months. Return to jogging may occur between 8 and 12 weeks. Cutting activities are to be avoided for 3 months. A supportive cloth ankle brace is used for 3 to 6 months after reconstruction.

Figure 12.17 (A) Intraoperative photograph of the lateral aspect of the ankle demonstrating the exposure just posterior to the fibula.


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Figure 12.17 Continued (B) The peroneal retinaculum has been incised 1 mm off the posterior aspect of the fibula; the periosteum is reflected off the fibula. (C) The chisel is inserted posteriorly to lift the fibrocartilaginous posterior wall. (D) The burr is inserted between the fibrocartilaginous flap and the posterior cancellous bone of the posterior fibula.



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Figure 12.17 Continued (E) The fibrocartilaginous flap is recessed anteriorly. (F) .045 in. Kirschner wires are used to create bone tunnels to reattach the posterior retinaculum into the fibula. The wires are placed, cut short, and left in the hole. Holes should be prepared at 1-cm intervals. (G) Using a 2-0 Ethibond suture and a modified Kessler technique, the superior retinaculum is secured to the lateral aspect of the deepened posterior fibular groove.


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FLEXOR DIGITORUM LONGUS

The FDL originates from the middle half of the posterior tibia below the soleal line. The tendon passes deep to the flexor retinaculum and then travels deep to the flexor digitorum brevis in the sole of the foot before dividing into four slips and inserting on the plantar proximal distal phalanx. It is a primary flexor of the toes and a secondary flexor of the ankle. It is in the deep posterior compartment of the leg and innervated by the tibial nerve. Spontaneous rupture of the common origin tendon of the FDL and attritional tendonitis have not been reported. Traumatic rupture after a closed tibial fracture has been reported [79]. Given the redundancy in the sole of the foot due to the interconnections with the FHL and the relatively good power of this tendon, it is an excellent candidate for transfer in the reconstruction situation. Laceration proximal to the knot of Henry would be difficult to pick up due to the preserved lesser toe plantar flexion power with the above mentioned interconnections. Distal to the knot of Henry, usually individual tendons are lacerated. Physical examination demonstrates an inability to flex the toes with the MTP joint held in a neutral position. Repair of the ruptured FDL is shown in Figure 12.18.

VIII. FLEXOR HALLUCIS LONGUS The FHL tendon arises from the lower two thirds of the interosseous membrane and the periosteum of the fibula. The tendon develops distally in the muscle and courses over the posteromedial distal tibia and talus, traveling beneath the sustentaculum before inserting on the distal phalanx of the hallux. The FHL courses plantar to the FHB tendon and sesamoids. FHL tenosynovitis can present with pain in the posterior ankle, arch, or plantar aspect of the MTP joint. Distinguishing between posterior ankle impingement and FHL tendinitis is challenging because the two structures are close to one another, and these conditions may coexist [80]. The trigonal or posterior ankle impingement usually occurs with passive full plantar flexion of the ankle,

Figure 12.18 FDL tendon rupture is noted plantarly after a laceration with glass. Preoperatively, the patient complained that the second toe was dorsiflexed in relation to the other toes, which made it difficult to put on socks and shoes. Inset: intraoperative exposure of the tendon. The larger photo demonstrates a plantar flexion immobilization of the second toe with suture penetrating the nail dorsally attached to a rubber band that is connected to the elastic wrap.



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whereas FHL tendinitis does not. Dorsiflexion of the great toe while in the fully plantar-flexed position does not usually induce symptoms in impingement conditions, but may in FHL tendinitis. The point of maximum tenderness in posterior impingement is usually posterolateral, whereas it is usually posteromedial in FHL tendinitis. Further distinction is possible with lateral radiographs of the ankle taken in neutral and full plantar flexion; these views show abutment of the trigonum between the tibia and the talus and calcaneus or subluxation of the talus and tibiocalcaneal abutment.

A.

Etiology

The etiology of the condition is unknown, but due to its frequency in ballet dancers it is likely an overuse phenomenon. The condition is also found following calcaneal fractures due to scarring of the FHL in the tunnel. Other associated conditions are synovial hypertrophy, tendon nodularity, hypertrophy of the tunnel causing a relatively stenotic area, and a low-lying FHL muscle belly causing the same [81].

B.


Nonoperative treatment is most often successful for cases diagnosed early. It consists of rest (boot brace or cast) followed by a gradual physical therapy. Occasionally, the careful use of steroid injection is warranted. Lidocaine alone can be a valuable tool in helping with the determination between posterior impingement and FHL tenosynovitis. Bone scan can be helpful as well in the diagnosis of impingement or symptomatic os trigonum.

C.

Operative Treatment

Operative treatment involves release of the FHL fibro-osseous tunnel. This is done with the patient in the supine position. A posteromedial incision is made along the course of the FHL tendon from behind the medial malleolus to just below the level of the sustentaculum. The neurovascular bundle is identified. Usually it is easiest to retract the bundle posteriorly by dissecting anterior to it. The variable branching of the posterior tibial nerve is avoided this way. The FHL sheath is readily identified once the bundle is retracted. The fibro-osseous sheath is entered sharply and released to its distal extent. Whenever possible, the surgery is performed under local ankle block with intravenous sedation. This permits dynamic evaluation of the release intraoperatively. It can be otherwise difficult to determine that there is no further stenosis, especially in ballet dancers. Occasionally, triggering is still noted, and the entire sheath has to be divided. The FHL is inspected and repaired if necessary (Figure 12.19). If the patient also has a symptomatic os trigonum or posterior impingement without an os the authors resect that from the same incision. The FHL and the bundle are taken posteriorly. The posterior process should be identifiable at that point. We then remove the os by careful dissection of the bone. The capsule and ligaments can be quite adherent. We assess the level of our resection by a lateral fluoroscopic image in neutral and full plantar flexion. FHL laceration occurs infrequently, but deserves mention. Spontaneous rupture has been reported as well. Direct laceration can occur anywhere along the length of the tendon. The zone of injury, etiology (spontaneous or traumatic), and length of time since rupture are all important factors in deciding on operative or nonoperative management and, in the case of operative management, what approach and what reconstruction options might be available. The key anatomic landmark is the knot of Henry. This is the crossing of the FHL and FDL in the arch of the foot. Laceration proximal to the knot will allow the proximal stump to retract longer distances than a laceration distal to that. Also, because of the interconnection of the FHL and the FDL, hallux interphalangeal (IP) flexion is sometimes preserved with the more proximal lacerations. Results of repair are variable. It appears that repair of traumatic lacerations usually has a better outcome with respect to IP flexion than to spontaneous ruptures. Active IP flexion is less


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Figure 12.19 A flap repair is noted in the FHL tendon distal to the talus in a dancer. This was debrided and repaired.

likely to be noted after repair of distal ruptures [82]. Romash [82] combined a case report with a review of the literature and noted: Closed flexor hallucis longus tendon injuries in the forefoot, repaired by suture, had no active IP joint motion. The tendon that ruptured in the hindfoot did regain pull-through. In open tendon lacerations that were sutured, 11 of 18 had active interphalangeal flexion. In none of those treated operatively was there a significant deformity of flexion contraction or contracture of the metatarsophalangeal joint or interphalangeal joint. Of the five open lacerations not sutured, only one needed a secondary procedure to correct interphalangeal joint deformity.

The authors’ results confirm these findings. Although no pull-through is noted in a large percentage of cases, we still feel that power is transferred with repair to the MTP and ankle joints. Postoperative care includes immobilization for 4 weeks in a splint, with early institution of passive flexion or active extension exercises.

IX.

POSTERIOR TIBIAL TENDON

The tibialis posterior muscle originates from the posterior surface of the tibia, fibular, and interosseous membrane. The tendon hugs the medial malleolus as it travels in a groove. It is held in place by the flexor retinaculum (lancinate ligament). It then inserts mainly on to the plantar medial pole of the navicular. Extensions travel to the cuneiforms, the cuboid, and the second, third, and fourth metatarsal bases as well. It is a primary inverter of the hindfoot and a secondary plantar flexor of the ankle. The innervation is from the tibial nerve (L4, L5). The muscle lies in the deep posterior compartment of the leg.

A.

Etiology

Traumatic posterior tibial tendon (PTT) injuries include rupture and dislocation. Other etiologies in the acute or subacute situation include symptomatic accessory navicular, tenosynovitis, longitudinal tearing, complete rupture, or avulsion with arch collapse. The PTT dysfunction is a common etiology in the development of adult acquired flat foot deformity. In this condition, the foot progressively collapses into a pes planum valgus position. Although it is typically seen in conjunction with pain and swelling along the course of the PTT, it may at times be insidious with minor symptomatology. The condition is described in middle-aged obese women, but has been seen



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in patients as young as 14 and in patients of advanced age. In the author’s experience, there are athletes or other healthy active individuals of both sexes that are affected by the condition. The diagnosis of tenosynovitis is usually made by noting swelling, warmth, pain, and occasionally crepitus along the course of the tendon. Resistance of the foot can be painful, but strength is generally not limited.

B.


This condition is generally treated with activity modification, bracing (the authors prefer an ankle stirrup style brace), NSAIDs, and physical therapy. Occasionally, a longitudinal arch support with medial heel posting is used. Surgical treatment is reserved for recalcitrant cases and consists of tenosynovectomy. If significant weakness is noted by manual examination or if the foot is not able to be inverted actively past the midline or if the patient is unable to perform a single stance heel raise, then tendonosis should be suspected. MRI is helpful if the diagnosis is in question. Initial treatment is the same as for tendonitis. Occasionally, a boot brace or cast is needed. Failure of conservative treatment often leads to the myriad of surgical procedures available for the treatment of PTT dysfunction. The choices and decision making involved are beyond the scope of this chapter, but are summarized below.

C.

Operative Treatment

Tendon degeneration in the absence of deformity can be treated with debridement or repair and transfer (FDL). The choice of tendon debridement þ/ transfer, debridement with repair þ/ transfer, or tendon resection with transfer is controversial. The authors use both the preoperative examination and the operative findings to direct our surgical decision making. If the tendon has power to the midline based on preoperative examination, is not severely degenerated, and shows excursion intraoperatively, we generally preserve the tendon and augment it with an FDL transfer. If the tendon does not have any function preoperatively, does not have intraoperative excursion, or is extremely degenerated, the authors resect the tendon. If the hindfoot alignment is greater than 108 of valgus either from acquired hindfoot deformity or from a preexisting congenital planovalgus deformity bilaterally, medial displacement calcaneal osteotomy in addition to the tendon augmentation is recommended [83]. A more severe, rigid deformity requires a triple arthrodesis. Critical review of the literature shows that an acute closed traumatic rupture of the tendon in a young healthy individual without prodromal symptoms is exceedingly rare. Laceration of the tendon is much more commonly reported. Both acute rupture and laceration should be treated in the acute setting to avoid long-term dysfunction. An incision over the PTT sheath, opening of the retinaculum, identification of the tendon, and exploration of the injury is recommended. Acute repair with #0 braided, nonabsorbable suture is recommended. Postoperative treatment is usually in a plantar-flexed splint for 2 weeks followed by a ROM walker boot with a dorsiflexion stop set at 208. The patient is allowed to bear weight and gradually passively work the ankle up to a neutral position by 6 weeks. At 6 weeks, the boot is locked in neutral and gentle active ROM is begun. At 12 weeks, strengthening exercises are started. There is a spectrum of injuries that can involve the os navicular. These include insertional tendonitis, avulsion of the os, or stress fracture through a previously asymptomatic os. Insertional tendonitis should be treated with the same regimen as described above as long as there is no concern for accessory navicular pathology. If there is concern for this, MRI or bone scan can further elucidate the pathology. If the fibrous bridge between the accessory navicular and the main fragment show increased signal on MRI or increased uptake on bone scan, many authors recommend excision of the os and advancement of the PTT to the navicular through a drill hole or with suture anchors (modified Kidner procedure). The authors have found this procedure to have a long rehabilitation and only fair to good results. In the face of a normal tendon (i.e., only pathology of the accessory navicular), the authors


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recommend drilling across the fibrous bridge and then percutaneous screw fixation. This procedure has a faster rehabilitation time and less morbidity than excision and advancement procedures.

D.

Dislocation of the Posterior Tibial Tendon

Dislocation of the PTT is thought to be a component of lateral subtalar dislocation. The flexor retinaculum is thought to be torn in this condition and the tendon dislocation can be a block to reduction [84]. Other authors have noted the retinaculum to be intact on surgical exploration [85]. Isolated PTT dislocation is rare, and when it occurs the diagnosis is frequently delayed. Most patients recall a specific injury event [86]. The senior author had two patients who presented after repeated steroid injections. They had one and three tarsal tunnel releases, respectively. Another patient had previously undergone exploration of the PTT with tenosynovectomy. In this case, it is speculated that a repair of the retinaculum was insufficient and the tendon dislocated postoperatively. Patients with this condition can have tremendous pain and even tibial neuralgia as a result of the local mechanical alterations. An MRI can demonstrate the dislocation (Figure 12.20). Repair of the posterior tibialis dislocation includes performing a groove-deepening procedure behind the medial malleolus in a fashion similar to the reconstruction for the peroneal tendon dislocation as noted previously. A new retinaculum is created using local tissues. The senior author has used the periosteum of the distal tibia as a turndown flap to create a new tendon sheath.

Figure 12.20 (A) Sagittal MRI demonstrating dislocation of the PTT. As a result of persistent severe symptoms, the tendon was placed back into a deepened groove behind the medial malleolus using a technique similar to that described for treating the peroneal dislocation. Nav, naviculum; MM, medial malleolus; FDL, flexor digitorum longus; Abd H, abductor hallucis; PTT, posterior tibial tendon. (B) Frontal MRI demonstrating PTT rupture medial to the medial malleolus.



Figure 12.20

X.

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Continued (C) Coronal MRI demonstrating the dislocation. (D) Intraoperative photo.

CONCLUSION

The ATT, EHL tendon, EDL tendon, Achilles tendon, peroneal tendons, FDL tendon, and FHL tendon are subjected to acute and chronic stresses that may result in laceration, rupture, and subluxation or dislocation. A variety of surgical options have been described for repair and reconstruction. Tendon transfers using local tendons or free grafts offer options when the dysfunctional tendon is beyond salvage. Recognizing the interplay between acute and chronic pathology and taking into consideration the local and systemic conditions that are unique to the particular patient will facilitate the proper choice of procedure and optimize the result.

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Mann, R.A., Holmes, G.B., Jr., Seale, K.S., and Collins, D.N., Chronic rupture of the Achilles tendon: a new technique of repair, J. Bone Jt. Surg., 73A, 214–219, 1991. 65. Sarrafian, S., Anatomy of the Foot and Ankle: Descriptive, Topographic, Functional, 2nd ed., Lippincott, Philadelphia, 1993, p. 218. 66. Edwards, M.E., Relations of the peroneal tendons to the fibula, calcaneus, and cuboideum, Am. J. Anat., 42, 213–253, 1928. 67. Purnell, M.L., Drummond, M.S., Engber, W.D., and Breed, A.L., Congenital dislocation of the peroneal tendons on the calcaneal valgus foot, J. Bone Jt. Surg., 65B, 316–319, 1983. 68. Davis, W., Sobel, M., Deland, J., Bohne, W.H., and Patel, M.B., The superior peroneal retinaculum: an anatomic study, Foot Ankle Int., 15, 271–275, 1994. 69. Pierson, J. and Inglis, A., Stenosing tenosynovitis of the peroneus longus tendon, J. Bone Jt. Surg., 74A, 440–442, 1992. 70. Thompson, F. and Patterson, A., Rupture of the peroneus longus tendon: report of three cases, J. Bone Jt. Surg., 71A, 293–295, 1989. 71. Sobel, M., DiCario, E., Bohne, W., and Collins, L., Longitudinal splitting of the peroneus brevis tendon: an anatomic and histologic study of cadaveric material, Foot Ankle, 12, 165–170, 1991. 72. Brodsky, J. and Krause, J., Pathophysiology and Surgical Reconstruction of Tears of Peroneus Brevis Tendon, paper presented at the 12th Annual Summer Meeting of the American Orthopaedic Foot and Ankle Society, Hilton Head, SC, June 29, 1996.


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73. Sobel, M., Geppert, M.J., Olson, E.J., Bohne, W.H., and Arnoczky, S.P., The dynamics of peroneus brevis tendon splits: a proposed mechanism, technique of diagnosis, and classification of injury, Foot Ankle, 13, 413–422, 1992. 74. Kilkelly, F.X. and Mchale, K.A., Acute rupture of the peroneal longus tendon in a runner: a case report and review of the literature, Foot Ankle Int., 15, 567–569, 1994. 75. Sobel, M., Pavlov, H., Geppert, M.J., Thompson, F.M., DiCarlo, E.F., and Davis, W.H., Painful os peroneum syndrome: a spectrum of conditions responsible for plantar lateral foot pain, Foot Ankle, 15, 112–124, 1994. 76. Eckert, W. and Davis, E., Acute rupture of the peroneal retinaculum, J. Bone Jt. Surg., 58A, 670–673, 1976. 77. Oden, R., Tendon injuries about the ankle resulting from skiing, Clin. Orthopaed., 216, 63–69, 1987. 78. McLennan, J., Treatment of acute and chronic luxations of the peroneal tendons, Am. J. Sports Med., 8, 432–436, 1980. 79. Korovessis, P., Spastris, P., Katsardis, T., and Sidiropoulos, P., Simultaneous rupture of the tibialis posterior and flexor digitorum longus tendons in a closed tibial fracture, J. Orthopaed. Trauma, 5, 89–92, 1991. 80. Hamilton, W., Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the os trigonum in ballet dancers, Foot Ankle, 3, 74–80, 1982. 81. McCarroll, J., Ritter, M., and Becker, T., Triggering of the great toe: a case report, Clin. Orthopaed., 175, 184–185, 1983. 82. Romash, M., Closed rupture of the flexor hallucis longus tendon in a long distance runner: report of a case and review of the literature, Foot Ankle Int., 15, 433–436, 1994. 83. Myerson, M.S. and Corrigan, J., Treatment of posterior tibial tendon dysfunction with FDL transfer and calcaneal osteotomy, Orthopaedics, 9, 383–388, 1996. 84. Waldrop, J., Ebraheim, N., Shapiro, P., and Jackson, T., Anatomic considerations of the posterior tibial tendon entrapment in irreducible lateral subtalar dislocation, Foot Ankle Int., 13, 458–461, 1992. 85. Mulroy, R.D., The tibialis posterior tendon as an obstacle to reduction of a lateral anterior subtalar dislocation, J. Bone Jt. Surg., 37A, 859–863, 1955. 86. Ouzounian, T.J. and Myerson, M.S., Dislocation of the posterior tibial tendon, Foot Ankle Int., 13, 215–219, 1992.


13 Posttraumatic Infections in the Foot and Ankle Maria Guidry Department of Orthopaedics and Rehabilitation, University of Texas Medical Branch, Galveston, Texas

Brian Hutchinson Wright State University, Dayton, Ohio

Richard T. Laughlin Wright State University, Dayton, Ohio

Hongbao Ma Department of Orthopaedics and Rehabilitation, University of Texas Medical Branch, Galveston, Texas

Jason H. Calhoun Department of Orthopaedic Surgery, University of Missouri-Columbia, Columbia, Missouri

CONTENTS I. Introduction ...................................................................................................................... 346 A. Classification.............................................................................................................. 347 B. Microbiology ............................................................................................................. 347 C. Diagnosis ................................................................................................................... 347 1. Clinical Evaluation.............................................................................................. 347 2. Laboratory Evaluation........................................................................................ 347 3. Evaluation for Blood and Oxygen Supply to Tissues.......................................... 348 4. Imaging Studies ................................................................................................... 348 D. Management .............................................................................................................. 349 1. Cultures ............................................................................................................... 349 2. Antimicrobial Therapy ........................................................................................ 350 3. Surgical Treatment .............................................................................................. 351 4. Adjunctive Therapy............................................................................................. 353 II. Posttraumatic Skin and Soft Tissue Infections.................................................................. 353 A. Puncture Wounds ...................................................................................................... 353 1. Clinical Evaluation.............................................................................................. 353 2. Treatment............................................................................................................ 353

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B.

Necrotizing Fasciitis .................................................................................................. 354 1. Clinical Presentation ........................................................................................... 354 2. Diagnosis............................................................................................................. 354 3. Treatment............................................................................................................ 355 C. Postoperative Wound Infections................................................................................ 355 D. Pin Track Infections .................................................................................................. 355 1. Clinical Presentation ........................................................................................... 356 2. Diagnosis............................................................................................................. 357 3. Management........................................................................................................ 357 III. Foot and Ankle Osteomyelitis........................................................................................... 357 A. Classification.............................................................................................................. 357 B. Etiology ..................................................................................................................... 357 C. Postoperative Osteomyelitis ....................................................................................... 358 D. Posttraumatic Osteomyelitis ...................................................................................... 359 E. Principles of Osteomyelitis Management ................................................................... 359 IV. Postoperative Infections Following Fractures ................................................................... 360 A. Fractures of the Plafond ............................................................................................ 360 1. Incidence and Risk Factors ................................................................................. 360 2. Treatment............................................................................................................ 360 B. Ankle Fractures ......................................................................................................... 361 1. Incidence and Risk Factors ................................................................................. 361 2. Treatment............................................................................................................ 361 C. Talus .......................................................................................................................... 362 1. Incidence and Risk Factors ................................................................................. 362 2. Treatment............................................................................................................ 364 D. Calcaneus................................................................................................................... 364 1. Incidence and Risk Factors ................................................................................. 364 2. Treatment............................................................................................................ 364 E. Midfoot and Forefoot ............................................................................................... 364 V. Conclusion ........................................................................................................................ 365 References .................................................................................................................................. 367

I.

INTRODUCTION

Infections following foot and ankle trauma remain a diagnostic and therapeutic challenge. Traumatic injuries such as nail punctures, lacerations, burns, and fractures are often contaminated with microorganisms introduced during the time of injury. The paucity of soft tissue coverage providing protection to the foot and the proximity of the skin to the bone increases the predisposition to posttraumatic infections, particularly to osteomyelitis. The risk for infection and inoculation of the organisms directly into bone is increased in open fractures, external and internal fixation, and during other surgical procedures. Therefore, early recognition of the infection and prompt management are essential to preserving a functional limb and preventing complications, such as sepsis and amputation. Development of infection is determined by multiple factors, including the type and extent of injury, the phenotypic characteristics of the invading microorganisms, and host factors (i.e., nutritional, immunologic, metabolic, and vascular status of the patient). A systematic approach to prevent, recognize, and treat infections can be accomplished by carefully considering the complex anatomy and biomechanics of the foot, host factors, etiologic organisms, and the various treatment options (antimicrobial and surgical) [1]. This chapter presents an overview of general topics as they relate to posttraumatic foot infections (i.e., soft tissue infections, bone infections) and postoperative infections following fracture treatment.


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A.

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Classification

Classification of foot and ankle infections may be based on site of involvement (cellulitis, abscess, necrotizing fasciitis, septic arthritis, osteomyelitis), pathogenesis (trauma, fractures, postoperative), etiologic agents (bacterial fungal), and the status of the host (diabetic or immunocompromised vs. normal hosts).

B.

Microbiology

Most infections following foot and ankle trauma are caused by normal skin flora, predominantly Gram-positive cocci, Staphylococcus spp., Streptococcus spp., and Enterococcus spp. Polymicrobial infections are more common in diabetic patients in whom both Gram-positive and Gram-negative aerobic organisms are frequently isolated from the wound [2]. Staphylococcus aureus, B-hemolytic Streptococcus, Pasteurella multocida, and other anaerobic bacteria have been commonly implicated in infected puncture wounds. If the patient was wearing athletic rubber sole shoes, Pseudomonas is recovered in 90% of cases, probably because the moist rubber environment facilitates growth of the organism [3]. Postoperative foot and ankle infection secondary to fungus (Coccidioides imitis and Cryptococcus neoformans, Aspergillus spp., Candida, Actinomycetes), Mycobacterium tuberculosis, and atypical mycobacteria (M. avium-intracellulare, M. marinum) are rare, but are seen in immunocompromised patients [4]. Other fungal infections occur in patients with diabetes, peripheral vascular disease, asplenia, or human immunodeficiency virus [5,6,7]. Madura foot is a chronic foot infection of mixed fungi causing soft tissue infections, sinus tracts, and osteomyelitis of the small bones of the foot. It is endemic to Mexico and South /Central America [8]. Miron et al. [9] described a case of M. fortuitum osteomyelitis of the calcaneus in a 14-year-old girl who had a nail puncture wound in her foot. The authors hypothesize that nontubercular mycobacteria colonize the skin and cause infection when there is skin and tissue disruption and devitalization. If foot trauma occurs in saltwater, freshwater, and other infected water (pools, brackish water, lakes, hospital sources of water), the common pathogenic organisms causing wound infection are Aeromonas spp., Edwardsiella tarda, Erysipelothrix rhusiopathiae, Vibrio vulnificus, and M. marinum. V. vulnificus is a common cause of wound infections and septicemia in immunocompromised patients, especially those with hepatic impairment. The clinical signs and symptoms are highly variable [10]. V. vulnificus usually causes significant bulla formation, abscess, and soft tissue necrosis. Infections due to M. marinum are commonly indolent with less systemic toxicity [11]. In open trauma with contaminated soil or plants, the pathogens commonly seen include Clostridium, Sporothrix schenkii, Bacillus, and Nocardia spp. Pasteurella multocida and Erysipelothrix sp. are commonly isolated from animal bite-related trauma, especially dog and cat bites.

C.

Diagnosis

The diagnosis of infection is based on clinical, laboratory, and imaging data. 1.

Clinical Evaluation

Signs of infection usually include warmth, redness, heat and pain, increased drainage, foul odor, and presence of necrotic tissue. Constitutional symptoms, such as fever, chills, and malaise, are not usually present. 2.

Laboratory Evaluation

Laboratory data are usually not very helpful in the evaluation of bone and soft tissue infections, although they may help confirm clinical suspicion. White blood cell (WBC) counts may be normal or elevated. Elevated WBC counts with left shift is highly suggestive of acute infection. However, diabetic and immunocompromised patients may not be able to mount an immune or inflammatory response, thus a low or normal WBC count is not predictive of the presence or absence of infection.


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Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are nonspecific markers of inflammation and are used to monitor response to treatment. Liver and renal function tests, coagulation studies, albumin, and prealbumin levels are needed for baseline studies and to monitor response to treatment, and have to be considered in dose adjustments for antibiotics (i.e., revised doses for renal failure and advanced liver disease). Glycosylated hemoglobin (HgbA1C) is useful to evaluate long-term glucose control in diabetics, a major determinant of wound healing and infection control. 3.

Evaluation for Blood and Oxygen Supply to Tissues

Determination of the vascular status and tissue oxygen tension in the lower extremities are important in developing a treatment plan and the choice of surgical intervention for foot ulcers and foot infections. Arterial insufficiency should be suspected when there is a history of coronary or cerebrovascular disease, hypertension, symptoms of intermittent claudication, or rest pain. Palpating for pulses in the lower limbs, measurement of capillary refill and venous filling time are helpful diagnostic tools for peripheral arterial disease. Decreased pedal or posterior tibial pulses, sluggish refill of toe capillaries, dependent rubor and pallor on elevation, thickened nails and scarcity of hair in the toes suggest arterial insufficiency. Ankle-brachial index (ABI), toe pressures, and transcutaneous oxygen tension (TcPO2) are commonly measured to assess the adequacy of perfusion to the extremity and estimate healing potential [12,13,14]. An ABI greater than 0.90 suggests normal arterial circulation. ABI of 0.8 to 0.9 suggests mild peripheral arterial occlusive disease, while an ABI greater than 0.50 but less than 0.80 suggests mild to moderate vascular disease and impaired wound healing. An ABI less than 0.50 suggests severe vascular disease and should prompt referral to a vascular surgeon and evaluation for revascularization. It must be noted that in diabetics and patients with chronic renal failure, the pulse examination and ABIs are not reliable because vessels may be calcified and noncompressible. In diabetics, toe pressure of digital plethysmography expressed as toe-brachial index (TBI) is the test of choice and more reliable than both ABIs and TcPO2. Studies documented very good correlation between the TBI and angiographic findings. Healing of foot ulcers or foot amputations in diabetics could be predicted by toe pressures greater than 10 mm Hg, or a TBI of 0.7. Transcutaneous oxygen measurements are used to assess oxygen delivery to tissues, serve as a guide to the location of adequately perfused tissues, and are predictive of healing potential [14,15,16]. TcPO2 values are useful guides in selecting surgical margins where healing can be expected to occur, as well as deciding on amputation levels. Cutaneous oxygen tensions are measured using a modified Clark electrode applied to the skin surface. A TcPO2 less than 20 suggests a poor prognosis of ulcer healing, while a TcPO2 greater than 30 suggests good healing potential. A TcPO2 less than 5 indicates insufficient oxygen to heal after amputation. However, TcPO2 measurements are inaccurate in the presence of cellulitis or leg swelling. 4.

Imaging Studies

Imaging techniques are of great value for the diagnosis of foot and ankle infection. Radiographs are the first choice for the evaluation of infection in the foot and ankle. Plain radiographs provide important information on the extent of tissue damage, existence of foreign bodies, subcutaneous gas, and fracture. In contiguous-focus and chronic osteomyelitis, the radiographic changes are subtle, are often found in association with other nonspecific radiographic findings, and require careful clinical correlation to achieve diagnostic significance. Periosteal thickening or elevation, osteopenia, and bony destructive changes can be observed in plain films. In acute osteomyelitis, these changes lag at least 2 weeks behind the evolution of infection. Radiographic improvement may also lag behind clinical recovery after receiving appropriate antimicrobial therapy. At least 50 to 75% of the bone matrix must be destroyed before radiographs show lytic changes. The more diagnostic lytic changes are delayed and often associated with an indolent infection of several months’ duration. When the diagnosis of osteomyelitis is ambiguous, other imaging studies may be obtained. These studies include radionuclide scans, computerized tomography (CT) scans, and magnetic resonance imaging (MRI) [17,18].



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Although not commonly used, computerized axial tomography can help to identify areas of devitalized bone and to assess the involvement of the surrounding soft tissues. It is very good at detecting bony cortical destruction, and shows increased marrow density in early osteomyelitis. In a recalcitrant infection, the CT scan may assist in identifying the surgical approach and augment debridement [19,20,21]. Adjacent bone changes secondary to osteomyelitis and nearby effusions are easily documented using CT [18]. MRI is a very useful modality for diagnosis of foot and ankle infection and has largely replaced the CT and bone scans as the imaging of choice in the diagnosis of diabetic ulcers and osteomyelitis. The spatial resolution of MRI makes it useful in differentiating between bone and soft tissue infection, often a problem with radionuclide studies. MRI can be used for detection of abscesses, septic arthritis, subcutaneous gas in the foot and ankle, and osteomyelitis extending into the marrow cavity [22] as a result of its highly accurate visual image of different structures. In evaluating foot osteomyelitis, MRI has slightly more sensitivity than the technetium (Tc) bone scan. Radionuclide scans are helpful when the diagnosis of osteomyelitis is ambiguous or when it is necessary to know the extent of the infection. Due to the high cost of the test, MRI may only be cost-effective for patients in whom there is a questionable/ambiguous diagnosis of osteomyelitis and to aid in planning the surgical approach [18,19,23]. The three-phase bone scan is ideal for evaluating suspected osteomyelitis when plain films are negative. Uptake of the tracer in all three phases is suggestive of osteomyelitis, whereas tracer uptake that is limited to only the early phases is suggestive of cellulitis and other soft tissue infections. Tc-99m polyphosphate used in a three-phase bone scan demonstrates increased isotope accumulation in areas of increased blood flow and reactive new bone formation. It is positive within 24 to 48 h of onset of symptoms, has a sensitivity of about 90%, but its specificity is relatively low. False positive findings can occur with posttraumatic injury, diabetic feet, septic arthritis, noninfectious inflammatory bone disease, and conditions with severe ischemia or increased bone turnover. Gallium Ga 67 citrate bone scan is very sensitive for the diagnosis of osteomyelitis. However it has a poor spatial discrimination, making it difficult to distinguish between bone and soft tissue inflammation. A Tc-99m scan can be performed in addition to the Gallium scan to increase the specificity of the study. Indium-labeled leukocyte scan uses WBCs labeled with radioactive indium as the tracer, which accumulates at sites of infection and inflammation in bone marrow. It was found to have better sensitivity and specificity than bone scans in diabetic feet infections, except for the hindfoot [24]. Indium-labeled leukocyte scans are less useful in the evaluation of osteomyelitis. Indium leukocyte scans are positive in approximately 40% of patients with acute osteomyelitis and 60% of patients with septic arthritis. Patients who have chronic osteomyelitis, bony metastases, and degenerative arthritis often have negative scans [25,26,27]. Dual tracer scans combine the specificity of the indium scan with the sensitivity of the bone scan and are most useful in localizing infection to bone or soft tissue [28]. There are several other nuclear medicine imaging procedures available, such as the leukocytelabeled Tc-99m hemethylpropylamine oxime (HMPAO) scan. This has been found to have limited value in recent fractures in which osteomyelitis is suspected, when Charcot osteoarthropathy is present, and in the postsurgical patient [29]. The treating physician must keep in mind that many of these studies will be positive when performed on a fracture or nonunion. The diagnosis of an infection requires all the clinical data available and should not be made solely on the results of any single test.

D.

Management

Infections of the foot and ankle are managed with appropriate antibiotic therapy, surgical debridement and dead space management, adequate drainage, aggressive wound care, as well as other surgical and adjunctive measures when indicated. 1.

Cultures

Isolation and identification of the causative agent by cultures (wound, tissue, bone) is paramount. Final culture results and the susceptibility of the microorganism dictate the choice of antibiotics.


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In cellulitis of the foot and ankle, cultures are unnecessary and often result in a low yield because of few microorganisms in the area. Swab cultures are only recommended when there is an open wound in the cellulitic area. In foot ulcers and deep soft tissue infections, curettage to obtain quantitative tissue cultures and/or bone cultures obtained at the time of irrigation and debridement is the recommended method [30]. Superficial swab cultures are inaccurate, unless the bacteria isolated is Staphylococcus aureus, and will not reflect the true pathogens. As with long bone osteomyelitis, open bone biopsy with histopathologic examination and cultures of necrotic bone is the gold standard in the diagnosis of osteomyelitis. Needle biopsy sensitivity is low in posttraumatic and postoperative patients, so a negative result does not exclude osteomyelitis. Positive blood cultures, combined with consistent radiological findings and a compatible clinical presentation, obviate the need for a bone biopsy to establish a microbiologic diagnosis. For patients not responding to routine antibiotic treatment, infections with other types of organisms should be considered. Special cultures for fungus and mycobacterium are recommended based on the index of suspicion. Histopathology to rule-out malignancy is also recommended for nonresponsive cases. 2.

Antimicrobial Therapy

Selection and duration of antibiotic treatment of infection in foot and ankle trauma depends on culture results and type of infections. Infections of superficial wounds may be treated with a 10- to 14-day course of oral antibiotics. Severe soft tissue infections may be treated with 2 weeks of parenteral antibiotics, and then may be switched to oral antibiotics with clinical improvement [31–33]. Patients suspected of, or diagnosed with, osteomyelitis should be treated empirically with a broad-spectrum antibiotic, taking into consideration the most likely pathogens. Table 13.1 to Table 13.3 list the recommended initial choice of antibiotics for suspected Gram-positive, Gram-negative, and anaerobic bone and joint infections. Once the organism is identified, the antibiotics may need to be modified based on culture and sensitivity results. Culture-directed antibiotics for 6 weeks, dating from the last major debridement surgery or initiation of antibiotic therapy, is the cornerstone of treatment. Osteomyelitis is usually treated with 4 to 6 weeks of parenteral antibiotics, or alternatively with 2 weeks of intravenous antibiotics and 4 weeks of oral antibiotics. Because of the need for prolonged antibiotic therapy, the ideal antibiotic should be bactericidal against the organism identified by culture, be chemically stable at the site of infection, have adequate bone concentrations, have low or minimal toxicity, be tolerated by the patient, and be cost-effective. The acidic pH of bone is a limiting factor in the bactericidal activity of certain antibiotics, such as the aminoglycosides. Penicillins and cephalosporins are more stable at a low pH. The ideal antibiotic must have serum concentrations eight times greater than its minimum inhibitory concentration (MIC) [34]. Adequate treatment of Staphylococcus aureus and coagulase-negative Staphylococcus is usually attained with penicillin G, nafcillin, clindamycin, vancomycin, or first-generation cephalosporins. Resistance of Staphylococcus aureus and coagulase-negative Staphylococcus to second-generation quinolones is increasing. They also have very poor activity against Enterococcus, Streptococcus, and anaerobes [22]. Third-generation quinolones (levofloxacin) cover Streptococcus and Gram-negative organisms, but have minimal anaerobic coverage. The fourth-generation quinolones (trovafloxacin) cover anaerobes and Gram-positive organisms, including Streptococcus. Coagulase-negative Staphylococcus may be treated with vancomycin, tetracyclines, clindamycin, Bactrim1 and rifampin, if sensitive. Enterococcus is treated with vancomycin or amoxicillin. Quinolones have good coverage against Gram-negative organisms in osteomyelitis of the foot. In osteomyelitis secondary to M. fortuitum that is preceded by a puncture wound, culturedirected therapy usually consists of a combination of two of the following agents for 4 to 6 weeks: amikacin, imipenem, meropenem, ciprofloxacin, or clarithromycin [9]. For M. marinum infections, the four regimens used are: clarithromycin, tetracycline, Bactrim, or rifampin þ ethambutol. The problem of antibiotic resistance is worsening. Methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis, and vancomycin-resistant Enterococcus


Posttraumatic Infections in the Foot and Ankle Table 13.1

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Gram-Positive Organisms: Initial Choice of Antibiotics for Therapy (Adult Doses)

Organism Staphylococcus aureus Coagulase-negative Staphylococcus sp. Staphylococcus aureus Coagulase-negative Staphylococcus sp. Group A Streptococcus Streptococcus pyogenes Group B Streptococcus Streptococcus agalactiae Streptococcus pneumoniae Streptococcus pneumoniae Streptococcus pneumoniae

Enterococcus sp.

Enterococcus faecium

Antibiotics of first choice Methicillin-sensitive Nafcillin 2 g every 4 h or clindamycin 900 mg every 8 h Nafcillin 2 g every 6 h or clindamycin 900 mg every 8 h Methicillin-resistant Vancomycin 1 g every 12 h or linezolid 600 mg every 12 h Vancomycin 1 g every 12 h or linezolid 600 mg every 12 h Penicillin G 2Mu every 4 h or ampicillin 2 g every 6 h Penicillin G 2Mu every 4 h or ampicillin 2 g every 6 h Sensitive Penicillin G 2Mu every 4 h Intermediate Cefotaxime 1 g every 8 h Resistant Vancomycin 1 g every 12 h or levofloxacin 500 mg daily Sensitive Ampicillin 1 g every 6 h,c or vancomycin 1 g every 12 h Resistant Quinupristin–dalfopristin linezolid 600 mg every 12 h

Alternative antibiotics Cefazolin, vancomycin Cefazolin, vancomycin SMZ–TMPa or minocycline + rifampin SMZ–TMPa or minocycline + rifampin, clindamycinb Clindamycin, cephalosporin, vancomycin clindamycin, cephalosporin vancomycin Clindamycin, erythromycin Clindamycin, erythromycin Quinupristin–dalfopristin linezolid Ampicillin-–sulbactam, linezolid Chloramphenicol þ rifampin

a

Sulfamethoxazole-trimethoprim. If sensitive to clindamycin. c In a serious Enterococcus sp. infection, ampicillin plus an aminoglycoside is used. Source: From Mader, J.T. et al., in Musculoskeletal Infections, Calhoun, J.H. and Mader, J.T., Eds., Marcel Dekker, New York, 2003, pp. 495–528. With permission. b

faecium (VRE) pose a problem in postoperative orthopedic patients, especially in diabetics. Pseudomonas resistance and Candidemia with residual bone seeding have also been observed. Treatment regimens for VRE include prolonged treatment with linezolid or quinupristin/dalfopristin. Preferred regimens for MRSA vary depending on the institution, and include vancomycin + rifampin or rifampin þ tetracyclines or Bactrim. In the case of infection following an acutely treated fracture with implanted hardware, the antibiotic treatment may need to be extended for the duration of fracture healing, after which the hardware can be removed. Thus, antibiotics are used to suppress the infection. As long as the hardware provides stable fixation it can be left in place; however, it is unlikely that the infection will be eradicated until the hardware is completely removed. 3.

Surgical Treatment

Some infections may require simple surgical procedures, such as irrigation and debridement of the wound, while other infections need emergency surgical exploration, debridement, or amputation. Appropriate surgical procedures are determined by many factors, such as site of infection, vascular status of the tissue, and the potential viability of the tissues proximal to the site of infection [35]. It is important to assess the vascularity of the tissue at the amputation site to determine the potential for successful wound healing. By performing early distal vascular bypass surgery, angioplasty, or


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Table 13.2 Gram-Negative Organisms: Initial Choice of Antibiotics for Therapy (Adult Doses) Organism

Antibiotics of first choice

Alternative antibiotics

Acinetobacter sp.

