Fractures of The Foot and Ankle PDF

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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
iv Preface
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,
Géza 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 ortho-
pedic 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 Infec-
tion 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. Steven A. Herbst, M.D.

Miller Orthopaedic Clinic Department of Orthopaedic Surgery
Charlotte, North Carolina Union Memorial Hospital
Baltimore, Maryland
Todd Arnold, M.D.
Thomas A. Brady Clinic Brian Hutchinson, M.D.
Methodist Sports Medicine Center Wright State University
Indianapolis, Indiana Dayton, Ohio
Jason H. Calhoun, M.D. R. Michael Johnson, M.D.

Department of Orthopedic Surgery Division of Plastic Surgery
University of Missouri–Columbia Department of Surgery
Columbia, Missouri Miami Valley Hospital
Wright State University
Kelly D. Carmichael, M.D. Dayton, Ohio
Department of Orthopaedics and
Rehabilitation Paul J. Juliano, M.D.
University of Texas Medical Branch Milton S. Hershey Medical Center
Galveston, Texas The Pennsylvania State University
Hershey, Pennsylvania
Bruce E. Cohen, M.D.
Miller Orthopaedic Clinic Géza F. Kogler, Ph.D.
Charlotte, North Carolina Department of Rehabilitation
School of Health Sciences
W. Hodges Davis, M.D. Jönköping University
Miller Orthopaedic Clinic Jönköping, Sweden
Charlotte, North Carolina
Richard T. Laughlin, M.D.
Maria Guidry, M.D. Wright State University
Department of Orthopaedics and Dayton, Ohio
Rehabilitation
University of Texas Medical Branch Hongbao Ma, M.D.
Galveston, Texas Department of Orthopaedics and
Rehabilitation
Bryan J. Hawkins, M.D. University of Texas Medical Branch
Central States Orthopaedic Specialists Galveston, Texas
Tulsa, Oklahoma
Arthur Manoli II, M.D.
Kent Heady, M.D. Michigan International Foot and
University of Texas Medical Branch Ankle Center
Galveston, Texas Pontiac, Michigan
viii Contributors
Sidney F. Miller, M.D., F.A.C.S. David A. Porter, M.D., Ph.D.

Department of Surgery Thomas A. Brady Clinic
Miami Valley Hospital Methodist Sports Medicine Center
Wright State University Indianapolis, Indiana
Dayton, Ohio
Steven Schmidt, M.D.
Stuart D. Miller, M.D. Division of Plastic Surgery
Department of Orthopaedic Surgery Department of Surgery
Union Memorial Hospital Miami Valley Hospital
Baltimore, Maryland Wright State University
Dayton, Ohio
Hoan-Vu Nguyen, M.D.
Milton S. Hershey Medical Center Lew C. Schon, M.D.
The Pennsylvania State University Department of Orthopaedic Surgery
Hershey, Pennsylvania Union Memorial Hospital
Baltimore, Maryland
Vinod K. Panchbhavi, M.D., F.R.C.S.
Matthew R. Talarczyk, M.D.
University of Texas Medical Branch
Department of Surgery
Galveston, Texas
Miami Valley Hospital
Wright State University
Mark D. Perry, M.D. Dayton, Ohio
Southwestern Medical Center
Department of Orthopaedic Surgery Daniel M. Thompson, M.D.
University of Texas Beaumont Bone and Joint Institute
Dallas, Texas Beaumont, Texas
Michael S. Pinzur, M.D. Saul G. Trevino, M.D.

Loyola University Medical School University of Texas Medical Branch
Maywood, Illinois Galveston, Texas
Jason H. Pleimann, M.D. William A. Vitello, M.D.

Ozark Orthopaedic and Sports Medicine Clinic Department of Surgery
Fayetteville, Arkansas 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
x Contents
17. Orthotic Management of Foot and Ankle Fractures ......................................................... 423