Ceftazidime 1 g 8 h þ levofloxacin 500 mg daily or imipenem 500 mg every 6 h Cefotaxime 1 g every 6 h or imipenem 500 mg every 6 h Ampicillin–sulbactam 3 g every 6 h

Ampicillin–sulbactam

Enterobacter sp. Escherichia coli Haemophilus influenza Klebsiella sp. Proteus mirabilis Proteus vulgaris, Proteus rettgeri, Morganella morganii Neisseria gonorrhea Providencia sp. Pseudomonas aeruginosa

Serratia marcescens

Cefotaxime 1 g every 8 h or ampicillin–sulbactam 3 g every 6 h Cefotaxime 1 g every 6 h or levofloxacin 500 mg daily Ampicillin 1 g every 6 h or levofloxacin 500 mg daily Cefotaxime 2 g every 8 h or imipenem 500 mg every 6 h or levofloxacin 500 mg daily Ceftriaxone 125 mg IM once þ azithromycin 1 g oral once Cefotaxime 2 g IV every 8 h or levofloxacin 500 mg daily Cefepimec 2 g every 12 h or piperacillin c 3 g every 6 h or imipenem 500 mg every 6 h Cefotaxime 2 g every 6 h

Levofloxacin, mezlocillin, ticarcillin–clavulanate Cefazolin, levofloxacin, gentamicin, SMZ–TMPa Levofloxacin, SMZ–TMPa ampicillin,b azithromycin Ampicillin–sulbactam, gentamicin Cefazolin, SMZ–TMP,a gentamicin Mezlocillin, gentamicin ticarcillin–clavulanate Levofloxacin þ azithromycin SMZ–TMP,a amikacin, imipenem Ticarcillin–clavulanate, tobramycin, amikacin, ciprofloxacind Levofloxacin, gentamicin, imipenem

a

Sulfamethoxazole–trimethoprim. Non-b-lactamase-producing strain of Haemaphilus influenza. c In a serious infection should be used with an aminoglycoside — gentamicin or tobramycin 5 mg/kg/day every 8 h. d Increasing resistance to the quinolones including ciprofloxacin. Source: From Mader, J.T. et al., in Musculoskeletal Infections, Calhoun, J.H. and Mader, J.T., Eds., Marcel Dekker, New York, 2003, pp. 495–528. With permission. b

angioplasty plus stenting it is often possible to provide enough blood flow to allow healing in the area to be debrided or ablated [36]. Postoperatively, once there is suspicion that a wound infection is present, the surgeon must make a decision whether or not to return to the operating room for exploration, cultures, irrigation, and debridement of the affected tissue. Superficial infection can generally be treated with a course of oral antibiotics [37]. However, in the case of a patient who has suffered a fracture and has retained hardware, there should be a very low threshold for simply admitting the patient to the Table 13.3 Anaerobic Organisms: Initial Choice of Antibiotics for Therapy (Adult Doses) Organism

Antibiotic of first choice

Alternative antibiotics

Bacteroides fragilis group

Clindamycin 900 mg every 8 h or metronidazole 500 mg every 8 h Clindamycin 900 mg every 8 h or metronidazole 500 mg every 8 h Penicillin G 2mu every 4 h or clindamycin 900 mg every 8 h Clindamycin 900 mg every 8 h or penicillin G 2mu every 4 h

Ampicillin–sulbactam, ticarcillin–clavulanic acid Ampicillin–sulbactam, cefotetan

Prevotella sp. Peptostreptococcus sp. Clostridium sp.

Clindamycin, metronidazole Ampicillin–sulbactam, metronidazole

Source: From Mader, J.T. et al., in Musculoskeletal Infections, Calhoun, J.H. and Mader, J.T., Eds., Marcel Dekker, New York, 2003, pp. 495–528. With permission.



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hospital for intravenous antibiotics. Deep soft tissue infection requires irrigation, debridement, and intravenous antibiotic therapy. The wound is usually loosely closed with a suction drain or left open postoperatively. Vacuum-assisted closure systems can be very helpful in managing these open wounds (see Chapter 10). 4.

Adjunctive Therapy

Hyperbaric oxygen (HBO) therapy has been used for many years as an adjunctive treatment for orthopedic infections. In infected wounds and other nonhealing wounds in patients with decreased systemic or segmental perfusion, oxygen plays an important role in angiogenesis, and raises tissue oxygen tensions to levels where wound healing can be expected. HBO therapy increases the killing ability of leukocytes, is lethal for certain anaerobic bacteria, and has been associated with antiinflammatory activity [38–41]. Several studies have shown the beneficial activity of HBO therapy in the treatment of diabetic foot ulcers, including those that are secondary to trauma. In one comparative study, Zamboni et al. showed a greater reduction of the wound surface area in the HBO-treated group compared with a group treated with antibiotics alone [42]. Also, Faglia et al. [43] demonstrated a reduction in the amputation rate in diabetic ischemic ulcers treated with HBO therapy compared with the group treated only with antibiotics.

II.

POSTTRAUMATIC SKIN AND SOFT TISSUE INFECTIONS

A.

Puncture Wounds

Puncture wounds usually result from penetrating trauma by a foreign object, most commonly a nail. Other objects such as glass, metal, and wood have been found as well. Most puncture wounds in the forefoot and metatarsophalangeal joints penetrate deeper, as these are weight-bearing areas [10]. In superficial wounds, there is usually spontaneous healing. However, more commonly, the wounds are of substantial depth and can injure soft tissue, deeper structures, and bone. Miron et al. [9] estimated that 3 to 18% of puncture wounds in children result in cellulitis or abscess, while 0.65 to 1.8% of these progress to osteomyelitis. If the penetrating object has broken off, there is a risk of retained foreign bodies in the wound, mandating further exploration and open surgical debridement. 1.

Clinical Evaluation

A thorough history should include the description of the foreign object, the environment where injury occurred, time elapsed since injury, depth of penetration, footwear, tetanus status, and patient risk factors (immune status, systemic illnesses, vascular status, etc.). Clinically, patients complain of foot pain and inability to bear weight. Edema, erythema, and drainage may be present. The involved limb should be extensively examined, paying attention to signs of infection and neurovascular compromise. After thorough wound exploration, the wound should be left open and observed for signs of infection. Surgical debridement is the cornerstone of infected puncture wounds, and specimens should be sent for microbiology. Radiographs are important to assess for retained foreign bodies, as well as to exclude fractures. When there is a high index of suspicion for a foreign body that is not apparent on radiographs, other techniques such as ultrasound, MRI, or CT are helpful. Tetanus toxoid and tetanus immune globulin should be administered if the patient’s booster is more than 5 years old, or if immunization is uncertain. 2.

Treatment

The use of antimicrobials in the management of puncture wounds should be individualized, considering the patient’s risk factors. There is no consensus recommending the prophylactic routine use of antibiotics for puncture wounds, unless the patient is immunocompromised or if


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osteomyelitis is strongly suspected. Clinical trials by Raz et al. [44] showed that a 7- to 14-day course of ciprofloxacin is effective when combined with surgical exploration and debridement. Osteochondritis was successfully healed by 2 weeks of therapy. The newer quinolones (levofloxacin and gatifloxacin) have enhanced Gram-positive activity and are preferred over ciprofloxacin when there is concomitant Pseudomonas and Staphylococcus aureus infection. Tetracyclines are the drug of choice for empiric therapy against noncholera Vibrio sp. and is indicated when a traumatic puncture wound is related to handling contaminated shellfish, or if there is associated exposure to contaminated seawater. Another drug regimen consists of ceftazidime plus a quinolone. Antibiotics may be modified based on culture results.

B.

Necrotizing Fasciitis

Necrotizing fasciitis is a surgical emergency characterized by progressive infection and necrosis of the subcutaneous tissue and fascia [45,46]. Without early diagnosis, followed by adequate antibiotic treatment and surgical intervention, the mortality rate of necrotizing fasciitis is very high [47]. Misdiagnosis is common in the early stage of the disease as a result of nonspecific clinical presentations. A high index of suspicion and aggressive surgical debridement is crucial in the diagnosis and treatment of necrotizing fasciitis. Minor injuries, such as scratches, lacerations, insect bites, puncture wounds, and needle sticks, can introduce microorganisms into subcutaneous tissue [48–50]. Several host factors have been associated with increased risk of necrotizing fasciitis, such as diabetes mellitus, renal failure, and vascular insufficiency. Common microorganisms are group A Streptococcus, anaerobic species such as Bacteroides and Peptostreptococcus spp., and other aerobes such as Streptococcus Pneumoniae and Staphylococcus spp. Infections involving lower extremities usually are more monomicrobial and include skin flora [48,51,52]. 1.

Clinical Presentation

Early skin changes of necrotizing fasciitis are similar to cellulitis, including redness, swelling, warmth, and tenderness. However, severe pain is usually out of proportion to other clinical presentations. Systemic changes including fever and chills can be observed. Characteristic skin changes of necrotizing fasciitis develop later from a smooth, tense, and shiny appearance to dusky, blue-gray blisters and bulla [53]. The presence of crepitus in physical examination is only found in less than one-half of patients. With rapid progression of the infection and necrosis of fat and fascia, patients develop signs and symptoms of sepsis, hypotension, tachycardia, mental status changes, and renal failure. Laboratory tests show elevated WBC count, blood urea nitrogen (BUN), and creatinine. Radiographic evaluation may aid in the evaluation of necrotizing fasciitis and should be performed in any suspected patients without delay. Soft tissue air in the infected area may be observed in plain films in patients with necrotizing fasciitis. Asymmetric thickening of deep fascia in association with gas may be observed on CT, which helps to differentiate necrotizing fasciitis from cellulitis. MRI has also been used in the evaluation of necrotizing fasciitis by demonstrating the thickening and tracking of deep fascial planes [54]. 2.

Diagnosis

Due to the lack of early specific clinical presentations, diagnosis is very difficult at the early stage of the infection. Patients may already be critically ill at the time of diagnosis. Diagnostic clues for necrotizing fasciitis include severe pain at the site of infection, prominent systemic toxicity, and poor response to conventional treatment. A high index of suspicion and adequate evaluation to confirm the diagnosis is crucial. Soft tissue air in plain radiographs observed in a patient with clinical signs and symptoms of necrotizing fasciitis prompt immediate surgical exploration. However, if radiographic evaluation cannot be performed immediately, surgical exploration should be made based on clinical presentation without any delay. Less invasive procedures to make tissue diagnosis, such as fine-needle aspiration and bedside incisional biopsy, have also been used [55].



3.

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Treatment

Treatment of necrotizing fasciitis includes parenteral antibiotics, surgical debridement, and HBO. Aggressive fluid replacement and other supportive measures in the surgical intensive care unit (ICU) may be necessary for management of acute renal failure and septic shock for critically ill patients. The selection of initial antibiotics should include broad coverage of aerobic and anaerobic microorganisms. The combination of a penicillin or cephalosporin, an aminoglycoside, and clindamycin or metronidazole is the common initial choice [53]. Modification of the antibiotics should be made after culture results become available. Aggressive surgical debridement of necrotic tissue plays an important role in the treatment of necrotizing fasciitis. Early and extensive debridement of infected skin, soft tissue, fascia, and muscle has been associated better outcome and survival. Repeated debridement is usually necessary to ensure that all necrotic tissue is removed without additional tissue damage. HBO treatment has been used for the treatment of necrotizing fasciitis. HBO treatment not only has effects on leukocytosis, bacterial killing, and spread of infective organisms in acute infection, but it also promotes tissue granulation and wound healing during recovery from the infection [56–58].

C.

Postoperative Wound Infections

Postoperative wound infections or surgical site infections (SSIs) continue to pose a challenge because they may compromise the results of surgery and cause devastating consequences. The number of postsurgical infections is estimated to be 500,000 per year, among roughly 27 million surgeries [59,60], and account for one-quarter of the 2 million nosocomial infections annually. Miller [61] estimated a 2.2% infection rate in 1841 patients after inpatient foot and ankle surgery. SSIs after foot and ankle surgery are divided into superficial (skin and subcutaneous tissue) and deep infections (fascia and muscle, and even possibly joints and bone). They may also be classified into incisional or organ/space infections (referring to the site manipulated during surgery) [62,63]. Postsurgical infections are more common after contaminated or traumatic injuries, open fractures, internal or external fixation, and with the use of indwelling hardware. They are rare after clean orthopedic procedures (less than 3%) and commonly involve nosocomial organisms; Staphylococcus aureus, coagulase-negative Staphylococcus, group B Streptococcus, and Gram-negative aerobes and anaerobes are the most common organisms [62,64]. It is believed that direct inoculation of endogenous normal flora during surgery is responsible for most cases. Exogenous sources of infection, however, should not be excluded. Postoperative infections after foot trauma are often a result of inadequate soft tissue coverage. When operating through injured or compromised tissue, the additional trauma of the surgery can cause necrosis and further compromise the soft tissue coverage. Necrotic tissue must be excised expediently, and viable soft tissue coverage must be obtained within 7 to 10 days to avoid bacterial colonization and the transition of the wound from acute to subacute or chronic [65]. Diagnosis of postoperative wound infection is based on clinical, laboratory, and radiographic data. Warmth, redness, heat, and pain point to the possibility of at least superficial infection. These infections are usually tender to palpation, but do not produce pain with joint movement, and are not fluctuant. Deep soft tissue infections are generally associated with an abscess that may be visible on plain radiographs or MRI and may be aspirated with a needle [37].

D.

Pin Track Infections

External fixation plays an important role in the treatment of foot and ankle injury [66–68]. Percutaneous insertion and long-term retention of the pin in the tissue provides a great opportunity for bacterial invasion and subsequent infection. Pin track infection is the major complication of external fixation [69]. Necrosis of tissue around the pin and excessive pin site tissue motion also contribute to the development of pin tract infections [70]. An animal model indicated that fluid accumulation around the interface is also an important factor in the spread of infection in the pin track [71]. Proper insertion technique, careful pin track care, and treatment of infection will improve the healing of the fracture and increase the success of the external fixation.


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Clinical Presentation

Initial signs and symptoms of pin track infection include redness of the skin around the pin site, swelling, and pain. Serous, serosanguious, or purulent drainage from the pin insertion site may be observed (Figure 13.1A and Figure 13.1B). In some patients, infection may spread to surrounding tissue and bone, causing cellulitis and osteomyelitis [72]. Efforts have been made to classify pin track infection. A system of classification of pin track infection has been proposed [73]). They are classified as minor and major infections, each of which is further subdivided into three subgroups. Minor infections can be managed as outpatients with pin site care and oral antibiotics while preserving the external fixator. Slight redness around the pin site with a little drainage is classified as grade I. More significant soft tissue infections around the pin site, with local signs and symptoms such as pain, swelling, and erythema are classified as grade II infections. They usually respond to

A

B

Figure 13.1 Ilizarov fixator placed to correct equinus and inversion contractures of the left ankle and foot in a 53-year-old female. She has a long history of synovial cell sarcoma treated by wide resection, radiation, and chemotherapy, followed by isolated limb perfusion with Adriamycin1 complicated by Adriamycin-related nerve damage, resulting in contractures. She developed a pin track infection during correction with the Ilizarov fixator. (A and B) There were large amounts of serous drainage around the posterior pins, with erythema and ecchymoses extending back into the Achilles tendon area. She was treated with culture-directed antibiotics and aggressive wound care.



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pin site care and antibiotic treatment. Those infections that do not respond to above treatment are classified as grade III. Grade IV infections involve multiple pin sites with extensive soft tissue infection. Infections involving bone are classified as grade V. Infections of pin track after the removal of the external fixators are grade VI. Grade IV to grade VI infections are considered major infections and the affected pins should be removed. Additionally, improving the stability of the frame should be considered because stable external fixation constructs with good pin care rarely have pin track problems. 2.

Diagnosis

Diagnosis of pin track infection can be made based on clinical presentation and local signs of soft tissue infection. Radiographic studies help to identify bone involvement and evaluate changes in the external fixator. Local wound and tissue cultures are important to guide selection of the appropriate antibiotics. Grading of infection based on the above classification may help to guide management of infection. 3.

Management

Many effective methods have been developed to reduce pin track infections, such as improved pin insertion techniques and the use of hydroxyapatite-coated pins [74,75]. Proper pin care is very important in the prevention and treatment of pin tract infection [73]. Minor infection like erythema around the pin can be treated with rest, wound care, and oral antibiotics. Significant infection with swelling, pain, and associated purulent drainage requires surgical incision and drainage, as well as parenteral antibiotics in the hospital setting. Removal of the pin may be indicated for significant infections. Chronic draining wound from the pin site is usually complicated with bone infection and requires long-term antibiotic treatment. Duration of antibiotic treatment is at least 6 weeks, with 2 weeks of parenteral antibiotics followed by 4 weeks of oral agents. Long-term suppression with antibiotics may be necessary for patients with chronic osteomyelitis. Selection of the antibiotics should be based on wound and tissue culture results. Initial antibiotics should cover at least aerobic and anaerobic organisms. Modification of antibiotics can be made when the culture results become available.

III. A.

FOOT AND ANKLE OSTEOMYELITIS Classification

Osteomyelitis is an infection of bone, which progressively results in inflammatory bone destruction. There are several different classification systems that can be used. Based on the pathogenesis of the infection, osteomyelitis is grouped into hematogenous or contiguous-focus osteomyelitis, with or without vascular insufficiency. Direct extension secondary to a contiguous focus is the most common form of osteomyelitis in the bones of the foot, especially in patients with vascular insufficiency, neuropathy, and segmental ischemia, as in diabetics [76]. Common predisposing factors for contiguous focus osteomyelitis without vascular insufficiency include trauma, open fractures, surgical procedures such as reduction and internal fixation of a fracture, chronic soft tissue infections, or an adjacent infected wound. The Cierny-Mader classification system for long bone osteomyelitis (Table 13.4) [76] stages infections based on their depth, the quality of overlying tissue, and the host status of the patient. This system makes treatment recommendations for each stage and is discussed in detail below.

B.

Etiology

Common pathogens in osteomyelitis secondary to traumatic injuries and in hematogenous seeding include normal skin flora, Staphylococcus aureus and Streptococcus epidermidis being the most common organisms. Hematogenous infections are usually monomicrobic, with Staphylococcus aureus being the most common isolate from bone and Gram-negative rods seen in 30% of cases.


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Table 13.4 Cierny-Mader Classification System Anatomical type Stage 1 Medullary Osteomyelitis Stage 2 Superficial Osteomyelitis Stage 3 Localized Osteomyelitis Stage 4 Diffuse Osteomyelitis Physiological class A Host: Normal host B Host: Systemic Compromise (Bs) Local Compromise (Bl) Systemic and local compromise (Bsl) C Host: Treatment is worse than the disease Systemic and local factors that affect immune surveillance, metabolism, and local vascularity Systemic (Bs) Local (Bl) Malnutrition Chronic lymphedema Renal, hepatic failure Venous stasis Diabetes mellitus Major vessel compromise Chronic hypoxia Arteritis Immune disease Extensive scarring Malignancy Radiation fibrosis Extremes of age Small vessel disease Immunosuppression or immune deficiency Neuropathy HIV/AIDS Alcohol and/or tobacco abuse From Mader JT, Calhoun JH. Adult long bone osteomyelitis. In: Calhoun JH, Mader JT (eds). Musculoskeletal Infections. New York: Marcel Dekker, 2003:150.

In contrast, contiguous focus osteomyelitis is usually polymicrobic. Staphylococcus and coagulase-negative Staphylococcus are the common isolates, followed by Gram-negative organisms and anaerobes (Bacteroides spp., Clostridium spp.). In diabetic foot osteomyelitis, a mixed or polymicrobic infection is seen with Staphylococcus aureus, coagulase-negative Staphylococcus, Streptococcus spp., Enterococcus spp., and aerobic and anaerobic Gram-negative bacilli. The incidence of osteomyelitis after puncture wounds is low (0.6 to 1.8%), with Pseudomonas being the most common offending agent [77,78]. Laughlin et al. studied adult patients who developed osteomyelitis of the calcaneus after a puncture wound to the heel [79]. Immunocompromised patients, including patients with systemic illness such as diabetes, were found to have a polymicrobial infection, whereas healthy, nonimmunocompromised patients developed only one pathogenic organism, Pseudomonas being the most commonly cultured, followed by Staphylococcus and Streptococcus.

C.

Postoperative Osteomyelitis

Postsurgical infections are more common in posttraumatic cases than after elective, clean surgical procedures. Staphylococcus aureus, Coagulase-negative Staphylococcus, and B-hemolytic Streptococcus usually cause postoperative osteomyelitis in uncompromised hosts. In the presence of orthopedic implants, Coagulase-negative Staphylococcus, Staphylococcus aureus, and Propionibacterium spp. are the common pathogens. Staphylococcus adheres to the implant forming a glycocalyx that makes them less susceptible to antibiotics. Prophylactic measures include antibiotic coverage and proper surgical technique, including minimal soft tissue stripping prior to placing the implant. When osteomyelitis is diagnosed, 6 weeks of culture-directed antibiotics and implant exchange or removal increase the chances of eradicating the infection [80]. When implants are retained, a longer course of antibiotic suppression may be required.



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Surgical management of postoperative osteomyelitis is similar to that of long bone osteomyelitis and includes adequate debridement, culture-directed antibiotics, and insertion of antibioticimpregnated beads, followed by the use of local or vascularized soft tissue grafts or bone grafts when indicated.

D.

Posttraumatic Osteomyelitis

Bacteria and other infective organisms may be inoculated into bone at the time of trauma, followed by bacterial proliferation and subsequent infection. Antrum and Solomkin [81] estimated that 70% of open fractures, such as those sustained from gunshot wounds, motor vehicle accidents, and lawn mower injuries, are likely contaminated at the time of injury, further increasing the risk for soft tissue and bone infections. Boucree et al. [82] reported a low incidence of osteomyelitis following gunshot wounds. Only 4 out of 81 patients with a Gunshot Wound and foot fracture developed osteomyelitis. These were found to have high-velocity wounds, with Staphylococcus epidermidis being the most common isolate. Patients with low-velocity GSW had an uneventful recovery following extensive debridement, delayed primary closure, and at least 3 days of intravenous cephalosporins. Patzakis et al. [77] reported a 13.9% infection rate in open fractures not treated with antibiotics, and 22.7% infection rate in those open fractures with extensive soft tissue damage. Posttraumatic osteomyelitis morphologically begins as necrosis of the outer tangential lamella of bone, followed by necrosis of fracture ends [83]. Diabetics are more prone to posttraumatic osteomyelitis because inadequate tissue perfusion inhibits the mounting of an inflammatory response to contain the infection. Patients present with localized bone and joint pain, redness, drainage, and localized swelling. Systemic symptoms such as fever and chills may be seen in the acute phase, but are uncommon in chronic osteomyelitis [22]. Surgical management of posttraumatic osteomyelitis involves careful debridement, maintaining bony stability, eliminating dead space and providing durable soft tissue and wound coverage. Bony stability may be achieved with screws, rods, and internal and external fixators. The Ilizarov fixation is commonly used to reconstruct difficult tibial deformities or nonunions that result from osteomyelitis. While it is true that internal fixation is necessary for fracture stability and union, infection has also contributed to the development of nonunion, delayed healing and loss of functionality of the foot [22].

E.

Principles of Osteomyelitis Management

Successful treatment of osteomyelitis involves aggressive surgical and medical management: adequate surgical drainage and debridement, obliteration of dead space, stabilization of bone, and culture-specific antibiotics. In some cases of osteomyelitis, antibiotic therapy alone is sufficient. For example, in acute hematogenous osteomyelitis in children, antibiotics may eradicate the infection. However, in diabetic foot infections and most chronic contiguous osteomyelitis in adults, adequate debridement and antibiotics are necessary for eradication of the infection [34]. In osteomyelitis localized to the large bones of the foot and ankle (i.e., calcaneus, talus) as well as the distal tibia–fibula, local debridement surgery and 4 to 6 weeks of antibiotic therapy may suffice, as long as patient has good vascular supply and tissue oxygen perfusion. Failure of wound healing after debridement (due to vascular insufficiency and other factors) may eventually lead to further surgery and ablative procedures. Ablative surgery, such as digital and ray resection, transmetatarsal amputation, midfoot disarticulation, and Syme amputation, are also done in extensive osteomyelitis involvement to allow ambulation without the need for a prosthesis. In extensive osteomyelitis, when infected bone is surgically transected, 4 weeks of antibiotics is required. If the patient undergoes ablative surgery, the duration of antibiotic treatment may be reduced to 2 weeks. If the infected bone is completely excised, but some residual soft tissue infection remains, 2 weeks of antibiotics is usually sufficient. If amputation is proximal to the site of osteomyelitis, a shorter course of antibiotics is sufficient (3 days). The patient may be offered suppressive antibiotics for osteomyelitis when a definitive surgical treatment is unacceptable to the patient or when patient is not a candidate for surgery because of


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coexisting medical conditions or poor vascular status. Intermittent or prolonged antibiotics may suppress acute exacerbations, but some patients eventually require amputation [22]. Clinical response, pharmacologic effects of treatment, adverse effects, and complications need to be monitored. Sequential periodic debridements combined with antibiotics increase the chances for suppression. To improve the outcome, host factors need to be maximized. Glucose control in diabetic patients, good nutrition, cessation of smoking, treatment of renal and hepatic failure, and revascularization for peripheral arterial disease are important variables that need to be addressed. A multidisciplinary team approach has improved outcomes in several institutions.

IV.

POSTOPERATIVE INFECTIONS FOLLOWING FRACTURES

Fractures of the foot and ankle comprise a large portion of fractures in adults. These include fractures of the plafond, ankle, talus, calcaneus, cuboid, cuneiforms, metatarsals, and phalanges of the foot. Fractures of this region are associated with high levels of disability and can result in a high level of functional loss. Infections can occur with these injuries when there is compromise of the protective barrier of the skin; whether by open fracture, surgical intervention, or a combination of the two. There are recurrent themes in the treatment of foot and ankle fractures regarding the avoidance of infection. Meticulous and gentle soft tissue techniques should be used. Additionally, timing of surgery should be delayed until soft tissues have stabilized. Tourniquet time should be minimized or eliminated, if possible, because it leads to further tissue injury. A tension-free closure should be achieved when possible, and flap procedures, when required, should be performed early rather than late. Open fractures should be irrigated and debrided repeatedly, if necessary, and treated with intravenous antibiotics.

A.

Fractures of the Plafond

1.

Incidence and Risk Factors

Pilon fractures are defined as fractures of the distal tibia involving the weight-bearing articular surface of the ankle [84]. These injuries are usually of a high-energy nature and are associated with other injuries to the soft tissue envelope. Surgically, they are treated with external fixation, open reduction and internal fixation (ORIF), or a combination of both. The timing of surgical intervention appears to have an impact on the postoperative incidence of infection. Whether or not the fracture is open may or may not have an impact. There is a large range of incidences of infection reported in fractures of the tibial plafond. Some of this may be attributable to the many degrees of soft tissue compromise and to the multitude of surgical treatment modalities. Studies have reported superficial postoperative infections in the range of 8 to 20%. Deep infection has been reported with a range of 0 to 55%. In more recent studies, using improved soft tissue handling techniques and timing protocols, rates of infection have generally been found to be less than 10% [85,86]. There has been conflicting data regarding open fractures as a risk factor for infection. Some studies have shown a link while others have not [87,88]. Most authors believe that the largest risk factor for infection is the degree of concurrent soft tissue injury. Other risk factors include contamination, comminution, ORIF during the acute phase of soft tissue injury, and the skill level of the operating surgeons [89,90]. In the case of external fixation as definitive treatment, pin site infections have been reported with a wide range of incidences: from as low as 5% to as high as 100%. Pin sites should be cleaned often, and loose pins should be addressed because pin loosening is associated with infection [91]. Loose pins should be removed or exchanged. Pin tract infections usually resolve with antibiotic treatment. These infections are discussed in more detail below. 2.

Treatment

Recent staged protocols combined with improved surgical techniques have probably helped to lower the incidence of postoperative infections in pilon fractures. Staged protocols generally



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involve early external fixation of the tibia with internal fixation of the fibula, followed by ORIF of the tibia at a later time when the acute injury phase has passed [92]. Improved techniques include meticulous soft tissue handling, including indirect reduction techniques and percutaneous hardware placement to avoid extensive approaches. Open fractures are treated for tetanus, given intravenous antibiotics, debrided early, stabilized, and receive closure or soft tissue coverage in the first week after the initial operation in order to reduce the risk of infection. Sutures are used in place of staples to allow for greater tissue expansion in hopes of avoiding tissue necrosis. In the unfortunate instance of deep infection, treatment involves irrigation and debridement of the wound. All necrotic tissue, including bone, must be removed. Hardware removal must be considered; however, in the case of stable hardware maintaining stability through an unstable fracture, one can make the argument for leaving the hardware in place until some bone healing has occurred. The most reliable way to sterilize a wound is to thoroughly debride it, fill the dead space with antibiotic impregnated beads and obtain stable, viable soft tissue coverage. Once the soft tissue envelope is reestablished and stable, bony reconstruction can resume (Figure 13.2A to Figure 13.2E). Regardless, cultures are taken and intravenous antibiotic therapy is given for at least 6 weeks based on culture results. Additionally, it is generally recommended that an infectious disease specialist be involved in the care of the patient.

B.

Ankle Fractures

1.


Ankle fractures include fractures of the posterior and medial malleoli, along with the distal fibula. They will not include fractures involving the tibial plafond, as these were discussed in the previous section. Both open and closed fractures will be covered. Incidences of postoperative infections after treatment of ankle fractures have been reported in a range of 1 to 9% for closed fractures [93]. A similar range has been reported for open fractures with most recent studies reporting rates of infection below 10% [94,95]. There are risk factors that can elevate risk for infection, including age more than 50 (11% rate), a history of alcohol abuse, and a diagnosis of diabetes mellitus [96–98]. In open fractures, the largest risk factors for infection are the severity of the trauma involved in producing the open fracture, and any large degree of contamination at the site. 2.

Treatment

The relative equivalence of infection rates of closed vs. open fractures of the ankle when treated with immediate ORIF has led to establishment of this method as the generally preferred treatment for both closed and open fractures of the ankle. In the case of fractures involving significant crush injuries, or greater then expected swelling, delayed internal fixation is recommended to allow soft tissue swelling to subside, as this facilitates effective closure and reduced incidence of infection. In the event of a deep infection, it is recommended that the surgeon debride, culture, irrigate, and close the incision over a suction drain to avoid fluid collection. Leaving the wound open for treatment with dressing changes and whirlpool therapy has been described as an option [99]; however, hardware must be covered, and this should be used only temporarily until definitive wound closure is possible. Vacuum-assisted closure is a more recently developed option and is discussed in Chapter 10. It provides a way of cleaning a wound, promotes granulation tissue, decreases interstitial edema and prepares a wound for skin grafting or tissue transfer. Intravenous antibiotics should be given with consideration of culture results. Additionally, the surgeon should consider a soft tissue flap if the wound cannot be closed at this time. There is some question about retention vs. removal of hardware at the time of debridement. In the case of ankle fractures, it is generally believed that there is a benefit to leaving the hardware in place until some bone stability is achieved, as the unstable ankle joint is felt to be an even greater detriment to clearing the infection and healing than is the potentially infected hardware. External fixation is also an option in this situation. With either choice, the ankle mortise must be maintained anatomically in order to preserve a viable ankle joint. Additionally, any time there is suspicion of a wound infection after


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fixation of an ankle fracture it is recommended that the surgeon perform an ankle arthrocentesis, because there is high risk for a septic arthritis.

C.

Talus

1.


Fractures of the talus are associated with increased risk of infection in the following circumstances: displaced fractures, open fractures, fracture-dislocations with significant tenting of the skin, fractures with a high degree of soft tissue injury, and fixation during the time of acute soft tissue reaction, or when there is significant swelling [84,100]. In open fracture-dislocations of the talus

A

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Figure 13.2 Infected calcaneal fracture with bone loss in a 55-year-old female multiple trauma patient. (A) Medial view of the foot with skin necrosis over the medial heel. The patient underwent open reduction internal fixation through an extensile lateral approach. The lateral wound healed without consequence. (B) Preoperative CT scan showing dislocation of the posterior facet of the calcaneus medially.



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C

D

E

Figure 13.2 Continued (C) Postoperative radiograph at 3.5 months when acute infection developed. (D) Hardware and necrotic posterior facet removed. Defect filled with polymethylmethacrylate beads impregnated with tobramycin. The patient received 6 weeks of culture-specific antibiotics and then underwent a subtalar fusion with iliac crest bone graft and antibiotic-impregnated resorbable beads. (E) Six-month follow-up radiograph showing solid fusion. The patient is free of infection at 3 years.


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there is reported to be a 38% infection rate [99]. There also appears to be an increased infection incidence when the talus protrudes from the skin in fracture dislocations. When treating closed fractures of the talus, one can expect significantly lower rates of acute infection if good soft tissue and fixation techniques are used. 2.

Treatment

Early reduction is necessary to avoid swelling and to preserve blood supply. All open wounds must be irrigated and debrided emergently. Additionally, open fractures are generally returned to the operating room in 3 to 5 days for an additional irrigation and debridement if necessary, along with definitive soft tissue closure. In the event of superficial tissue necrosis, it is recommended that the surgeon remove all necrotic tissue, both superficial and subcutaneously. However, dry eschar often represents only partial thickness skin loss. As long as this is dry and there are no other surrounding signs of infection, it can often be left to reepithelialize. Close follow-up is required in these cases. When the infection enters the bone, options are limited. These include removal of the talus; whether total or subtotal, or once the infection is controlled, either a Blair type fusion or a tibial–calcaneal fusion.

D. 1.

Calcaneus Incidence and Risk Factors

Fractures of the calcaneus can be a debilitating injury, especially in the event of postoperative wound infection. Incidences of superficial wound infections range from 10 to 27%, while deep infection ranges are 1.3 to 2.5% [101]. Some factors associated with increased wound dehiscence after calcaneus fracture repair are single layer closure, high body mass index, greater than 14 days between injury and surgery, diabetes, and open fractures [102–104]. Additionally smoking is associated with increased incidence of wound dehiscence, but has been reported as a nonfactor in wound infection incidence. Factors directly related to postoperative wound infection include timing of surgery, preoperative control of swelling, careful surgical technique, and avoidance of the use of retractors during surgery [105]. 2.

Treatment

Delay of surgery until acute phase of tissue reaction has passed is recommended in the treatment of calcaneus fractures [106]. It is also recommended that all methods of reducing swelling be performed preoperatively. There is some indication that intermittent pressure stockings can assist in this, along with ice and elevation. Recommendations previously mentioned for the treatment of fractures of the foot and ankle also apply to the calcaneus. In the event of deep infection, repeated aggressive debridement and irrigation is recommended. Implants can be retained, unless there is evidence of deep osteomyelitis (i.e., into the body of the calcaneus) [105]. At least 6 weeks of culture-directed intravenous antibiotic therapy is recommended. Hardware can usually be removed after 3 months if infection persists. Bony defects can be filled with antibiotic impregnated beads, and then bony reconstruction with fusion and bone grafting can be done when soft tissue is stable (Figure 13.2A to Figure 13.2E). Achieving stable soft tissue coverage is critical to the success of any salvage, and the soft tissue envelope should be reestablished before proceeding with bony reconstruction. Despite efforts, however, rotational flaps often do not provide durable coverage, leading to chronic breakdown of tissues (Figure 13.3A to Figure 13.3D).

E.

Midfoot and Forefoot

Open fractures of the midfoot and forefoot should be treated with timely irrigation and debridement. If this is performed quickly, and there is adequate soft tissue coverage, then the surgeon can



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immediately fix the fracture. It is recommended that the patient stay in the hospital for a 2-day treatment of intravenous antibiotics, then receive another 3 weeks of oral antibiotics after discharge [107]. Fractures in this part of the foot are otherwise treated in the same manner and with the same precautions as other fractures of the foot and ankle in an attempt to avoid postoperative infection. As with infections in other regions of the foot and ankle, if the infection becomes chronic, eventual definitive therapy may include amputation.

V.

CONCLUSION

Evaluation and treatment of patients with traumatic injury to the foot and ankle is challenging. Clinical presentation of infection in patients with foot and ankle trauma varies greatly, depending on the interplay of various host factors, location of infection, and pathogenic organisms. With modern surgical techniques and perioperative care, rates of infection after surgery involving fractures of the foot and ankle have been reduced. Infection involving these bones and soft tissue, however, still occur with reasonable incidence and, in many cases, with poor outcomes. Preoperative care, timing of surgery, meticulous surgical techniques including adequate soft tissue coverage,

A

B

Figure 13.3

(A) Chronic open wound. (B) Sural artery-based rotational flap.


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C

D

Figure 13.3 Continued (C) Insetting the flap. (D) Skin graft donor site. Although this flap healed, the patient persisted with chronic breakdown at the distal end of the flap. It did not provide durable coverage, and the patient eventually chose to undergo a below-knee amputation rather than a free-tissue transfer.

and postoperative care all have a significant impact on the rates of postoperative infection. While these factors can be controlled to some extent, there are also many factors that cannot be controlled, including physiological factors such as age, diabetes, and vascular status; as well as the degree of comminution and soft tissue injury of each individual injury, exposure of bone to the environment, and any local contamination at that time. It is therefore necessary to maximize the chance of healing without injury by attempting to control those factors that can be manipulated, to the highest possible degree. Additionally, once infection has occurred, there are factors that are under the control of the surgeon, and should be addressed, such as early diagnosis, adequate debridement and irrigation, culture-based antibiotic therapy, and early recognition of soft tissue coverage problems with appropriate flap procedure planning. Infection in the foot and ankle after trauma or surgery is a significant problem and can lead to disastrously poor outcomes. For this reason it is of the utmost importance to minimize its possibility of occurrence whenever possible.



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14 Complex Regional Pain Syndrome or Reflex Sympathetic Dystrophy William A. Vitello Department of Surgery, Wright State University, Dayton, Ohio

CONTENTS I. Introduction ................................................................................................................... 371 II. History............................................................................................................................ 372 III. Definitions ...................................................................................................................... 372 IV. Pathophysiology ............................................................................................................. 372 V. Stages.............................................................................................................................. 373 A. Stage I (Acute) ........................................................................................................ 374 B. Stage II (Dystrophic) .............................................................................................. 374 C. Stage III (Atrophic) ................................................................................................ 374 VI. Clinical Diagnosis........................................................................................................... 374 VII. Diagnostic Testing .......................................................................................................... 375 A. Radiographs............................................................................................................ 375 B. Three-Phase Radionuclide Bone Scan..................................................................... 375 C. Sympathetic Blockade............................................................................................. 376 D. Thermoregulatory Testing ...................................................................................... 376 E. Psychological Evaluation ........................................................................................ 376 VIII. Treatments...................................................................................................................... 376 A. Pharmacological Treatment .................................................................................... 376 1. Antidepressants ................................................................................................ 377 2. Narcotic Analgesics .......................................................................................... 377 3. Oral Nifedipine................................................................................................. 377 B. Nerve Blocks ........................................................................................................... 377 C. Intravenous Regional Blocks .................................................................................. 377 D. Surgical Sympathectomy......................................................................................... 378 E. Physical Therapy..................................................................................................... 378 IX. Summary ........................................................................................................................ 378 References .................................................................................................................................. 378

I.

INTRODUCTION

Complex regional pain syndrome (CRPS), also called reflex sympathetic dystrophy (RSD), is the term applied to a variety of disorders that have similar clinical features and physiology. RSD, a

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poorly understood symptom complex, may occur after major lower extremity trauma or may complicate minor injuries or surgical procedures. Regardless, this can be one of the most dreaded complications and challenges to the orthopedic surgeon. Early signs and symptoms of these processes are frequently not recognized or are ignored. Delay in the diagnosis of RSD or failure of conventional pain management results in frustration for both the patient and clinician. Early treatment is important because of the difficulty in managing more chronic syndromes, which may contribute to the extent of permanent disability.

II.

HISTORY

Mitchell et al. [1], a Civil War physician, first described the clinical symptoms now known as RSD. He reported a syndrome of intense pain and vasomotor dysfunction that accompanied partial nerve injuries caused by gunshot wounds to the upper extremities. Many others have since added their descriptions and opinions to the literature. Sudek [2] described the osteoporosis that is associated with long-standing RSD. In 1916, Leriche [3] reported the role of sympathetic nervous system in the syndrome. In 1930, Schutzer and Gossling [4] performed the first successful surgical sympathectomy for the cure of RSD. Livingston [5] expanded the ‘‘vicious cycle’’ hypothesis to a concept of abnormal firing in self-sustaining loops in the dorsal horn provoked by an irritative focus in small nerve endings or major nerve trunks. In 1952, Bonica [6] coined the term RSD, which is now being used to describe the syndrome of pain and dysfunction that can develop after extremity trauma, nerve injury, or surgery.

III.

DEFINITIONS

Many terms have been used to describe the syndrome that is currently referred to as RSD. Causalgia is a Greek term that means ‘‘burning pain.’’ It has been used historically to describe an RSD that follows partial or complete injury to a peripheral nerve trunk [7]. RSD is characterized by constant, spontaneous, severe burning pain and is usually associated with hypesthesia and hyperesthesia, hyperpathia, and allodynia. Vasomotor disturbances, if persistent, may result in trophic changes. Changing of concepts and taxonomy was put forth by a special consensus conference that was convened on this topic. The changes were based on the patient’s history, presenting history, symptoms, and findings at the time of diagnosis [8]. The disorders are grouped under the umbrella term CRPS. This overall term requires the presence of regional pain and sensory changes following a noxious event. Further, the pain is associated with findings such as abnormal skin color, temperature changes, abnormal sudomotor activity, or edema. The combination of these findings exceeds their expected magnitude in response to known physical damage during and following the inciting event. Two types of CRPS have been recognized: type I, which corresponds to RSD and occurs without a definable nerve lesion, and type II, formerly called causalgia, which refers to cases where a definable nerve lesion is present. The term sympathetically maintained pain (SMP) was also evaluated and considered a variable phenomenon associated with a variety of disorders, including CPRS types I and II. These revised categories have been in the Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, 2nd ed. (IASP Press). Table 14.1 [9] lists various other terms used to describe RSD.

IV.

PATHOPHYSIOLOGY

The sympathetic and parasympathetic nervous systems are the two divisions of the autonomic nervous system. The sympathetic nervous system is mostly an efferent (central-to-peripheral) system, but there are some afferent (peripheral-to-central) fibers. The two main ganglionic trunks are the cervical and lumbar trunks. However, there are many other ganglia throughout the paraspinal area, which form complex interconnections within the sympathetic nervous system and between it and the brain. Preganglionic fibers arise from the cell bodies in the gray matter of


Complex Regional Pain Syndrome or Reflex Sympathetic Dystrophy Table 14.1

373

Terms Used to Describe Reflex Sympathetic Dystrophy

Acute atrophy of bone Algodystrophy Algodystrophy mineures Algodystrophy reflexes Causalgia Chronic traumatic edema Complex regional pain syndromes Mimo-causalgia Minor causalgia Neurodystrophy Pain-dysfunction syndrome Posttraumatic dystrophy Posttraumatic osteoporosis Posttraumatic pain syndromes Reflex neurovascular dystrophy Shoulder-hand syndrome Sudeck’s atrophy Sympathalgia Sympathetic overdrive syndrome Traumatic vasospasm

the spine. They exit the spinal cord in the ventral roots of the spinal nerves, and they either reenter the spinal cord through the white rami communicans at the same or an adjacent level, or they connect to a peripheral sympathetic ganglion. Postganglionic fibers may reenter the corresponding spinal nerve through the gray rami communicans to innervate viscera or to travel with blood vessels. They also may move to a higher or lower level and may cross the midline at multiple points. The confusion and complexity of the clinical terminology of sympathetic nervous system dysfunction are largely due to an incomplete understanding of its actions [10]. It has long been believed that sensitization of peripheral mechanoreceptors and nociceptors can be a cause of SMP [11]. Recently, there have been studies that suggest that there is a sympathetic-afferent coupling at sensory nerve endings mediated through sensitive alpha-adrenergic receptors. Norepinephrine is released from sympathetic terminals in response to increased sympathetic tone. This mediator release can stimulate the peripheral sensory nerves of the afferent spinothalamic tract, which transmit intense pain and temperature signals to the neocortex [12,13]. A direct injury to the nerve may allow for an epileptic type discharge of electrical energy in the area of the injured nerve. This may either directly stimulate sensory nerves or allow for excessive neurotransmitter release, which may stimulate pain fibers [14]. Another mechanism explaining the pathogenesis is deafferentation, which is a substantial decrease in afferent signal to the spinal cord and to other neurological centers. Continuous and normal sensory input is thought to suppress sympathetic activity. When the extremity becomes painful it will be used less and the patient will avoid contact. This will lead to increased skin sensitivity and decreased afferent activity. The decreased afferent activity limits the normal inhibition of the sympathetic discharge. Such a mechanism can explain the positive clinical results seen with massage and desensitization of a body part affected by SMP [15].

V.

STAGES

It is important to remember that CRPS is not a static event with predictable sequelae, but rather a dynamic process that starts in the periphery with reversible physiologic responses to the initiating incident. Over time, these events produce irreversible end-organ adaptations or permanent injury. The following staging of acute, dystrophic, and atrophic provides a simplistic view of a dynamic and complex process. The progression from one stage to another will also vary from patient to patient, and the recognition of this variation is critical for successful treatment or intervention.


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A.

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Stage I (Acute)

Classically, stage I is the first 3 months after injury. Symptoms develop within days to weeks, but this could be a more insidious process. The pain is more severe or persistent than would be expected from the magnitude of the injury, and it is often described as burning or aching. The pain will be aggravated by dependency, motion, physical contact, and emotional anxiety and will not respond to narcotics. Hypersensitivity and allodynia over an injured nerve (posterior tibial nerve in the tarsal tunnel) may be elicited early in the process. Once the dystrophy is established, the entire extremity may be so hypersensitive that identifying a painful cutaneous nerve or ligamentous injury may be impossible [16]. Vasomotor abnormalities resulting in hyperthermia or hypothermia may also be seen, and radiographic signs of disuse are often apparent by 3 or 4 weeks.

B.

Stage II (Dystrophic)

This stage is typically seen at 3 to 6 months after injury, and the pain is constant and unremitting. The subcutaneous tissues and periarticular areas may change consistency and become firm and indurated. The skin may be cool to the touch or even appear cyanotic. Without early recognition and appropriate treatment, hindfoot varus and ankle equinus will result. Localization of pain and a specific lesion become more difficult. Diffuse osteopenia becomes more pronounced, and a threephase bone scan may be positive at this point.

C.

Stage III (Atrophic)

Atrophic changes become more pronounced during the period 6 months to 1 year after the injury. The changes that occur in the soft tissues, nerves, and blood vessels during this period may become permanent. The skin appears shiny, thin, and hypothermic, and radiographs will show marked osteopenia.

VI.

CLINICAL DIAGNOSIS

The history given by patients with sympathetically mediated pain may vary widely. The initiating noxious event or injury may be as seemingly trivial as an ankle sprain or may be the result of high energy, massive foot and lower extremity trauma. If the patient has an unusual amount of pain immediately after surgery or injury, and healing is not progressing as would otherwise be expected, then sympathetic dysfunction should be suspected. Early recognition of this process is critical to the patient’s ultimate outcome and morbidity. The SMP has a variable presentation. Lankford [17] has described four cardinal signs and symptoms and six secondary signs and symptoms required to establish the diagnosis. The four cardinal signs are pain, edema, stiffness, and discoloration. The secondary signs are demineralization, pseudomotor changes, thermoregulatory changes, vasomotor instability, trophic changes, and palmar fibromatosis. The pain is typically in a nonanatomical distribution and usually does not follow the distribution of a single peripheral nerve. However, the CPRS type II causalgia is defined as burning pain and allodynia in the hand or foot after partial injury of a nerve or one of its major branches. One of the earliest and most helpful signs of early sympathetic dysfunction is intolerance to cold [18]. There is usually an increase in sweating and color changes in the extremity ranging from blue to dusky red. Allodynia and hyperpathia, which are pathologic pain responses, are frequently seen early in the syndrome and make aggressive physical therapy difficult. These patients’ pain usually does not respond to narcotic analgesics that are usually appropriate for the extent of trauma or injury. Later in the course of the process there are trophic changes that include dystrophic, smooth and shiny skin, osteoporosis, fast growing, brittle nails, and hypertrichosis, with muscular and subcutaneous atrophy [19]. A mechanical or systemic cause of the patient’s extremity pain should be pursued. Some of these problems can be easily managed and treated if looked for and considered. It is important to rule out stress fractures, chronic posttraumatic synovitis, peripheral vascular disease, tendinitis,


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avascular necrosis, compressive neuropathies, osteochondral lesions, and impingement syndromes. With evaluation of the patient by careful history and physical examination followed by the appropriate laboratory studies, radiographic evaluations, and scintigraphic information, the correct diagnosis should be obtained [20].

VII.

DIAGNOSTIC TESTING

There is no single reliable, sensitive, and specific diagnostic test for CRPS. Because it is primarily a clinical diagnosis, undue reliance on diagnostic testing is not warranted. Objective measures that appear to be useful in the evaluation of CRPS include plain radiographs (weight-bearing, if possible) of the foot and ankle, three-phase bone scan, vasomotor/thermoregulatory assessment, and differential neural blockade.

A.

Radiographs

Three-view weight-bearing radiographs of the foot and ankle are an important first diagnostic test in the assessment of CRPS. These are useful to rule out other diagnoses and to identify sources of persistent pain. Early in the course of the disease, 3 to 5 weeks after symptoms, the radiographs classically show diffuse osteopenia. Periarticular and juxta-arterial osteoporosis, soft tissue swelling, and subchondral bone changes also may be seen. Sudeck’s atrophy has been used to describe these bony changes. However, osteopenia is not a prerequisite for the diagnosis of CRPS. Of the patients with definite CRPS, 30% have been found to be without bony resorption by radiographs [21].

B.

Three-Phase Radionuclide Bone Scan

The three-phase bone scan analysis has assumed an important role in the assessment of CRPS and RSD. The standard technique uses a 20-mCi injection of technetium-99m methylene diphosphonate into a vein. The bone scan involves three separate phases: 1. Phase I (dynamic component) is performed immediately after injection of the radionucleotide bolus and is continued every 5 seconds for 40 seconds. This segment of the test allows assessment of regional perfusion characteristics. 2. Phase II (blood pool component) is recorded immediately after the first phase and is reflected by radiotracer activity. 3. Phase III (delayed, metabolic component) is done 3 to 4 hours later and provides information about chronic changes. Kozin et al. [22] established a criteria system for diagnosis of RSD and reported a sensitivity of 67%, a specificity of 92%, a positive predictive value of 86%, and negative predictive value of 67%. The most comprehensive diagnostic criteria for interpreting the TPBS were set forth by Holder and MacKinnon [23]. They stated that the abnormal increased activity must be diffuse. This was differentiated from multifocal uptake, which is not RSD, and from focal uptake, as a possible initiating lesion, upon which diffuse uptake of RSD is superimposed. The pattern of increased flow on the radionuclide angiogram, diffuse increased blood pool phase activity, and diffuse increased delayed activity may be most suggestive of RSD. However, abnormality in all the three phases is seen in less than half of the patients. The diffuse increased activity with juxta-articular accentuation on the delayed images appears to be the most suggestive and sensitive scintigraphic findings. Further work by Holder [24] was done to on a more homogenous group of patients having symptoms in the foot consistent with RSD. The criteria used were nonanatomic pain, autonomic vasomotor signs, dermal changes, and positive response to sympathetic blockade. With these clinical criteria, he demonstrated a scintigraphic pattern similar to that in the hand with diffuse increased activity in the hind-, mid- and forefoot with juxta-articular accentuation. His overall sensitivity and negative predictive value was 100%. The specificity of 80% and positive predictive value of 54% was attributed to the large number of patients with diabetes mellitus in their population who presented with infection in whom there was no clinical suspicion of RSD [24].


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C.

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Sympathetic Blockade

Sympathetic blockade has been cited as the best method for the diagnosis of SMP [25]. If complete sympathetic blockade does not relieve pain, the disorder most likely is not SMP. There are a variety of ways to achieve a sympathetic block; the most common method is the intravenous administration of an alpha-blocker such as phentolamine [26]. This creates a complete sympathetic blockade and so the pain relief should correlate closely with the degree of SMP. However, this method of blockade is of short duration and does not help in the treatment of the condition. Differential spinal sympathetic blockade is done with the use of a spinal puncture and requires delivery of the anesthetic agent to the appropriate area as documented by an increase of 2 to 38C in the skin temperature of the involved extremity. Visual analog pain scales should be used to measure the amount of pain relief achieved with the blockade. A decrease in pain of at least 50% must be documented in order for the physician to be confident of a diagnosis of SMP.

D.

Thermoregulatory Testing

Early in the course of RSD, abnormal thermoregulation may be manifested by increased or decreased total blood flow and asymmetric responses to isolated cold-stress testing. It has been demonstrated that normal, local, and reflex central mechanisms of vascular reactivity exist in patients with RSD [27]. Long-standing RSD is associated with abnormally reduced vascular activity, despite apparently normal total blood flow. Symptoms of pain and cold intolerance correlate with abnormal vascular control as demonstrated by isolated cold-stress testing or laserDoppler velocimetry. Lower extremities with RSD manifest consistently abnormal thermoregulatory and nutritional flow patterns. In acute stages of RSD, total flow may be elevated, yet nutritional flow may be barely sufficient for tissue survival. Analysis of a painful lower extremity or foot is incomplete without assessment of thermoregulatory capacity in a stressed state.

E.

Psychological Evaluation

The psychological assessment is conducted to obtain understanding of stressors that may adversely affect treatment and to obtain information about the psychological distress patients may be experiencing as a result of the pain and subsequent loss of function. The evaluation may consist of a clinical interview and personality measures such as the Minnesota Multiphasic Personality Inventory (MMPI). Research has indicated that, as RSD progresses, patients’ MMPI profiles tend to resemble those of patients experiencing chronic pain, as revealed by the increasing evaluations on the hypochondriasis, depression, and hysteria scales. Phase I patients also report more pessimism than do patients in the second and third phases of the disorder, which suggests that patients have more difficulty adjusting to the disorder in the early phases. Younger patients with RSD tend to report more pessimism and symptoms of depression than do older patients [28].

VIII. TREATMENTS Because the Pathophysiology of RSD is predominantly a hyperactivity of the regional sympathetic nervous system, pain management in such patients should focus on interrupting the activity of the sympathetic nervous system. This can be accomplished by different modalities such as pharmacologic agents, nerve blocks, chemical sympathectomy, surgical, and physical therapy. The literature on RSD treatments is difficult to interpret because of the lack of uniformity on quantification of treatment outcomes as defined by a change in pain or improvement in function [29].

A.

Pharmacological Treatment

Many drugs are used in the treatment of RSD. A wide variety of unrelated agents have been used in treating RSD because a patient with this syndrome go through phases of severe pain, limited function, and depression. Sympathetic hyperdysfunction causes vasoconstriction, pain, and swell-



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ing necessitating sympathetic blockade with local anesthetics, sympathetic blocking drugs, or vasodilating drugs. A myofascial pain component is common in RSD so a nonsteroidal antiinflammatory agent or muscle relaxants are often used [29]. 1.

Antidepressants

There are three effects of tricyclic antidepressants that make this class of drugs valuable in the treatment of RSD: sedation, analgesia, and mood elevation. The analgesic action of the tricyclics may be related to inhibition of serotonin reuptake at nerve terminals of neurons that act to suppress pain transmission, with resultant prolongation of serotonin activity at the receptor [30]. Amitriptyline has the most potent effect on amine production and should be the most effective of the tricyclics. It is used most often in a 25 to 50 mg dose at bedtime. 2.

Narcotic Analgesics

Narcotics have a high abuse potential by those who have chronic pain. These agents will do little to relieve pain once tolerance develops. When given epidurally in combination with local anesthetics in an acute inpatient setting, these agents can be extremely effective analgesics. Both morphine and fentanyl have been used by continuous infusion in doses of 0.5 mg/h and 0.03 to 0.05 mg/h, respectively. For chronic pain, narcotics should only be used sparingly. Morphine and methadone may be used effectively in a carefully ordered schedule to promote progress in physical therapy. 3.

Oral Nifedipine

It has been reported that oral nifedipine was successfully used in the treatment of Raynaud’s phenomenon and RSD [31]. Nifedipine is a calcium channel blocker that relaxes smooth muscle, increases peripheral blood flow, and antagonizes the effect of norepinephrine on arterial and venous smooth muscle. It is suggested that nifedipine is given in a dose of 10 to 30 mg orally three times a day for the treatment of RSD. Because of the vasodilatory end-organ effects of this drug, headaches are a frequent side effect [29].

B.

Nerve Blocks

Sympathetic blockade and physical therapy are the mainstays of current treatment for RSD. Many patients respond to sympathetic blockade, and the effects may be permanent. A series of blocks should be performed before they are declared unsuccessful. If repeated injections are not possible in this manner, then admission to the hospital for continuous infusion of local anesthetic at the appropriate site is indicated. For the lower extremity, the lumbar sympathetic chain or epidural space is the preferred site. Conduction of nerve impulses through the various size nerves can be controlled by the concentration of local anesthetic used. A low concentration of lidocaine (1%) or bupivacaine (0.25%) blocks the C-fibers, which conduct visceral afferent impulses and dull, aching somatic pain impulses. A moderate concentration of lidocaine (1.5%) or bupivacaine (0.5%) blocks A-delta fibers, which conduct sharp somatic pain impulses [29].

C.

Intravenous Regional Blocks

Intravenous or intra-arterial infusion of ganglionic blocking agents into the affected extremity has gained prominence in the treatment of RSD. Guanethidine, an antihypertensive agent, inhibits the presynaptic release of norepinephrine by displacing it from its source site on the nerve endings and preventing its reuptake [32]. Guanethidine creates a sympathetic block pharmacologically. Using a Bier block technique, guanethidine is infused into the affected extremity. After 30 to 45 min, the tourniquet is slowly released. For the lower extremity, 20 mg of guanethidine is diluted in 50 cc of 0.25% lidocaine. Intravenous reserpine has also been used as a blocking agent with this same technique.


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D.

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Surgical Sympathectomy

Surgical sympathectomy has been advocated for patients who do not experience permanent relief from sympathetic blocks or other conservative measures. Before electing sympathectomy, the following criteria should be met [29]: 1. 2. 3. 4.

E.

The patient should experience pain relief from sympathetic block on several occasions. Pain relief should last at least as long as the vascular effects of the sympathetic block last. Placebo injection should produce no pain relief, or the relief should be less pronounced and of shorter duration than that achieved with local anesthetic sympathetic blocks. Possible secondary gain motives and significant psychopathology should be ruled out as possible causes of pain complaints.

Physical Therapy

Physical therapy is an important adjunct to sympathetic blocks and may be effective alone for the treatment of mild cases of RSD. For long-standing cases, rehabilitation may be necessary. Active and active-assisted range of motion exercises, muscle strengthening and conditioning, massage, and heat (whirlpool, paraffin, or radiant heat) are particularly useful [33]. Vigorous passive range of motion exercises and the use of heavyweights may trigger symptoms. Exercises are best performed during analgesic periods following sympathetic blocks. Patients may require hospital admission and aggressive analgesia with epidural, intravenous, or oral routes in order to participate in an effective physical therapy program [29].

IX.

SUMMARY

Early diagnosis of RSD is essential. It is a clinical diagnosis that may be supplemented by digital temperature, three-phase bone scan, and radiography. A thorough examination is necessary to identify untreated or inadequately treated sources of RSD. Once diagnosed, prompt treatment is beneficial. Patients should be started on a pharmacological agent and then undergo a series of sympathetic blocks, with ongoing physical therapy. Surgical treatment is considered after failure of all other conservative measures. A multidisciplinary approach with all available modalities and personnel should be used to achieve the best success in breaking the cycle of pain and returning the patient to normal productive function.

REFERENCES 1. Mitchell, S.W., Morehouse, G.R., and Keen, W.W., Gunshot Wounds and Other Injuries of the Nerves, Lippincott, Philadelphia, 1864. 2. Sudek, P.H.M., Uber die acute entzundliche Knockenatrophie, Arch. Klin. Chir., 62, 147, 1900. 3. Leriche, R., The Surgery of Pain (Young, A., trans, Ed.), Williams & Wilkins, Baltimore, 1939. 4. Schutzer, S.F. and Gossling, H.R., The treatment of reflex sympathetic dystrophy syndrome, J. Bone Jt. Surg., 66A, 625–629, 1984. 5. Livingston, W.K., Pain Mechanisms: A Physiological Interpretation of Causalgia and its Related States, Macmillan, New York, 1943. 6. Bonica, J.J., The Management of Pain, 1st ed., Lea & Febiger, Philadelphia, 1953, p. 13. 7. Mitchell, S.W., On the diseases of nerves resulting from injuries, in Contributions Relating to the Causation and Prevention of Disease, and to Camp Diseases: Together with a Report of the Diseases, etc., among Prisoners at Andersonville, GA, Flint, A., Ed., Hurd and Houghton, New York, 1867, pp. 412–468. 8. Stanton-Hicks, M., Janig, W.S., Hassenbusch, S., Haddox, J.D., Boas, R., and Wilson, P., Reflex sympathetic dystrophy: changing concepts and taxonomy, Pain, 63, 127–133, 1995. 9. Merskey, H. and Bogduk, N., eds., Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, Seattle, Wash: IASP Press, 1994. 10. Dzwierzynski, W.W., Reflex sympathetic dystrophy, Hand Clin., 10, 29–44, 1994. 11. Roberts, W.J., Sympathetic activation of A-delta nociceptors, Somatosens. Res., 3, 33–44, 1985.



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12. Duncan, K.H., Lewis, R.C., Jr., Racz, G., and Nordyke, M.D., Treatment of upper extremity reflex sympathetic dystrophy with joint stiffness using sympatholytic Bier blocks and manipulation, Orthopaedics, 11, 883–886, 1988. 13. Katz, M.M. and Hungerford, D.S., Reflex sympathetic dystrophy affecting the knee, J. Bone Jt. Surg., 69B, 797–803, 1987. 14. Sunderland, S., Nerves and Nerve Injuries, 2nd ed., Churchill Livingstone, New York, 1978, pp. 377–472. 15. Wall, P.D. and Devor, M., The effect of peripheral nerve injury on dorsal root potentials and on transmission of afferent signals into the spinal cord, Brain Res., 209, 95–111, 1981. 16. Teasdall, R.D., Koman, L.A., Wessinger, P., Pollock, F.E., Jr., Smith, B.P., and Marr, A.W., Reflex sympathetic dystrophy of the foot and ankle, Foot Ankle Clin., 3, 485–509, 1998. 17. Lankford, L.L., Reflex sympathetic dystrophy, in Rehabilitation of the Hand-Surgery and Therapy, 3rd ed., Hunter, J.M., Schneider, L.H., and Mackin, E.J., Eds., Mosby, St. Louis, MO, 1990, pp. 763–786. 18. Koman, L.A., Nunley, J.A., Goldner, J.L., Seaber, A.V., and Urbaniak, J.R., Isolated cold stress testing in the assessment of symptoms in the upper extremity: preliminary communication, J. Hand Surg., 9A, 305– 313, 1984. 19. Lindenfeld, T.N., Bach, B.R., Jr., and Wojtys, E.M., Reflex sympathetic dystrophy and pain dysfunction in the lower extremity, Instr. Course Lect., 46, 261–268, 1997. 20. Kozin, F., Reflex sympathetic dystrophy syndrome, Bull. Rheum. Dis., 36, 1–8, 1986. 21. McDougall, I.R. and Keeling, C.A., Complications of fractures and their healing, Semin. Nucl. Med., 18, 113–125, 1988. 22. Kozin, F., Soin, J.S., Ryan, C.M., Carrera, G.F., and Wortmann, R.L., Bone scintigraphy in reflex sympathetic dystrophy syndrome, Radiology, 138, 437–443, 1981. 23. Holder, L.E. and MacKinnon, S.E., Reflex sympathetic dystrophy in the hands: clinical and scintigraphic criteria, Radiology, 152, 517–522, 1984. 24. Holder, L.E., Reflex sympathetic dystrophy in the foot: clinical and scintigraphic criteria, Radiology, 184, 531–535, 1992. 25. Roberts, W.J., A hypothesis on the physiological basis for Causalgia and related pains, Pain, 24, 297–311, 1986. 26. Arner, S., Intravenous phentolamine test: diagnostic and prognostic use in reflex sympathetic dystrophy, Pain, 46, 17–22, 1991. 27. Christensen, K., The reflex sympathetic dystrophy syndrome: an experimental study of sympathetic reflex control of subcutaneous blood flow in the hand, Scand. J. Rheumatol., 12, 263–267, 1983. 28. Raj, P.P. et al., Management protocol of reflex sympathetic dystrophy, in Pain and the Sympathetic Nervous System, Stanton-Hicks, M., Ed., Kluwer, Boston, 1989. 29. Raj, P.P., Pain Medicine: A Comprehensive Review, Mosby, St. Louis, MO, 1996, pp. 466–480. 30. Hollister, L., Tricyclic antidepressants, N. Engl. J. Med., 299, 1106–1109, 1978. 31. Prough, D.S., McLesky, C.H., Poehling, G.G., Komar, L.A., Weels, D.B., Whitworth, T., and Semble, E.L., Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy, Anesthesiology, 62, 796– 799, 1985. 32. Hannington-Kiff, J.G., Intravenous regional sympathetic block with guanethidine, Lancet, 1, 1019–1020, 1974. 33. Pak, T.J., Martin, G.M., Magness, J.L., Kavanaugh G.J., Reflex sympathetic dystrophy: review of 140 cases, Minn. Med., 53, 507–512, 1970.



15 Late Reconstruction Mark D. Perry Southwestern Medical Center, Department of Orthopaedic Surgery, Dallas, Texas

Arthur Manoli II Michigan International Foot and Ankle Center, Pontiac, Michigan

CONTENTS I. Introduction ...................................................................................................................... 381 II. General Considerations ..................................................................................................... 382 III. Late Reconstruction .......................................................................................................... 382 IV. Specific Injuries ................................................................................................................. 383 A. Talus Fractures .......................................................................................................... 383 B. Calcaneus................................................................................................................... 384 C. Midfoot...................................................................................................................... 387 D. Cuboid ....................................................................................................................... 387 E. Syndesmotic Injuries.................................................................................................. 389 F. Compartment Syndrome ........................................................................................... 389 G. Flexion Contractures ................................................................................................. 390 V. Summary ........................................................................................................................... 390 References .................................................................................................................................. 390

I.

INTRODUCTION

Complex foot and ankle injuries are occurring more frequently. Traditionally, victims of severe automobile accidents succumbed to their injuries [1]. However, even though the number of automobile accidents increases by approximately 2% per year, the percentage of fatalities is decreasing [2]. This results in an increase in the number of people with significant high-energy foot and ankle fractures. Past considerations have focused on prevention of head and thoracic injuries whereas today there is more focus on prevention of the collapse of the foot box during an accident. The demographics of the injured have changed from several decades ago as well. The population continues to be older and more patients are on medications that affect bone quality (e.g., steroids). Injuries to the feet are not without significant cost.If a worker has a major foot injury and is no longer able to return to work as before, significant economic effects result. Several studies looking at return to work for lower-extremity injuries show that the injured return to work later than when the physician feels appropriate, but the workers themselves feel that they have returned at an appropriate time [3,4]. This shows that both physicians’ and patients’ perceptions of the injury need to be improved.

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The goals following reconstruction need to be realistic [5]. There is no guarantee of preinjury function even if bony alignment can be perfectly reestablished. The energy placed into the soft tissue results in more than just injury to bones. It has been shown that patients with Lisfranc dislocations have a poorer result if there is no fracture [6]. In addition to bone quality, patient comorbidities have a significant effect on overall outcome [7,8]. It has been shown that diabetes (insulin-dependent and non-insulin-dependent) greatly delays union time in the lower extremities. Diabetes also results in worse surgical outcomes even after the fractures heal [9]. Some authors advocate using stronger internal fixation in the diabetic population than in the nondiabetic population [10,11]. Similarly, the effects of smoking are also significant in the overall outcome of fracture healing [12]. Some authors report a 50% increase in complication rates in smokers compared with nonsmokers [13]. This chapter focuses on late reconstruction techniques.

II.

GENERAL CONSIDERATIONS

The authors feel that there are several general technical considerations that should be followed in foot reconstruction. As a rule, cannulated screws do not provide adequate strength for fixation. In the past, a solid 3.5-mm cortical screw has been the ‘‘workhorse’’ hardware, although the new 4-mm cortical screw provides extremely strong and rigid fixation and is being used more frequently. The foot exhibits much variability in bone morphology or fracture fragments. For this reason, it is recommended that a wide variety of equipment be available and familiar to the surgeon. The modular handset with very small plates is useful in foot reconstruction, as are 2.7-mm dynamic compression plates (DCPs) with long 2.7-mm screws. Recent work shows that when placing a screw in cancellous bone, there is a significant loss of pullout strength if the hole is tapped [14]. For this reason, tapping of cancellous screws is not recommended. Posttraumatic reconstructions require careful evaluation and preoperative planning. Radiographs and careful clinical evaluation [15] are the foundation of surgical intervention. Weightbearing radiographs, which include an anteroposterior (AP) view of the ankles (both sides on one film), an AP view of the feet (both sides on one film), and a combined lateral view of each side (a combination of the lateral ankle and a lateral foot), are preferred. This allows the surgeon to accurately determine hindfoot malalignment, height lost, and forefoot alignment.

III.

LATE RECONSTRUCTION

Late reconstructions are performed if the injured foot is not a candidate for acute reconstruction, as often happens in patients with diabetes or renal failure, or if patients were originally treated nonoperatively but require surgery because of significant symptoms. Communication with the patient concerning the expected outcome is paramount. Patients, especially smokers, need to understand that amputations are likely to follow painful nonunions or severe infections. Patients with significant deformities or soft tissue risk should be informed that they are undergoing a stage procedure, with the last stage being an amputation. We disagree with Ouzounian and Kleiger [16] and feel that arthrodesis should be performed under a tourniquet. Surgery in a bloodless field allows for attention to be directed at more important issues. In some cases of more distal trauma, a calf tourniquet provides effective hemostasis [17]. In general, the patients’ best interests are served if they are comfortable with, and have consented to, amputation before a reconstructive trial is undertaken. A study addressing tibial fractures showed that the patients with amputations had no complaints and were more pleased than the patients who underwent attempted surgical union. Amputation is not a defeat but may provide the patient with significant improvement in mobility and pain. Foot reconstructions need to be performed within a 2-year period from the date of injury. If final treatment is provided after this time, the symptoms linger and do not respond as well to definitive treatment, whether it be an arthrodesis or an amputation.


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Figure 15.1 Dorsal talar spur after trauma that resulted in nerve irritation.

There are several late and seemingly minor complications that provide substantially irritating symptoms. Although the effect on foot architecture may be minimal, they still greatly hinder the patients’ final abilities or outcomes. An example of this would be talonavicular or naviculocuneiform spurring or osteophytes (Figure 15.1). These can cause a superficial nerve irritation, which is quite disabling to the patient. Tight heel cords are discussed later.

IV. A.

SPECIFIC INJURIES Talus Fractures

Nondisplaced talar neck fractures should be stabilized acutely. In this circumstance, two cannulated screws placed parallel from a posterolateral incision are recommended. If there is any displacement of the fracture, or rotation, seen on plain films or computed axial tomography (CAT) scans, then a two-incision technique (medial and lateral) is necessary to assess fracture alignment. It is important for the talus to be anatomically reduced; typically there is medial comminution of the talar neck. If this cannot be stably held by screws, a small plate is placed medially. A talar osteotomy may be needed in order to eliminate symptoms if the talus heals with a significant malreduction [18]. In general, displaced talar neck fractures are treated with two parallel screws, one from the medial side and the other from the lateral side. However, sometimes the fracture plane will be based more proximally and laterally, involving the lateral process [19]. In this instance, the lateral screw will be placed in more of a crossing pattern to the medial screw. Stainless-steel screws are preferred over titanium screws for fixation because the increased screw strength provides better protection during ankle motion. In the environment of the traumatized foot, mixing metals is not contraindicated unless the screws are in direct contact. Posttraumatic arthritis of the tibiotalar joint may be successfully treated with arthrodesis. The final result of the fusion may not be known until 1 year after the surgery [20], and the patients continue to have good results for as long as 25 years. The goal would be to achieve a painless ankle and functional position. If the arthritis occurs because of articular step-off with little resulting bone loss, then we favor an inside-out technique for the introduction of the internal fixation. An anterior incision is made exposing the ankle joint, articular cartilage is removed taking care to leave the subchondral bone and, subsequently, multiple perforations are made in the bony surface. The ankle is dislocated to reveal the surface of the tibial plafond. A drill bit is then placed from a distal to proximal direction. A suction tip is placed through the hole to delineate the posterior exit. At this point the ankle is re-reduced and from the posterior to anterior direction the drill track is made into the talus, and then an appropriate screw is used to provide internal compression across the arthrodesis. At this point, placing the screws from the lateral fibula into the talus and from the medial malleolus into the talus is technically much easier (Figure 15.2). If however, there is significant bone loss with subsequent subtalar arthritis, a lateral incision technique is preferred. This involves osteotomies in the fibula, with a posterior rotation to provide


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Figure 15.2

(A) AP view of an ankle fusion. (B) Lateral view of an ankle fusion.

excellent visualization of the tibiotalar joint. Local bony deficiencies are easily corrected as they only involve the preparation of the surfaces to be fused. This approach gives excellent working access to the joint and allows careful scrutiny of alignment. Provisional alignment is obtained using a medium distractor. The medium distractor is strong enough to provide a significant distraction force across the fusion site and precise enough to allow fine corrections in alignment, and it provides good working access by having decreased bulk when compared with the femoral distractor. After the tibia and talus have been fixed with internal fixation, the fibula is halved to provide bone graft as necessary and also forms a plate to cover the fusion site laterally. If the ankle fusion is being done because of talar avascular necrosis, frequently both the tibiotalar and the subtalar joints are involved. Although the talar body is dead, the talar neck normally maintains its blood supply. Traditional Blair fusion leaves a space for the talar body, therefore we employ a method of aligning the talar neck to the distal anterior tibia by filling the void from the distal tibial articular surface to the posterior facet of the calcaneus for iliac crest bone graft. Chou et al. [5] reported results of 55 ankles that underwent tibiotalocalcaneal arthrodesis. The goal of surgical treatment was a painless and plantigrade foot. The authors agreed with Papa and Myerson [21] that ‘‘it is a complex and technically demanding procedure, but a reasonable alternative to amputation.’’ The position of fusion is as recommended by Buck et al. [22], with neutral flexion and 58 of valgus with 5 to 108 of external rotation. We use a sterile metal equipment tray to provide a ‘‘sterile floor’’ to judge foot alignment.

B.

Calcaneus

Calcaneus fractures are approached laterally. This involves a vertical limb of Letournel with a horizontal limb at the distal lateral aspect of the foot, which runs parallel to the sole of the


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foot that is approximately at the level of the top of the small toe. Great care is taken with the soft tissues and this flap is elevated thickly and sharply. The use of tenotomy scissors to spread the tissues through the incision is discouraged. This causes necrosis of the subcutaneous fat and will lead to dimpling of the incision. Careful dissection with pickups and a #15 blade, which provides thick flaps without undermining the superficial edges, is preferred. If there is still tension on the wound after closure of the flap using Allgower–Donati sutures, the flap is pie-crusted just through the dermis but not deeper, using a #15 blade in multiple areas to provide relaxation. This is sometimes necessary when treating calcaneus fractures with significant preoperative loss of height. Late treatment of calcaneal fractures involves addressing arthrosis from the subtalar joint or correction of deformities caused by loss of height, lateral impingement, or varus heel deformity. Stephens and Sanders [23] classified calcaneal malunions into three types. Patients with type I malunions have lateral impingement symptoms; with type II malunions, subtalar arthritis; and with type III malunions, an additional varus heel. If the subtalar joint is to be fused because of pain associated with arthrosis, the standard lateral sinus tarsi incision is preferred. If however there is significant height loss, or despite undergoing operative fixation, the subtalar joint is painful, then the medium distractor and the posterior limb of the standard calcaneal incision are used to access the subtalar joint. It is recommended that the height be restored during subtalar fusion by using a subtalar bone block distraction arthrodesis [24]. Although this is an unusual approach at first, familiarity with the technique allows minimal soft tissue insult and a good visualization of the posterior facet. Careful preoperative planning and use of the distractor allows a structural iliac crest bone graft of the appropriate size to reconstitute hindfoot height (Figure 15.3). If the patient is experiencing calcaneal complications other than subtalar arthrosis, several smaller procedures may be used to provide significant symptom relief. The blowout of the lateral wall of the calcaneus often results in peroneal tendinitis. Sanders type I complication responds well to a calcaneal exostectomy for impingement of the peroneals and provides significant symptomatic relief (Figure 15.4). An incision over the peroneals often reveals significant stenosis of the tendons at the peroneal tubercle as well as significant synovitis. Removal of the inflamed synovium, freeing of the tendons, and removal of impinging bone provide significant symptomatic relief. A calcaneus after fracture may cause symptoms of a varus and heel or subtle cavus foot. If the subtalar joint is really correctable as shown by the Coleman block test, then valgus heel slide is a small procedure that is able to improve hindfoot alignment.

Figure 15.3 Lateral view of a subtalar bone block.


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Figure 15.4 Calcaneus malunion. (A) Arrows highlight swelling of peroneals. (B) Tight fibrous band over the peroneal does not allow passage of a thin surgical probe. (C) Tendons retracted inferiorly to reveal peroneal tubercle as a fibrotic and bony spike.


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Figure 15.4 Continued (D) Note the decreased diameter of the peroneus brevis even after release.

C.

Midfoot

The path of energy should be appreciated and a stable medial column reestablished. If there is significant comminution, which does not afford the surgeon the ability to fix with screws alone, thin plates designed for the modular handset, or 2.7-mm plates, are employed. Fractures of the tarsometatarsal joint must be anatomically reduced. This can only be done under direct visualization. Past methods for fixation of the joint after realignment with Kirschner wires have fallen out of favor. The use of cortical screws, without overdrilling, to hold the reduction is recommended. The screws can be removed after 4 months, if desired. If there is any evidence of significant cartilage loss or injury, early fusion is advocated. Late fusions for arthrosis should be based on pain, not bone scan activity [25]. Horton and Olney [26] show that medial plating may correct deformity and provide excellent results. The complication of splitting the thick cortex of the metatarsal when placing screws at an angle must be avoided. For this reason, the technique of bone preparation using a burr to make a cutout for the screw head, as previously described, is advocated [27]. This prevents it from levering against the inferior cortex and causing a crack propagation through the metatarsal shaft. The Seattle group [6] reviewed 48 patients, 15 of whom had purely ligamentous involvement. Higher average American Orthopaedic Foot and Ankle Society (AOFAS) scores were seen in the patients with an anatomic reduction (82.1 vs. 70.6). However, there were no significant differences seen comparing purely ligamentous with ligamentous and osseous involvement. This suggests that it is the injury, rather than the treatment, that had more of an impact on overall patient outcome. Arthrodesis may be a better option for purely ligamentous injury; however, more research would be needed to better support this view.

D.

Cuboid

Cuboid fractures can be challenging to treat. The weak spongy bone of the cuboid is easily fractured in a nutcracker-type configuration, resulting in bone loss. Although bone grafting for calcaneal fractures is not recommended, many cuboid fractures need grafting. Whenever possible, autografts should be used. If a structural graft is needed, such as in a subtalar bone block distraction, a tricortical iliac crest graft is obtained. If, however, the graft site can be covered by one cast, then harvesting from the calcaneus or the metaphyseal region of the distal tibia is preferred. An instrument that can be used during bone grafting is a gouge, which is normally used in preparation of the proximal tibia for insertion of a tibial nail. Lateral column length is obtained by placing a small distracter or fixator from the calcaneus to the proximal fourth and fifth metatarsals (Figure 15.5). If only the fifth metatarsal is used to


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Figure 15.5 Cuboid fracture. (A) Lamina spreaders restore cuboid length. (B) Screw placed to hold joint in alignment after provisional fixation. (C) C-arm appearance of the plate before screw placement. (D) A 2.7-mm DCP sliding under tension to span the cuboid.


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provide the distal base for spanning the cuboid, the distraction will dislocate the fifth metatarsal from the fourth metatarsal. Also placing the half-pin into the fourth metatarsal provides a stable base and will provide the much-needed lateral column lengthening without difficulty. Once the cuboid has been adequately bone grafted, the lateral column needs continued support, otherwise this will recrush the cuboid. Sometimes there is enough cortical bone in the cuboid to provide significant support for a plate. Usually, the cuboid must be bridged. Although an external fixator can be left in place to provide this lateral column bridging, there are instances when support will be needed for more than 6 weeks. Under these circumstances, the use of a 2.7-mm DCP is recommended. This is a sufficiently strong plate with somewhat of a low profile. This plate can be removed after fracture healing. The plate often breaks if left in place; therefore, a planned hardware removal is recommended. The incision that is used to treat cuboid fractures puts the sural nerve at risk. Sural neuromas are common and symptomatic for the patient if extreme care is not taken during the surgical approach. This should be anticipated and looked for, in addition to avoiding excessive traction on the wound edges. With these caveats, the incidence of sural neuritis is minimal.

E.

Syndesmotic Injuries

The majority of syndesmotic injuries are successfully treated acutely. However, there are instances when late syndesmotic reconstruction is necessary. Diabetics often have some syndesmotic injury not appreciated on initial injury films. Posterolateral comminution at the joint line is an evidence of ankle instability, which may increase the stress on the syndesmosis in an ankle fracture that is a delayed union. Syndesmotic reconstruction is a significant undertaking. Typically, the fibula is shortened and malrotated, which must be corrected [28]. Fibular length is corrected by ensuring that there is equal joint space around the talus, that the fibular spike points to the articular cartilage of the tibia, and that Shenton’s line of the ankle is unbroken. The medium distractor is used to help with alignment; the fibula is osteotomized, and the fibrous tissue within the distal tibial fibular space is removed. Before this, the medial joint line is also checked for soft tissue interposition [29]. Although this procedure is rarely performed, these patients are extremely happy after receiving a stable ankle.

F.

Compartment Syndrome

Compartment syndrome is another entity, which is easier to treat acutely than its late consequences. The Mubarak chart has been modified to include foot compartment syndrome (Table 15.1). The only subjective indicator for compartment syndrome is the presence of a tense, shiny, and swollen foot and a history of trauma. Release of the hindfoot compartments by medial incision, with dorsal incisions to release the forefoot, is preferred (Figure 15.6). If compartment syndrome has been unrecognized or has been chosen not to be treated acutely, late treatment is aimed at obtaining and preserving joint mobility in conjunction with accommodative shoe wear with or without corrective bracing. Shoe modification may be used to treat claw toes and contractures addressed nonoperatively. Surgical options address mainly the release of contractures, myotendinous lengthening, and muscle resection or tenotomy or tendon transfers.

Table 15.1

Differential Diagnosis Based on Clinical Signs and Symptoms

Clinical signs and symptoms Pressure increase Pain with stretch Paresthesia Paresis or paralysis Pulse intact

Foot compartment syndromes

Other compartment syndromes

Arterial occlusion

Neuropraxia

þ þ

þ þ þ þ þ

þ þ þ

þ þ þ

Source: From Perry, M.D. and Manoli, A., II, Orthoped. Clin. North Am., 32, 103–111, 2001. With permission.


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Figure 15.6 Release of the hindfoot compartments by medial incision with dorsal incisions to release the forefoot. (From Manoli, A., II and Weber, T.G., Foot Ankle Int., 10, 267–275, 1990.)

Sometimes the fibrous deformity can be resected; however, severe involvement requires osteotomies and fusions with capsular releases to place the foot in a neutral position. More importantly, foot compartment syndrome can result in compartment syndrome of the deep posterior calf with a wellknown sequela.

G.

Flexion Contractures

Tight heel cords may cause an insertional Achilles tendonitis or metatarsalgia even after the appropriate acute management of trauma. Postoperatively, great attention is placed on having the foot in the neutral position. Even a slight 58 tightness of the gastrocnemius tendon may cause symptoms. If, after operative fixation of the Lisfranc dislocation, there is any evidence of a tight heel cord, a gastrocnemius slide is performed. This will greatly decrease the forces across the midfoot joints. Attention to detail during release and closure leaves a cosmetically pleasing scar. Like in calcaneal incision, scissors are not used to spread, and thereby destroy, subcutaneous fat. This is critical if dimpling of the skin is to be avoided. If the gastrocnemius and soleus are both tight, a percutaneous lengthening is performed.

V.

SUMMARY

Treatment of the traumatized foot has significant complications and must have appropriate surgical timing. The goal of treatment should be to provide the patient with a plantigrade, painless foot. Soft tissue must be carefully handled to prevent serious complications. A thorough appreciation of the injury and the anatomy, along with realistic goals, provide the patient with the most optimal results.

REFERENCES 1. Manoli, A., II, Prasad, P., and Levine, R.S., Foot and ankle severity scale (FASS), Foot Ankle Int., 18, 598– 602, 1997.