Géza F. Kogler
18. Treatment of Foot and Ankle Deformities with the Ilizarov Fixator ................................ 439
Daniel M. Thompson and Jason H. Calhoun
Index........................................................................................................................................... 459
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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
1
2 Miller and Herbst
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 displace-
ment 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 meas-
urements, 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].
Ankle Fractures 3
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 liga-
ment (PITFL), the tibiofibular interosseous ligament, and the inferior transverse tibiofibular
ligament. The fibula will externally rotate approximately 128 and displace posterolaterally with
4 Miller and Herbst
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) Arbeits-
gemeinschaft für 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 observa-
tions 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 excep-
tion 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 repre-
sent 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.
6 Miller and Herbst
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 inter-
vention.
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 long-
term 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 < 1 mm or > 4 mm, similar to distance between talar dome and tibia
Talocrural angle More than 2 to 58 difference from contralateral side
Talar tilt > 2 mm, > 58
Tibiofibular clear space > 5 mm
Tibiofibular overlap < 10 mm on AP view, < 1 mm on mortise
Ankle Fractures 7
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,
8 Miller and Herbst
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.
Ankle Fractures 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 surface-
bearing 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 syndes-
mosis [52]. Stabilization of the syndesmosis when in doubt is recommended.
10 Miller and Herbst
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 controver-
sial. 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. Displacement (lateral or posterior > 2 or 3 mm) in any direction or a talocrural angle > 58
than that of the opposite side
2. Significant medial-sided tenderness and swelling
3. Any appreciable talar shift (medial clear space > 4 mm)
4. 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
Ankle Fractures 11
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 satisfac-
tory 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
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, indicat-
ing 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 syndes-
mosis 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 13
H. 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-weight-
bearing 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
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 dehis-
cence. 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
Ankle Fractures 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 drill-
and-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.
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
Ankle Fractures 17
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.
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 demon-
strate 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.
Ankle Fractures 19
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 poster-
olateral 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 cannu-
lated 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
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.
Ankle Fractures 21
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.
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 23
XIII. 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 asymp-
tomatically 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.
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2
Pilon Fractures
Richard T. Laughlin
Wright State University, Dayton, Ohio
CONTENTS
I. Introduction .................................................................................................................... 27
II. Fracture Classification..................................................................................................... 28
III. Soft Tissue Classification ................................................................................................. 28
IV. Temporary Fixation ........................................................................................................ 30
V. Fixation of The Tibial Articular Surface ......................................................................... 33
VI. Plate Fixation .................................................................................................................. 36
VII. External Fixation............................................................................................................. 37
VIII. Postoperative Care .......................................................................................................... 43
IX. Results ............................................................................................................................. 44
X. Complications.................................................................................................................. 45
XI. Conclusion....................................................................................................................... 46
Acknowledgment......................................................................................................................... 46
References ................................................................................................................................... 46
I. 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
28 Laughlin
Lateral Anteroposterior Axial
A A A
B B B
C C C
Figure 2.1 Ruedi–Allgöwer classification of pilon fractures [4,5].
II. FRACTURE CLASSIFICATION

Many classification schemes have been proposed for this injury. The system of Ruedi and Allgöwer 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 displace-
ment 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 extra-
articular, 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.
Pilon Fractures 29
A B C
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 Simple G Superficial
r Fracture r abrasion
a configuration (shaded area),
a mild to
d with little or d moderately
e no soft tissue
injury
e severe
fracture
0 I configuration
Deep, G Extensive
G
contaminated contusion
r r
abrasion local or crushing
a contusional a of skin or
d damage to d destruction
e skin/muscle e of muscle
moderately (shaded
II severe III area),
fracture severe
configuration fracture
Figure 2.3 Tscherne [11] classification of soft tissue injury.