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2. National Highway Traffic Safety Administration, 2000 Annual assessment of motor vehicle crashes Online: www-nrd.nhtsa.dot.gov/departments/nrd-30/NCSA/ Content/Assess2K.html 3. Arangio, G.A., Lehr, S., and Reed, J.F., III, Reemployment of patients with surgical salvage of open, highenergy tibial fractures: an outcome study, J. Trauma, 42, 942–945, 1997. 4. Lee, R.H., Length of sickness absence from work after minor fractures, Int. J. Rehabil. Res., 5, 499–506, 1982. 5. Chou, L.B., Mann, R.A., Yaszay, B., Graves, S.C., McPeake, W.T., III, Dreeben, S.M., Horton, G.A., Katcherian, D.A., Clanton, T.O., Miller, R.A., and Van Manen, J.W., Tibiotalocalcaneal arthrodesis, Foot Ankle Int., 21, 804–808, 2000. 6. Kuo, R.S., Tejwani, N.C., Digiovanni, C.W., Holt, S.K., Benirschke, S.K., Hansen, S.T., Jr., and Sangeorzan, B.J., Outcome after open reduction and internal fixation of Lisfranc joint injuries, J. Bone Jt. Surg., 82A, 1609–1618, 2000. 7. Tonnesen, H., Pedersen, A., Jensen, M.R., Moller, A., and Madsen, J.C., Ankle fractures and alcoholism. The influence of alcoholism on morbidity after malleolar fractures, J. Bone Jt. Surg., 73B, 511–513, 1991. 8. Nyquist, F., Berglund, M., Nilsson, B.E., and Obrant, K.J., Nature and healing of tibial shaft fractures in alcohol abusers, Alcohol, 32, 91–95, 1997. 9. Bibbo, C., Lin, S.L., Beam, H.A., and Behrens, F.F., Complications of ankle fractures in diabetic patients, Orthoped. Clin. North Am., 32, 113–133, 2001. 10. Dunn, W.R., Easley, M.E., Parks, B.G., Trnka, H.-J., and Schon, L.C., A new fixation method for fibular fractures in elderly patients: a biomechanical evaluation with clinical correlation, J. Orthopaed. Trauma, in press. 11. Perry, M.D., Taranow, W., and Manoli, A., II, Multiple Syndesmotic Fixation for Neuropathic Ankle Fractures with Failed Traditional Fixation, American Orthopaedic Foot and Ankle Society Winter Meeting, Dallas, Texas, Feb 16, 2002. 12. Raikin, S.M., Landsman, J.C., Alexander, V.A., Froimson, M.I., and Plaxton, N.A., Effect of nicotine on the rate and strength of long bone fracture healing, Clin. Orthopaed., 353, 231–237, 1998. 13. Easley, M.E., Trnka, H.J., Schon, L.C., and Myerson, M.S., Isolated subtalar arthrodesis, J. Bone Jt. Surg., 82A, 613–624, 2000. 14. Chapman, J.R., Harrington, R.M., Lee, K.M., Anderson, P.A., Tencer, A.F., and Kowalski, D., Factors affecting the pullout strength of cancellous bone screws, J. Biomech. Eng., 118, 391–398, 1996. 15. Myerson, M., Soft tissue trauma: acute and chronic management, in Surgery of the Foot and Ankle, 7th ed., Coughlin, M.J. and Mann, R.A., Eds., Mosby, St. Louis, MO, 1999, pp. 1367–1368. 16. Ouzounian, T.J. and Kleiger, B., Arthrodesis in the foot and ankle, in Disorders of the Foot and Ankle, 2nd ed., Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1991, pp. 2614–2646, chap. 95. 17. Michelson, J. and Perry, M., Clinical safety and efficacy of calf tourniquets, Foot Ankle Int., 17, 573–575, 1996. 18. Monroe, M.T. and Manoli, A., II, Osteotomy for malunion of a talar neck fracture: a case report, Foot Ankle Int., 20, 192–195, 1999. 19. White, R.R. and Babikian, G.M., Tibia: Shaft, in AO Principles of Fracture Management, Ruedi, T.P. and Murphy, W.M., Eds., Thieme Medical Publishers, New York, 2000, chap. 4.8.2. 20. Morgan, C.D., Henke, J.A., Bailey, R.W., and Kaufer, H., Long term results of ankle arthrodesis following trauma, J. Bone Jt. Surg., 67, 546–550, 1985. 21. Papa, J.A. and Myerson, M.S., Pantalar and tibiotalocalcaneal arthrodesis for post-traumatic osteoarthrosis of the ankle and hindfoot, J. Bone Jt. Surg., 74A, 1042–1049, 1992. 22. Buck, P., Morrey, B.F., and Chao, E.Y.S., The optimum position of arthrodesis of the ankle: a gait study of the knee and ankle, J. Bone Jt. Surg., 69A, 1052–1062, 1987. 23. Stephens, H.M. and Sanders, R., Calcaneal malunions: results of a prognostic computed tomography classification system, Foot Ankle Int., 17, 395–401, 1996. 24. Bednarz, P.A., Beals, T.C., and Manoli, A., II, Subtalar distraction bone block fusion: an assessment of outcome, Foot Ankle Int., 18, 785–791, 1997. 25. Komenda, G.A., Myerson, M.S., and Biddinger, K.R., Results of arthrodesis of the tarsometatarsal joints after traumatic injury, J. Bone Jt. Surg., 78A, 1665–1676, 1996. 26. Horton, G.A. and Olney, B.W., Deformity correction and arthrodesis of the midfoot with a medial plate, Foot Ankle, 14, 493–499, 1993. 27. Manoli, A., II and Hansen, S.T., Jr., Screw hole preparation in foot surgery, Foot Ankle, 11, 105–106, 1990. 28. Beals, T.C. and Manoli, A., II, Late syndesmosis reconstruction: a case report, Foot Ankle Int., 19, 485–488, 1998. 29. Rosen, H. (Late), Reconstructive procedures about the ankle joint, in Disorders of the Foot and Ankle, 2nd ed., Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1991, pp. 2593–2613, chap. 94.



16 Traumatic Amputations of the Foot and Ankle Jason H. Pleimann Ozark Orthopaedic and Sports Medicine Clinic, Fayetteville, Arkansas

Robert B. Anderson, W. Hodges Davis, and Bruce E. Cohen Miller Orthopaedic Clinic, Charlotte, North Carolina

CONTENTS I. Introduction ...................................................................................................................... 394 II. Initial Assessment and Acute Treatment........................................................................... 395 A. Foot Salvageability .................................................................................................... 395 B. Acute Management — Preoperative .......................................................................... 396 C. Acute Management — Operative .............................................................................. 397 III. Subacute Management ...................................................................................................... 398 IV. Chronic Management........................................................................................................ 401 A. Rehabilitation ............................................................................................................ 401 B. Complications............................................................................................................ 402 V. Specific Amputation Levels ............................................................................................... 404 A. Terminal Syme........................................................................................................... 404 1. Technique ............................................................................................................ 404 2. Complications ..................................................................................................... 405 3. Orthotic and Prosthetic Issues............................................................................. 405 B. Great Toe Amputation .............................................................................................. 405 1. Technique ............................................................................................................ 406 2. Complications ..................................................................................................... 406 3. Orthotic and Prosthetic Issues............................................................................. 406 C. Lesser Toe Amputation ............................................................................................. 406 1. Technique ............................................................................................................ 406 2. Complications ..................................................................................................... 406 3. Orthotic and Prosthetic Issues............................................................................. 407 D. Ray Resections .......................................................................................................... 407 1. Technique ............................................................................................................ 408 2. Complications ..................................................................................................... 408 3. Orthotic and Prosthetic Issues............................................................................. 410 E. Transmetatarsal Amputations ................................................................................... 410 1. Technique ............................................................................................................ 410 2. Complications ..................................................................................................... 413 3. Orthotic and Prosthetic Issues............................................................................. 413

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Lisfranc’s Amputation ............................................................................................... 413 Chopart’s Amputation............................................................................................... 413 1. Technique............................................................................................................ 414 2. Complications ..................................................................................................... 415 3. Orthotic and Prosthetic Issues............................................................................. 416 H. Syme’s Amputation ................................................................................................... 417 1. Technique............................................................................................................ 417 2. Complications ..................................................................................................... 418 3. Orthotic and Prosthetic Issues............................................................................. 419 VI. Conclusion ........................................................................................................................ 420 References .................................................................................................................................. 421

I.

INTRODUCTION

Trauma is the third leading cause of partial and complete amputations of the foot, after only diabetes mellitus and peripheral vascular disease. The mechanisms of injury are diverse and include crush injuries often encountered in the industrial setting, lawn mower and other lacerating trauma, high-energy combination injuries seen with motorcycle crashes, high-velocity gunshot wounds, and thermal injuries from burns or frostbite (Figure 16.1). Although one of the oldest forms of surgery, foot amputation often carries with it a stigma of failure. This is especially true in the traumatic situation where there is no prodromal period of decreased function and increased pain as is often seen in the diabetic or vascular insufficiency populations. Rather, the trauma victim is often suddenly and unexpectedly faced with the possibility of losing part or all of a previously fully functional extremity. Advances in reconstructive techniques, including free-tissue transfer, skeletal fixation, hyperbaric medicine, and

A

Figure 16.1

B

(A) Clinical appearance and (B) radiograph of a severe lawn mower injury to the foot.


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vascular reconstruction, have added to this stigma, making previously unsalvageable situations manageable. Nevertheless, one must ultimately decide what is really best for the patient. This must be assessed on a case-to-case basis. From a medical point of view, a well-functioning, painless amputation is preferable to a poorly functioning and painful foot. As has been stated, ‘‘to save a poorly functioning foot is to have won the battle and lost the war, because the goal is to enhance the function and quality of the life for the patient, not the limb’’ [1]. One must also take into account the significant amount of time, effort, and expense that is often required to achieve foot salvage. Certainly, some patients are better served by proceeding to a more reliable proximal-level amputation, allowing them to return quickly to an acceptable quality of life. While amputation does not equate to failure, it is a salvage procedure, and maintaining a functional foot and ankle is important when possible. In the traumatic situation, this can often be achieved through a variety of partial foot amputations. A thorough understanding of the indications, techniques, and potential pitfalls of these procedures is mandatory for the surgeon dealing with foot and ankle trauma. Many partial foot amputations are very functional and allow patients to ambulate with orthotic devices and shoe wear modifications rather than prosthetic devices (Figure 16.2). In addition, significantly less energy is expended during the gait cycle than with more proximal amputations [2,3,4]. While partial foot amputations are more commonly performed for infection or peripheral vascular disease, those done in the traumatic setting provide unique challenges. These include performing ‘‘nonstandard amputations,’’ the need for fracture healing, creative soft tissue coverage, tendon balancing, as well as the potential problems of painful neuroma formation, chronic regional pain syndrome (CRPS), and bony overgrowth. It is useful to consider these issues in their respective time frames, i.e., in the acute, subacute, and chronic management settings.

II.

INITIAL ASSESSMENT AND ACUTE TREATMENT

A.

Foot Salvageability

Many factors weigh into the decision whether to attempt foot or partial foot salvage, or to proceed to a more proximal-level amputation. First and foremost is an accurate assessment of overall patient stability. Will life-threatening concomitant injuries impact the feasibility of a prolonged operative procedure or of subsequent procedures? Next, if possible, one must obtain a thorough history to evaluate the patient’s overall health status before injury. Diabetes mellitus, peripheral vascular disease, malnutrition, and other systemic conditions can significantly hinder a patient’s ability to heal following a foot-level amputation. Another important part of the history is the mechanism of injury. The zone of injury in crush or blast injuries is often underestimated at the time of initial assessment. An initial debridement followed by a second-look debridement should be standard protocol for these injuries. Important features of the physical examination include detailed evaluation of associated ipsilateral and contralateral limb injuries. While the foot injuries alone may be manageable, there may be more significant proximal injuries that prohibit limb salvage. In addition, if the contralateral limb is to be amputated at a proximal level, it becomes even more important to salvage a portion of the injured foot; energy expenditure during gait increases significantly with bilateral amputations above the ankle [4] (Figure 16.3). When assessing the injured foot, particular attention should be paid to the level of traumatic injury, the vascular supply and bony configuration of the residual foot, the presence or absence of plantar sensation, and the degree of plantar soft tissue loss. All of these factors have significant influence on the ability to salvage a functional and durable partial foot amputation. While there is no magic formula that adds up to salvage vs. amputation, there have been several attempts to objectively evaluate these injuries. Predictive indices, such as the Mangled Extremity Severity Score (MESS), have been developed to assist the surgeon in the decision-making process [5]. However, these scoring systems are not a substitute for sound clinical judgment [6,7].


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A

B

Figure 16.2

B.

(A) Partial foot amputation and (B) custom-molded orthotic device.

Acute Management — Preoperative

The acute management of partial foot amputation begins in the emergency department. Initial emphasis should be on the probability of foot salvage as described above. However, this decision often cannot be definitively made until the patient is in the operating room. Initially, a rapid, accurate history of the injury and physical examination of the injured limb should be performed. Multiple examinations are to be avoided as they are often painful and increase the risk of wound contamination and subsequent infection [8]. Any history of a crushing mechanism warrants a thorough evaluation to rule out compartment syndrome of the foot, including measurements of intracompartmental pressures [9,10]. Standard



397

Figure 16.3 This bilateral below-knee amputee required the use of a motorized wheelchair for mobility.

radiographs are obtained, looking specifically for bony injuries at and proximal to the perceived level of injury. Once the decision for foot salvage has been provisionally made, a plan for acute management is developed. Prophylactic intravenous antibiotics should be administered in the emergency department. As a general rule, these antibiotics should be continued for 2 to 3 days postoperatively or until definitive wound coverage is performed. At the authors’ institution, clean or mildly contaminated wounds are managed with a first-generation cephalosporin (cefazolin) to provide Gram-positive coverage. For injuries with severe contamination, a second antibiotic with Gram-negative coverage is added (gentamycin). Wounds with a history of agricultural exposure or other risk factor for clostridial infection warrant the further addition of aqueous penicillin G. Tetanus prophylaxis is also provided [11]. Wounds with gross contamination or any significant delay in operative debridement require an initial thorough irrigation in the emergency department, thereby reducing the chance of subsequent infection. This can be facilitated by the use of standard ankle block anesthesia. A simple and effective method of irrigation is used [12]. Multiple holes are punched in the cap of a plastic bottle of normal saline with an 18-gauge needle, which provides streams of irrigation under mild pressure when squeezed. Sterile dressings and a splint, if indicated, are then applied.

C.

Acute Management — Operative

After the stability of the patient has been ensured, operative debridement should follow in a timely fashion. Before operative intervention, however, it is important to communicate with the patient or family, if possible. A realistic description of the severity of the injury and the potential for foot salvage should be given. Since demarcation of soft tissue injuries may take several days to occur, the possibility of proceeding to a more proximal-level amputation after further evaluation should be discussed during the initial consultation as well. Once in the operating room and once adequate anesthesia has been achieved, a careful repeat examination is performed and the findings subsequently recorded in the operative note. Assuming partial foot salvage remains a viable option, a careful debridement and thorough irrigation should follow. Tourniquet use facilitates visualization of foreign material, but should be discontinued before closure or placement of dressings to ensure adequate hemostasis. An Esmarch bandage used about the supramalleolar region provides an effective and safe tourniquet during partial foot amputations [13,14]. While obviously necrotic tissue should be eliminated, it is important to maintain any potentially viable soft tissue flaps, even if irregular. These may be necessary for creative soft tissue coverage at the time of definitive closure (Figure 16.4).


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Figure 16.4 A lawn mower injury with large, irregular soft tissue flaps.

Exposed nerves should be sharply resected and allowed to retract into deep soft tissues to minimize the risk of painful neuroma formation. Exposed fractures are identified and stabilized or resected at an appropriate level depending on available soft tissue coverage and the proposed amputation level. In the case of partial metatarsal resections, a dorsal distal to plantar proximal bevel is created at the end of the residual bone to avoid plantar prominence (Figure 16.5). Occasionally, external fixation may be necessary to facilitate wound care and secondary coverage. At this time, primary closure or coverage may be performed if possible and if the zone of injury is well understood. Otherwise, a repeat debridement should be done 48 to 72 hours later as demarcation of marginally viable tissue occurs [11]. An important exception to this protocol of early surgical intervention is frostbite injuries. Unless gross infection is present, debridement should be delayed in these patients because there is often recovery of the soft tissues over time, which will allow a more distal-level amputation than initially thought. The process of demarcation may take months to occur [15]. This allows time to perform appropriate vascular studies that may provide guidance in determining a level of amputation with reasonable healing potential. Postoperatively, the foot should be splinted and elevated and perioperative antibiotics given according to the guidelines previously described.

III.

SUBACUTE MANAGEMENT

The subacute management phase encompasses the variable time period between the initial surgery and complete healing of the amputation. When a primary closure of an amputation has been



399

Figure 16.5 Illustration of the line of metatarsal resection using a dorsal distal to proximal plantar bevel.

performed in the acute setting, there may be little else to do but ensure timely wound healing. However, in many cases, this stage presents a plethora of unique challenges to the surgeon. As in the acute stage, the salvageability and potential function of the residual foot should be carefully reassessed. Areas of borderline viability should be reexamined after adequate time for demarcation, especially in those amputations associated with a crush or blast component (Figure 16.6). Repeat debridement is performed as indicated for persistent wound contamination, necrosis, or infection. In patients with a history of peripheral vascular disease and nonpalpable pedal pulses, it is important at this stage to accurately assess the vascular status of the limb. Several noninvasive techniques are used to determine if adequate local circulation is present to support healing. However, no method has demonstrated 100% sensitivity and specificity. Therefore, all should be considered as screening tests and not absolute predictors of healing potential. Arterial Doppler ultrasound pressure measurements are the most frequently used method. An ankle-brachial index of greater than 0.35 for nondiabetics and 0.45 for diabetics is considered a general guideline for healing [16,17]. However, calcific vessels are less compressible, which can lead to a falsely elevated ratio. The role of toe pressures has been debated, although measurements of 40 mmHg or greater seem to be predictive of healing in forefoot-level amputations [1]. Transcutaneous oxygen tension measurements appear to be somewhat more accurate predictors of wound healing. Readings greater than 30 mmHg at the proposed level of amputation seem to correlate well

Figure 16.6 Severe degloving injury to the plantar foot in a 14-year-old girl. After initial irrigation and debridement, third toe amputation and final debridement were delayed for 2 weeks to allow for demarcation of nonviable tissue.


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with healing [17,18,19]. However, alterations in skin temperatures can cause significant variability in measurements. Results of any of the above tests suggesting poor healing potential should prompt immediate vascular surgical consultation if partial foot salvage will be pursued. For dysvascular patients who are not revascularization candidates, hyperbaric oxygen therapy can be considered. This has been shown to improve wound healing in both normal and dysvascular tissues [20]. Poor nutrition should not be overlooked as a potential barrier to wound healing. Laboratory assessments of nutritional status can be predictive of successful wound or amputation healing [16,21]. General parameters have been described in Table 16.1. Once a reasonable chance for wound healing has been established, adequate debridement performed, and a level of partial foot amputation selected, wound coverage can be addressed. In the event that a tension-free primary closure of the amputation is not possible, several options for wound coverage exist. These include skeletal shortening with primary closure, ‘‘creative wound coverage’’ utilizing nonstandard amputation techniques, skin grafting, and local or free-tissue transfer. The multitude of injury patterns seen with traumatic amputations creates an equal number of challenges in soft tissue coverage. The surgeon must be willing to be creative with amputation techniques and wound coverage in order to maximize residual foot function. Therefore, no hard and fast rules apply to this stage of management. However, several guidelines can prove helpful. In general, the simplest method of wound coverage should be employed. This is often best done through skeletal shortening and primary wound closure. However, preservation of length leads to more functional ambulation and less excessive prosthetic needs [2]. Therefore, when the amount of shortening necessary to achieve closure significantly compromises the weight-bearing characteristics or function of the foot, alternate methods of coverage should be considered. The emphasis on length preservation applies to the individual digits as well. Maintenance of a portion of the proximal phalanx of the lesser toes can prevent significant varus or valgus drift of the adjacent digits with resultant transfer metatarsalgia. In the hallux, preservation of at least 8 mm of the proximal phalanx and the associated sesamoid complex allows the windlass mechanism to remain intact [22]. This has been shown to be advantageous in avoiding gait dysfunction, first-ray instability, and transfer metatarsalgia seen with more proximal-level hallux amputations [23,24]. For residual dorsal foot skin loss with an adequate soft tissue bed, split-thickness skin grafting is an effective method of covering even large wounds [25] (Figure 16.7). Because of the significant weight-bearing and shear stresses present during ambulation, split-thickness skin grafts typically are not durable enough for plantar coverage (Figure 16.8). However, limited use in non-weightbearing plantar areas has been reported [26]. Another option for wound coverage is split-thickness skin excision, where split-thickness grafts are obtained from potentially nonviable skin flaps [27]. Options for more significant soft tissue loss include local rotational flaps or free-tissue transfer. Numerous local muscle flaps have been described, including the abductor hallucis, flexor digitorum brevis, abductor digiti minimi, extensor digitorum brevis, and extensor hallucis brevis flaps. The use of these is generally limited to smaller full-thickness defects. For coverage of larger areas, free-tissue flaps such as the latissimus dorsi, rectus abdominis, and gracilis flaps can be considered (Figure 16.9). While these are often capable of covering significant areas of tissue loss, their use requires adequate vessels at the recipient site, which may have been damaged in the initial injury. A final issue that deserves careful consideration during the subacute management phase is the overall tendon balance about the residual foot, and the effect this will have on the ability of the limb to maintain a functional plantigrade posture. This issue is especially important when considering more proximal partial foot amputations that compromise the attachments of the tendons about the Table 16.1 Basic Laboratory Parameters of Nutritional Status Parameters Hemoglobin Hematocrit Total lymphocyte count Total protein Albumin

Concentrations >11 g/dl >32% >1500/ml >6.2 g/dl >3.5 g/dl



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Figure 16.7 Healed dorsal wound after split-thickness skin grafting.

Figure 16.8 Breakdown of split-thickness skin graft used for plantar wound coverage.

foot and ankle. The loss of function of these tendons alters the biomechanical balance about the ankle [28]. This, in turn, leads to predictable changes in foot posture based on the relative position of these tendons to the axis of ankle joint motion. Specific techniques can be employed at the time of amputation to ‘‘rebalance’’ the forces about the ankle, maintaining a plantigrade posture. These are described in the ‘‘Specific Amputaion Levels’’ section.

IV. A.

CHRONIC MANAGEMENT Rehabilitation

Although it is beyond the scope of this chapter to fully address the long-term management and rehabilitation of partial foot amputations, this is perhaps the most challenging phase of care. The


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A

B

Figure 16.9 This severe lawn mower injury required a (A) latissimus flap and (B) split-thickness skin grafting for coverage.

treating physician faces multiple issues and potential complications. These include not only limbspecific issues such as maintaining a functional position and range of motion but also more global issues such as the patient’s self-image and return to work. To address these concerns, we have employed a multidisciplinary approach that includes physiatrists, physical therapists, orthotists, prosthetists, and social workers.

B.

Complications

Despite an initially successful amputation, numerous potential complications may occur. These include, among others, loss of functional limb position, recurrent wound breakdown, infection, painful neuroma formation, bony overgrowth, phantom limb pain, and CRPS. However, attention to the principles of acute and subacute management will minimize the risk of these problems. In addition, some complications are more characteristic of certain amputation levels. These are discussed in more detail in the ‘‘Specific Amputation Levels’’ section. One of the most common complications is wound breakdown. This is often seen in areas of skin grafting or tissue transfer, especially in the plantar weight-bearing areas. Shoe wear or orthotic modifications can often reduce pressure or shear forces in these areas. Occasionally, bony prominences may need to be surgically revised to allow adequate soft tissue coverage. Loss of functional plantigrade position may occur. This is usually due to tendon imbalance and is a common cause of distal stump breakdown. If bracing and orthotic adjustments fail, various



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combinations of tendon lengthenings, tenotomies, tendon transfers, and arthrodeses may be required to address these problems. Another common scenario is the painful residual limb. The causes of this are numerous, and an accurate diagnosis is the key to successful treatment. The nature and character of the pain, its location, chronicity, and relation to weight-bearing, activity, or shoe wear are all important factors to elicit from the history and from the physical examination. Radiographs should be obtained to rule out osteomyelitis, posttraumatic degenerative disease, and bony overgrowth. A history of fevers, recurrent swelling, redness, or drainage should raise suspicion of chronic infection. Useful adjuncts in diagnosis include magnetic resonance imaging (MRI), bone scan, and laboratory studies (white blood cell count, erythrocyte sedimentation rate, and C-reactive protein). In patients with documented neuropathy, a combined bone scan and labeled leukocyte study may be an effective means of differentiating between osteomyelitis and Charcot neuroarthropathy [29]. Adequate surgical debridement and culture-directed antibiotic therapy are required to treat osteomyelitis, while cast immobilization is the mainstay of treatment for acute Charcot neuroarthropathy (Figure 16.10).

A

B

Figure 16.10 (A) After successful transmetatarsal amputation. Severe swelling and warmth of the residual foot in a diabetic patient. (B) Radiograph showing bony fragmentation consistent with acute Charcot neuroarthropathy.


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Focal pain of an electric or burning nature should alert one to the possibility of painful neuroma formation. While orthotic or shoe wear changes can be effective, surgical resection of the neuroma with redirection of the proximal nerve stump into deep soft tissues may be required. Another cause of focal pain, especially in children, is bony overgrowth. Radiographs utilizing markers over the area of maximal tenderness will identify the offending prominence. Again, orthotic management often will provide adequate relief. However, occasionally bony revision is needed. When a more diffuse pain pattern exists without an obvious anatomic cause, the diagnosis of CRPS should be considered. Keys to diagnosis include pain of a burning nature, allodynia, hyperemia, and diffuse osteopenia when in the acute stage. Three-phase radionuclide bone scanning has been reported to be quite sensitive in establishing the diagnosis, and early diagnosis and treatment are critical to successful management [30]. Consultation with painmanagement specialists is an important part of a multidisciplinary approach to treatment. A comprehensive review of this entity and its treatment is found elsewhere in this book.

V.

SPECIFIC AMPUTATION LEVELS

As mentioned previously, traumatic amputations of the foot and ankle often require the surgeon to be creative when managing these injuries. ‘‘Nonstandard’’ amputations are often used; therefore, the following sections should not be considered exhaustive. Nevertheless, a thorough understanding of the more commonly performed amputations is necessary for the surgeon dealing with foot and ankle trauma.

A.

Terminal Syme

(See Figure 16.11) Indications for this procedure include severe, chronic nail deformity, osteomyelitis of the distal phalanx, or toe-tip necrosis due to frostbite or burns (after adequate time for demarcation). It is rarely performed in the acute traumatic setting. 1.

Technique

The nail plate is removed and an elliptical excision of the entire sterile and germinal matrix is performed, exposing the distal phalanx. Complete excision of the germinal matrix should be done to avoid partial nail regrowth. Using a bone cutter or microsagittal saw, an adequate portion of

Figure 16.11

Healed terminal Syme’s amputation of the great toe.



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distal phalanx is resected to allow easy soft tissue and skin closure. The skin flap is reshaped as necessary to avoid excessive ‘‘dog ears’’ and then closed loosely with a single layer of interrupted sutures. 2.

Complications

The most common early complication is wound dehiscence due to insufficient resection of bone and subsequent skin closure under tension. Improper shaping of the ellipse may result in a bulbous appearance at the end of the toe. Incomplete excision of the germinal matrix can result in partial nail regrowth, which may be painful (Figure 16.12). Finally, extensor lag can occur due to compromise of the extensor hallucis longus insertion. 3.

Orthotic and Prosthetic Issues

None.

B.

Great Toe Amputation

Amputations of the great toe may be required in a multitude of traumatic situations including frostbite, crush injuries, and lawn mower accidents. While the level of amputation is often dictated by the injury, it is important to preserve length when possible. Preservation of at least 8 mm of proximal phalanx has been shown to allow a more normal pattern of plantar weight-bearing

Figure 16.12

Partial, medial, and lateral nail regrowth after terminal Syme’s amputation.


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distribution. The risk of transfer lesions over the remainder of the forefoot is therefore theoretically reduced. In addition, preservation of the sesamoid complex and plantar fascia improves push-off during gait [23,24]. 1.

Technique

A ‘‘fishmouth’’ or ‘‘racquet-shaped’’ incision is created, encircling the area of nonviable tissue, which is removed. In general, viable skin must remain at the level of the distal portion of the proximal phalanx in order to cover an amputation at the metatarsophalangeal (MP) joint or base of the proximal phalanx. Therefore, any areas of viable skin are left intact, as they may prove necessary to allow creative closure. If the racquet incision is used, it can be extended proximally along the medial border of the toe, raising full-thickness flaps to expose the level of bony resection, which is completed with a microsagittal saw. The bone edges are beveled. Again, preservation of at least 8 mm of the proximal phalanx is preferred. If an MP joint disarticulation is required, however, the cartilage cap should be left intact as a barrier to potential infection. The sesamoids are not removed unless clinically indicated (fractured, infected, or degenerative). Interrupted monofilament sutures are used to achieve full-thickness closure utilizing creative flaps as necessary. 2.

Complications

As with other distal-level amputations, wound breakdown may occur because of skin closure under tension or an inadequate blood supply. Long-term varus drift of the second toe with hyperextension at the MP joint may occur. This can ultimately lead to second toe pressure lesions and pain on the dorsum of the proximal interphalangeal joint and on the plantar surface of the MP joint. 3.


Following wound healing, an accommodative insole is used to prevent excessive pressure transfer to the lateral forefoot. For amputations at the base of the proximal phalanx or at the MP joint, toe filler is added to prevent varus drift of the second toe.

C.

Lesser Toe Amputation

As with the great toe, amputations of the lesser toes may be required in a number of situations. These can be done through a bony resection or a disarticulation as determined by the skin available for coverage. Retention of a portion of the proximal phalanx is desirable as this serves to prevent migration of adjacent toes and theoretically preserves push-off strength. This is especially important with second toe amputations as progressive severe hallux valgus can occur with MP joint disarticulation [31]. 1.

Technique

Partial toe amputations are usually best addressed through fishmouth type incisions (Figure 16.13). The skin flaps may be fashioned either dorsoplantar or side-to-side. If proximal extension of the incision is required, side-to-side flaps are preferable. This avoids extending the incisions over the medial and lateral neurovascular bundles. Disarticulation or bony transection is then performed as dictated by skin coverage. The flaps are then approximated with interrupted sutures. 2.

Complications

The most common early complication is wound dehiscence due to inadequate soft tissue coverage and closure under tension. This is avoided by preservation of all distal viable skin and adequate bony resection.



Figure 16.13

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Outline of planned fishmouth incision for second toe amputation.

As mentioned previously, migration of adjacent digits into the dead space left after toe amputation may occur. This is most common with second toe amputations, and severe hallux valgus may develop (Figure 16.14). Maintenance of a portion of the proximal phalanx may help to prevent this. When this is not possible, more proximal resection of the second metatarsal can be considered. This will provide immediate narrowing of the forefoot and gap closure. Another potential late deformity seen with partial toe amputations is progressive hyperextension of the MP joint. When symptomatic, this is treated with revision amputation at the MP joint level or extensor tenotomy and MP joint release. 3.


For isolated amputations, soft or semirigid toe fillers should be used alone or in conjunction with a custom-molded orthotic device to prevent adjacent toe migration. In the rare instance when all the toes are disarticulated at the MP joints, a custom orthotic device is utilized to unload the metatarsal heads and provide arch support. Cosmetic toe prostheses can also be fabricated.

D.

Ray Resections

Ray resections involve an amputation of a toe and a portion or its entire associated metatarsal. They are durable and may be performed on border or central rays in a variety of traumatic situations, including gunshot wounds and lawn mower injuries. While this does result in foot narrowing, residual foot length is maintained, allowing easier pedorthic management than with more proximal-level amputations.


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Figure 16.14 Severe hallux valgus and a transfer lesion developed years after a second toe MP joint disarticulation.

Multiple-ray amputations may be performed as well. However, with each successive ray removal, the transfer of forefoot pressure to the remaining toes is increased. This is especially true with medial-sided resections. Therefore, it is generally recommended that if greater than one medial ray resection or greater than two lateral ray resections are required, a more proximal-level amputation [1,32] should be carefully considered. 1.

Technique

Ray resections performed in the traumatic setting commonly require the use of creative flaps to allow primary skin closure. Therefore, when planning single- or multiple-ray resections, it is advisable to preserve more viable skin from the digit than would seem necessary for closure. An example of this is the fillet flap, where a full-thickness soft tissue flap is created after bony removal from the digit. This can then be rotated to cover a more proximal soft tissue defect. When addressing border digits, a racquet incision is utilized with the proximal limb extending over the medial border of the first ray or the lateral border of the fifth ray. When resecting central rays, the proximal limb of the incision is made dorsally. Full-thickness flaps are raised, and the metatarsals are transected with a microsagittal saw at a level that will allow tension-free skin closure (Figure 16.15). A dorsal distal to plantar proximal bevel is created at the end of the residual metatarsal to avoid plantar prominence. Wound closure of central resections can be significantly more difficult than that of the border rays because there is less soft tissue mobility (Figure 16.16). Again, leaving as much viable skin as possible from the amputated digit minimizes this problem. If wound closure remains a problem, a more proximal-level metatarsal resection can be performed, allowing easier narrowing of the foot. The base of the metatarsal should be left intact for maintenance of midfoot stability. 2.

Complications

Wound dehiscence or slow healing may occur, especially with central ray resections. Revision metatarsal resection may be required to achieve tension-free closure. More chronic problems include difficulty with balance, transfer lesions under the residual forefoot, and deformities of the



Figure 16.15

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Well-healed first-ray amputation.

Figure 16.16 Healed second- and third-ray amputation. Note the broad scar that developed due to difficulty achieving wound closure.


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Figure 16.17

Transfer lesion under the lateral forefoot following first- and second-ray amputation.

remaining digits (Figure 16.17). These are often best addressed through pedorthic modifications. However, persistent transfer ulcerations, especially when three or fewer toes remain, may ultimately require revision to a transmetatarsal or Chopart’s amputation. 3.


Appropriate shoe wear, often incorporating custom-molded insoles, is critical to the long-term care of these very functional partial foot amputations. Shoes should have extra depth to accommodate the insoles and any deformities of the residual toes. The insoles themselves should balance pressure over the residual forefoot and include fillers to prevent medial and lateral shifting of the narrowed forefoot in the shoe (Figure 16.18).

E.

Transmetatarsal Amputations

The transmetatarsal amputation was first described in 1855 and remains one of the more common foot-level amputations. It may be done in the acute traumatic setting or as a salvage for failed attempts at a more distal-level amputation. A significant advantage of this over more proximallevel foot amputations is that the insertion and function of the anterior tibialis tendon are preserved. This allows improved foot clearance during the swing phase of gait and helps to prevent equinus contracture due to imbalance with the gastrocnemius–soleus complex. Nevertheless, distal weight-bearing pressures are increased following this procedure [33]. 1.

Technique (See Figure 16.19)

A curvilinear incision is made dorsally just distal to the planned level of metatarsal transections and a full-thickness flap is made to the level of bone. Plantarly, the skin incision is made more distally to produce a long plantar flap for eventual closure. Tendons and nerves are identified and divided sharply at the proximal edge of the wound under tension to allow retraction into deeper soft tissues. The metatarsals are transected using a microsagittal saw, beginning with the first metatarsal and progressing laterally. Each successive metatarsal is cut 2 to 3 mm shorter than the previous one to produce a gentle cascade of length. Again, a dorsal distal to plantar proximal bevel is created at the end of each residual metatarsal to avoid plantar prominence. The medial aspect of the first and lateral aspect of the fifth rays should be beveled as well. Care must be taken to preserve the anterior tibialis insertion.



Figure 16.18

Custom-molded insole utilized following fourth- and fifth-ray amputations.

Figure 16.19

Technique of transmetatarsal amputation: (A) incision

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Figure 16.19 Continued Technique of transmetatarsal amputation: (B) level and direction of bony resections, (C) tension-free closure.



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The forefoot is then removed and the plantar flap debulked to allow tension-free closure over a drain. Finally, if 58 of passive ankle dorsiflexion cannot be achieved intraoperatively, either a gastroc slide or lengthening of the Achilles tendon is performed. A splint should be applied with the ankle in approximately 108 of dorsiflexion. This is subsequently replaced with a cast to protect the lengthened Achilles tendon. 2.

Complications

The most common complication is recalcitrant ulceration of the distal stump (Figure 16.20). Occasionally, plantar ulcerations are caused by bony overgrowth of a residual metatarsal and may require local revision to achieve healing (Figure 16.21). More commonly, however, this is due to the development of subtle equinus. If a trial of casting fails to achieve lasting improvement, this situation is best addressed with Achilles tendon lengthening. Painful neuromas may also occur and are managed with excision and diversion of the proximal stump. 3.


While many transmetatarsal amputees do not require a prosthesis for short-distance walking or transfers, forefoot pressures are increased, placing them at risk for ulceration. In addition, maximum ankle dorsiflexion is diminished. The simplest solution for these problems is a shoe insert with a toe filler, often in combination with a high-top shoe. The insert should be fairly rigid but well padded at its distal end. The shoe must have a fairly rigid sole as well, to prevent increased pressure at the distal stump during terminal stance. A rocker sole may be added to aid in pressure reduction.

F.

Lisfranc’s Amputation

Amputations performed through the tarsometatarsal joints are managed similarly to those through the transverse tarsal joints (see ‘‘Chopart’s Amputation’’ section below). Because a portion of the anterior tibialis insertion remains intact at the medial cuneiform, however, the risk of equinovarus is less. Therefore, rather than performing a complete Achilles tenotomy, an Achilles tendon lengthening is performed. The remainder of the operative technique, the postoperative management, and the potential complications closely mirror those of Chopart’s amputation as described below.

G.

Chopart’s Amputation

Disarticulations at the level of the transverse tarsal joints (talonavicular and calcaneocuboid) have fallen into disfavor because of problems with progressive equinovarus deformity due to the

Figure 16.20 Ulceration of the distal plantar stump following transmetatarsal amputation.


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Figure 16.21 Bony overgrowth of the second metatarsal after transmetatarsal amputation.

unopposed action of the Achilles tendon. More recently, however, there has been renewed interest as techniques to minimize this problem have been developed [28,34,35]. An amputation at this level has several advantages over more proximal amputations (Syme’s and below-knee). First, unlike below-knee amputations, it preserves both limb length and the weight-bearing surface of the heel pad, allowing limited end bearing without a prosthesis (i.e., getting out of bed to go to the bathroom). Second, it is technically easier to perform than Syme’s amputation. Finally, patients with Chopart’s amputation require only an ankle–foot orthosis (AFO), rather than the knee-high prostheses needed by Syme’s or below-knee amputees. 1.


A fishmouth incision is used, creating dorsal and plantar skin flaps as distal as is possible to allow tension-free closure. The tendons of the extensor digitorum longus are cut proximally under tension, allowing them to retract into the deep soft tissues. The anterior tibialis and peroneus brevis tendons are transected at the most distal aspect of their insertions and preserved for later transfer. Disarticulation is performed at the desired level. As previously mentioned, late equinovarus is the primary cause of failure for this amputation. It is at this stage that efforts are made to avoid this complication. First, an open Achilles tenotomy or tenectomy (excision approximately 2 cm of tendon) is performed. In addition, the anterior tibialis tendon is transferred to the neck of the talus to assist in ankle dorsiflexion. Similarly, the peroneus brevis tendon may be transferred to the anterior calcaneal process to provide an eversion force.



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Wound closure is achieved over a drain and a splint is applied with the ankle held in a mild degree of dorsiflexion. This is subsequently changed to a total-contact cast, and non-weight-bearing status is maintained for 4 to 6 weeks. 2.

Complications

Intraoperatively, the most common pitfall is failure to fashion flaps of appropriate length to adequately cover the wound. This is due to the significantly large cross-sectional area of the foot at the level of the transverse tarsal joints. Care must be taken to account for this. Equinovarus is best addressed proactively through Achilles tenotomy or tenectomy and transfer of the anterior tibialis and peroneus brevis tendons at the time of amputation. Late equinus

Figure 16.22

Technique of Chopart’s amputation: (A) incision, (B) level of disarticulation,


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D

Figure 16.22 Continued (C) transfer of anterior tibialis tendon to talar neck, (D) clinical appearance after healing.

can lead to recurrent ulcerations of the distal stump. If orthotic adjustments fail to achieve healing, an Achilles tenotomy can be performed, followed by bracing with an AFO. 3.


After wound healing, the patient is fitted with an AFO and custom-molded insole (Figure 16.23). The complexity of this construct depends on the anticipated activity level of the patient. Typically, this orthosis will include a semirigid toe plate to allow for better transition of weight transfer at the end of stance phase.



Figure 16.23 insole.

H.

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Orthosis used for Chopart’s amputation, consisting of an AFO with a custom-molded

Syme’s Amputation

Syme’s amputation involves disarticulation of the ankle with preservation of the plantar heel pad and skin. Although considered more technically demanding to perform than a below-knee amputation, Syme’s amputation produces a durable terminal stump that is capable of partial end bearing. In addition, there is less energy consumption during ambulation with this compared with a below-knee amputation [2]. Prosthetic fitting can be difficult due to the bulbous end, however, and requires an experienced prosthetist [36] (Figure 16.24). An absolute contraindication to performing this amputation is trauma that significantly involves the heel pad. Loss of heel pad integrity dooms this procedure to failure. 1.


Syme’s amputation is described in the literature as being performed in one or two stages [1,37]. It was previously thought that the two-stage technique yielded better healing results. However, a recent study has shown comparable rates of healing with either method, and most surgeons experienced with this procedure perform it in a single stage [38]. A fishmouth type incision is utilized, with the apices placed approximately 1 cm anterior and 1 cm distal to the tip of the malleoli. The incisions are carried down to bone, creating full-thickness flaps. Anteriorly, the tendons and nerves are cut proximally under tension, allowing them to retract, and the anterior tibial artery is ligated. With plantar and distal traction on the talus, the medial and lateral collateral ligaments of the tibiotalar joint are divided. Care is taken to avoid damage to the


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Figure 16.24 Clinical appearance of Syme’s amputation. Note bulbous end with intact plantar heel pad.

medial neurovascular structures, which lie just posterior to the flexor hallucis longus tendon. The posterior tibial artery provides blood supply to the heel pad, and damage to it can doom the procedure to failure. As the talus is exposed anteriorly, a bone hook is placed over its posterior body to aid in dissection of the calcaneus. Using blunt and sharp dissection alternately, the calcaneus is subperiosteally dissected free of the Achilles tendon and surrounding soft tissues, again avoiding the posterior tibial artery medially. This portion of the procedure is technically demanding and requires meticulous attention to detail, as penetration of the posterior or plantar skin damages the heel pad, which often leads to failure of the amputation. Once the calcaneus is removed, the medial and lateral malleoli are resected at the level of the tibial plafond. However, the cartilage at the distal tibia may be left intact. The heel pad fascia and plantar fascia are then sutured through drill holes to the anterior tibial plafond to prevent postoperative heel pad migration. Wound closure is performed over a drain, utilizing inverted absorbable sutures in the subcutaneous tissue and sutures or staples in the skin. A splint is applied, and at the first follow-up visit it is replaced with a cast. The patient should remain non-weight-bearing for 4 to 6 weeks. 2.

Complications

A review of the literature reveals a success rate of 50 to 90% for Syme’s amputation, although the majority of these studies involved diabetic and dysvascular patients [36,37,39,40]. Early failure is usually due to failure to heal. Adequate preoperative vascular evaluation is critical, as is maintenance of the blood supply to the heel pad.



Figure 16.25 and closure.

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Technique of Syme’s amputation: (A) incision, (B) dissection of the talus and calcaneus

The next most common problem with this procedure is heel pad hypermobility, which can cause the heel pad to migrate medially or laterally. This is best addressed through prevention. If the heel pad seems too mobile at the time of amputation, excess soft tissue at the distal end of the heel pad flap should be excised. Suturing the heel pad to the distal tibia through drill holes also aids in heel pad stability. Common sources of pain in the traumatic Syme’s amputee include neuroma formation and chronic heel pain. Neuromas can be localized with selective injections and may require excision if prosthetic adjustments fail. Chronic heel pain is occasionally seen when this procedure is performed for crush injuries with damage to the heel pad. These patients often require revision to a below-knee amputation. 3.


As mentioned previously, prosthetic fitting for Syme’s amputation can be difficult, usually due to the bulbous shape of the distal stump. This makes achieving a snug fit more proximally a challenge.


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Figure 16.26 stump.

Syme’s amputation prosthesis with distal window to accommodate entry of bulbous

To accommodate this, a hinged window is usually made in the distal portion of the prosthesis (Figure 16.26). A solid ankle–cushioned heel (SACH) is often added. A significant advantage of Syme’s amputation over below-knee amputation is the ability to partially end bear in the prosthesis. This minimizes the problem of proximal skin breakdown seen with fully patellar-tendon-bearing prostheses. In addition, energy usage is lowered, and gait velocity is higher [2].

VI.

CONCLUSION

Although recent advances in the management of severe foot and ankle trauma have made foot salvage a possibility in previously unsalvageable situations, amputation remains a viable option for a significant number of patients. While still considered a salvage procedure, amputation does not equate to failure. In appropriately selected patients, partial foot amputations provide a functional, painless residual limb with a rapid return to ambulation and daily activities. Numerous obstacles may be encountered when managing the traumatic amputee. However, careful attention to the principles of acute, subacute, and chronic management will minimize these potential problems. In the authors’ experience, a multidisciplinary approach to both limb and overall patient care has proven to be of significant benefit in this regard. When these efforts are successful, partial foot amputations provide patients with the opportunity to return to a high level of function.



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REFERENCES 1. Brodsky, J.W., Amputations of the foot and ankle, in Surgery of the Foot and Ankle, Coughlin, M.J. and Mann, R.A., Eds., Mosby, St. Louis, MO, 1999, pp. 971–995. 2. Waters, R., Perry, J., Antonelli, D., and Hislop, H., Energy cost of walking of amputees: the influence of level of amputation, J. Bone Jt. Surg. Am., 58, 42–46, 1976. 3. Pinzur, M., Gold, J., Schwartz, D., and Gross, N., Energy demands for walking in dysvascular amputees as related to the level of amputation, Orthopaedics, 15, 1033–1037, 1992. 4. Fisher, S. and Gullickson, G., Energy cost of ambulation in health and disability, Arch. Phys. Med. Rehabil., 59, 124–133, 1978. 5. Johansen, K., Daines, M., Howey, T., Helfet, D., and Hansen, S.T., Jr., Objective criteria accurately predict amputation following lower extremity trauma, J. Trauma, 30, 568–572, 1990. 6. Bonanni, F., Rhodes, M., and Lucke, J.F., The futility of predictive scoring of mangled lower extremities, J. Trauma, 34, 99–104, 1993. 7. Roessler, M.S., Wisner, D.H., and Holcroft, J.W., The mangled extremity: when to amputate?, Arch. Surg., 126, 1243–1249, 1991. 8. Tscherne, H., Management of open fractures, in Fractures with Soft Tissue Injuries, Tscherne, H. and Gotzen, L., Eds., Springer-Verlag, Berlin, 1984, pp. 10–32. 9. Myerson, M.S., The diagnosis and treatment of compartment syndrome of the foot, Orthopedics, 13, 711– 717, 1990. 10. Manoli, A., Compartment syndromes of the foot: current concepts, Foot Ankle, 10, 340–344, 1990. 11. Norris, B.L. and Kellam, J.F., Soft-tissue injuries associated with high-energy extremity trauma: principles of management, J. Am. Acad. Orthopaed. Surg., 5, 37–46, 1997. 12. Myerson, M.S., Soft tissue trauma: acute and chronic management, in Surgery of the Foot and Ankle, Coughlin, M.J. and Mann, R.A., Eds., Mosby, St. Louis, MO, 1999, pp. 1330–1372. 13. Biehl, W.C., Morgan, J.M., Wagner, F.W., Jr., and Gabriel, R.A., The safety of the Esmarch tourniquet, Foot Ankle, 14, 278–283, 1993. 14. Brodsky, J. and Chambers, R., Effect of tourniquet use on amputation healing in diabetic and dysvascular patients, Perspect. Orthoped. Surg., 2, 71–76, 1991. 15. Britt, L.D., Dascombe, W.H., and Rodriguez, A., New horizons in management of hypothermia and frostbite injury, Surg. Clin. North Am., 71, 345–370, 1991. 16. Wagner, F.W., Jr., Amputation of the foot and ankle: current status, Clin. Orthopaed., 122, 62–69, 1977. 17. Oishi, C.S., Fronek, A., and Golbranson, F.L., The role of non-invasive vascular studies in determining levels of amputation, J. Bone Jt. Surg. Am., 70, 1520–1530, 1988. 18. Wyss, C.R., Harrington, R.M., Burgess, E.M., and Matsen, F.A., III, Transcutaneous oxygen tension as a predictor of success after amputation, J. Bone Jt. Surg. Am., 70, 203–207, 1988. 19. Pinzur, M.S., Sage, R., Stuck, R., Ketner, L., and Osterman, H., Transcutaneous oxygen as a predictor of wound healing in amputations of the foot and ankle, Foot Ankle, 13, 271–272, 1992. 20. Uhl, E., Sirsjo, A., Haapaniemi, T., Nilsson, G., and Nylander, G., Hyperbaric oxygen improves wound healing in normal and ischemic skin tissue, Plast. Reconstr. Surg., 93, 835–841, 1994. 21. Dickhaut, S.C., DeLee, J.C., and Page, C.P., Nutritional status: importance in predicting wound-healing after amputation, J. Bone Jt. Surg. Am., 66, 71–75, 1984. 22. Mann, R.A., Biomechanics, in Disorders of the Foot, Jahss, M.H., Ed., W.B. Saunders, Philadelphia, 1982, pp. 37–67. 23. Mann, R.A., Poppen, N.K., and O’Konski, M., Amputation of the great toe: a clinical and biomechanical study, Clin. Orthopaed., 226, 192–205, 1987. 24. Levine, S.E., Myerson, M.S., and Cook, W.P., Management of hallux amputation, Orthopedics, 21, 330– 333, 1998. 25. Attinger, C., The use of skin grafts in the foot, J. Am. Podiatr. Med. Assoc., 85, 49–56, 1995. 26. Avellan, L. and Johanson, B., Full thickness skin graft from the dorsum of the foot to its weight-bearing areas, Acta Chir. Scand., 126, 497, 1963. 27. Myerson, M.S., Split-thickness skin excision: its use for immediate wound care in crush injuries of the foot, Foot Ankle, 10, 54–60, 1989. 28. Early, J.S., Transmetatarsal and midfoot amputations, Clin. Orthopaed., 361, 85–90, 1999. 29. Splittgerber, G., Speigelhoff, D., and Buggy, B., Combined leukocyte and bone imaging used to evaluate diabetic osteoarthropathy and osteomyelitis, Clin. Nucl. Med., 14, 156–159, 1989. 30. Fealy, M.J. and Ladd, A.L., Reflex sympathetic dystrophy: early diagnosis and active treatment, J. Musculoskelet. Med., 13, 29–36, 1996. 31. Seligman, R.S., Trepal, M.J., and Giorgini, R.J., Hallux valgus secondary to amputation of the second toe, J. Am. Podiatr. Med. Assoc., 76, 89–91, 1986. 32. Myerson, M.S., Bowker, J.H., Brodsky, J.W., and Trevino, S., Symposium: partial foot amputations, Contemp. Orthopaed., 29, 139–157, 1994. 33. Garbaloza, J.C., Cavanagh, P.R., Wu, G., Ulbrecht, J.S., Becker, M.B., Alexander, I.J., and Campbell, J.H., Foot function in diabetic patients after partial amputation, Foot Ankle, 17, 43–48, 1996.


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34. Letts, M. and Pyper, A., The modified Chopart’s amputation, Clin. Orthopaed., 256, 44–49, 1990. 35. Lieberman, J.R., Jacobs, R.L., Goldstock, L., Durham, J., and Fuchs, M.D., Chopart amputation with percutaneous heel cord lengthening, Clin. Orthopaed., 296, 86–91, 1993. 36. McElwain, J.P., Hunter, G.A., and English, E., Syme’s amputation in adults: a long-term review, Can. J. Surg., 28, 203–205, 1985. 37. Spittler, A.W., Brennan, J.J., and Payne, J.W., Syme amputation performed in two stages, J. Bone Jt. Surg. Am., 36, 37–42, 1954. 38. Pinzur, M.S., Smith, D., and Osterman, H., Syme ankle disarticulation in peripheral vascular disease and diabetic foot infection: the one-stage versus two-stage procedure, Foot Ankle, 16, 124–127, 1995. 39. Francis, H., III, Roberts, J.R., Clagett, G.P., Gottschalk, F., and Fisher, D.F., Jr., The Syme amputation: success in elderly diabetic patients with palpable ankle pulses, J. Vasc. Surg., 12, 237–240, 1990. 40. Jany, R. and Burkus, J., Long-term follow-up of Syme amputations for peripheral vascular disease associated with diabetes mellitus, Foot Ankle, 9, 107–110, 1988.


17 Orthotic Management of Foot and Ankle Fractures Ge´za F. Kogler Department of Rehabilitation, School of Health Sciences, Jo¨nko¨ping University, Jo¨nko¨ping, Sweden

CONTENTS I. Introduction ...................................................................................................................... 423 A. Prefabricated vs. Custom-Molded ............................................................................. 424 B. Mechanical Function and Control Mechanisms........................................................ 424 1. Arch Support Mechanisms.................................................................................. 424 2. Wedges ................................................................................................................ 425 3. Heel Lifts and Elevations .................................................................................... 425 C. Orthotic Principles and Biomechanical Considerations ............................................. 425 D. Diagnostic Tests to Determine Pain Reduction Potential.......................................... 426 1. Medial Column Load-Bearing Test..................................................................... 426 2. Lateral Column Load-Bearing Test .................................................................... 426 3. Hindfoot Load-Bearing Test ............................................................................... 428 E. Negative Impression Technique Considerations ........................................................ 428 II. Orthotic Treatment of Fractures ....................................................................................... 429 A. Phalanges ................................................................................................................... 429 B. Metatarsals ................................................................................................................ 430 1. Stress Fractures ................................................................................................... 430 C. Sesamoid Bones of the Great Toe.............................................................................. 430 D. Navicular, Cuneiforms, and Cuboid.......................................................................... 431 E. Talus .......................................................................................................................... 432 F. Calcaneus................................................................................................................... 433 G. Ankle ......................................................................................................................... 433 III. Conclusion ........................................................................................................................ 436 References .................................................................................................................................. 437

I.

INTRODUCTION

Certain fractures of the foot and ankle can be treated through external support with various types of orthoses. They are primarily used to immobilize and hold the injured segment following reduction of the fracture. Stabilization and maintenance of the fracture reduction is accomplished with a variety of materials such as plaster of Paris, fiber resin tape, metals, and plastics. Despite the variety of materials used, the three-point force system, hydrostatic pressure, and total-contact fit are common principles employed in orthotic fracture devices. While techniques for orthotic

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management of long bone fractures are well established [1], their applicability for fractures of the foot and ankle often require different considerations. Moreover, there are few studies that have assessed the effectiveness of fracture orthoses specific to the foot. Accordingly, this chapter reviews clinically accepted orthotic principles for fracture management and provides a practical guide for orthotic treatment of specific types of fractures.

A.

Prefabricated vs. Custom-Molded

An orthosis is an external force system applied to a segment of the body to control motion, and correct or prevent deformity. Specific to the treatment of foot and ankle fractures, orthoses are often designed to hold the fractured segment after it is reduced and stable. Orthoses may be used for all phases of fracture treatment, depending on the severity, type of injury, and location. For shortterm, acute, and subacute orthotic intervention, prefabricated nonmolded orthoses are commonly used, whereas custom-molded devices are prescribed for more definitive use in healed fractures with residual symptoms or when deformity is present. Orthoses are commonly classified as nonmolded, custom-fitted and custom-molded. Prefabricated orthoses that are nonmolded and do not require a model (i.e., negative impression, mold) of the body segment usually rely on a standard sizing system based on measurements or shoe size (i.e., small, medium, large, etc.). Off -the-shelf systems that require some modifications to the device for proper fit and function are further described as ‘‘custom-fitted.’’ ‘‘Custom-molded’’ orthoses necessitate a negative impression or measurements to produce a positive model for the orthoses to be constructed from. Prefabricated systems are best suited for the management of stable fractures, with the primary function being to limit ankle–foot motion in a specific plane (i.e., frontal, sagittal, transverse). While these types of devices are effective for motion control of the talocrural and subtalar joints, their generic or noncontoured foot components are not as efficient as custom-molded plantar foot interfaces for resisting joint movements within the foot. Contraindications for prefabricated orthoses are: nonstable fractures, edema or swelling, deformity, loss of protective sensation, definitive orthotic management, obesity, and patient compliance.

B.

Mechanical Function and Control Mechanisms

The primary objectives of an ankle–foot orthosis (AFO) for the treatment of foot and ankle fractures are immobilization of the fractured segments and control of joint movements. AFOs (with an anterior or a posterior clamshell design) are not considered major load-bearing devices, experiencing less than 20% of the axial loads the leg is subjected to [2]. Custom-molded foot orthoses can influence plantar foot pressures and alter load transmission pathways through the foot. While the contribution of foot orthoses to healing of fractures is not fully known, clinical symptoms of pain often improve with orthotic intervention, allowing earlier return to functional activities. Control mechanisms are the regional portions of an orthosis that perform a specific function (i.e., metatarsal support, medial arch support) and orthotic control mechanisms may be incorporated into the design of an orthosis, depending on the individual needs of a patient. Mechanisms that alter the load transmission pathways in the foot can be classified into primary and secondary control elements. Medial arch supports and varus and valgus wedges are categorized as primary, while lifts, metatarsal pads, and pressure relief zones are considered secondary control elements. Although these orthotic control mechanisms can be used to treat a variety of foot pathologies, only their relevance to the management of foot fractures is discussed. 1.

Arch Support Mechanisms

An appropriately designed medial longitudinal arch support increases loading to the medial midarch tarsal skeletal structures. Arch support mechanisms are capable of minimizing the medial truss action of the foot by transferring loads from the medial aspect of the heel and the first metatarsal head (MTH) to the navicular and adjacent tarsal bones [3]. For fractures of the talus,


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navicular, and medial cuneiform where the compressive forces exuded by the truss action of the foot may be associated with symptoms of pain, the alternative load pathway produced with the medial longitudinal arch may lessen pain and permit an increase in functional activities. The medial longitudinal arch is also effective in controlling subtalar valgus and resisting pronation, which is often an important orthotic objective for the management of fractures to the ankle. In general, arch support mechanisms are more tolerable and effective as a treatment when they are fabricated with materials that have a viscoelastic property of low durometer (hardness) rather than a rigid material. Therefore, arch supports should ideally be considered mechanisms that resist undesirable foot movements rather than block them. 2.

Wedges

Varus and valgus wedges are inclined surfaces in the coronal plane that raise a portion of the foot higher with respect to another. They are often descriptively referenced in terms of the region of foot they interface with (i.e., forefoot valgus wedge). The influences of varus and valgus wedges require utilization of the two primary polymodus support systems of the foot, the medial truss, and the lateral locking mechanism of the calcaneocuboid joint [4]. Effective at altering the load transmission pathways in the foot, they can be used to reduce loading of midfoot and forefoot fractures. In general, varus forefoot wedges are used for lateral forefoot and midfoot injuries and valgus forefoot wedges for medial forefoot and midfoot problems. Clinicians not familiar with the biomechanical rationale of this approach might conclude that a forefoot varus wedge may increase loading to the lateral aspect of the foot. However, instead of a lateral shift in load transmission the medial support of the foot’s truss bears a greater portion of the load. A series of orthotic diagnostic tests (see ‘‘Navicular, Cuneiforms, and Cuboid’’ section below) may be used to determine the potential of pain relief benefit afforded by a forefoot varus or a valgus wedge. 3.

Heel Lifts and Elevations

Heel lifts elevate the calcaneus higher than plantar forefoot structures. Lifts and elevations of the heel serve a variety of fracture-related problems. For fractures of the ankle where pain is associated with end-range dorsiflexion, a heel elevation may potentially alleviate symptoms. Temporary plantar flexion contractures or fixed equines deformities can be accommodated with an appropriate heel-height elevation. A standing diagnostic block test may be used to determine the potential benefit of a heel lift (see ‘‘Navicular, Cuneiforms, and Cuboid’’ section below).

C.

Orthotic Principles and Biomechanical Considerations

The orthotic principles used to manage fractures of the foot and ankle are dependent on the goals of treatment. Common objectives are to reduce loading through the fracture site, support the fracture, and restrict joint movements. Several fundamental orthotic principles may be employed to accomplish these aims. Hydrostatic pressure, total-contact fit, three-point force systems, and altering load transmission pathways through the foot are techniques used in the orthotic management of fractures. Hydrostatic pressure is produced when an orthosis applies circumferential and uniform compression to soft tissue structures to support skeletal segments. Externally applied pressure from orthoses can also be effective in controlling postfracture swelling [5,6]. Internal hydrostatic pressure provides stability to a fracture but is not effective at any significant axial unloading. Since structural loading of the orthosis is not a major function for these types of orthoses, lightweight and relatively thin materials can be used. The efficiency of a hydrostatic pressure system is reliant on the shape of interface components, the rigidity of the material, and the ability to regulate pressure. Thin plastics that have anatomically contoured interfaces are more effective than compliant cloths. The circumferential wrap and bivalve clamshell are the two common design integrations. Both systems require adjustable closures (i.e., Velcro1, etc.) to regulate the amount of pressure applied to the body segment. Pneumatic air compression systems available with some prefabricated orthoses


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(Aircast1, Summit, NJ) capitalize on this principle and have been successful in treating various types of ankle fractures [6,7,8,9,10]. Theoretically optimum orthotic control and comfort is achieved when pressure is evenly distributed. Therefore the premise of custom-molded orthoses is to provide a ‘‘total-contact’’ fit with the intent that uniform pressure is imparted to the limb and foot. The orthotic interface may have to assume a different shape than the natural anatomic morphology of the body segment to achieve this objective, particularly if compression soft tissue is required to support a skeletal structure. A metatarsal support is an example of an orthotic interface contour that differs from the foot’s plantar surface. Successful orthotic fracture management requires a thorough understanding of both foot and ankle biomechanics and the diversity of load transmission pathways the foot and ankle can assume during standing and walking. Orthotic-ground reaction forces can be applied to the foot in a prescribed manner via an orthosis to alter the load transmission patterns. This capability allows the clinician to determine a therapeutic load transmission pattern that protects a healing foot fracture and decreases pain.

D.

Diagnostic Tests to Determine Pain Reduction Potential

Several tests that simulate certain orthotic conditions in stance are useful clinical tools to assess the potential therapeutic response of an orthosis for alleviating pain. The tests evaluate different load transmission pathways in the foot to determine if an orthotic condition can divert a portion of load away from the injured segment, thereby reducing pain in weight-bearing. Three orthotic diagnostic tests that replicate primary orthotic control mechanisms (i.e., valgus forefoot wedge) and encourage load transmission pattern shifts during stance are described. Orthotic diagnostic tests are generally conducted in the same way. With the patient standing on an orthotic test block under the affected foot and a flat block under the uninvolved side, the examiner asks if the patient notices an ‘‘increase,’’ ‘‘decrease,’’ or ‘‘no change’’ in pain symptoms. A ‘‘decrease in pain’’ response denotes a positive (þ) test, an ‘‘increase in pain’’ response indicates a negative () test, and ‘‘no difference’’ is neutral (ø). Patients are evaluated in single- and doublelimb stance. If standing balance is of concern, or a partial weight-bearing test is preferred, the tests can be conducted with the aid of parallel bars or a walker. The location of the fracture and physical examination will determine the appropriate diagnostic test (see ‘‘Orthotic Treatment of Fractures’’ section for recommendations). One must be cautious on how negative and positive results are interpreted by the orthotic diagnostic tests described. Negative results only suggest that the orthotic condition simulated by the respective diagnostic test may not contribute to a reduction in pain. Other orthotic control mechanisms (i.e., arch support mechanisms) not evaluated with this test may be effective in pain relief and should still be considered. 1.

Medial Column Load-Bearing Test

A medial column load-bearing test elevates the first and second MTHs higher (0.6 to 0.8 cm) than other plantar foot structures (Figure 17.1). The test simulates the use of a varus forefoot wedge or platform to increase structural loading of the foot’s medial truss mechanism and decrease loading of lateral column skeletal structures. Thus, a medial column load-bearing test assesses pain relief potential for cuboid and metatarsal (fourth and fifth) fractures. A positive (less pain) test result suggests that an orthosis with a varus forefoot wedge or platform may contribute to reduction in pain during weight-bearing. A negative test suggests that a varus forefoot wedge or platform may not decrease pain or even increase symptoms. 2.

Lateral Column Load-Bearing Test

A lateral column load-bearing test elevates the fourth and fifth MTHs higher (0.6 to 0.8 cm) than other plantar foot structures (Figure 17.2). The test simulates use of a forefoot valgus wedge or



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Figure 17.1 Photograph of a medial column load-bearing test that elevates the first and second MTHs higher (0.6 to 0.8 cm) than other plantar foot structures. The test evaluates the pain reduction potential of an orthotic varus forefoot wedge or platform.

platform to increase structural loading of the lateral column. The test engages the calcaneal cuboid ‘‘lock’’ and decreases loading of the foot’s medial truss mechanism. Pain associated with fractures of the medial aspect of the foot such as the medial metatarsals (first to third), navicular, and cuneiforms may be evaluated for pain relief with this diagnostic test. A positive test (less pain) result suggests that an orthosis with a valgus forefoot wedge or platform may contribute to reduction in pain during weight-bearing. A negative test (more pain) suggests that a valgus forefoot wedge or platform may not decrease pain or even increase symptoms.

Figure 17.2 Photograph of a lateral column load-bearing test that elevates the fourth and fifth MTHs higher (0.6 to 0.8 cm) than other plantar foot structures. The test evaluates the pain reduction potential of an orthotic valgus forefoot wedge or platform.


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Hindfoot Load-Bearing Test

A hindfoot load-bearing test elevates the heel higher (0.5 to 1.5 cm) than other plantar foot structures (Figure 17.3). The test simulates use of an orthotic heel elevation to encourage increased loading of the calcaneus and decrease loading of the forefoot. A complete test may require sequential heel elevation blocks to determine the appropriate heel-height prescription. Pain associated with fractures of the ankle, metatarsals, and midtarsal bones may be evaluated with this diagnostic test. A positive test (less pain) result suggests that a heel elevation or lift may contribute to reduction in pain during weight-bearing. A negative test (more pain) result suggests that a heel elevation or lift may contribute to an increase in pain during weight-bearing.

E.

Negative Impression Technique Considerations

Custom-molded orthoses require a positive model of the limb segment to construct and fabricate a device. The positive cast is created from a negative impression (mold) taken of the patient’s leg and foot. The negative impression is a means to transfer and duplicate the three-dimensional shape and contours of the respective body segment accurately, to produce an orthosis that achieves a totalcontact fit. Therefore, the method used to obtain a mold is key to proper fit, function, and comfort. Numerous techniques and materials are employed to obtain a negative impression. However, manipulation of soft tissue for efficient transfer of orthotic corrective forces to structural bone elements and skeletal positioning are crucial procedures in all techniques. Negative impressions for AFOs require the ankle be positioned at 908 of flexion to prevent an equinus deformity and contractures of the posterior musculature. In the coronal plane the subtalar should be positioned at neutral. If angulatory deformity is of concern in ankle fractures, compression of proximal soft tissues where corrective forces (three-point force system) are applied by the orthosis need to be incorporated into the impression during the molding procedure. Measurements (M-L) of soft tissue compressibility for application of corrective forces may also be helpful for later reference to estimate modification parameters to the positive model. For an improved fit of in-shoe AFOs, a contoured footplate that simulates the shank profile of a shoe may also be used. To obtain an impression of the foot’s plantar surface, the alignment of the foot’s medial longitudinal arch is of primary importance. In general, the medial longitudinal arch should be clinically positioned at its maximum height when an impression is taken. The manipulation may be accomplished in several ways, but the final positioning results in external rotation of the tibia, forefoot adduction, calcaneal inversion, and a relative shortening of foot length. The technique

Figure 17.3 Photograph of a hindfoot load-bearing test that elevates the heel higher (0.5 to 1.5 cm) than other plantar foot structures. The test evaluates pain reduction potential of an orthotic heel elevation at various heights.



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described by Campbell and Inman [11] for the University of California Berkeley Laboratory, UCBL shoe insert employs the basic principles of foot positioning to raise and lower the foot’s arch. Plaster or fiber resin tape impressions allow for plantar soft tissue molding and clinical compression to specific regions where a load-bearing support is desired (i.e., metatarsal support, sustentaculum tali support). Polystyrene foam impressions and foot digitizers do not permit targeted compression of plantar soft tissues of the foot during the measurement and molding process. If the impression technique does not allow the clinician to hand mold supportive features, modifications to the positive model may be necessary to include these orthotic control elements in the finished orthosis.

II.

ORTHOTIC TREATMENT OF FRACTURES

A.

Phalanges

Fractures of the toe phalanges pose unique orthotic challenges due to the natural fore and aft displacements the toes engage in during walking. Suspension of single-digit splints and lack of comfort are common problems associated with phalangeal orthoses. A plantar phalangeal toe sulcus support is a simple intervention that may provide some relief from symptoms (Figure 17.4). Prefabricated versions that affix to the toe with an elastic loop permit displacement of the toes while maintaining continued plantar support even during metatarsal–phalangeal joint dorsiflexion. Fixed custom sulcus supports built into an orthosis are effective only when the device or shoe restricts or blocks metatarsal–phalangeal joint movements. If pain is present with movement of the metatarsal– phalangeal joint, foot orthoses designed to restrict movement via a rigid toe plate, rigid-soled shoe, or a full-sole graphite plate fitted to a shoe may be of benefit. In instances where a shoe or an orthosis is prescribed to resist dorsiflexion of the toes, a rigid rocker sole is recommended for additional unloading and improved comfort during ambulation. A rocker axis placed at 65% of shoe length can decrease plantar pressure to the toes by approximately 20% at the hallux, 40% at the second toe, and 37% at the lateral toes (third to fifth) [12]. Shoes with an extradeep toe box may also be considered if swelling and toe contact with the shoe aggravate symptoms.

Figure 17.4 A prefabricated phalangeal sulcus support.


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Metatarsals

Fractures of the metatarsals disrupt the foot’s function as an anterior lever arm during standing and the natural transfer of loads from the hindfoot to the forefoot during propulsion. The objective of orthotic intervention is to resist excessive loading of the fractured segment and transfer the loadbearing function to another region of the foot. Thus, an orthosis should encourage loading of either the medial truss or the lateral calcaneal locking mechanism based on the location of the injury. A foot orthosis designed to treat a fracture to the shaft of the first, second, or third metatarsals should encourage loading of the lateral column of the foot via a valgus forefoot wedge to decrease the loading of the medial column’s truss. In contrast, a midshaft fracture of the fourth or fifth MTs would necessitate increased loading of the medial truss with a forefoot varus wedge that would decrease loading of the lateral column. Further orthotic control can be obtained by incorporating a load-bearing support area (i.e., metatarsal support), with the apex of the support’s convex contours positioned at the level of the fracture site. A rigid rocker-soled shoe may contribute to pain reduction and theoretically reduces loading through the metatarsal shafts as evidenced by decreases in plantar pressure measurements. A rocker axis for a rigid rocker-soled shoe at 55 to 60% of shoe length has the potential to decrease plantar pressures 40% at the first MTH, 55% at the second MTH, and 57% at the lateral MTHs [12]. Metatarsal fractures that require open reduction and internal fixation (ORIF) may involve more than one type of orthotic intervention for postoperative management. Depending on the type of fixation, a solid ankle AFO with rigid toe plate may be used postoperatively or after initial immobilization with a cast. Ambulation can be considered at 4 to 6 weeks with the use of a custommolded foot orthoses and a rigid-soled shoe. Distal metatarsal fractures (i.e., fractures of the metatarsal head) may require a longer duration of orthotic treatment for complete recovery and relief of symptoms compared with more proximal fractures. A rigid rocker-soled shoe and a foot orthosis can be of benefit for residual metatarsalgia pain due to forefoot fractures [13]. 1.

Stress Fractures

Stress fractures to the metatarsals usually respond to plantar control with the combination of a medial arch and a metatarsal support. Patients tolerate treatment best when the orthotic interface is fabricated out of a soft viscoelastic material. Mild to moderate symptoms of pain may be treated using conventional footwear that can accommodate an orthosis. For more severe pain or when excessive swelling is present the orthosis can be used with a rigid rocker-soled surgical shoe. In certain instances the use of a simple rocker-soled shoe may be the only treatment needed [14,15]. A Morton’s extension on a foot orthosis that incorporates a full-length foot section at the hallux than at the lateral toes may be of benefit for stress fractures of the second MT when the first MT is anatomically shorter than the second MT [16]. Stress fractures are often a result of overuse injuries from sports, activity, and dancing [17]. The use of foot orthoses for the treatment of stress fractures may provide a prophylactic benefit in reducing injury in the active person. Simkin et al. [18] reported a significant reduction in the occurrence of metatarsal stress fractures in military recruits with low-arched feet with the use of a rigid type of foot orthosis (Langer military stress orthosis) that provides an additional shockabsorbing function along with the foot. The treatment of dancers with metatarsal fractures ranges from a soft support type foot orthosis [19] to an AFO for a specific type of stress fracture to the second MT involving the Lisfranc’s joint [20].

C.

Sesamoid Bones of the Great Toe

Sesamoid fractures are generally associated with symptoms of point-specific pain on the plantar aspect of the first MTH. Physical examination by palpation can often differentiate whether the lateral or the medial sesamoid is affected, with the latter most common. The objective of orthotic treatment is to redistribute plantar foot pressures with a focal concave relief that accommodates the first MTH. Orthotic intervention is based on a custom medial longitudinal arch whose contours hold the skeletal arch at its maximum height. In addition to an arch support mechanism, a relief



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Figure 17.5 A right-foot orthosis designed to decrease loading to fractured sesamoids during weightbearing. The orthosis includes a medial longitudinal arch support mechanism and a concave relief zone at the first MTH. Configured with an appropriate relief depth, the orthosis can accommodate for plantar flexion deformities of the first MT.

zone (negative concavity) at the first MTH is usually required depending upon the magnitude of pain associated with weight-bearing (Figure 17.5). Patients that present with a plantar flexion angulatory deformity of the first ray require further orthotic adaptations. Plantar flexion of the first ray relative to the other metatarsals (second to fifth) usually puts undue pressure on the sesamoids of the first MTH and is a factor that predisposes the foot to sesamoid stress reactions and fractures. Unless the orthosis accommodates for relative plantar flexion (first MT), patients tend to be resistant to treatment with just a conventional custom-molded arch support and a first MTH relief. To redistribute pressures more equitably, an orthotic ‘‘platform’’ can accommodate for the plantar flexion of the first ray and reallocate a portion of the pressure from the first MTH to the second through fifth MTHs [21]. To limit metatarsal head contact time during gait, shoes can be modified with a rigid rocker sole. Resistant cases usually respond with the combination of the orthosis and a modified shoe.

D.

Navicular, Cuneiforms, and Cuboid

Fractures of the navicular and cuneiforms utilize the same orthotic treatment principles as metatarsal fractures. As with fractures to the medial metatarsals, the orthosis should redirect a portion of the load the foot is subjected to from the medial skeletal structures to the lateral column. An orthosis that elevates the fourth and fifth MTHs relatively higher (0.5 cm) than the medial metatarsal heads (i.e., valgus forefoot wedge, MTH [fifth, sixth] elevation platform) is usually effective in reducing symptoms of pain (Figure 17.6). The lateral column load-bearing test can determine the potential response of this treatment. In addition to the lateral MTH elevation platform, plantar support at the fracture site with a medial longitudinal arch support and a metatarsal support provides stability during weight-bearing activities. Orthotic treatment is optimal with custommolded orthoses that can achieve a total-contact fit. Cuboid fractures with mild to moderate symptoms of pain respond to an orthosis that has an MTH (first to third) elevation platform or a varus forefoot wedge. The potential response to this treatment is assessed with a medial column load-bearing test. The inclusion of a medial arch support is desirable but not as critical as it is for the treatment of navicular and cuneiform fractures.


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Figure 17.6 Orthosis with a valgus forefoot platform that elevates the fourth and fifth MTHs relatively higher (0.5 cm) than the medial metatarsal heads. The orthosis often reduces residual pain and inflammation associated with fractures of the medial metatarsals (first to third), cuneiforms, and navicular.

When severe pain is present, a custom-molded UC-BL shoe insert may be the alternative treatment for effective resolution of symptoms. During the negative impression procedure for the UC-BL shoe insert, the forefoot should be positioned in adduction relative to the hindfoot to achieve maximum stress relief of the fracture for weight-bearing activities. Heel lifts (i.e., 0.5 to 1 cm) that extend just proximal to the location of the fracture may also provide additional relief from pain. A load-bearing test that simulates the heel-lift effect can determine the potential response of this treatment. Stiff-soled shoes with shock-attenuating soles impart greater comfort during standing and walking when wearing a foot orthosis. Fractures to the accessory ossicle, os peroneum, may utilize several orthoses for treatment. Initial immobilization with an AFO walking boot can assist with reduction of acute pain and inflammation while a foot orthosis with an appropriate wedge may assist with the management of residual pain symptoms [22]. Requejo et al. [22] hypothesize that a 48 inclined valgus wedge may decrease tension within the peroneal tendon, thereby decreasing inflammation symptoms. A rigid rocker-soled shoe may also provide pain relief since this form of immobilization is believed to be effective in transferring forefoot loads [23].

E.

Talus

An important function of an orthosis for treatment of talus fractures is to reduce stress through the talus. This is particularly challenging since the superior portion of the talus and the talonavicular joint are major load-bearing regions of the foot and arch, respectively. While unloading the body of the talus is technically difficult and rarely attempted with an orthosis, plantar support of the navicular and sustentaculum tali can maintain stability of the fracture and reduce pain. Talus fractures of the neck and head have the potential for some load reduction by transferring a portion of the load through the arch support portion of an orthosis. Several orthotic control mechanisms may need to be incorporated into a foot orthosis for the treatment of talus fractures. A custom-molded arch support is critical to relief from pain. Direct orthotic support of the talus is not possible due to its anatomic orientation. Control of the talus is achieved through support of the calcaneus and the navicular via adequate compression of plantar soft tissues to resist arch depression and elongation. A sustentaculum tali support is a convex prominence on the medial arch support region of an orthosis that is situated beneath the respective calcaneal protuberance. This orthotic addition requires accurate placement for optimal support and has gentle contours for comfort.



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Nonoperative treatment of talus fractures often includes some form of orthotic management. The type of orthosis used to manage fractures of the talus varies considerably and is dependent on the stage of fracture healing and the type and location of injury. In general, immobilization of the entire foot and ankle with a rigid orthosis may be indicated during the first stages of healing, with more compliant devices that permit ankle movement considered as symptoms subside. A solid ankle AFO calms acute inflammation and swelling while custom foot orthoses are therapeutic for residual or persistent pain after the fracture has healed. With stable nondisplaced fractures, orthotic intervention assists in reducing pain and permits relatively comfortable ambulation. Compression fractures of the navicular that consequentially produce an impact fracture to the head of the talus are well suited for orthotic treatment with a custom-molded foot orthosis and a rigid-soled shoe. Orthoses are often of considerable benefit as an adjunct treatment for postoperative care of fractures that require ORIF. Postoperative care following open reduction of the neck of the talus involves initial immobilization with a series of casts (i.e., non-weight-bearing, weight-bearing) followed by a rigid-soled orthopedic shoe and custom foot orthosis. A calcaneotibial fusion for a displaced fracture of the body of the talus can be managed with a solid ankle AFO to provide protection after cast immobilization for another 2 to 3 months.

F.

Calcaneus

During standing, 65 to 70% of the loads transmitted through the foot are borne by the heel [24]. Thus, the common orthotic intention of altering the load transmission pathway in the foot is technically difficult for calcaneal fractures. Another complicating factor is that most calcaneal fractures involve the subtalar joint. So, any attempt to transfer loads from the hindfoot to midfoot and forefoot structures still necessitates loading of the injured talus. Of the variety of methods used to treat these fractures, orthotic management includes both primary treatment of nondisplaced fractures and secondary adjunctive intervention for postoperative care of displaced fractures. In general, the underlying principles of orthotic treatment are fundamentally similar, with plantar foot pressure redistribution and restriction of joint movement being common objectives. Calcaneal fractures that do not involve the subtalar joint or need an open reduction can be managed by an initial period of cast immobilization followed by treatment with a prefabricated AFO that limits ankle motion. Patients that respond well to cast immobilization may only need additional treatment with a custom-molded foot orthosis with an arch support. If an AFO is considered, versions that have a contoured foot bed with an arch support are better than noncontoured flat interfaces. Custom-molded arch supports provide additional control in prefabricated AFOs and are useful following treatment with an AFO. For injuries requiring ORIF, orthoses are used during initial healing and after healing is complete. AFOs can often lessen the time of cast immobilization, maintain the reduction, and improve patient comfort during ambulation. After treatment with an AFO, patients often have persistent pain with ambulation that can be treated with custom foot orthoses and an athletic or a running shoe. Patients tolerate orthoses fabricated out of viscoelastic rather than rigid materials better. However, if plantar orthotic control is not considered adequate for a particular fracture, a UCBL shoe insert offers greater stability to the calcaneus through its plastic heel cup design. In addition, posting of the heel on a UC-BL shoe insert is effective if subtalar motion needs to be controlled. Calcaneal fractures can produce residual pain in the ankle and foot even after union of the fracture. Multiple injuries of the foot and ankle that include the calcaneus may require definitive orthotic treatment. A foot orthosis with shoe modifications can ease symptoms for patients with activities that require extended periods of standing. Custom footwear has proven to be useful for rehabilitation following land mine injuries that often involve fractures of the calcaneus combined with other foot–ankle fractures [25].

G.

Ankle

Orthotic management of ankle fractures includes a broad range of treatment interventions that encompass the spectrum of fracture management from acute to postoperative rehabilitation. Orthoses may be considered within the first week following the injury in nondisplaced fractures,


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4 to 6 weeks after a period of cast immobilization, or 1 week postoperatively following ORIF for displaced fractures. The range of designs for orthotic management of ankle fractures includes a high-laced stabilizing shoe for treatment of closed lateral ankle fractures [26] to AFOs that are similar to tibial fracture orthoses [27,28]. An AFO (push brace medium) made of a compliant cloth with control straps may also be effective in treating supination–eversion stage II ankle fractures [29]. The use of AFOs provides patients with the advantage of early mobilization during healing and rehabilitation compared with delayed rehabilitation and limited ankle dorsiflexion range that may result from cast immobilization and non-weight-bearing protocols [27,30,31,32]. Evidence from several studies suggests that AFOs may provide a prophylactic benefit to prevent ankle fractures and sprains [33,34,35]. In general, the orthoses should permit full range of motion at the ankle joint while limiting rotation of the talus within the mortise. Excessive subtalar joint motion related to fracture alignment or degenerative changes may require further biomechanical design considerations. A foot orthosis with an arch support mechanism made of a viscoelastic material provides shock attenuation and can limit pronation to resist extraneous movements of the talus within the ankle mortise [36]. The medial longitudinal arch with a sustentaculum tali support may also be incorporated into an AFO’s foot piece section to compliment the hinged joints in restricting motion in the frontal plane. A rigid hinged AFO with an anterior or a posterior clamshell proximal section is an established design for management of ankle fractures [27]. Transverse and frontal plane control (i.e., rotation, eversion, inversion) is the most common prescription requirement. Some fractures require an initial period of both frontal and sagittal plane control, with gradual increases in movements permitted in one or both planes as symptoms of pain lessen. Ankle stiffness is a common complication of ankle fractures that is often associated with cast immobilization and non-weight-bearing treatment regimes [37,38,39,40]. Ankle dorsiflexion is the most frequent movement limitation. To avert such problems, some surgeons advocate early mobilization with the use of AFOs, particularly after ORIF [27,30,41,42]. However, the ability to improve ankle motion with an AFO and early mobilization is still not conclusive. The potential ankle dorsiflexion motion following treatment with an AFO is reported to be greater than 108 by Segal et al.[27] and 158 by Cimino et al. [41] and Tropp and Norlin [43] while other investigations have not shown any significant changes in ankle-joint movements [39,44]. Investigations into the use of ankle stirrup type AFOs for treatment of ankle fractures have shown that certain versions are capable of producing clinically acceptable results for specific types of fractures. Aircast air stirrup orthoses have successfully been used for stable lateral malleolar fractures [6,8,9]. When frontal plane control of inversion and eversion is the biomechanical objective of an orthosis, some stirrup type AFOs can provide mild M-L stability and relief from pain. Studies evaluating motion control in the coronal plane demonstrate that pneumatic ankle stirrup orthoses can significantly reduce range of motion at the subtalar joint [45,46]. A stirrup type AFO has medial and lateral support components that are connected distally by a band of material that fits under the heel of the foot, hence the descriptive category of ‘‘stirrup’’ (Figure 17.7A). Compressive forces are applied to both malleoli via anatomically contoured side panels secured with a series of straps. Stability and motion control is achieved in part from hydrostatic pressure and multiple three-point force elements. Stirrup-type AFOs primarily restrict motion in the coronal plane. Some include a foot piece and have a joint that articulates at the talocrural joint to permit free dorsiflexion and plantar flexion. Other versions may have no joint or foot piece but may still permit movement. To ensure maximum fit, function, and comfort, interface systems employ air, gel, liquids, and various foams to apply supportive forces to the foot and ankle. Although custom versions of stirrup type AFOs can be fabricated, the majority dispensed are prefabricated stock devices. Prefabricated walking boot type AFOs are also effective in treating certain type ankle fractures (Figure 17.7B and Figure 17.7C). Designs vary greatly between manufacturers, with varying features such as rigid ankles, variable range motion control ankle joints, gel interfaces, pneumatic hydrostatic compression systems, and various rigid rocker sole configurations. The use of walking boot type AFOs is often considered for postoperative care of ankle fractures [7,17]. The DonJoy1 R.O.M. walker (Figure 17.7C) was compared with Aircast ankle stirrup orthosis (Figure 17.8A) and proved to have a similar treatment outcome for stable lateral



435

Figure 17.7 Prefabricated nonmolded AFOs used to treat fractures of the ankle and foot. (A) Air stirrup orthoses (Aircast). (B) Walking boot with pneumatic rigid rocker sole (Aircast). (C) Ankle fracture orthosis with hinge articulation (DonJoy).


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Kogler

Figure 17.8 Custom-molded AFOs used to treat fractures of the ankle and foot. (A) Solid ankle AFO with rigid rocker sole. (B) AFO with free-motion ankle joint, foot piece, and a plantar flexion stop.

malleolar fractures [9]. Postoperative treatment of internally fixed ankle fractures with a flexible arthrodesis boot type AFO has demonstrated improved function and accelerated venous flow compared with cast immobilization [48]. Custom AFOs offer optimal fit and control compared with prefabricated fracture orthotic systems. They are often the only option when deformity is present. Traditional thermoplastic AFO designs can be used for fracture management with appropriate design features. To encourage mobility, dorsiflexion, and plantar flexion movement with closed or open (ORIF) stable fractures, AFOs with a hinged ankle joint, proximal clamshell tibial section, and a foot piece are advocated [28]. When motion in all planes needs to be restricted, solid-ankle AFOs perform best with padded ankle-control straps and structural reinforcements at the ankle. Clamshell designs that consist of a posterior rigid shell (i.e., polypropylene) with a more compliant anterior shell (i.e., polyethylene) provide maximum hydrostatic compression and control. Designs where the medial lateral trimlines of the AFO are posterior to the anatomic ankle axis can permit greater movement at the ankle without the use of a hinge with successful treatment results [31]. Custom AFOs can be fabricated to fit within a shoe or be designed as a boot with its own sole (Figure 17.8A and Figure 17.8B) [49]. Soft-soled shoes with a cushioned heel are recommended to absorb some of the impact during heel strike for AFOs that restrict plantar flexion.

III.

CONCLUSION

Functional treatment of foot–ankle fractures with orthoses is an established method of management within orthopedics. The scope of orthotic intervention is broad, encompassing the full



437

spectrum of applications that include acute, primary, and postoperative care. An understanding of foot–ankle biomechanics, fracture mechanics, and orthotic principles of fracture management is essential to achieve a successful clinical outcome. Biomechanical data supporting orthotic design principles for specific types of foot–ankle fractures are limited compared with the body of knowledge that exists for orthotic management of long bone fractures. Future investigations that evaluate the biomechanical design features of fracture orthoses could widen the therapeutic options available for orthotic treatment.

REFERENCES 1. Sarmiento, A., A functional below-the-knee cast for tibial fractures, J. Bone Jt. Surg., 52A, 295–311, 1970. 2. Sarmiento, A. and Latta, L.L., Closed Functional Treatment of Fractures, Springer-Verlag, New York, 1980. 3. Kogler, G.F., Solomonidis, S.E., and Paul, J.P., Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain, Clin. Biomech., 11, 243–252, 1996. 4. Kogler, G.F., Veer, F., Solomonidis, S.E., and Paul, J.P., The influence of medial and lateral placement of orthotic wedges on loading of the plantar aponeurosis. In vitro study, J. Bone Jt. Surg., 81A, 1403–1413, 1999. 5. Matsen, F.A. and Krugmire, R.B., The effect of externally applied pressure on post-fracture swelling, J. Bone Jt. Surg., 56A, 1586–1591, 1974. 6. Stuart, P.R., Brumby, C., and Smith, S.R., Comparison study of functional bracing and plaster cast treatment of stable lateral malleolar fractures, Injury, 20, 323–326, 1989. 7. Dietrich, A., Lill, H., Engel, T., Scho¨nfelder, M., and Josten, C., Conservative functional treatment of ankle fractures, Arch. Orthopaed. Trauma Surg., 122, 165–168, 2002. 8. Richter, J. and Muhr, G., Die funktionell konservative therapie von stabilen außenkno¨chelfrakturen, Ambulant Operieren, 3, 94–98, 1998 (in German) (as quoted by Dietrich et al.). 9. Brink, O., Staunstrup, H., and Sommer, J., Sable lateral malleolar fractures treated with Aircast ankle brace and Don Joy R.O.M. walker brace: a prospective randomized study, Foot Ankle Int., 17, 679–684, 1996. 10. Stover, C.N., Air stirrup management of ankle injuries in the athlete, Am. J. Sports Med., 85, 360–365, 1980. 11. Campbell, J.W. and Inman, V.T., Treatment of plantar fasciitis and calcaneal spurs with the UC-BL shoe insert, Clin. Orthopaed., 0, 57–62, 1974. 12. Van Schie, C., Ulbrect, J.S., Becker, M.B., and Cavanagh, P.R., Design criteria for rigid rocker shoes, Foot Ankle Int., 21, 833–844, 2000. 13. Ivanic, G.M., Trrnka, H.J., and Homann, N.C., Post-traumatic metatarsalgia. Early results of treatment with a new insole, Unfallchirurg, 103, 507–510, 2000 (in German). 14. Kadel, N.J., Goldstein, J., Newberg, A.H., and Trepman, E., Salter-Harris III stress fracture of the proximal first metatarsal: a case report, Foot Ankle Int., 22, 252–255, 2001. 15. Mizel, M.S., Marymont, J.V., and Trepman, E., Treatment of plantar fasciitis with a night splint and shoe modification consisting of a steel shank and anterior rocker bottom, Foot Ankle Int., 17, 732–735, 1996. 16. Zechman, J.S., Stress fracture of the second metatarsal after Keller bunionectomy, J. Foot Surg., 23, 63–65, 1984. 17. Drez, D., Young, J.C., Johnson, R.D., and Parker, W.D., Metatarsal stress fractures, Am. J. Sports Med., 8, 123–125, 1980. 18. Simkin, A., Leichter, I., Giladi, M., Stein, M., and Milgrom, C., Combined effect of foot arch structure and an orthotic device on stress fractures, Foot Ankle, 10, 25–29, 1989. 19. Hardaker, W.T., Margello, S., and Goldner, J.L., Foot ankle injuries in theatrical dancers, Foot Ankle, 6, 59–69, 1985. 20. Michelli, L.J., Sohn, R.S., and Solomon, R., Stress fractures of the second metatarsal involving Lisfranc’s joint in ballet, J. Bone Jt. Surg., 67A, 1372–1375, 1985. 21. Duddy, R.K., Duggan, R.J., Visser, H.J., Brooks, J.S., and Klamet, T.G., Diagnosis, treatment and rehabilitation of injuries to the lower leg and foot, Clin. Sports Med., 8, 861–876, 1989. 22. Requejo, S.M., Kulig, K., and Thoradson, D.B., Management of foot pain associated with accessory bones of the foot: two clinical case reports, J. Orthopaed. Sports Phys. Ther., 30, 580–594, 2000. 23. Wu, K., Foot Orthoses Principles and Clinical Application, Williams & Wilkins, Baltimore, 1990. 24. Cavanagh, P.R., Rodgers, M.M., and Liboshi, A., Pressure distribution under symptom-free feet during barefoot standing, Foot Ankle, 7, 262–267, 1987. 25. Jacobs, L.G.H., The landmine foot: its description and management, Injury, 22, 463–466, 1991. 26. Zeegers, A., Van Ray, J., and van der Werken, C., Ankle fractures treated with a stabilizing shoe, Acta Orthopaed. Scand., 60, 597–599, 1989.


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18 Treatment of Foot and Ankle Deformities with the Ilizarov Fixator* Daniel M. Thompson Beaumont Bone and Joint Institute, Beaumont, Texas

Jason H. Calhoun Department of Orthopaedic Surgery, University of Missouri, Columbia, Missouri

CONTENTS I. Introduction ...................................................................................................................... 439 II. Classification of Deformities ............................................................................................. 440 III. Simple Deformities ............................................................................................................ 440 A. Equinus Contracture.................................................................................................. 440 B. Distal Tibial Angular Deformity ............................................................................... 443 C. Osteotomy with Internal Fixation ............................................................................. 444 D. External Fixation Technique ..................................................................................... 446 E. Simple Nonunion....................................................................................................... 448 F. Arthrodesis ................................................................................................................ 450 IV. Complex Deformities ........................................................................................................ 450 A. Complex Equinus Deformity ..................................................................................... 450 B. Cavus Deformity ....................................................................................................... 450 C. Rocker-Bottom Deformity ........................................................................................ 451 D. Infection..................................................................................................................... 453 E. Amputation ............................................................................................................... 455 F. Special Patient Populations ....................................................................................... 455 V. Summary ........................................................................................................................... 457 References .................................................................................................................................. 458

I.

INTRODUCTION

Deformities of the foot and ankle are common and are among the most challenging problems faced by surgeons. Rigid contractures caused by soft tissue deformity can be caused by nerve, muscle, or skin pathology and are commonly seen in patients with conditions such as poliomyelitis, Charcot– Marie–Tooth disease, and burns. Bony deformities are typically the result of high-energy trauma *From Thompson, D. and Calhoun J.H., Advanced techniques in foot and ankle reconstruction, Foot Ankle Clin., 5, 417–442, 1998. With permission.

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and include malunion, nonunion, and infection. Many deformities, such as congenital malformations, occur with combined soft tissue and bony pathology. Techniques to address these varied problems include casting, soft tissue release and transfer, osteotomies with internal or external fixation, external fixation techniques, arthrodesis, and amputation. This chapter reviews advanced techniques of external fixation with selected internal fixation applications for the treatment of foot deformities.

II.

CLASSIFICATION OF DEFORMITIES

Preoperatively, it is necessary to have a thorough understanding of the deformity under consideration. To do this, it is helpful to classify foot and ankle deformities by origin (malunion or nonunion, arthritic, burn, neuromuscular, infection, or congenital or developmental) and by type, such as a simple or complex presentation of an angular, rotational, translational, length, or union deformity. Simple deformities occur in one plane and in one tissue, such as an equinus soft tissue contracture, angular malunion, or simple nonunion. More complex deformities involve more than one plane, more than one tissue, or a deformity at more than one location. Complex deformities include the equinocavus contracture, rocker-bottom deformity, many bony nonunions, and most burn contractures. Deformities also can be divided on the basis of the age of the patient. Children younger than 8 years can often undergo successful correction of deformities without osteotomy because of the plasticity of their bone, but deformities may recur with growth [1,16]. Older children and adults are more likely to require osteotomy to maintain correction. The presence or absence of fixed bony deformity helps to further classify the deformity and helps guide the decision as to whether osteotomy is indicated.

III. A.

SIMPLE DEFORMITIES Equinus Contracture

Equinus contracture is probably the most common deformity encountered by the foot and ankle surgeon. The causes of these deformities include burns, trauma, neuromuscular disease, and congenital conditions. Mild (< 158) and moderate (15 to 308) equinus contractures usually respond to the accepted techniques of physical therapy, manipulation, casts, and soft tissue surgery. More severe corrections typically require more advanced techniques. It is important to realize that severe equinus contractures involve more than a tightened heel cord; all periarticular structures are contracted, including the medial neurovascular bundle. Rapid or intraoperative correction of a severe deformity places the soft tissues, including the neurovascular bundle, at risk. These deformities are treated best with gradual techniques and are especially well suited for the use of Ilizarov techniques with a circular fixator [2–6]. The Galveston equinus frame was developed for the treatment of burned children. It consists of a tibial ring, one calcaneal half-ring, and one metatarsal half-ring (Figure 18.1). The tibial ring is positioned approximately at the junction of the middle and distal thirds of the leg. It is secured with a single posterolateral-to-anteromedial wire and three half-pins attached to the ring anteriorly with the Rancho cube system (hybrid technique). The remaining half-rings are connected to bone with 1.5- or 1.8-mm wires (for children and adults, respectively) that are tensioned to 90 kg of force on the half-rings. The calcaneal wire is directed from the medial to lateral side to avoid the posterior neurovascular bundle. The wire is located relatively proximally and posteriorly in the calcaneus to prevent wire cutout and increase its biomechanical advantage. The metatarsal pin is directed medial to lateral from the first metatarsal to the fifth metatarsal. Only the first and fifth metatarsals are pinned so that a synostosis does not develop between adjacent metatarsals. Half-rings are connected to the calcaneal and metatarsal wires. The calcaneus half-ring is connected to the tibial ring with threaded distraction rods, and the metatarsal half-ring is connected with threaded compression rods. Calcaneus distraction requires only proximal hinges without distal hinges to allow posterior translation of the calcaneus pin as the calcaneus moves plantarly. Metatarsal dorsiflexion requires hinges on the metatarsal ring and a rotating post at the tibial ring to allow the metatarsal


Treatment of Foot and Ankle Deformities with the Ilizarov Fixator

441

Figure 18.1 Galveston frame for equinus correction. (A) The tibial ring is secured with one wire from the fibula to the tibia. The calcaneal wire and half-ring allow distraction of the calcaneus and ankle joint. The metatarsal wire and half-ring allow for correction of the equinus. (B) The frame is applied on a patient.


442


pin to translate anteriorly as the deformity is corrected. The ankle joint must be distracted before deformity correction and is performed at the time of frame placement. In a simple equinus correction, the ankle should be distracted 2 to 5 mm compared with preoperative radiographs. This limits cartilage compression and midfoot dorsiflexion deformity (rocker-bottom deformity). Distraction of the hindfoot must be done in a posteriorly inclined direction. If distraction is performed in a purely axial direction, parallel to the tibia, the talus tends to sublux anteriorly [4]. Postoperatively, deformity correction is started as soon as the patient can tolerate it comfortably, which usually is in 1 to 3 days. The calcaneus is pushed distally and the metatarsals are pulled proximally at a rate of 1 to 3 mm per day. Because the forefoot lever arm (metatarsal pin) is further from the axis of rotation (ankle) than the posterior lever arm (calcaneal pin) a difference in angular correction occurs if all telescoping rods are distracted and compressed at the same rate. Theoretically, it is possible to compensate for this tendency by increasing the rate of dorsiflexion of the metatarsal ring in relation to the distraction of the calcaneal ring. In practice, however, doing so has been unnecessary. The distraction of the calcaneus is the primary driver of correction and the dorsiflexion of the metatarsals is of secondary importance. Postoperative radiographs taken at 1, 2, 4, and 6 weeks are important; they are used to follow deformity correction and to ensure that the ankle remains distracted 2 to 5 mm without any subluxation (Figure 18.2).

Figure 18.2 (A) Resultant rigid equinus contracture in a 23-year-old woman 7 years after severe muscle injury to the thigh. (B) After application of an older version of the equinus frame. Note the difficulty encountered by placing hinges distally at the calcaneus half-ring.



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Figure 18.2 Continued (C) Correction nearing completion. (D) Deformity corrected with the frame held in a static position.

After correcting to between 5 and 108 of ankle dorsiflexion, the frame is left in place for 2 to 6 weeks, depending on the soft tissue rigidity. After frame removal, a short leg walking cast typically is applied for 6 weeks. Alternatively, an ankle–foot orthosis (AFO) can be constructed with 108 of built-in dorsiflexion that is removed only for range of motion exercises. Depending on the cause of the deformity, orthoses and tendon transfer or joint fusion may be needed to prevent recurrence. Two technical points of frame application deserve special mention: 1. An unconstrained technique (as previously described), in which the correction is done around the natural axes of rotation of the joints and soft tissue hinges [3], is much easier to use and more flexible than a constrained technique, which attempts correction through a precisely placed pair of hinges along the defined anatomic axis of the joint. The two keys to the use of an unconstrained technique are that distraction must be applied to the ankle joint before any attempted correction and that hinges are placed proximally for the calcaneal ring and distally for the metatarsal ring to allow translational movement. 2. Frames for the correction of a simple equinus contracture require much less rigidity than those typically described for bony instability. It has been the authors’ experience that frames classically described as equinus frames are also more rigid than is required. A single tibial ring with a single wire and three half-pins (hybrid technique) has proven to be more than adequate proximal fixation. The use of a footplate or connecting bars between the calcaneal and metatarsal half-rings has not been needed for simple equinus correction.

B.

Distal Tibial Angular Deformity

Distal tibial angular deformities are usually the result of posttraumatic malunion. The ultimate goal of treatment is the avoidance of long-term degenerative changes. There are few long-term natural


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history studies to guide treatment, but there are biomechanical studies that can help guide treatment. Joint-contact forces have been shown to increase progressively with increasing angular deformity and proximity to the articular surface [7]. Acceptable limits of coronal and sagittal angulation typically are reported as 10 to 158, but patients with extremely distal malunions or limited subtalar motion may not tolerate this degree of deformity. Occasionally, these deformities present with purely vans or valgus angulation, but they commonly appear to have components of malalignment in multiple planes. Although these multiplanar deformities can initially be intimidating, it is important to realize that they actually represent a single deformity that occurs on an oblique plane [5]. The axis of this oblique plane can be determined trigonometrically, but is determined most easily graphically or with the use of nomograms (Figure 18.3). Oblique radiographs taken at orthogonal angles to the calculated axis of the deformity provide confirmation of this analysis. Preoperatively, a complete understanding of the deformity is necessary before any realignment procedure can be undertaken. Multiple techniques are available and have been used with excellent results. Osteotomy with internal fixation and the use of circular frames (Ilizarov techniques) with corticotomy are the two commonest techniques and can be used successfully, depending on soft tissue integrity, infection, and the surgeon’s preference or experience.

C.

Osteotomy with Internal Fixation

Opening and closing wedge osteotomies are techniques with which most surgeons are familiar. These techniques have been described for the management of distal tibial malalignment, and it is possible to obtain excellent results with each method. Multiple osteotomy configurations also have been described, each with their own proponents. When planning an osteotomy it is important to recognize distinct advantages and disadvantages of various techniques. Closing wedge osteotomies offer greater initial stability because of bony apposition but require the sacrifice of some length. Opening wedge osteotomies are able to preserve length but at the expense of stability and often require the use of bone grafting with its additional morbidity. The opening wedge technique also requires a soft tissue envelope that accommodates any potential increase in length. The shape of the osteotomy influences stability and available bone surface for healing. Relatively transverse osteotomies are stable in compression but offer little resistance to rotational displacement and relatively small areas of bony surface for healing. Oblique osteotomies offer greater resistance to torsional stresses and provide greater surface area for healing but less axial support. Dome, barrel, or

Figure 18.3 Oblique plane deformity. Angular deformity in the anteroposterior radiograph is measured and marked on the x-axis. Deformity in the lateral radiograph is marked on the y-axis. Oblique angulation is the vector sum of these two lines. Magnitude of oblique angulation in degrees is determined by measurement of this line. Orientation of the oblique plane relative to the frontal plane can be measured on the graph (a); 1 mm ¼ 18



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‘‘banana’’ osteotomies are technically more demanding to perform but offer more stability and good bony surface area for healing. The preferred osteotomy at the authors’ institution has been a closing dome osteotomy. The shape of the osteotomy is inherently stable, and less length is lost than with a simple closing wedge osteotomy. It is performed in line with the axis of deformity and can be used for varus and valgus malalignment. The apex of the osteotomy is placed at the apex of the deformity on its concave side, and its base lies along the convex side of the deformity. The osteotomy is centered over a line that bisects the axes of the proximal and distal bony fragments. The shape of the osteotomy is first outlined by the placement of multiple Steinmann pins placed perpendicular to the long axis of the bone along an arc (Figure 18.4). Bone cuts then are performed with a narrow, sharp osteotome between adjacent pins. The anterior cortex is removed piecemeal to gain access to the posterior cortex. The entire anterior cortex is scored with the osteotome before the canal is exposed so that cracks will occur along the arc. The pins are used to perforate the cortex and help prevent propagation of cracks away from the desired path of the osteotomy. After removal of the desired bone, the osteotomy is compressed and fixed with a plate and screws. To allow the distal tibial fragment to move, it is necessary to perform an osteotomy of the fibula. For varus deformities it is usually necessary to remove a section of fibula to allow for the shortening that accompanies the closing tibial wedge. Although not always necessary, fibular shortening may be necessary for valgus deformities, depending on the degree of shortening required at the tibia and the amount of fibular abutment at the lateral mortise. When possible, the fibular osteotomy site is compressed rigidly with a plate and screws to add lateral stability to the tibial osteotomy. Bone grafting (from the tibial

Figure 18.4 Dome osteotomy for valgus deformity.


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Figure 18.5 Radiographs. (A) Preoperative view of a 60-year-old woman with a 2-year history of distal tibial malunion after nonoperative treatment. (B) Postoperative view at 12 weeks with the patient weightbearing.

resection) sometimes is necessary if a gap exists at the osteotomy site (Figure 18.5). This fibular fixation provides additional stability but is not an absolute requirement and is not always possible. Postoperatively, patients are placed into a non-weight-bearing cast until evidence of bony union is present clinically and radiographically.

D.

External Fixation Technique

Distal tibial angular deformities can be managed successfully with external fixation techniques. A number of unilateral fixation devices are available, and although they are used most commonly for the management of acute pilon fractures, many are capable of deformity correction. Ring fixators combined with the use of Ilizarov techniques have been used more widely in deformity correction [2–6]. Circular fixators have some biomechanical benefit because of pin placement, flexibility, and the ability to apply immediate and gradual compression. Many surgeons feel circular fixators offer greater versatility and adaptability to match specific deformities. External fixation offers several well-recognized advantages and disadvantages. External fixation is particularly valuable and is used most often for deformities that require lengthening as a component of correction. Percutaneous corticotomy, when used with external fixation techniques, offers another advantage by minimally disrupting the soft tissue envelope. This minimal disruption makes external fixation especially appropriate for patients who have sustained significant soft tissue trauma, such as open fractures, burns, or multiple operative procedures. The small wires or pins used with external fixation, when placed under tension and in multiple planes, allow fixation of poor quality bone and very small fragments that otherwise can be very difficult to control. External fixation with gradual correction also offers the advantage of precise correction that can be modified throughout the postoperative course. Because of the rigidity provided by circular fixators, the possibility of free motion at the ankle and subtalar joints is possible and almost immediate ambulation with weight-bearing can be encouraged. The most prevalent disadvantages associated



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with external fixation are related to pin sites. Infection is the commonest complication and can be seen in some series at rates greater than 30%. Most of these infections respond to local pin site care or short-duration oral antibiotic regimens but occasionally pin removal may be necessary, which can diminish frame rigidity dramatically. Pin locations can be painful in many patients, limiting their ability to bear weight. Psychologically, some patients are incapable of tolerating external fixation for extended periods of time, and others are incapable of participating in routine pin-site care or frame adjustment. These patients are poor candidates for external fixation regardless of the suitability of the deformity and every effort should be made to identify these patients preoperatively. At the authors’ institution, the frame used for correction of distal tibial malalignment is similar to the classical equinus frame but additional wires are placed in the distal tibia. The tibial segment consists of two full rings placed proximal to the deformity. The ring block is fixed to the bone using a hybrid technique with one wire at each ring and multiple half-pins placed anteriorly. A distal ring is placed parallel to the tibial plafond. The ring usually is fixed to the distal tibia with either two or three wires and an anterior half-pin. This procedure is the typical ring fixation used more commonly for high-energy fractures of the plafond. In patients with poor quality or minimal bone at the distal fragment, wire fixation can be achieved through the talus. In patients with severe deformity or minimal bone, a calcaneal half-ring and a metatarsal half-ring can be used to provide additional stability and fixation. Hinges are oriented perpendicularly to the plane of maximum deformity along the convex cortex when no lengthening is required. Correction is started after a 7- to 10-day latency period. Distraction is applied with telescoping rods placed on the concave side of the deformity at a rate of 1 to 2 mm per day, divided into four increments. Ambulation with crutches is encouraged throughout the correction but is not always easily tolerated by the patient. After correction has been achieved, the fixator is left in place until evidence of bony union is present clinically and radiographically (Figure 18.6). Removal of the

Figure 18.6 (A) Intraoperative view of shortened varus malunion of the distal tibia and tibiofibular synostosis in a 27-year-old woman 3 years after a motor-vehicle accident (MVA). (B) Two months after frame application with correction of angulation and maturing regenerate. (C) One year after frame removal with the correction maintained.


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frame can be performed in the clinic with minimal discomfort to the patient. A combination of intravenous or intramuscular analgesics and local anesthetics can be used when necessary. At the authors’ institution, simple angular deformities of the distal tibia are treated preferentially with osteotomy and internal fixation. This technique seems to be better tolerated and acceptable to most patients. When combined with fixation of the fibula, it offers excellent stability with minimal complications. Indications for the use of external fixation with Ilizarov techniques include [2–6,8]: .

.

.

Soft tissue envelopes that will not tolerate the exposure necessary for internal fixation, such as those seen in burns patients, patients who have had multiple operative procedures, and patients with old, open injuries with severe soft tissue injury or loss. Severe deformities that require gradual distraction to maintain the viability of soft tissues on the distraction side of the deformity. Deformities in which closing wedge osteotomy would result in an unacceptable degree of limb shortening (> 2 cm).

Internal and external fixation techniques have been successful at the authors’ institution. Results ultimately depend on the operating surgeon’s comfort and experience with the chosen technique.

E.

Simple Nonunion

Nonunions rarely are seen in the foot but, with the increasing frequency of high-energy pilon fractures nonunions, have become a more frequently encountered deformity of the distal tibia. It is important to realize that nonunions of the distal tibia (and elsewhere) are not a homogenous group. Multiple classification systems have been proposed and can be useful but cannot replace an understanding of the personality of each individual nonunion. Nonunions can be divided on the basis of geometry (transverse vs. oblique), biological activity (hypertrophic vs. atrophic), the presence or absence of infection, and the degree of bone loss. Nonunions associated with less than 1 cm of bone loss and without evidence of infection usually can be managed with internal fixation techniques. Surgical principles include atraumatic handling of the soft tissue envelope, debridement of fibrous tissue and necrotic bone at the nonunion site, use of autogenous cancellous bone graft, and adequate bony stability with compression provided by plates and screws. Fibular osteotomy usually is required to allow compression and can be performed at the nonunion site or preferably at a midshaft location that allows the intraosseous membrane to provide greater stability. Stable fixation allows early, protected weight-bearing and range of motion exercises at the ankle, which promote union. For patients with compromised soft tissue, osteomyelitis, more extensive bone loss, or hypertrophic pseudarthroses, external fixation with the use of Ilizarov techniques can be more effective. Frame application is similar to the frame described for correction of angular deformity. Two rings are placed proximally and fixed to the bone using the hybrid technique. One ring is placed distal to the nonunion site, and the foot is fixed with a calcaneal half-ring and a metatarsal half-ring or less commonly with a foot plate. Hinges can be added if any additional deformity is present (Figure 18.7). Hypertrophic pseudarthroses are capable of biological reaction and typically progress to union if stability can be provided. An external fixator is especially appropriate for these nonunions because stability and compression can be provided without disruption of the vascularity at the nonunion site. Autogenous bone grafting, with its inherent potential for morbidity, often can be avoided. In contrast, atrophic pseudarthroses typically require debridement of tissue at the nonunion site and the use of autogenous bone graft. After application of the frame, the proximal and distal ring blocks are compressed intraoperatively. If less than 158 of angular deformity is present and the nonunion is mobile preoperatively or following debridement, it can be corrected acutely before compression. If there is significant shortening (> 2 cm), proximal metaphyseal tibial lengthening can be performed at the same time. Oblique nonunions require the use of more advanced techniques. Standard axial compression of the ring blocks actually creates significant shear forces at an oblique fracture or nonunion. To produce interfragmentary compression at the deformity it may be necessary to use opposed, tensioned olive wires placed adjacent to or through the nonunion site. This ‘‘dueling’’ olive wire technique is



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Figure 18.7 (A and B) A distal tibia or fibula fracture treated with open reduction and internal fixation in a 42-year-old man 1 year after MVA. (C) Nonunion frame with patient ambulating. (D) Frame removed reveals bony union of tibia and fibula.


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biomechanically strong. Overtensioning of the wires, which can actually pull the olive through the bone or create fractures, should be avoided.

F.

Arthrodesis

Ankle arthrodesis typically is performed using well-described internal fixation techniques. Although internal fixation is an extremely successful technique, there are times when its use can be undesirable. Patients with previously failed arthrodesis, significant bone loss, infection, or compromised soft tissues are often poor candidates for internal fixation, but these patients often can have ankles fused successfully with the use of an external fixator and Ilizarov techniques [9,10,14,15]. The technique is similar to that described for nonunion. Modifications to the frame include the use of multiple wires placed through the body of the talus to provide tibiotalar compression and the placement of a ring at the proximal tibial metaphysis for lengthening, if necessary. Fixation of the foot can be used to provide greater stability. Intraoperatively, the distal end of the tibia and the talar dome are debrided to bleeding (paprika sign) bone. The tibial frame and the foot frame are then compressed 1 to 2 cm. A sterile Doppler device is used to ensure that the dorsal pedal and posterior tibial arteries have not collapsed. If extensive bone loss has occurred, it may not be possible to achieve immediate bony apposition, and shortening of the extremity more than 2 cm is undesirable. Postoperatively, the tibia and talus are compressed 1 mm per day until they contact. Compression is then continued at the rate of 1 mm per week. This weekly compression can be gradual (0.25 mm every 2 days) or acute (1.0 mm every 7 days). If there is significant shortness (> 2 cm) from distal tibial or talar bone loss the tibia is lengthened proximally (Figure 18.8). Weight-bearing is encouraged because it promotes healing of the fusion and regenerates and decreases pain and edema. The frame is removed in the clinic when there is clinical and radiographic evidence of fusion and proximal regenerate maturity. The fusion typically is protected after frame removal with a walking cast for approximately 6 weeks.

IV.

COMPLEX DEFORMITIES

Complex deformities involve multiple locations, multiple planes, or multiple tissue types. They are encountered more commonly in patients with neuromuscular disease, severe trauma, burns, or infection. Although techniques such as soft tissue transfer, traditional osteotomies, internal fixation, and fusion can be effective in patients with these deformities, external fixation with Ilizarov techniques often can be more successful and often are indicated. Because of the underlying causes of these deformities, postcorrection surgery (fusion) often is indicated to maintain correction.

A.

Complex Equinus Deformity

Equinus deformities frequently are encountered as a component of a more complex deformity pattern. Patients with neuromuscular disease, severe trauma, or burns typically present with additional deformities of the foot. Equinovarus and equinocavus deformities frequently are seen and equinovalgus deformities have been reported. Occasionally, rocker-bottom feet present with an equinus contracture, usually after a failed equinus correction that occurred through the midfoot rather than the ankle. These complex deformities are more difficult to correct and require more complex strategies for correction.

B.

Cavus Deformity

Cavus deformities can be classified as mild, moderate, or severe based on the metatarsal–calcaneal angle. Cavus deformity is defined as mild when the metatarsal–calcaneal angle is 135 to 1508, moderate when the angle is 120 to 1358, and severe when the angle is < 1208. Mild cavus deformities occasionally respond to stretching, casts, or soft tissue release. Moderate midfoot cavus usually does not respond to manipulation and casting but can be treated with soft tissue release and



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Figure 18.8 (A) Radiograph of a 29-year-old man 3 years after a pilon fracture with severe posttraumatic degenerative changes at the ankle joint. (B) Frame applied with wire fixation of the talus and extension to calcaneus before compression. (C) Frame fully compressed with tibiotalar fusion.

midfoot osteotomy; however, the recurrence rate is high. Severe cavus deformities are treated more successfully with the Ilizarov technique. The frame used for the equinocavus foot uses the previously described equinus frame with modification. Threaded rods are used to connect the calcaneal and metatarsal half-rings medially and laterally. The medial column is distracted at rate of 1 mm per day. The lateral rod is typically static during correction because the majority of the deformity is medial (Figure 18.9). If needed, the lateral column can be distracted. Toe flexion contractures occasionally are encountered and are best treated with flexor tenotomy and pinning for 6 weeks.

C.

Rocker-Bottom Deformity

The rocker-bottom deformity occasionally is encountered as a result of dorsal soft tissue contracture (burns) but has been more commonly seen at the authors’ institution as the result of overcorrection of the forefoot during equinus correction. Rocker-bottom feet have been treated


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Figure 18.9 (A) Preoperative view of severe equinocavus deformity secondary to burns in an 11-yearold boy. (B) Equinus frame with cavus modification and knee bracing to prevent flexion contracture secondary to tendo Achilles lengthening. (C) The cavus frame. The calcaneal half-ring is distracted from the metatarsal half-ring with a threaded rod. (D) Three and one-half years after surgery, the patient has maintained a plantigrade foot and participates in all sports.



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classically with capsulotomy and midfoot osteotomies but severe deformities (metatarsal–calcaneal angle > 2008) are well suited to correction with Ilizarov techniques. The surgical technique for the Ilizarov rocker-bottom frame is similar to the cavus frame with modification. An additional midfoot half-ring is secured with a single wire placed through the cuboid and cuneiforms. This half-ring is connected to the tibial ring block with telescoping compression rods and pulled dorsally at a rate of 1 to 3 mm per day to recreate the arch (Figure 18.10). As in all foot deformities, this nonosteotomy technique is especially effective in young children in whom bony remodeling can be expected to maintain the correction.

D.

Infection

Osteomyelitis remains one of the most difficult problems encountered by the foot and ankle surgeon. Unfortunately, these deformities rarely present as an isolated infection. An infected pseudarthrosis is the rule rather than the exception. These patients typically have some bone loss

Figure 18.10 (A) Radiograph of a rocker-bottom deformity secondary to dorsal burn contractures and failed equinus correction in a 12-year-old boy. (B) Equinus frame with wires placed through the cuboid and cuneiforms. (C) Arch has been recreated by pulling the midfoot wires dorsally.


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and commonly have a concomitant angular, rotational, or translational deformity. Because most of these deformities are the result of high-energy open fractures, the soft tissues at the deformity frequently are compromised. Although many segmental defects of bone and soft tissue can be treated with the Ilizarov technique by closing a distal defect and lengthening proximally (bifocal osteosynthesis), many of these injuries have had some type of soft tissue transfer during their acute management that further complicates their treatment. Traditional operative techniques for the treatment of osteomyelitis have focused on four basic principles. They include debridement of all necrotic tissue and avascular bone, providing bony stability, eliminating dead space, and providing adequate soft tissue coverage [11]. According to Ilizarov, debridement may not always be necessary. It was believed that revascularization of the osteomyelitis center and the resultant biological stimulation of corticotomy could be effective in controlling infection without radical debridement because ‘‘osteomyelitis burns in the fire of regeneration’’ [6]. Unfortunately, the experience of most centers is that, although bony union can be achieved with this technique, it cannot be used reliably for suppression of the infection. Thorough (radical) debridement often requires en bloc resection of bone. Obviously, this usually results in significant bony instability and significant loss of length. Occasionally, when less than 2 cm of bone is excised, it is possible to perform an acute limb shortening that provides relative bony stability and compression. More often, a dead space that requires treatment is present. Circular fixators, used with Ilizarov techniques, are especially well suited to these deformities. They provide excellent stability, do not require the placement of implants at the infection site, allow bone transport or lengthening to eliminate the dead space, and allow access to the soft tissue for monitoring and wound care. Operatively, debridement can be performed before or after frame placement depending on the surgeon’s preference. At the authors’ institution, debridement usually is performed before frame placement. Debriding before frame placement allows greater access to the debridement site and a rough estimate of the ability to acutely correct minor angular, rotational, or translational deformity. Because many of these infections are polymicrobial, and intraoperative cultures often do not correspond with cultures taken preoperatively from sinuses, it is important to take multiple cultures during the procedure [12]. The authors routinely send a minimum of three cultures: one of fluid, one of soft tissue, and one of bone. Another important point is that whenever possible the intramedullary canal should be debrided. It is typically closed at the deformity and often contains sequestrum. Reestablishing the canal obviously can decrease bacterial load, but its most important function is increasing blood flow to the deformity. All sinuses are excised. The frame used for infection of the distal tibia is similar to the ones previously described for nonunions and arthrodeses. A ring is placed at the proximal tibial metaphysis to allow bifocal osteosynthesis. Rings are then placed proximal and distal to the debridement site to provide stability. When possible, a distal ring is placed at the distal tibial metaphysis, but extension of the frame to the foot is also commonly done. The proximal rings are connected with telescoping rods to apply distraction at a corticotomy performed at the proximal metaphysis. The proximal ring block is then connected to the ring distal to the debridement site with telescoping rods to apply compression at the deformity. The distal two rings are connected statically (Figure 18.11). Postoperatively, broad-spectrum intravenous antibiotics are administered and, with the help of an infectious disease expert, switched to more culture-specific medications when that information becomes available [13]. At the authors’ institution, intravenous antibiotics are continued for 2 weeks and oral antibiotics are continued for an additional 4 weeks. Patients routinely complete the intravenous portion of this regimen at home with the help of a home health agency. Following a latency period of 7 to 10 days, the proximal ring block is distracted and the deformity is compressed at a rate of 1 mm per day in divided increments. After ‘‘docking,’’ when compression has occurred at the debridement site, the frame is maintained until clinical and radiographic evidence of fusion is present. On average, fusion can be expected at approximately 6 months, but longer periods are not unusual. Distraction, of 0.25 mm daily for 2 weeks, followed by compression of 1 mm daily may initiate more rapid healing. If union seems to be progressing slowly it can be encouraged by minimally debriding the bony gap and autografting the site. Before removing the frame it is dynamized by removing stabilizing elements or loosening wires. If the patient is able to tolerate weight-bearing in the clinic, the frame is removed and the patient typically is allowed to partially bear weight on the extremity with a walking cast.



E.

455

Amputation

Amputation as an alternative in the treatment of severe deformity often is overlooked and, rarely discussed with patients. Many surgeons view amputation as a failure on their part to provide effective reconstruction of a diseased limb. This view is unfortunate. For many patients, amputation offers the best opportunity for an early return to maximal function. Modern prosthetics combined with aggressive rehabilitation can rapidly allow patients to return to work and easily participate in activities of daily living. Many patients are not psychologically capable of enduring multiple surgeries, long treatments with external fixators, or extended antibiotic regimens with the potential for recurrence. These patients are especially well suited for amputation, and it should be discussed as an option with the patient before the decision to proceed with reconstruction is made.

F.

Special Patient Populations

Two patient populations deserve special consideration when planning correction of complex deformities. Patients with neuromuscular disease and patients with burns to the extremities

Figure 18.11 (A) Intraoperative radiograph of a 21-year-old man injured in a hunting accident; 6 cm of the distal tibia and the talar dome are absent. The frame is constructed to allow proximal tibial lengthening through a metaphyseal corticotomy. (B) Clinical demonstration of the frame before lengthening.


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Figure 18.11 Continued (C and D) Radiographs taken after frame removal with demonstration of mature proximal regenerate. (E) Mature tibiotalar fusion is present with slight shortening of the fibula.

typically present with the most severe deformities encountered by surgeons. The most difficult part of reconstruction for these patients often is not achieving correction but maintaining it. Neuromuscular deformity is typically the result of unbalanced muscle actions and often is seen with severe arthritic changes (Figure 18.12). After deformity correction these forces are still present and are likely to cause recurrence if no additional steps are taken. Postoperative bracing can occasionally be effective but soft tissue balancing procedures, such as a split posterior tibial tendon transfer or fusion in the postcorrection period, should be considered strongly. Alternatively, distraction osteotomies can be performed on the foot. Paley and Tetsworth [5], Grant et al. [3], and others have described these techniques, and, although they are technically demanding, they may provide a lasting correction through bone fusion rather than mobile joints. Burn patients’ deformities are similarly prone to recurrence. Unlike patients with neuromuscular disease, however, these patients are extremely poor candidates for soft tissue transfer or osteotomy because of their compromised soft tissues. Corrections may be maintained with postoperative bracing and a supervised physical therapy program but the patient and family should be prepared for repeat application of an Ilizarov device if the deformity recurs [2]. The most successful technique for the treatment of burn contractures is their prevention.



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Figure 18.12 (A) Severe equinocavovarus deformity in a 42-year-old woman with a history of poliomyelitis since age 14. (B) Radiograph of affected deformity with severe degenerative changes. (C) Application of equinus frame with cavus modification and anterior threaded rods designed to derotate the forefoot. (D) After frame removal, the patient maintained a plantigrade foot and normal shoe wear.

V.

SUMMARY

Complex deformities of the foot and ankle remain a difficult problem for even the most experienced surgeon. Many techniques are available to provide correction, and no single one is appropriate in all cases. Identical deformities often can be treated with different techniques, with equally successful outcomes. Each deformity is unique, and the surgeon should be capable of using multiple


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techniques to provide the most appropriate treatment for the patient and the deformity. Simple deformities often can be handled with simple techniques, but more complex problems often require more complex solutions. The techniques discussed here have worked well at the authors’ institution but are undergoing constant reevaluation and occasional modification. It is important that the surgeon and the patient understand that with these techniques it is usually possible to provide a functional outcome but never possible to provide a normal foot or ankle. If appropriate goals are set, correction of these challenging deformities can be satisfying to surgeon and patient.

REFERENCES 1. Paley, D., The correction of complex foot deformities using Ilizarov’s distraction osteotomies, Clin. Orthopaed., 293, 97–111, 1993. 2. Calhoun, J.H., Evans, E.B., and Herndon, D.N., Techniques for the management of burn contractures with the Ilizarov fixator, Clin. Orthopaed., 280, 117–124, 1992. 3. Grant, A.D., Atar, D., and Lehman, W.B., The Ilizarov technique in correction of complex foot deformities, Clin Orthopaed., 280, 94–103, 1992. 4. Laughlin, R.T. and Calhoun, J.H., Ring fixators for reconstruction of traumatic disorders of the foot and ankle, Orthoped. Clin. North Am., 26, 287–294, 1995. 5. Paley, D. and Tetsworth, K., Mechanical axis deviation of the lower limbs. Preoperative planning of uniapical angular deformities of the tibia or femur, Clin. Orthopaed., 280, 48–63, 1992. 6. Villa, A., Pseudarthroses, in Advances in Ilizarov Apparatus Assembly, Maiocchi, A.B., Ed., Medicalpiastic srl, Milan, Italy, 1994, pp. 59–83. 7. Tarr, R.R., Resnick, C.T., Wagner, K.S., and Sarmiento, A., Changes in tibio-talar joint contact areas following experimental induced tibial angular deformities, Clin. Orthopaed., 199, 72–80, 1985. 8. Calhoun, J.H. and Mader, J.T., Use of the Ilizarov fixator, in Current Therapy in Foot and Ankle Surgery, Myerson, M.S., Ed., Mosby, St. Louis, MO, 1993, pp. 288–297. 9. Cierny, G., III, Cook, W.G., and Mader, J.T., Ankle arthrodesis in the presence of ongoing sepsis: indications, methods, and results, Orthoped. Clin. North Am., 20, 709–721, 1989. 10. Kitaoka, H.B., Anderson, P.J., and Morrey, B.F., Revision of ankle arthrodesis with external fixation for nonunion, J. Bone Jt. Surg. Am., 74, 1191–1200, 1992. 11. Cierny, G., III, Classification and treatment of osteomyelitis, in Surgery of the Musculoskeletal System, Evarts, C.M., Ed., Churchill Livingstone, New York, 1990, pp. 4337–4381. 12. Patzakis, M.J., Wilkins, J., Kumar, J., Holtum, P., Greenbaum, B., and Ressler, R., Comparison of the results of bacterial cultures from multiple sites in chronic osteomyelitis of long bones, J. Bone Jt. Surg. Am., 76, 664, 1994. 13. Mader, J.T. and Calhoun, J.H., Antimicrobial treatment of musculoskeletal infections, in Surgery of the Musculoskeletal System, Evarts, C.M., Ed., Churchill Livingstone, New York, 1990, pp. 4323–4336. 14. Misson, J.R., Anderson, J.G., Bahay, D.R., and Weinfeld, S.B., External fixation techniques for foot and ankle fusions, Foot & Ankle Clin., 9(3): 538–539, 200. 15. Calif, E., Steen, H., and Lerner, A., The Ilizarov external fixation frame in compression arthrodesis of large, weight bearing joints, Acta. Orthop. Belg., 70(1): 51–56, 2004. 16. Kirienka, A., Villa, A., and Calhoun, J.H., Ilizarov Ttechnique for Complex Foot & Ankle Deformities, New York: Marcel Dekker, 2004.

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Index

A Abduction forefoot, 121, 126, 143, 156 midfoot, 126 Abduction III, pronation (PAB), 9 Abductor digiti, 400 hallucis, 400 hallucis fascia, 109 Ablative surgery digital and ray resection, 359 midfoot disarticulation, 359 Syme amputation, 359 transmetatarsal amputation, 359 Abnormalities gait, 275 hormone, 180 Abscess, foot, 180, 349 Accident(s), motor vehicle, 123, 200, 381 Acetabulum pedis, 51, 146 Achilles tendon, 310, 317–328; see also Tendon chronic rupture, 323–328 operative treatment, 325–328 prerupture conditions and treatment, 318–321 nonoperative treatment, 318 operative treatment, 319 rupture, 321–323 conservative treatment, 322 comparison of operative and nonoperative treatment, 322 operative treatment, 323 percutaneous repair, 323 Aching, 109 Acid hydrofluoric, 307 polyglycolic, 18 Acinetobacter sp., 352 Acticoat, 293–294 Actinomycetes, 347 Activities of daily living (ADL), 199 Activity, afferent, 373 Adduction, 239 Adduction I, supination (SAD), 9 Adductor hallucis, 206 Adductus metatarsus, 212 Adjunctive therapy, 353 hyperbaric oxygen therapy (HBO), 353

Aeromonas spp., 347 Agent(s) antihypertensive, 377 ganglionic blocking, 377 vasoconstricting, 289 Algodystrophy, 373 mineures, 373 reflexes, 373 Alloderm, 294 Allodynia, 372, 374, 404 Allograft, 71, 82, 109, 294 cadaveric, 294 American Orthopaedic Foot and Ankle Society (AOFAS), 312, 387 Amikacin, 350 Aminoglycosides, 350 Amitriptyline, 377 Amoxicillin, 350 Amputation Chopart’s, 410, 413–417 foot and ankle, 394–421; see also Foot and ankle forefoot, 143 great toe, 405–406 lesser toe, 406–408 Lisfranc’s, 413 nonstandard, 395 Syme’s, 414–417 transmetatarsal, 410–414 Amputee, transtibial, 46 Analgesia, 377 aggressive, 378 Analgesics, narcotic, 377 Anastomosis, 247, 274–275, 327–328 microvascular, 267 Anesthesiology (ASA), 275 Angiogenesis, 267, 297, 353 Angiogram, radionuclide, 375 Angiography, 267 Angle Bohler’s, 94, 97, 101–103, 108; see also Bohler’s angle Gissane’s, 97, 101–103, 105; see also Gissane’s angle talocrural, 6, 10 talometatarsal, 132 tuber, 94 Angle bone of Gissane, 94

459


460 Ankle anatomy, 2, 212 arthrodesis, 14, 77–78 arthroplasty, 21 diastasis, 12 dorsiflexion, 4, 434 equines, 58 equinus, 374 fracture, 1–23; see Ankle fractures fracture classification Danis–Weber, 4 Lauge–Hansen, 4 injuries, 3, 213 ipsilateral, 82, 246 joint, 3, 6, 14, 38, 41, 57 lesser saphenous vein, 14 saphenous nerve, 14 ligaments, 2 sprain, 89 stability, 11 stiffness, 434 stirrup-style brace, 339 subluxation, 12 syndesmosis, 21 Ankle–foot motion, 424 Ankle–foot orthosis (AFO), 325, 416, 424 Ankle fractures, 1–23, 361 anatomy, 2–4 classification of ankle fractures, 4–5 dislocation, 21–22 examination (physical, radiographic), 5–7 incidence and risk, 361 osteoporosis, 19–21 postoperative infections, 360–367 results (operative, nonoperative, operative intervention), 8–9 subtypes and treatment, 9–13 closed reduction and care, 13 isolated lateral malleolus, 9–10 medial malleolar, 11 open fractures, 12 osteochondral injury, 12 posterior malleolar, 10–11 syndesmosis involvement, 11–12 talar shift, 12 surgical techniques, 13 bimalleolar, 15–19 lateral malleolus, 13 medial malleolus, 14–15 trimalleolar, 19 treatment, 361 Anorthosis, 430 Antalgia, 139 Anterior colliculus, 2 Anterior inferior tibiofibular ligament (AITFL), 4, 9, 197; see also Ligament(s) Anterior talofibular ligament (ATFL), 2, 197 Anterior tibial tendon (ATT), 64, 310 Anterograde flap, 277 Anterolateral tibial tubercle, 33

Index Anteversion excessive femoral, 212 Antibiotics, topical antimicrobial therapy, 352 foot and ankle infections, 352 mafamide, 293 sulfamylon, 293 transcyte, 293 xeroform, 293 Antidepressants, 377 Apligraf, 294 integra, 294 Aponeurosis plantar, 254, 271, 317 Approach anteromedial, 62, 249 dorsomedial extensile, 136 surgical, calcaneal fractures, 108 lateral approach, 108 medial approach, 108 Arbeits-gemeinschaft fur OsteosynthesefragenOrthopaedic Trauma Association (AO-OTA), 4 Arch plantar arterial, 121 Arizona bracevarus, 76 Arrhythmias, cardiac, 307 Artery(ies) anastomotic loop of, 247 anterior tibial, 5, 269, 316 arcuate, 121 dorsalis pedis, 54, 121, 132, 143–146, 247 lateral calcaneal, 269 lateral plantar, 143 peroneal, 54 posterior tibial, 5, 54–55, 143, 146 sinus tarsi, 54 thoracodorsal, 279 Arthritis, 8–9, 21, 50, 77, 246 ankle, 76, 87 degenerative, 145 inflammatory, 311 injuries talar, 50 osteo-, 70 posttraumatic, 9, 45, 55, 69, 89, 246, 383 septic, 349 subtalar, 59, 62, 87, 114, 383, 385 Arthrodesis, 12, 76, 108, 151, 382, 403, 450 ankle, 77–78 Blair type, 65 hindfoot, 76 pantalar, 65 primary subtalar, 94 primary, 106 talonavicular, 155 tibiotalocalcaneal, 384 triple, 114 Arthropathy Charcot foot, 180, 183, 185, 188 acute, 181 osteo-, 190 Arthroplasty, 14 abrasion, 251


Index ankle, 21, 76 joint, 14 interpositional, 159 Arthroscope, 81 Arthroscopy, 12 subtalar, 76 Arthrosis, 7, 45, 84, 166, 175, 196 pseudo-, 65, 78 posttraumatic, 13, 15, 139, 145, 155 subtalar, 251, 385 talonavicular, 147, 152 Arthrotomies, 151 Arthrotomy, 15, 158 anterolateral, 231, 241 anteromedial, 222 Articulation Lisfranc’s, 122 talonavicular, 50 TMT, 121 Aspergittus spp., 347 Asplenia, 347 Astragalus, 50 Athlete(s), 140, 149, 256 Atrophy, 109 muscular, 374 subcutaneous, 374 Sudeck’s, 373, 375 Autogenous graft, 79 Autograft, 288, 295, 313, 387 osteochondral, 82 Autoimmune disorders, 5 Autologous grafting, 325 Avascular necrosis (AVN), 55, 70, 75, 207, 249–250 of distal tibia/talus, 198 of talar body, 80 of talar head, 67 Avulsion fracture, 2 Axial compression injuries, 214 loading, 147 load mechanism, 27 B Bacillus, 347 Bacteroides fragilis, 352 Bacteroides spp., 358 Bactrim, 350 Bandage Ace, 150 Esmarch, 397 Bent bone type fracture, 213 Bier block technique, 377 Biking, 84 Bimalleolar fracture fixation, 8 Biobrane, 294 Bites, dog and cat, 348 Blair fusion, 384 Blair type arthrodesis, 79 Blindness, 179

461 Blister(s), 6, 101, 109 clear fluid-filled, 5 fracture, 45 Blockade differential neural, 375 sympathetic, 375–377 Blocker calcium channel, 377 Blocks intravenous regional, 377 nerve, 377 sympathetic, 378 Blood sugar, 180 Bohler’s angle, 94, 97, 101–103, 108, 252 Bone absorption, 257 acute atrophy of, 373 cancellous, 15, 34, 97, 382 cement, 73 chondroosseus, 247 contusions of tibia/talus, 198 cuboid, 105, 108 density, 19 elastic, 212 graft, 35, 65, 109, 158 grafting, 15, 175, 246 autogenous, 448 healing, 44 loss, 50, 73, 180, 383, 387 metaphyseal, 215 navicular, 105, 147 necrotic, 84 osteochondral, 212 osteopenic, 185 osteoporotic, 15 scan, 82, 375, 403–404 subchondral, 82, 84, 153, 159, 383 transport, 38–39 triple arthrodesiscuboid, 94 weak, 19 Bone marrow edema, 82 Bony stability, 2 Boot(s) brace or cast, 337 flexible arthrodesis, 436 silicone, 300 soft-shelled, 88 walker, 13 Box within a box alignment, 197 Brace stirrup, 13 Bracing, 325, 402 functional, 322–323 Bronchoscopy, 289 Buckle fracture pattern, 213 Buddy taping, 177, 257 Bunk bed injury, 253 Bupivacaine, 377 Burn(s), 394, 404 management, 297 plantar, 274 wounds, 269


462 Burns, to the feet, 288–307 complications, 303–304 dystrophic calcification, 303 Marjolin’s ulcers, 303–304 osteoporosis, 303 pigmentation, 303 initial evaluation, 289 inhalation injury and associated injuries, 289 of burn wound, 289–292 pathophysiology of burn injury, 289–290 modern burn care, burn team concept, 288–289 prevention, 307 reconstruction and rehabilitation, hypertrophic scars, and contractures, 297–302 classification of contractures, 299–300 treatment, 300–302 special orthopedic issues, 302–303 bone and Achilles tendon exposure, 302 fractures, 302 involved joints, 303 special types of burns, 305 chemical burns, 306–307 electrical burns, 305–306 treatment, 291–297 definitive wound coverage, 294–296 escharotomy, 292 hyperbaric oxygen, 296–297 initial wound care, 292–294 resuscitation, 291–292 C Cadaveric feet, 56 Caisson disease, 297 Calandruccio clamp, 79 Calcaneal, 99 anatomy, 94–95 classification, 98–101 Essex-Lopresti system, 98 Soeur and Remy system, 98 Warrick and Bremner system (modified), 98 complications, 109, 114 definitive management, 104 extra-articular fractures, 104–106 intra-articular fractures, 106–108 fractures, 56, 93–115 groove, 94 initial presentation, 101 management, 101 mechanism of injury, 95–97 open calcaneal fractures, 114 postoperative management, 109 preferred method of treatment, 108–113 radiographic examination, 101–103 salvage procedures, 114 sulcus, 96 surgical approach, 108 lateral/medial, 108 tuberosity, 33 Calcaneofibular ligament (CFL), 2, 197 Calcaneus, 302, 317, 328 distraction, 440

Index fractures, 364 ankle, 2 incidence and risk factors, 364 pilon, 30–31, 37–38 treatment, 364 midfoot fractures, 158 paediatric foot, 247, 252 talar, 78 Lisfranc (TMT) injuries complications, 143 Syme’s amputations complications, 418 well, 103 Calcification dystrophic, 303 Caliper patella-bearing, 75 Cancellous, 94, 153 Cancellous bone, 143 Candida, 347 Cannulated cancellous screws, 175 Cantilever effect, 56 Capsule joint, 33 Capsulotomy, 153 talonavicular, 153 Carbonic anhydrase inhibitor, 293 Carboxyhemoglobin, 297 Carcinoma basal cell, 303 squamous cell, 303 Cast(ing) acrylic, 300 immobilization, 229, 322, 434, 436 mallet, 94 long leg, 216, 222, 231 serial, 298 short leg, 105, 151, 155, 216, 252–255 walking, 150, 156, 254 total-contact, 185, 188, 191 Causalgia, 372–374 Cavus, 301 Cedell’s fracture, 85 Cefazolin, 397 Cefoxitin, 73 Cells, white blood, 180, 347, 403 Cellular injury by acids, 307 by alkali agents, 307 lipid saponification, 307 liquefaction necrosis, 307 protein denaturation, 307 Coagulation necrosis, 307 Cellulites, 349–350 Center(s) accessory ossification, 229, 254 distal fibula ossification, 212 epiphyseal ossification, 212 Cephalosporin, 350, 397 Cerclage wire, 23 Cervical ligaments, 56 Charnley compression device, 79 Checkreins, 2 Chondrocyte autologous, 89 Chopart’s amputation, 410, 413–417


Index Chronic hypoxia, 358 lymphedema, 358 Ciprofloxacin, 350, 354 Circulation extraosseous, 54–55 interosseous, 54–55 Clamp(s), 94 bone reduction, 241 percutaneous bone, 228 reduction, 231 Weber, 153 Clarithromycin, 350 Classification AO comprehensive, 29 Hawkins, 70 of periarticular fractures AO, subtypes, 28 complete articular, 28 Claw toes, 299, 389 Clawing of lesser toes, 109 Clindamycin, 350, 352 Closed reduction, 8; see also Reduction Clostridium sp., 347, 352, 358 Closure single-layered, 109 tension-free, 43 vacuum-assisted wound (VAC), 71 Coalition calcaneonavicular, 155 Coccidioides imitis, 347 Cold intolerance, 376 stress, 376 Collagen deposition, 297 fibers, 301 Collapse, 89 Colliculus anterior, 54 posterior, 52, 54 Comminution, 28, 41, 89, 147, 176, 243 central, 38 degree of, 62 Comorbidities, 5, 274, 313, 320–322, 382 Compartment syndrome, 101, 257 Complete transverse fractures, 213 Complex ankle joint, 19 gastrocnemius–soleus, 410 lateral subtalar ligamentous, 200 Complex Lisfranc, 121, 126–128, 132, 145 joint, 143 ligament, 134 midfoot–forefoot, 200 sesamoid, 196, 203, 205, 400, 406 TMT, 156, 159 TMT-Lisfranc joint, 118 Complex plantar plate-sesamoid (CPPS), 205 Complex regional pain syndrome (CRPS), 371–378

463 Complications in fractures amputation, 27 infection, 27 nonunion, 27, 45 malunion, 45 osteoarthritis, 45 Soft tissue, 73 Compression arthrosis, 130 fracture of cuboid, 134 Computed axial tomography (CAT) scan, 332 Computer tomography, 33 Configuration Ilizarov, 41 Congruency joint, 130 Contact forces, 2 Continuous passive motion (CPM), 298 Contracture(s), 297–302, 389 burn, 297 classification, 299–300 dorsiflexion, 299 equinus, 41, 410 plantar flexion, 425 rigid causes of, 439 treatment, 300–302 external fixators, 300 garments, 301 limb suspension, 301–302 orthotics, 302 Corrective orthotics, 318 Corticotomy percutaneous, 446 proximal, 36 Cosmesis, 78 Cranioplast, 228, 246 Crash(es) motorcycle, 394 motor vehicle, 43 C-reactive protein (CRP), 348 Crepitans, peritendinitis, 311 Crepitus audible and palpable, 319 sensation of, 311 Crescents, tibial and talar, 6 Crest anterior tibial, 33 iliac, 65, 155, 158 metaphysis, 34 proximal tibiailiac, 143 Chronic regional pain syndrome (CRPS), 402 Crush(ing) injuries, 394 ipsilateral, 46 Cryptococcus neoformans, 347 Cuboid, 118, 127–128 Cuff, pressure, 6 Cuneiform(s), 41, 118–121, 127–128 medial, 167 Roman arch configuration of, 119 Curettes, 143 Cuts axial, 33


464 Cycling low-resistance, 83 Cysts subchondral, 84 D Damage articular, 45 bone and ligamentous, 5 cartilage, 27 contusional, 30 iatrogenic, 220 neurovascular, 274 soft tissue, 9, 45, 123, 167 Danis–Weber classification, 5 Deafferentation, 373 Debridement, 65, 134, 257 surgical, 353 Debulking, 275 Defect(s) calcaneal, 271 cancellous, 35 metaphyseal, 35–36, 39 osteochondral, 79 Definitive fixation, 114, 131, 152 reduction, 131 wound coverage, 294–296 Deformation cavus, 123 Deforming forces abduction, 4 adduction, 4 external rotation, 4 Deformit(y)ies angulatory, 428, 431 bony, 439–440 burn, 301 cavus, 450 Charcot midfoot, 189 chronic nail, 404 classification simple/complex, 440 complex bony nonunions, 440 contractures, 301, 440 equinocavus, 440, 452 equinus, 450 rocker-bottom deformity, 440, 451–453 congenital malformations, 440 planovalgus, 339 donor site, 279 equines, 425, 428 fibrous, 390 foot, 101, 143, 179, 311 flat foot, 338 foot and ankle, 439 forefoot, 109 hallux, 176 hallux valgus, 145 heel varus, 385 hindfoot, 76, 339 interphalangeal joint, 338

Index loss of height, 385 lateral impingement, 385 midfoot dorsiflexion, 442 neuromuscular, 456 neuropathic (Charcot) foot, 180 osteomyelitis, 180 persistent, 220 planus foot, 121 planovalgus, 145 progressive, 246 flatfoot, 311 residual, 220, 243 rotational, 246 simple, 440 arthrodesis, 450 distal tibial angular deformity, 443–444 equinus contracture, correction, 440–443 external fixation technique, 446 osteotomy with internal fixation, 444 simple nonunion, 448 techniques to address, 440 tibial, 359 toe, 312 varus, 36, 155, 185 Degeneration collagen, 318 mucoid, 319 tendon, 339 Deltoid ligament, 2, 61 complex, 2 Denervation, 143 Depression, 376 Destruction Charcot type, 123 Devascularization, 143 Device(s) bridging, 36 buttress, 36 Doppler, 450 Diabetes, 5, 115, 274, 288, 311 mellitus, 375, 395 Diaphysis, 172 Diabetic foot osteomyelitis, 358 Diabetic patients, foot and ankle fractures, 179–191 Diastasis, 98, 126, 131, 140, 121 ankle joint, 214 distal tibiofibular, 212 recurrent, 136 residual, 132 subtle, 126–127 tibia–fibula, 231 Diffuse osteopenia, 374 Direct-force injury, 157 Disc herniation, 310 Discharge sympathetic, 373 Disease(s) autoimmune, 318 cast, 15 cerebrovascular, 348 ischemic peripheral vascular, 180 peripheral arterial, 348 peripheral vascular, 5, 132, 374, 394–395, 399


Index posttraumatic degenerative, 403 vascular, 274 Disimpaction with mallet casting, 94 Dislocation, 3, 42 ankle, 196–199, 243 clinical findings, 197–198 epidemiology and anatomy, 197 pathogenesis and history, 197 prognosis and long-term follow-up, 199 radiographic findings, 198 treatment options, 199 dorsal or plantar, 123 great toe MTP dislocation, 203–207 clinical findings, 204 epidemiology and anatomy, 203 pathogenesis and history, 203–204 prognosis and long-term outcome, 207 radiographic findings, 205–206 treatment options, 205–207 hindfoot (talus, navicular), 185 Lisfranc fracture, 134, 170, 203, 382, 390 midfoot (tarsometatarsal), 188 MTP, 127–128, 130, 207 peroneal, 333 peroneus brevis, 331 plantar, 124 posterior tibialis, 340 stalonavicular, 153 subluxation or frank, 59 subtalar, 60, 252 clinical findings, 200–201 epidemiology and anatomy, 200 joint, 199–203 long-term results and prognosis, 203 pathogenesis and history, 200 radiographic findings, 200–201 treatment options, 201–202 subtalar, 340 subtle Lisfranc, 127–128 talar, 50–89 head, 58 talonavicular, 56, 87 talus, 68 tarsometatarsal joint, 183 toe, 301 Displacement(s), 2, 10, 28, 59, 231 articular, 222 initial, 9 intra-articular, 6 physeal, 243 posterior tibiofibular joints, 40 residual, 11, 132 risks of, 13 rotatory, 173, 176 sagittal plane, 167 subtalar, 68 ankle dislocation, 56 congruous ankle, 56 TMT joints, 139 Disruption, 21 deltoid ligament, 6, 9

465 joint, 126 Lisfranc’s ligament, 126, 131, 147, 139 naviculocuneiform, 155 posterior tibial tendon, 127–128 synchondrosis, 149 syndesmosis, 231, 237 Dissecans, 156 Dissection subperiosteal, 133 Distal joint, 2 Distal reverse flow flap, 277 Distal tibial, 8 metaphyseal region, 213 physis, 212–213 Distraction, 241 Distractor, 384–385, 389 AO, 33 external, 152 Divers ‘‘bends,’’ 297 Dog ears, 405 Doppler device, 450 examination, 6 laser flowmetry, 317 studies, 267 Dorsalis pedis artery, 54, 136, 143 Dorsiflexion, 121, 126, 166, 197, 331, 337 ankle, 11, 18, 413–414 force, 56 of ankle, 88 forced, 248 metatarsal, 440 Dorsiflexor, 310 Drainage, 45 Dressing biosynthetic, 294 alloderm, 294 apligraf, 294 apligraf integra, 294 biobrane, 294 compression, 45 Jones, 101 postoperative, 44 topical, 294 Drift valgus, 400 varus, 400, 406 Drilling transmalleolar, 84 Dry skin, 180 Dynamic compression plates (DCPs), 382 Dysfunction, 121 leukocyte, 185 progressive posterior tibial, 126 sympathetic nervous system, 373 vasomotor, 372 Dysrhythmias, 305 Dystrophy posttraumatic, 373 reflex neurovascular, 373 reflex sympathetic, 145, 371–378, 247


466 E Ecchymosis, 56, 148 plantar, 126, 204 Edema, chronic traumatic, 373 Edwardsietta tarda, 347 Effect, medial buttressing, 44 Enterobacter sp., 352 Enterococcus sp., 347, 350–351, 358 E. faecium, 351 Entrapment nerve, 143 sural nerve, 323 Epiphyseodesis, 228, 246 Equines, 31 resting, 323 Equinocavus, 311 Equinovarus, 413–415 Equinus, 59, 85, 301 subtle, 413 Erysipelothrix sp., 347 E. rhusiopathiae, 347 Erythema, 289 Erythrocyte sedimentation rate (ESR), 348 Eschar burn wound, 288 Escharotomy, 292 Escherichia coli, 352 Ethambutol, 350 Eversion, 241 passive, 132 stresses, 2 Examination Doppler, 6 neurovascular, 6 radiographic, 6 Excision early wound, 288 Exostectomy, 177 calcaneal, 385 Exostosis, 329 painful bony, 145 Exposure bone and Achilles tendon, 302 Extended steel shank, 136 Extensile dorsomedial approach to midfoot, 137–138 Extensive scarring, 358 Extensor digitorum brevis, 62, 313, 400 digitorum longus (EDL), 62, 64, 310, 414 hallucis brevis, 136, 313, 400 hallucis longus (EHL), 136, 310 Extensors, long toe, 312 External fixator, 101 Extremes of age, 358 Extremity contralateral, 246 F Falls from heights, 147, 253 Fascia, 136 Fascia plantar, 406 Fasciocutaneous flap, 280 Fasciotomy, 109 Feet neuropathic, 126, 288 Femur, distal, 34

Index Fentanyl, 377 Fibers, soleus, 317 Fibrosarcoma, 303 Fibula, 2–23, 28, 30–41, 50 displacement, 2 distal, 15, 21 fracture, 5 periosteum, 14 shortening fixation of, 32 Fixation, 9, 11, 17, 23 absorbable pin, 224 antegrade, 62 anatomic reduction, 118 AO Association for the Study of Internal Fixation (ASIF), 9 arthroscope-assisted, 85 bimalleolar, 12 circular, 34 definitive, 30–31, 37, 152, 249 delay of, 30 delayed, 12 extensive, 15 external, 73, 346, 398 in Lisfranc injuries, 132, 143 in midfoot fracture, 153 in pilon fracture, 35–45 fibular, 22–21, 33 half-pin, 39 hybrid, 39 initial, 34, 69 interfragmentary screw, 170 internal, 94, 241, 346, 382 arthroscope-assisted, 89 in ankle fracure, 12–13 in Lisfranc injuries, 132, 144 in metatarsal and phalanges fracture, 167, 173 in midfoot fracture, 150, 153, 156 in pilon fracture, 32–44 in talar fractures and dislocations, 50, 59, 78, 83 intramedullary screw, 174 Kirschner wire, 249, 252 in Lisfranc injuries, 140, 153 metatarsal and phalanges fracture, 167, 170, 175 lag screw, 36–39, 151 medial, 15 multiple-plane, 41 open reduction, 106 open reduction and internal (ORIF), 360–361, 434 in ankle fracture, 10, 12, 19, 21 in calcaneal fracture, 106, 114 in pediatric foot and ankle fracture, 229–243, 249–253 in talus fracture, 62, 76, 85, 87, 89 operative, 94 percutaneous pin, 170 screw, 59 pin, 59, 143 plaster, 131 plate, 33–36, 77 plate and screw, 170


Index primary, 115 rigid internal, 50, 106, 151, 188 ring, 41 screw, 77, 152 smooth-wire, 217 stable, 15 surgical, 155 syndesmotic, 19–21 temporary, 30 tibiotalar pin, 69 Fixator(s) external, 106, 167, 301 arthrodesis external, 12 hybrid external, 42–44 in Lisfranc injuries, 132–134 in midfoot fracture, 152–153, 157 in pilon fracture, 30, 31, 38–39, 42 in talar dislocation, 77 medial external, 30, 33 medial spanning external, 32, 34 ring external, 43–44 Ilizarov, 39, 246, 301 internal, 157 lateral, 132 Flap(s) cross leg, 274 free, 276–281 gracilis, 279–280, 400 lateral arm flap, 280–281 latissimus dorsi, 278–279, 400 paxascapulax, 279–280 radial forearm flap, 276–277 reconstruction, 273–276; see also Reconstruction rectus abdominis, 277, 400 serratus anterior, 279, 281 lateral arm, 280 rectus femoris, 280 scapular, 280 temporal parietal fascia, 280 tensor fascia lata, 280 lateral calcaneal, 270 latissimus, 402 local (pedicle), 269–273 dorsalis pedis artery, 273 lateral calcaneal artery, 269–271 medial plantar, 271–272 sural fasciocutaneous, 271, 273 muscle, 400 abductor digiti minimi, 269, 400 abductor hallucis brevis, 269, 400 extensor digitorum brevis, 271, 400 extensor hallucis brevis, 400 flexor digitorum brevis, 269, 271, 400 intrinsic muscle, 269 pedicle muscle, 269 neurosensory fasciocutaneous, 275 osteocutaneous, 280 pedicle muscle, 269 peroneus brevis, 269 soleus, 269

467 tertius flaps, 269 tibialis anterior, 269 radial forearm, 276 sensate fascial, 275 skin, 414 suitability for a free, 275 sural artery, 271 thrombosed, 275 walking tube, 274 Fleck sign, 128 Flexion interphalangeal (IP), 337 neutral, 102 planta, 84, 147, 239 Flexor ankle, 336 digitorum brevis, 269, 271, 400 digitorum longus (FDL) tendon, 310 hallucis longus (FHL) tendon, 52, 94, 310 Flowmetry laser, Doppler, 317 Fluid requirements, 291 synovial, 228 Fluoroquinolone, 318 Fluoroscopy, 132 intraoperative, 109 Fools, 2, 23 Foot abscess, 180 burns, 292 cavovarus, 155 Charcot, 185, 190–191 compartment syndrome, 396 contralateral, 6 crushed, 133 deformity, 179 dorsiflexed, 311 dorsiflexion of, 85 dorsum of, 6 dysvascular, 198 equinovarus deformity of, 77 eversion of, 148 fractures, 50, 165–177, 213 fractures of I metatarsal, 167–169 fractures of lesser metatarsals, 167, 170–175 metatarsals, 167–175 phalanges, 175–177 injured, 126 injury, 148 insensate, 274 inversion, 310 ischemic, 143 narrowing, 407 orthoses, 185 orthosis, 432 plantar, 399 plantargrade, 143, 185, 191, 384 position (supination or pronation), 145 pronation of, 145 pump, 101 residual, 395, 399–400


468 Foot (continued) socket, 51 supination of, 94, 99, 145 truss action, 425 ulcers, 179, 348 varus hind, 250 with varus inclination, 76 Foot and ankle fractures in diabetic patients, 179–191 calcaneus, 185–188 Charcot foot, 185 displaced or unstable, 182, 184 forefoot, 188 hindfoot, 185, 188–189 midfoot (tarsometatarsal), 188 susceptibility, 180–181 undisplaced, 180–183 wound healing, 179–180 fractures, orthotic management, 423–437 determination of pain reduction potential, 426 mechanical function and control mechanisms, 424 negative impression technique considerations, 428 orthotic principles and biomechanical considerations, 425 orthotic treatment of fractures, 429 prefabricated vs custom-molded, 424 infections, 352 antimicrobial therapy, 352 posttraumatic infections, 346–365 soft tissue coverage, 266–282 mechanism, 267 nonoperative coverage of wounds, 268 nonoperative treatment, 267–268 operative treatment, 268–282 patient evaluation, 266–267 reconstruction, 267 wound evaluation, 266 wound management principles, 267 trauma, 346 traumatic amputations, 394–421 assessment and acute treatment, 395–399 chronic management, 401–404 specific amputation levels, 404–420 subacute management, 398–402 Football, 203 Footwear, therapeutic/protective, 184–185, 191 Force(s) avulsion, 147 compressive, 97 crushing, 123 external rotation, 236 Forefoot, 126, 165, 191, 364–365 Fracture ankle, 1–23 incidence and risk factors, 361 operative/nonoperative treatment, 8 outcome, 7 poor fixation, 7 Weber classification, 9

Index articular, 114 avulsion, 85, 105, 156, 215, 254 displaced, 106 dorsal, 146–148 of metatarsal, 128 midfoot, 147–151 tuberosity, 146, 148 type, 10 blisters, 5, 45 fluid-filled and blood-filled, 5 Boyd’s classification of talar body, 70 calcaneal, 93–115, 384–385, 433 in children, 252 incidence and risk factors, 364 treatment, 364 closed, 30, 42 grades 0, I, II, and III, 29 coding and classification of OTA committee for, 28 common signs distortion of the normal anatomy, 101 ecchymosis, 101 swelling, 101 tenderness, 101 complications after calcaneus early and late, 109 compression, 105, 156–157 coronal, 70 cuboid, 127–128, 253, 387, 389 compression, 156–157 cuneiform, 127–128, 156 diaphysisintra-articular, 28 posterior, anterolateral and anteromedial, 28 dislocation, 9 displaced, 216, 249 foot or ankle, 183 minimally displaced, 96 distal fibula, 18, 21, 23 isolated, 13 supination-external rotation, 13 distal tibial pilon, 13, 15 dorsal avulsion, 147–148, 150 extra-articular, 104 extremities, 190 fibula, 17, 20, 197, 212, 241 long spiral, 229 transverse, 216 foot, 50, 213, 247 foot and ankle, 381 in diabetic patients, 179–191 orthotic management, 423–437 pediatric, 212–257; see also Pediatric foot and ankle forefoot, 126, 191, 364–365 growth plate, 241 Hawkins III, 65 impact, 9 intra-articular, 96, 98, 104, 106 ipsilateral tibia, 237 ipsilateral tibial shaft, 243 joint depression type, 97


Index juvenile Tillaux, 229, 241 Lisfranc, 183 malalignment, 2 malleolar, 23, 436 bimalleolar, 8, 10, 15, 22–23 medial, 12, 15 multi, 9 trimalleolar, 3, 11 unimalleolar, 9 malleolus, 9–10, 13 posterior, 19 metaphyseal, 39, 237 metatarsal [MT], 156, 167–175, 203, 430 metatarsals and phalanges, 165–177 anatomy, 166 mechanism of injury, 166 phalangeal fractures, 167, 175–177 radiographic evaluation, 166–167 midfoot, 126, 364–365 navicular, 56, 133, 156 nondisplaced, 11, 96, 151, 173 nutcracker type, 156, 253 open, 29, 56, 257, 346 ankle, 5, 12 calcaneal, 114 pilon, 35 osteochondral, 83, 251 pattern, 2, 28 Essex-Lopresti, 96 fibular, 28 phalanges, 175–177 hallucal fractures, 175 lesser toe fractures, 176 pilon type, 10, 27–46, 243, 360; see also Pilon fractures plafond incidence and risk factors, 360 treatment, 360–361 postoperative infections, 360–367 pronation-external rotation simulated, 12 reduction, 423 rigidly fixed fibular, 9 sagittal plane, 36, 70 Salter-Harris types I and II, 213, 215 III and IV, 222, 224 sesamoid, 430 spine, 190 stabilization and maintenance, 423 plaster of Paris, fiber resin tape, metals, and plastics, 423 stress, 180, 183, 185, 255–257, 374, 430 subtle compression, 127–128 talar, 50–89 talar neck, 56, 248 talus, 42, 383 tarsal bone, 93, 125 tarsometatarsal joint, 387 tibial, 28, 197 shaft, 9, 311 tillaux type, 214, 222, 236, 241

469 tongue type, 97, 99, 252 transitional, 222, 229 transverse, 241 triplane, 214, 229, 236–237, 241 tuberosity, 252 undisplaced, 106, 180–181 Weber types B, 9, 21, 197 C, 9, 12 14, 83, 197 Fragment(s) anterolateral epiphyseal, 229, 237, 241 anteromedial (sustentaculum or constant), 96 avulsed, 106 larger avulsion, 150 depression of, 98 metaphyseal, 217, 224, 237 osteochondral, 134 posterolateral (tuberosity), 96 superomedial, 99 sustentacular, 108 talonavicular, 153 thalamic, 97 Thurston-Holland, 216 tuberosity, 96, 99, 108 unreconstructable, 153 Fragmentation, 89 Frame(s) cavus frame, 452 equinus, 452 Galveston equines, 440 Ilizarov, 78 shalf-pin, 132 Taylor spatial, 42 Frostbite, 394, 404 Frustrum, 50, 52 Fulcrum, Achilles tendon, 97 Fusion Blair-type, 70, 384 delayed, 65 interpositional, 159 primary subtalar, 65, 89, 114 tibiotalar, 65 talonavicular, 152 tibiocalcaneal, 65, 70, 78 tibiotalocalcaneal, 80 G Gait, 94, 145 abnormalities, 145, 275 analysis, 8, 139 biomechanics of, 50 cycle, 166 dysfunction, 400 impairing, 156 stance phase of, 159 velocity, 420 Gastroc slide, 413 Gastrocnemius, 201, 317, 390 Gentamycin, 397 Gissane, angle of, 97


470 Gissane, boneangle of, 94 Gissane’s angle, 101–103, 105 Glycocalyx, 358 Gracilis, 279, 400 Graft(ing) autogenous, 78 cancellous, 158 interpositional arthroplasty, 143 keratinocytes, 295 local bone, 76 polytetrafluoroethylene, 274 skin, 257, 402 sliding tendon, 313 tendon, 316 tibial, 78 tricortical, 158–159 iliac crest, 387 Gram-negative organisms, 347 Gram-positive cocci, 347 Greenstick (bent bones) fracture, 213 Groove, calcaneal, 94 Growth disturbance, 228 Growth factor, platelet-derived (PDGF), 267–268 Growth plate crush (Salter-Harris type V), 214 injuries, 213 Guanethidine, 377 Guidewire, 19, 84, 134, 224 H Haemophilus influenza, 352 Hallux, 175, 313–317, 336–337, 400 rigidus, 207 valgus, 406–408 Hardcastle’s classification, Lisfranc disruptions, 125 types A, B, C, 125 Hawkins classification scheme, 248 types I, II, III, 89 Hawkins classification Heel lifts, 425, 432 pad plantar, 417, 419 varus-valgus alignment, 109 Hematoma(s), 14, 30, 109, 134, 323 subungual, 176 Hemoglobin glycosylated, 348 Hemoglobin, 305 Hemostasis, 382, 397 Hernia, transverse rectus abdominis myocutaneous [TRAM], 277 Hindfoot, 57, 139, 201, 338, 430 calcaneus, navicular, 200 dislocations of the (talus, navicular), 185 eversion, 2 varus, 374 Hockey players, 310 Human immunodeficiency virus (HIV), 347 Humerus, 280 Hydrocholecalciferol, 180 Hydrotherapy, 303

Index Hyperbaric oxygen (HBO), 267–268, 296–297 therapy, 353 Hyperdysfunction sympathetic, 376 Hyperemia, 404 Hyperesthesia, 372 Hyperflexion, 156, 302 plantar of forefoot, 123, 124 Hyperglycemia, 179–180, 288, 305, 307 Hypermobility heel pad, 419 Hyperparathyroidism, 180 Hyperpathia, 372, 374 Hypersensitivity, 374 Hypertension, 348 Hyperthermia, 374 Hypertrichosis, 374 Hypertrophic pseudarthrosis, 448 Hypertrophic scars, 297–302 Hypertrophysynovial, 337 Hypesthesia, 372 Hypocalcemia, 307 Hypochondriasis, 376 Hypoplasia, 197 Hypothermia, 374 Hypothesis vicious cycle, 372 Hypovolemia, 289 Hypoxia, 180 Hysteria, 376 I Ilizarov construct, 42 Images, plain stress, 128 Imaging, magnetic resonance (MRI), 311, 348, 403 in ankle dislocation, 198 in ankle fracture, 11, 213 in talar fracture, 58 Lisfranc injuries, 118 Imipenem, 350 Immobilization cast, 255 postoperative, 299 Immune deficiency, 185, 358 Immune disease, 358 Immunosuppression, 358 Impaction, 28 degrees of, 27 Impaired immune response, 180 Implants, 36 artificial tendon, 323 carbon fiber, 323 collagen tendon, 323 Marlex mesh, 323 prosthesis, 323 bioabsorbable, 89 Incision(s), 65 dual, 76 fishmouth type, 406, 414, 417 Oilier, 66, 77, 88 tibial, 33 Incisura fibularis, 6 Incongruity articular, 222, 231, 241, 246


Index Index ankle-brachial (ABI), 348, 399 high body mass, 109 toe-brachial (TBI), 348 Infection(s), 29, 50, 55 erythema, 357 foot and ankle abscess, 347 bacterial, 347 bone infections, 346 cellulitis, 347 classification, 347 constitutional symptoms, 347 diabetic, 347 diagnosis, 347 fractures, 347 fungal, 347 host factors, 346 immunocompromised, 347 necrotizing fasciitis, 347 osteomyelitis, 347 postoperative, 347 posttraumatic, 346–365 septic arthritis, 347 soft tissue infections, 346 trauma, 347 pin track, 39, 45, 355 postoperative infections, 190, 360 pseudomonal, 257 soft tissue, 297 Inferior retinaculum, 310 Inflammation, 45 nonspecific markers of, 348 Inflow, vascular, 183, 185 Influenza, haemophilus, 352 Injury(ies) acid, 307 acute neglected, 126 sprain, 125 ankle extent, 5 pattern, 5 associated injuries, 5 alkali, 307 athletic, 126 avulsion, 274 axial load mechanism of, 27 primary articular cartilage damage, 27 blast, 395 blunt, 311 burn pathophysiology, 289–290 calcaneocuboid, 155 calcaneus, 198 associated, 101 chronic neuropathic, 125 chronic repetitive, 147 crush, 213, 228, 257 pilon, 44 industrial setting, 394

471 lawn mower, 394 Lisfranc, 123 talus, 70 cuboid, 156 deep deltoid, 10 deltoid ligament, 12 direct, 123–124 displaced Lisfranc, 123, 139 distracting, 126 divergent, 126 dorsiflexion, 50 pronated, 85 electrical, 302, 305 extensor hallucis longus, 205 external rotation, 12, 241 extra-articular, 44 falls from ground level/height, 123 fibula, 12 flexor hallucis longus, 205 foot, 46 foot and ankle, 45, 381 frostbite, 297, 394, 398 Gustilo type, 114 gunshot, 394 Hawkins type IV, 67 head and thoracic, 381 high-energy, 126, 394 calcaneal, 96 midfoot, 148, 156 talar body, 70 indirect-force, 123–124 industrial setting, 394 inhalation, 289 intra-articular growth plate, 257 ipsilateral, 205 ischemiavascular, 143 lacerating trauma, 394 lawn mower, 257, 394, 407 ligamentous, 9, 197, 199, 214, 387 Lisfranc, 118, 124, 156, 159 neuropathic, 132 pediatric foot, 253 mechanism of, 5, 229, 394 midfoot, 213 hindfoot/midfoot bones, 126–128 low-energy, 95 lower leg, 45 maisonneuve, 213 medial diastasis, 144 malleolar, 11 motorcycle, 197, 394 nerve, 372 neuropathic, 123 neurovascular, 199 occult tendon, 127, 198 open, 30, 139 os trigonum, 198 osteochondral, 9, 12, 213, 251 overuse, 311 pattern, 139


472 Injury(ies) (continued ) pediatric burn, 302 pronation-external rotation (PER), 9 renal, 305 Salter-Harris type, 214, 228 Sanders classification types, 114 severe degloving, 399 sites of, 200 soft tissue, 196, 252 Lisfranc, 127–128, 139 pilon, 27–30, 35, 41–42 sports, 123 subtle, 126 subtle joint, 140 supination-adduction, 10 supination-external rotation (SER), 9–10, 214 supination-inversion (SI), 214 syndesmosis, 6, 11, 212, 241, 389 talar, 67, 80 talar neck, 50–51 tarsometatarsal, 253 tendon, 9 thermal, 394 turf toe, 203 types, 214, 228 calcaneal, 114 great tow, 205, 207 talar, 76 venous, 199 Insertion Achilles tendon, 97, 252 extensor hallucis longus, 405 tibialis anterior, 121 tendinosis, 325 Instability ankle syndesmotic, 18, 20 chronic, 199 hindfoot, 203 midfoot, 126 MTP joint, 207 Insulin, 180 Integrity plantar plate, 205 Interobserver reliability, 5 Interposition soft tissue, 131 Intervention operative, 13, 241 orthotic, 430 surgical, 21, 109 aggressive surgical, 13 Intraepiphyseal, 224 Inversion passive, 132 plantar, 239 Iontophoresis, 318 Irrigation, copious, 14 Irritation posterior tibial tendon, 13 Ischemia, 46 J Joint ankle, 52, 316, 383

Index ankle and subtalar, 55, 76 anterolateral, 229 aviculocuneiform, 152 calcaneal cuboid (CCJ), 62, 97, 103, 109, 425 midfoot, 145–147, 156–159 calcaneus, 147 subluxation of, 147 capsule, 2 Chopart’s, 145, 156 contractures of the toes and ankles, 268 debri, 196 dislocation tarsometatarsal, 183 dislocation ankle, 196–199 great toe metatarsal-phalangeal (MTP), 203–207 subtalar, 199–203 hallux MTP, 313 inter cuneiform, 145, 151 interphalangeal (IP), 175, 299, 338, 406 Lisfranc, 131, 430 metatarsocuboid, 172 metatarsocunieform, 118 metatarsophalangeal (MTP), 166, 175, 299, 317, 338 great toe, 205, 406 lesser toe, 407 orthotic treatment, 429 paediatric foot, 254 metatarsophalangeal-interphalangeal, 257 midfoot or forefoot TMT, 126 naviculo cuneiform, 139, 145, 153, 155 subtalar, 200–201, 384, 424 ankle, 61 calcaneal, 94, 99, 108 midfoot, 155 surgical treatment, 78 talar, 84, 88–89 talar neck, 50, 59 subtaloid, 98 talocalcaneal, 200 talocrural, 197, 424, 434 talofibular, 89 talonavicular, 50, 62, 67, 200–201 midfoot, 145, 147, 151–155 orthotic treatment, 432 tarsometatarsal (TMT), 130, 140, 156–159, 413 tibiofibular, displacement, 40 tibiotalar, 50, 78, 383–384, 417 transverse tarsal talonavicular and calcaneocuboid, 413 transverse tarsal, 145 Jones dressing, 101 fractures, 172 Junction metaphyseal-diaphyseal, 45, 255 musculotendinous, 317 naviculocuneiform, 134 Juvenile osteonecrosis, 79


Index K Keratinocytes, 267–268, 294 Keratosis, 175 Kirschner wire in ankle fracture, 15, 17, 22 in calcaneal fracture, 108–109 in metatarsal fracture, 167, 173 in midfoot fracture, 136, 152–153 in pediatric fracture ankle, 217, 220, 228, 231 foot, 249, 254 in talar fracture, 84 in treatment of Lisfranc injury, 132 Klebsiella sp., 352 L Lacerating trauma, 394 Laceration(s), 83, 323 acute indirect, 311 tendon, 339 Latissimus dorsi, 279, 400 Leg distal, 30 Lesions anterolateral, 251 grade III and IV, 83 of talus chondral, 80 osteochondral, 80 osteochondral, 198, 375 posteromedial, 251 stage III and IV, 84 tibial, 84 transchondral, 82 Levofloxacin, 350 Lidocaine, 337, 377 Ligament(s) ankle, 21 anterior inferior tibiofibular (AITFL), 3, 197, 229 anterior talofibular (ATFL), 87, 105, 197, 200 bifurcate, 87 calcaneofibular (CFL), 108, 197, 200, 328 calcaneonavicular (spring), 146 calcaneus talocalcaneal, 52 cervical, 52–53, 87, 200 deltoid, 146, 197, 200, 247 in ankle, 6, 11, 13, 15, 21 in talar, 52, 54 intercuneiform, 118 intermetatarsal, 118–119 interosseous, 94–96, 167, 200 talar, 52–56 tibiofibular, 3 intersesamoid, 203, 205 lancinate, 338 Lisfranc, 118–120, 134, 136, 139–140 medial subtalar talonavicular, 200 naviculocuneiform, 147 otaxis, 33, 152 posterior inferior tibiofibular (PITFL), 3, 9, 197

473 posterior talocalcaneal, 52 posterior talofibular (PFL), 52, 84, 197 posterior tibiofibular, 19, 40 remodeling of the ruptured, 131 sprains, 213 spring, 200 superomedial calcaneal navicular, 51 syndesmotic, 11 talocalcaneal, 94 talofibular, 328 talonavicular, 146, 147 tarsometatarsal, 140 tibiafibula, 328 tibionavicular, 146, 147 Ligation, 134 Limb contralateral, 246 vascular status of, 185 Line sagittal fracture, 237 Linked toe, 128, 130 Liposarcoma, 303 Lisfranc disruptions types divergent injuries, 125 partially incongruent injuries, 125 totally incongruent injuries, 125 Lisfranc injuries classification displacement in the coronal plane, 125 divergent dislocations, 125 homolateral dislocations, 125 partial dislocations, 125 Loss of bone, 383, 387 of eversion, 76 of fixation, 155 of motion, 146 of protective sensation, 180–181, 185, 190 of supination, 156 of soft tissue, 274 Low contact dynamic compression plate (LC-DCP), 14 Lower extremity trauma, 374 Lucency subchondral, 249 Lund-Browder chart, 290 M Madura foot, 347 Mafamide, 293 Major vessel compromise, 358 Malalignment, 50 forefoot, 151 hindfoot, 382 lower-extremity, 212 rotational, 66 sagittal, 65 talar neck, 65 varus, 250 Malignancy, 358 Malleolar medial, 17, 56, 62, 83, 231 medial osteotomies, 70 osteotomy, 64, 73


474 Malleoli (growth plates), 27, 78, 213 instability residual, 10 rotational, 10 translational, 10 medial and lateral, 9 medial and posterior, 20 Malleolus, 102, 108, 271, 328–331 ankle, 18 lateral, 94, 229, 269 ankle, 9, 11, 13 medial, 338, 340, 383 ankle, 13–15, 18, 22, 197 midfoot, 152 paediatric foot and ankle, 212, 222, 237, 248 pilon, 33, 41 talar, 50, 55, 62, 78 pilon, 34 posterior, 33 talar, 85 Malnutrition, 358, 395 Malreduction, 383 degenerative joint disease, 2 Malunion(s), 45, 55, 59, 80, 250 calcaneal, 385 equinus, 246 progressive, 246 sagittal plane, 246 talar neck, 76 valgus, 45 varus, 45 Management nonsurgical, 228 orthotic, 404, 76 Mangled extremity severity score (MESS), 395 Mannitol, 305 Mapping of physeal bars, 213 Marjolin’s ulcers, 303–304 Maturity, skeletal, 258 Mechanism(s) axial load, 27 calcaneal locking, 430 flexor and extensor, 175 gastrocnemius–soleus, 94 plantar flexion, 85 soft tissue coverage of foot and ankle, 267 Mechanism of injury, calcaneal fracture, 96 displacement with the sustentaculum tail, 96 joint depression, 96 tongue type, 96 Melanoma, malignant, 303 Menopause, 19 Meropenem, 350 Mesotendon, 310, 317, 319 Metabolic acidosis, 293 Metadiaphysis, 38 Metaphyses, 172, 215, 241 comminution of, 35 distal tibial, 27, 237 in pilon, 35–36, 38 supra-articular, 27

Index tibial, 15 Metatarsal(s), 165 base, 31 forefoot, 118 Metatarsalgia, 143, 167, 390, 400, 430 Metatarsophalangeal (MTP) joint, 310, 336 Methadone, 377 Methicillin, 350 Metronidazole, 352 Microorganisms, invading, 346 Midfoot, 139 anatomy, 145 bone, 118 dislocation (tarsometatarsal), 188 fractures, 145–159 postoperative infections, 364–365 navicular fractures, 146 classification and mechanism of injury, 146 diagnosis, 148 treatment, 150–159 Migration, keratinocyte, 267–268 Minimum inhibitory concentration (MIC), 350 Minnesota Multiphasic Personality Inventory (MMPI), 376 Model, cadaveric fibular malunion, 10 Molding, closed manual, 94 Mood elevation, 377 Morbidit(y)ies, 175, 177, 185, 297 donor-site, 276 fracture-associated, 190 Morganella morganii, 352 Morphine, 377 Mortise, 118 ankle, 197, 200, 201 ankle fractures, 2–4, 11, 13, 20–23 pilon fractures, 33, 38 Mosaicplasty, 82 Motion sagittal, 121 subtalar, 145 Motor vehicle accidents, 101 Mubarak chart, 389 Mucosa tracheobronchial, 289 Muscles gastrocnemius, 305 interosseous, 127–128, 130 Musculotendinous junction, 310 Mycobacterium tuberculosis, 347 M. avium-intracettulare, 347 M. fortuitum, 347, 350 M. marinum, 347 Myofibroblasts, 297 Myoglobin, 305 Myonecrosis, 305 Myonecrosis bacterial, 305 N Nafcillin, 350 Nails brittle, 374


Index Navicular, 2, 118 fractures basic types of, 146–148 body, and stress, 146 dorsal avulsion, 146 tuberosity avulsion, 146 sustentaculum tali, 432 Naviculum, 58 Necrosis avascular, 50, 247, 375 in midfoot fracture, 145–146, 151, 155 pressure, 70 skin, 106, 132 talar avascular, 384 tissue, 69 toe-tip, 404 wound-edge, 45 Necrotizing fascitis, 354 clinical presentation, 354 radiographic evaluation, 354 diagnosis, 354 treatment, 355 HBO, 355 parenteral antibiotics, 355 surgical debridement, 355 Neisseria gonorrhea, 352 Neocortex, 373 Neoplasm, 310 Nerve(s) conduction disease, 180 entrapment, 143 of foot and ankle, 6 plantar, 6 saphenous medial and lateral, 6 sural, 6 medial plantar, 327 peroneal, 6, 313, 316–317 Lisfranc, 121, 123, 132–133, 136, 143 saphenous, 121 superficial peroneal, 14 sural, 85, 108, 121, 271, 389 midfoot, 157 tibial, 336 Neuralgia, tibial, 340 Neuritis, sural, 109, 389 Neuroarthropathy, Charcot, 403 Neurodystrophy, 373 Neuroma, 132, 398, 402, 404, 419 sural, 389 Neuropathy(ies), 132, 358 autonomic vasomotor, 180 compressive, 375 diabetic, 274 motor peripheral, 188 peripheral, 180, 183, 185, 188, 191 vasomotor, 185 vasomotor and motor, 180 vasomotor autonomic, 183 Neuropraxia, 198, 389 Neurovascular dysfunction, 101 Nifedipine, oral, 377

475 Night walker fracture, 166 Nocardia spp., 347 Nociceptors, 373 Nondisplaced fractures, 56 Nonoperative treatment, 267–268 Nonunion, 173, 185, 359, 382 midfoot fractures, 145 147, 150–151 of V metatarsal, 175 pediatric foot and ankle fractures, 213, 246 pilon fractures, 44–45 talar fractures and dislocations, 55, 76, 85 Norepinephrine, 373, 377 Nutcracker type fractures, 253 O Obes(e)ity, 185, 338, 424 Occlusion arterial, 389 Open fracture dislocation, 5 Open reduction and internal fixation (ORIF), 360–361, 434 in ankle fracture, 10, 12, 19, 21 in calcaneal fracture, 106, 114 in pediatric fracture ankle, 231, 241, 243 foot, 249, 252, 253 in talus fracture, 76, 85, 87 Orthopaedic Trauma Association, 5 Orthoses, 423 custom-fitted, 424 custom-molded, 424, 428 nonmolded, 424 Orthosis, 136, 155, 416 aircast ankle stirrup, 434 ankle-foot, 140, 414 patella tendon bearing (PTB), 75 total-contact, 140 Orthotic(s), 302 foot, 276 intention, 433 management, 404, 433 of ankle fractures, 434 sheel wedge, 329 Os calcis, 93 naviculare, 147, 149 peroneum, 329 subtibiale, 212 trigonum, 52, 84–85, 252, 337 vesalianum, 254 Ossicles, 84 Ossification pattern, 247 Osteoarthritis, 45, 70 Osteoarthropathy, 190 Charcot osteoarthropathy, 349 Osteochondral lesions (OCLs), 79 Osteochondritis, 156, 354 dissecans, 79 Osteochondroma, 329 Osteomyelitis ankle dislocation, 199 burnt feet reconstruction, 297


476 Osteomyelitis (continued ) calcaneal fracture complications, 114 chronic, 359 Cierny-Mader classification system, 357–358 diffuse, 358 localized, 358 medullary, 358 superficial, 358 contiguous focus, 358 diabetic patients, 180 diagnostic techniques, 349 computerized axial tomography scan, 349 gallium scan, 349 hemethylpropylamine oxime (HMPAO) scan, 349 magnetic resonance imaging, 349 radionuclide scan, 349 technetium (Tc) bone scan, 349 etiology, 357 foot and ankle deformities treatment, 448, 453–454 operative treatment of soft tissue coverage, 269 posttraumatic infections, 346–348, 350, 353–358 traumatic amputations, 403–404 hematogenous, 357 in subtalar dislocation, 203 in talar complications, 71 management, 359–360 postoperative, 358 posttraumatic, 359 Osteonecrosis, 89 talar neck, 54–59, 61, 248 Osteopenia, 155, 181, 185, 348 calcaneal fracture, 106 diffuse, 375, 404 Osteophyte, 311, 383 Osteoporosis, 372, 374–375 ankle fracture, 19, 22 calcaneal fracture, 94 diabetic patients, 180 feet burns, 303 in talar complications, 75 posttraumatic, 373 Osteosynthesis, bifocal, 454 Osteotomes, 143 Osteotomy(ies), 62, 78, 79, 83, 220, 246, 298, 333, 390, 440 banana, 445 calcaneal, 339 closing dome, 445 closing wedge, 76, 444 corrective, 185 derotational, 80 fibular, 19, 61–62, 64, 79, 83 in fibula, 383 late, 250 malleolar, 61–64, 73, 78, 83 medial malleolar, 61–62 oblique, 444 opening wedge, 76, 444 relatively transverse, 444

Index supramalleolar, 246 talar, 383 talar neck, 66 OTA Committee for Coding and Classification of fractures, 28 Overdistraction, 45 Overgrowth bony, 402–403, 413 Overlap tibia–fibula, 213 tibiofibular, 6 Oxygen hyperbaric (HBO), 30, 267–268, 296, 297 molecular, 267 tension arterial (PAO2), 297 tension tissue (PTO2), 297 transcutaneous, 267–268 P Pain aching midfoot, 143 burning, 372, 374 chronic disabling, 147 myofascial, 377 palmaris longus, 276 pancytopenia, 293 pantalar arthrodesis, 65 paralysis, 389 complete, 305 phantom limb, 402 sympathetically maintained (SMP), 372–374 Paratendinitis, 319 Paratenon, 317, 323 Paresis, 389 Paresthesia, 305, 389 Parkland Formula, 291 Pasteurella multocida, 347 Patella, 42 Pathogens, skin, 6 Pathognomonic for calcaneal fractures, 101 Patient(s) burn, 289 diabetic, 267–268, 418 dysvascular, 400, 418 evaluation, 266–267 ischemic, 185 neuropathic, 185 Pediatric foot and ankle fractures ankle fractures, 212–247 anatomy of distal tibia and fibula, 212 classification systems, 214–215 complications, 246–247 etiology, prevalence, diagnosis, and natural history, 213 transitional fractures, 229, 231, 235–245 treatments, 215–234 foot fractures, 247–258 anatomy, 247–248 calcaneus fractures, 252–253 lesser tarsal fractures and tarsometatarsal injuries, 253


Index metatarsal fractures, 254–257 phalanx fractures, 257–258 talus fractures, 247–252 Pedorthotists, 302 Penicillin G, 350 Peptostreptococcus sp., 352 Perfusion, 6 Periosteum, 302, 331 ankle, 14 fibular, 333 pediatric ankle, 212, 217 pilon, 33 Peripheral vascular disease, 347 Peritendinitis, 311, 318 Peritenon, 323 Peroneal, 6, 247, 385 longus brevis, 329 nerve palsy, 310 tendons, 2, 310 Peroneus brevis, 254, 325 longus, 331 teritus, 62, 64, 316 PGA pins, 84 Phalangeal fractures fractures of the lesser toes, 175 hallucal fractures, 175 Phalanges, 165, 257, 429 Phalanx, 166, 400, 406 Phalanxdistal, 336 Phentolamine, 376 Phonophoresis, 318 Physeal injuries, 213 Physis distal tibial, 246 Pigmentation abnormal, 303 Pilon fractures, 27–46 classification, 28 soft tissue classification, 28–29 complications, 45–46 fixation, 30–37 external, 37 methods, 35 of tibial articular surface, 33–36 plate, 36 temporary, 30–32 postoperative care, 43–44 treatment results, 44–45 Pin(s) bioabsorbable, 83, 153 calcaneal, 61 guide, 132 infection, 39 talar or the calcaneal, 39 track infections, 355 clinical presentation, 356 diagnosis, 357 management, 357 skin and soft tissue, 355–357 traction, 94 transfixion, 30–31, 37 Pinning

477 intramedullary (of metatarsal shaft), 170 technique, antegrade–retrograde, 170–171 Plafond, 27 tibial, 7, 383 Plane(s) coronal, 99, 147 dorsoplantar, 132 frontal, sagittal, transverse, 424 navicular, 150 sagittal, 97, 143, 147 sagittal and transverse, 65 sagittal and coronal, 72 transverse, 143 Plantar ecchymosis, 101 flexion, 126 ligaments, 119 plates, 203 Planum, pes, 338 Planus, pes, 143 Plaster, 300 Plate(s) buttress, 37 cloverleaf, 36 dynamic compression (DCPs), 382 locking, 36 plantar, 203 surgical reconstruction, 207 posterior buttress, 41 spanning, 167 Platelet-derived growth factor (PDGF), 267–268 Plethysmography, 348 Poisoning carbon monoxide, 297 Polymicrobial infection, 347, 358 Position decubitus, 108 lateral decubitus, 65 plantigrade, 41 valgus, 338 Posterior colliculus, 2 inferior tibiofibular ligament (PITFL), 9, 197 malleolar, 2 fixation, 3 fragment, 6 subluxation, 3 talofibular ligament (PFL), 2, 197 tibial nerve, 374 tendons, 6 tuberosity, 109 Posterolateral tubercle, 52 Posttraumatic infections, 50 in foot and ankle, 346–365 Pressures, joint-contact, 10 Prevotella sp., 352 Procedure(s) anchovy, 143 modified Kidner, 339 salvage, 143 Process, anterolateral, 97


478 Pronation passive, of midfoot and forefoot, 126 Propionibacterium spp., 358 Proteus P. mirabilis, 352 P. rettgeri, 352 P. vulgaris, 352 Providencia sp., 352 Pseudohernia, 277 Pseudomonas sp., 347, 358 P. aeruginosa, 352 Pulsed electromagnetic fields, 175 Pulses nonpalpable pedal, 399 palpable pedal, 268 palpation of, 6 pedal, 185 Pump foot, 101 Puncture wounds, 353 clinical evaluation, 353 treatment, 353 R Radiation fibrosis, 358 Radiograph(s), 353 anteroposterior (AP), 6 positive stress, 10 Radiography, image intensifier, 33 Rami communicans gray, 373 white, 373 Range-of-motion (ROM), 199, 268 Ray resections, 407–411 Raynaud’s phenomenon, 377 Receptors alpha-adrenergic, 373 mechano, 373 Recognition, compartment syndrome, 101 Reconstruction, 34 deltoid, 9 free-flap, 273–276; see also Flaps diabetes and free-tissue transfer, 274 failures and revisions, 275 free flaps and the elderly, 275 gait, 275–276 long-term results of free-flap foot reconstruction, 275 sensitivity and foot and ankle reconstruction, 274–275 vascular disease and free-tissue transfer, 274 lateral ankle ligament, 5 soft tissue coverage of foot and ankle, 267 specific injuries, late, 383–390 calcaneus, 384–386 compartment syndrome, 389–390 cuboid, 387–389 flexion contractures, 390 midfoot, 387 talus fractures, 383–384 syndesmotic injuries, 389 syndesmotic, late, 389

Index synthetic options, 325 collagen tendon prosthesis, 325 dacron vascular graft, 325 Marlex mesh, 325 polyglycol threads, 325 polymer and carbon fiber, 325 tendon, 325 Achilles turndown, 325 fascia lata, 325 plantaris tendon, 325 V–Y advancement, 325 Reconstruction and rehabilitation, 297–302 Recovery, soft tissue, 37 Rectus abdominis, 277, 400 Reduction, 33 anatomic, 167, 251, 387 in ankle fractures, 15, 23, 228 Lisfranc injuries, 118, 132, 136, 139 anatomic bone, 15 closed, 106, 167, 170 anatomic, 9, 131, 150 in ankle fractures, 12, 222 in pilon fractures, 33 in talar fractures and dislocations, 59, 61, 69, 76 definitive, 198 Essex-Lopresti, 252 fibular external rotation reduction of talus, 10 initial open, 12 nonanatomic, 139 open, 173, 228 in calcaneous fractures, 94 in Lisfranc injuries, 131–132 in pilon fractures, 32–35, 44 in talar fractures and dislocations, 59 operative, 9 Reepithelialization, 267, 289, 293–294 Reflex sympathetic dystrophy (RSD), 145, 247, 371–378 definitions, 372 diagnosis, clinical, 374–375 diagnostic testing, 375–376 psychological evaluation, 376 radiographs, 375 sympathetic blockade, 376 thermo regulatory testing, 376 three-phase radionuclide bone scan, 375 pathophysiology, 372–373 stages, 373–374 stage I (acute), 374 stage II (dystrophic), 374 stage III (atrophic), 374 treatments, 376–378 intravenous regional blocks, 377 nerve blocks, 377 pharmacological treatment, 376–377 physical therapy, 378 surgical sympathectomy, 378 Regranex, 268 Relative avascularity, 320 Remodeling, 220


Index Renal failure, hepatic, 358 myoglobinuria-induced, 305 Repair calcaneus, 325 medial malleolus, 6 tendon repair, 325 Rerupture rates, 322 sural nerve, 323 Resection(s) metatarsal, 399 physeal bar, 228, 246 Ray, 407–411 Residual diastasis, 132 displacements, 132 foot, 407 forefoot, 410 functional deficits, 7 hindfoot, 108 metatarsal, 413 toes, 410 Response, inflammatory, 180 Resuscitation, 291–292 Retinaculum, 328, 331, 333, 336, 339 extensor, 52 flexor, 338, 340 inferior, 317, 329 stenotic, 328 superior, 317, 329 superior peroneal (SPR), 328 Retinopathy, diabetic, 179–180 Rifampin, 350 Rigid internal fixation, 2 Rocker bottom, 301 ROM, 328; see also Range-of-motion walker boot, 339 Rotation external, 13, 229, 241 pronation-eversion-external (PEER), 214 pronation-external (PER) injuries, 9 supination and external, 14 Rugby, 203 Rule of Nines, 290 Running long-distance, 147 Rupture deltoid ligament, 12–13, 15 frank nerve, 198 neglected, 311 peroneus longus, 329 spontaneous, 311 spring ligament, 127–128 syndesmosis, 13, 197 S SAD type fibula fracture (Weber type A), 9 Sagittal alignment, 59 malalignment, 65

479 Salter–Harris type fractures I and II, 215 III and IV, 222, 224 injuries V, 228 Sanders classification, 108 Scan bone, 404 computed axial tomography (CAT), 19, 34, 98, 383 computed tomography (CT), 58, 202, 213, 348 hemethylpropylamine oxime (HMPAO), 349 radionuclide, 348–349 technetium (Tc) bone, 349 Scaphoid, 54 Scar epiphyseal, 34 hypertrophic, 297–302 Scarring, 44 Score(s) American Orthopaedic Foot and Ankle Society (AOFAS), 8, 387 Mangled Extremity Severity (MESS), 395 Olerud and Molander ankle, 8 syndesmosis outcome, 9 Screw(s) antegrade compression, 62 bioresorbable, 15 syndesmotic, 17 breakage, 174 cancellous, 86, 130, 152 cannulated, 382, 383 in ankle fractures, 15, 19 in Lisfranc injuries, 132, 139 in paediatric foot and ankle fractures, 224, 228, 235 cannulated pediatric hip, 78 compression, 76, 150, 173 cortical, 152, 382, 387 countersunk, 62, 83 fixation, 79 lag, 150 headless, 62, 83 Herbert, 83 intramedullary, 174 lag, 19, 35, 78 cortical, 132 in Lisfranc injuries, 130, 152, 155 in paediatric foot and ankle fractures, 229 malleolar, 15, 174 noncompression, 76 Steinmann, 108 syndesmotic, 21 titanium, 58 cancellous, 153 Sedation, 377 Semitendinosis, 313 Sensory changes, 109 Sepsis, 180, 346 Seroma, 296


480 Serotonin, 377 Serratia marcescens, 352 Serratus anterior, 279 Sesamoidectomy, 207 Sesamoids, 203, 205–206, 257, 336 Shaft ipsilateral tibia, 236, 241 metatarsal, 133 tibial, 7, 35, 39 Shear fractures of talar body, 70 Sheath synovial, 317 tenosynovial, 328 Shell, metaphyseal, 41 Shenton’s line of ankle, 389 Shock burn wound, 288–289 Shoe extended steel shank, 140, 143 rigid-soled, 433 Short leg cast (SLC), 13–14, 59, 85 Shortening fibular, 10 lateral shift, 2 skeletal, 400 Shunt, arteriovenous, 185 Shunting, arteriovenous, 183 Silver sulfadiazine cream (SSD), 293 Sinus tarsi, 84, 103 Skate blade, 310 Skin blistering, 101 grafting, 202, 289, 297, 400 in paediatric foot and ankle fractures, 257 Lisfranc injuries, 145 soft tissue coverage of foot and ankle, 269, 274 ischemia, 200 lacerations, 310 loss, 400 necrosi, 56, 71, 145 slough, 56 Skin-tenting, 145 Sleeve periosteal, 11 Slide gastrocnemius, 390 Slough, 45, 56 Sloughing, 106 Small vessel disease, 358 Smok(ers)ing, 109, 115, 382 Snowboarding, 87, 251 fracture, 251 Soft tissue coverage, 266 foot and ankle, 266–282; see also Foot and ankle paucity, 346 injury, 114 Space fibulocalcaneal, 97 intercuneiform, 126 intermetatarsal, 126 medial clear, 6, 10, 13, 18, 20 syndesmotic, 6 tibiofibular clear, 6

Index Spinal cord, 317 Splint stirrup, 13 Splinting, 45 Sporothrix schenkii, 347 superior peroneal retinaculum (SPR), 328, 333 Sprain, 212, 328 ankle, 105, 148, 156 midfoot, 126, 140 syndesmotic, 13 Springiness, 328 Stability, midfoot, 408 Stabilization, syndesmotic, 12 Stance phase, gait, 2 Staphylococcus sp., 347, 351, 358 S. aureus, 347, 350–351, 357–358 S. epidermidis, 350 Status altered mental, 126 fibula, 35 neurovascualar, 198, 202, 237 nutritional, 400 vascular, 6 Steida’s process, 52, 84 Steinmann pin, 108 Stenosis, 337 of tendons, 385 Steroids, 381 injection, 311, 340 Stiffness, 101, 109, 166, 175 ankle and foot, 44 in ankle dislocation, 196 in great toe MTP dislocation, 203 in subtalar joint dislocation, 199 Strain, 328 Streptococcus spp., 347, 350, 358 S. agalactiae, 351 S. epidermidis, 357 S. pneumoniae, 351 S. pyogenes, 351 Stress(es) advanced age, 320 chronic steroid use, 320 contact, 10 diabetes, 320 external rotation, 12, 19 fracture, 339, 374 hindfoot, 166 midfoot, 147, 149–150, 155 inflammatory arthopathy, 320 inversion, 222 lateral translation, 12 test, 126 valgus, 205 varus, 205 views, 12, 213 Study(ies) Doppler, 267 labeled leukocyte, 403 Subluxation, 150, 157 dorsolateral peritalar, 185


Index midtarsal, 150 peroneal, 333 peroneus brevis, 331 posterior, 19 subtalar, 200 talonavicular, 56 Suboptimal operative fixation, 8 Subtalar joint, 109, 433, 652 Subtalar valgus, 425 Sudeck’s atrophy, 373, 375 Sulcus, 84, 99, 197, 328 calcaneal, 96, 247 interosseous, 94 support, 429 talus, 247 Sulfamylon, 293 Superior extensor retinaculum, 310 Supination, 239, 241, 248 foot, 94 injuries, 213 Supination-plantar flexion (SPF), 214 Supine position, 14 Sural nerve, 85, 108, 121, 271, 323, 389 Surgery ablative digital and ray resection, 359 midfoot disarticulation, 359 Syme amputation, 359 transmetatarsal amputation, 359 Surgical debridement, 353 techniques, 84 intervention, 109 ligation, 199 reapproximation, 2 techniques, 310 debridement, 310 repairs, 310 reconstructions, 310 tendon transfers, 310 treatment posttraumatic infections in foot and ankle, 351 treatment, complications delayed union, 174 failure of intramedullary fixation, 174 refracture, 174 Surgical site infections (SSIs), 355 diagonosis, 355 Sustentaculum, 336–337 Sustentaculum tali, 52, 94, 98, 103, 434 Suture(s) Allgower-Donati, 109, 385 Bunnell, 323 Ethibond, 327 Kessler, 323 Kessler–Tajima, 313 Krackow, 313, 323 Swimming, 83–84 Syme’s amputation, 414, 417–419

481 terminal, 404–405 Sympathalgia, 373 Sympathectomy, 378 surgical, 372 in RSD, 378 Sympathetically maintained pain (SMP), 373–374 cardinal signs, 374 edema, 374 pain, 374 stiffness, 374 secondary signs demineralization, 374 palmar fibromatosis, 374 pseudomotor changes, 374 thermoregulatory changes, 374 trophic changes, 374 vasomotor instability, 374 Symptoms of pain, 376 cold intolerance, 376 peroneal paratendinitis, 329 Synchondrosis, 85 Syndesmosis, 197, 389 in ankle fractures, 3, 5, 9, 11–12, 18, 20 in pilon fractures, 33 involvement, 9, 11 level of the Weber B or C, 10 rupture, 197 tibiotalar, 197 widening, 12 Syndesmotic ligament complex, 3 Syndrome chronic regional pain (CRPS), 395 compartment, 389–390, 396 in Lysfranc injuries, 127–128, 143–144 complex regional pain, 371–378 impingement, 375 lateral, 109 ostrigonum, 85 pain-dysfunction, 373 posttraumatic pain, 373 shoulder–hand, 373 sympathetic overdrive, 37 Synovitis, 81, 385 chronic posttraumatic, 374 Synovium, 385 Synthesis collagen, 267 System Ruedi and Allgower, 28 Shin, 237 T Talar body, shear fractures, 70 type I (coronal/sagittal fracture) displacement at the trochlea, 70 simple nondisplaced, 70 trochlear fracture with dislocations of subtalar and tibiotalar joint, 70 type II (horizontal), 70 Talar dome, 75, 81–83


482 Talar head, 147, 153, 155, 200 depressed, 185 Talar injuries, 50 Talar neck, 2, 152, 247, 383–384 fracture, 33, 56–57 displacement, 57 Hawkins talar neck fracture, 57–58 joint sub talar subluxation, 57 malalignment of, 65 Lisfranc injury, 133 impaction or breakage, 56 osteotomy of, 66 Talar shift, 2, 6, 10, 12 tilt, 6–7 Talectomy(ies), 65–70, 73, 250 canis, 50 limping, 78 residual pain, 78 shortness, 78 Talotibial joint, 2 Talus, 146, 197, 247, 424 anatomy, 51–55 blood supply, 52–55 body, 52 head, 51 neck, 51–52 complications, 70–76 avascular necrosis (AVN), 75 malunions of talar neck, 76 nonunion, 75 osteomyelitis, 71–75 posttraumatic arthritis, 76 skin problems, 70–71 dislocation, 68–70 fractures of talar neck, 55–62 categories, 58–62 classification, 56 clinical features, 56 imaging studies, 56–58 fractures of the lateral process, 87–89 clinical evaluation, 87–89 mechanism of injury, 87 treatment, 89 fracture of the medial tubercle (Cedel’s fracture), 85–87 fractures of the posterior process, 84–85 anatomy, 84 clinical features, 85 mechanism of injury, 84–85 treatment, 85 Hawkins III open fractures, 65–67 Hawkins type IV injuries, 67 in ankle fractures, 2–7, 10–15, 19, 21 osteochondral lesions (OCLS) of talus, 79–84 prognosis, 84 treatment, 82–84 postoperative infections, 362–364 incidence and risk factors, 362 treatment, 364 shear fractures of talar body, 70

Index surgical techniques, 62–65 surgical treatment, 76–79 principles of arthrodesis, 76–78 talectomy and tibiocalcaneal fusion, 78–79 tibiotalar fusion with partial talectomy, 78 Tarsal bones, 133 lesser, 253 midfoot, 118 navicular, the cuboid cuneiforms, 253 Tarsal tunnel, 374 Tarsals occult fractures of, 247 Tarsometatarsal (TMT/Lisfranc) injuries, 118–145 anatomy, 118–121 articular complex, 120, 124 biomechanics, 121–122 classification, 124–126 complications, 143–145 devascularization, 143 other complications, 145 skin compromise, 145 diagnosis, 126–129 disruption, 133 type III, 133 history, 118 mechanism of injury, 122–124 midfoot sprains in athletes, 140 postoperative care, 135–136 prognosis, 136, 139 salvage procedures, 143 treatment, 129–135, 137–142 closed reduction and casting, 131 closed reduction and percutaneous fixation, 131 extensile dorsomedial approach to the midfoot, 132 external fixation, 132 open reduction and internal fixation, 132 principles, 129 timing of surgery, 130 Taxillus, 50 Tear periosteal, 216 Tears peroneus brevis, 329 Technique(s), 406, 408, 414, 417 Bier block, 377 Bunnell, 323 closed reduction, 94 end-to-end repair, 323 external fixation technique, 446–448 fluoroscopic dye, 84 free-flap, 45 Kessler-style suture, 323 Krackow, 323 Ilizarov, 440, 448 imaging, 348 nonstandard amputation, 400 olive wire, 448–449 osteotomy, 62 reconstruction, 382, 394–396; see also Reconstruction free-tissue transfer, 394 hyperbaric medicine, 394


Index skeletal fixation, 394 vascular reconstruction, 395 replacement, 89 splinting, 300 surgical, 13 corticocancellous inlay grafts, 175 reversed trapezoid grafting, 175 sliding local grafting, 175 Tendinitis, 337 peroneal, 385 Tendinopathy, calcifying, 319 Tendinosis, 319, 323, 329 asymptomatic, 318 Tendolipomatosis, 319 Tendon Achilles, 185, 302, 413–414, 418 in calcaneal fractures, 106 in free flaps, 249, 279 in talar fractures and dislocations, 65, 85 rupture and lacerations, 317–328 allograft interposition, 313 anterior tibialis, 62, 74, 121, 131, 316, 410 etiology of rupture, 311 nonoperative treatment, 311–312 operative treatment, 313–315 autograft interposition, 313 degeneration, 310 extensor digitorum longus, 62, 64, 310, 317, 414 ruptures of the EDL, 317 extensor hallucis brevis, 133 extensor hallucis longus, 133, 205, 249, 313, 316 etiology of rupture, 313 nonoperative treatment, 313 operative treatment, 316 flexor carpi radialis, 276 flexor digitorum longus, 87, 310, 336 flexor hallucis longus (FHL), 52, 65, 94, 205, 418 etiology, 337 nonoperative treatment, 337 operative treatment, 337–338 function, 6 healing, 322 integrity, 325 laceration, 310 lengthenings, 403 loss, 316 of continuity, 323 malleolus of, 318 nodularity, 337 periosteum of, 318 peroneal, 97, 328–335 anatomy, 328 chronic repairs, 333–335 os perineum and peroneus longus tears, 329–332 peroneus brevis subluxation or dislocation, 331–332 peroneus brevis tears, 172–173, 329–330

483 peroneal tenosynovitis, attritional tears, and rupture, 328–329 posterior tibial tendon, 15, 121, 147–148, 150 dislocation of the posterior tibial tendon, 340 etiology, 338–339 nonoperative treatment, 339 operative treatment, 339–340 ruptures and lacerations, 310–341 Achilles tendon, 317–328 anterior tibial tendon, 310–315 extensor digitorum longus tendon, 317 extensor hallucis longus tendon, 313, 316 spontaneous disruption of, 318, 336 autoimmune disease, 318 cavovarus, 318 collagen abnormalities, 318 corticosteroid use, 318 fluoroquinolone usage, 318 infectious disease, 318 neurological abnormalities, 318 pronation, 318 weakness and stiffness of gastrocsoleus complex, 318 stenosing tenosynovitis, 310–311 transfers, 403 vincular system, 310 Tendonitis, 322, 336, 339, 374 FHL, 336 insertional, 339 Achilles, 390 Tendonosis, 339 Tenectomy, 385, 389 Achilles, 413–416 extensor, 407 Tenodesis, 313, 327 Tenosis, 329 Tenosynovectomy, 329, 339–340 Tenosynovitis, 328–329, 338–339 FHL, 336–337 stenosing, 310–311 Tenotomies, 403 Tension cutaneous oxygen, 348 transcutaneous oxygen, 348, 399 Tenting skin, 106 Tertius, peroneus, 317 Tetanus immune, 353 toxoid, 353 Tetracycline, 350 Theory, neurotraumatic, 185 Therapy(ies) adjunctive, 353 antimicrobial, 348, 350 cytokine, 274 hyperbaric oxygen (HBO), 353, 400 leech, 275 nonoperative, 267 physical, 297, 377–378 in RSD, 378


484 Tibia, 30–37, 41, 78, 94 ankle fracture, 2, 6, 11–12, 15, 19, 21, 27 distal, 15 proximal, 34 Tibial graft, 79 incisura, 6 nerve, 337 damage, 85 plafond, 83, 85 plateau, 42 Ticarcillin-clavulanic acid, 352 Tilt, talar, 6–7 Tobramycin, 73 Toe(s), 180 active motion of, 6 contracture or rotation of, 269 dislocation, 301 distal phalanx, 166 lesser, 400 middle phalanx, 166 pressures, 348 proximal phalanx, 166 stubbing, 176 Tomography, 81 computed (CT), 7, 30, 58, 98 Tourniquet, 84 Tourniquet calf, 382 Trabeculae compression, 94 pattern of, 94 sparse, 94 Tract, afferent spinothalamic, 373 Traction, 94 axial, 61 calcaneal, 33 skeletal, 300 Transchondral fractures, 79 Transcyte, 293–294 Transfer abductor hallucis tendon, 207 free-tissue, 30, 269, 274, 400 peroneus brevis tendons, 415 tendons, 313, 316, 389, 403 anterior tibialis, 415 Transformation, malignant, 303 Transitional fractures of ankle Tillaux and triplane fractures, 258 Transplant, renal, 274 Transverse fibula fractures, 213 Traps, sterile finger, 132 Trauma, 394 blunt, 328 direct-blow, 156 distal, 382 high-energy, 123, 203 inner, 311 lower energy, 203 lower extremity, 372 mechanical, 328 motor vehicle, 197

Index Traumatic injuries burns, 346 fractures, 346 nail punctures, 346 tendon injury, 318 Treatment calcaneal fracture, 107 modalities, soft tissue (unroofing, aspirating, leaving intact), 5 orthotic, 185 plafond fracture open reduction and internal fixation (ORIF), 360–361 RSD, 376–378 intravenous regional blocks, 377 nerve blocks, 377 pharmacological treatment, 376–377 surgical, 351 surgical sympathectomy, 378 Trochlea, 50 Trovafloxacin, 350 Truss medial, 430 Tuber angle, 94 Tubercle Chaput, 33–34 Gerdy’s, 62, 70 hypertrophic peroneal, 329 peroneal, 328 Tuberosity, 103–106, 252 calcaneal, 153 medial, 147 navicular, 146, 149, 151 V metatarsal, 172 Tunnel cuboid, 329 FHL fibroosseous, 337 tarsal, 15 U UC-BL shoe, 432 Ulceration, 289 Ulcers, 185 foot, 179 Marjolin’s, 303–304 stasis, 269 trophic, 275 Union, delayed, 246 of V metatarsal, 175 Ustentaculum, 100 V Valgus, 30, 37, 96, 301, 339 alignment, 32, 114 of heel, 109 drift, 33, 400 forefoot wedge, 430 genu, 212 malunions, 45 orientation, 33 wedge, 432 Vancomycin, 73, 350


Index Variant intramalleolar, 241 Varus alignment of heel, 109 angulation, 44, 62, 76 collapse, 35, 38, 44 deformity, 36, 155, 185 drift, 400 fractures B type (partial articular), 35 genu, 212 heel, 385 hindfoot, 250 malalignment, 59, 76–77, 108, 250, 301 malunions, 45, 51 shift, 147 Vascular disease, 180 Vasculogenesis, 297 Vasomotor abnormalities, 374 Vasospasm traumatic, 373 Velocimetry, laser-Doppler, 376 Venae comitantes, 271, 274 Venous engorgement pallor, or cyanosis, 6 Venous stasis, 358 Venus, 50 Vessels calcific, 399 intramedullary, 172 metaphyseal, 172 Vibrio vulnificus, 347 View(s) anteroposterior (AP) ankle, 75 Broden (s), 59, 62, 102–103, 109 Canale, 58, 62, 248 Canale pronation, 59 coned-down, 149 Kelly, 248 mortise, 103, 109, 213 stress, 213 abduction-pronation, 126 transverse, 77 weight-bearing, 126 W Walker boot range-of-motion (ROM), 318 Walking boot, 136, 156, 183, 236 aircast, 199 Walking cycle, 166 Weakened warrior, 321 Weakness, 109 Web space, 6 Weber fracture classification, 13, 197 Wedge(s), 425 heel, 318 valgus, 424–425 forefoot, 431 varus, 424–425 Weight-bearing capacity, 2

485 Widening, physeal, 217 Wire(s) calcaneal, 41 cerclage, 23 guide, 15, 19, 139 Kirschner, 333, 387 ankle, 217, 220, 228, 231 foot, 249, 254 in ankle fracture, 15, 17, 22 in calcaneal fracture, 108–109 in metatarsal fracture, 167, 173 in midfoot fracture, 136, 152–153 in talar fracture, 84 in treatment of Lisfranc injury, 132 percutaneous Kirschner, 252 tensioned, 39 transfixion, 34, 43 Wound(s), 44–45 breakdown, 35, 402 care, 69, 292–294 compression, 150 coverage, 400 dehiscence, 14, 109 delayed closure, 12 edge necrosis, 45 failure, 185 foot, 274 foot and ankle management principles, 267 nonoperative coverage of, 268 gunshot, 372, 394, 407 healing, 45, 180, 399 high-velocity gunshot, 394 infection, 109, 185 clostridial infection, 397 management, 183 open, complications, 5, 34, 199 abrasions, 29 contusions, 29 necrosis, 29 slough, 74 puncture, 353 surgical management, 199 X Xenograft, 294 Xeroform, 293 gauze, 294 Z Zone of hyperemia, 289 hypovascularity, 317 necrosis, 289 stasis, 289 Z-plasties, 299


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