30 Laughlin
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.
Pilon Fractures 31
A 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.
A B
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.
32 Laughlin
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.
Pilon Fractures 33
V. 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 Allgöwer [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 distrac-
tion 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.
34 Laughlin
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 ante-
rolateral 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.
Pilon Fractures 35
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 Joint or rigid spanning
Locking screw or plate systems Joint-spanning or articulated
Precontoured, percutaneous plates Non-joint-spanning
Small wire — hybrid
Small wire — Ilizarov
36 Laughlin
A B
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.
Pilon Fractures 37
B C
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 5-
mm 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
38 Laughlin
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 compres-
sion 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.
Pilon Fractures 39
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 half-
pins (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 multiple-
trauma 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 biomech-
anics 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.
40 Laughlin
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.
Pilon Fractures 41
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 half-
pin. 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.
42 Laughlin
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 43
A 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-weight-
bearing.
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].
44 Laughlin
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-weight-
bearing 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 recon-
structive 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.
Pilon Fractures 45
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
46 Laughlin
bundle, and the foot is ischemic, immediate amputation is often necessary. In cases with multiple-
joint 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.
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delphia, 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 Allgöwer, M., Fractures of the lower end of the tibia into the ankle-joint, Vol 1, Injury,
92–99, 1969.
5. Ruedi, T.P. and Allgöwer, 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.
Pilon Fractures 47
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.
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the tibia, Clin. Orthopaed., 298, 221–228, 1994.
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treatment of pilon fractures, J. Orthopaed. Trauma, 6, 195–200, 1992.
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contributing to poor results and complications, Clin. Orthopaed., 292, 108–117, 1993.
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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,
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lower extremity trauma, J. Orthopaed. Trauma, 7, 270–274, 1993.
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33. Borrelli, J., Jr., Torzilli, D.A., Grigiene, R., and Helfet, R., Effect of impact load on articular cartilage:
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Foot and Ankle Trauma, Sanders, R., Ed., 1999, pp. 487–497.
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3
Talar Fractures and Dislocations
Saul G. Trevino and Vinod K. Panchbhavi
University of Texas Medical Branch, Galveston, Texas
CONTENTS
I. Introduction .................................................................................................................... 50
II. History............................................................................................................................. 50
III. Anatomy.......................................................................................................................... 51
A. The Head of the Talus ............................................................................................. 51
B. The Neck of the Talus.............................................................................................. 51
C. The Body of the Talus ............................................................................................. 52
D. Blood Supply ........................................................................................................... 52
1. Posterior Tibial Artery ...................................................................................... 54
2. Dorsalis Pedis Artery and Peroneal Artery ....................................................... 54
3. Intraosseous Circulation.................................................................................... 54
IV. Fractures of the Talar Neck ............................................................................................ 55
A. Clinical Features ...................................................................................................... 56
B. Classification ............................................................................................................ 56
C. Imaging Studies........................................................................................................ 56
D. Categories ................................................................................................................ 58
1. Group I Fractures ............................................................................................. 58
2. Group II Fractures ............................................................................................ 59
3. Group III Fractures........................................................................................... 61
V. Surgical Techniques ......................................................................................................... 62
VI. Hawkins III Open Fractures............................................................................................ 65
VII. Hawkins Type IV Injuries ............................................................................................... 67
VIII. Total Dislocation of the Talus......................................................................................... 68
IX. Shear Fractures of the Talar Body .................................................................................. 70
X. Complications.................................................................................................................. 70
A. Skin Problems .......................................................................................................... 70
B. Osteomyelitis............................................................................................................ 71
C. Avascular Necrosis (AVN)....................................................................................... 75
D. Nonunion................................................................................................................. 75
E. Malunions of the Talar Neck................................................................................... 76
F. Posttraumatic Arthritis ............................................................................................ 76
XI. Surgical Treatment .......................................................................................................... 76
A. Principles of Arthrodesis.......................................................................................... 76
1. Ankle Arthrodesis ............................................................................................. 77
49
50 Trevino and Panchbhavi
B. Tibiotalar Fusion with Partial Talectomy................................................................ 78

C. Talectomy and Tibiocalcaneal Fusion ..................................................................... 78
XII. Osteochondral Lesions (OCLS) of the Talus ................................................................... 79
A. Treatment................................................................................................................. 82
B. Prognosis.................................................................................................................. 84
XIII. Fractures of the Posterior Process ................................................................................... 84
A. Anatomy .................................................................................................................. 84
B. Mechanism of Injury................................................................................................ 84
C. Clinical Features ...................................................................................................... 85
D. Treatment................................................................................................................. 85
XIV. Fracture of the Medial Tubercle (Cedell’s Fracture) ....................................................... 85
XV. Fractures of the Lateral Process ...................................................................................... 87
A. Clinical Evaluation................................................................................................... 87
B. Mechanism of Injury................................................................................................ 87
C. Clinical Evaluation................................................................................................... 89
D. Treatment................................................................................................................. 89
XVI. Conclusion....................................................................................................................... 89
References ................................................................................................................................... 89
I. 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 attach-
ment 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 biomech-
anics 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 plantar-
directed 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
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 segmen-
ted, 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
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, Phila-
delphia, 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.
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 commu-
nicating 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
Anterior tibial artery

Posterior tubercle artery Posterior tibial
Deltoid branches artery
Deltoid branches
Artery of the tarsal canal Tarsal sinus
branches Posterior tibial artery
Lateral plantar Artery of

artery the tarsal
Medial plantar artery canal
A
Posterior tubercle vessels
Artery of the
tarsal canal
Deltoid branches
Tarsal sinus
branches
Lateral Medial
Superior neck
vessels
(dorsalis pedis artery)
B
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 anasto-
motic 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
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. Anatom-
ically, 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 down-
ward 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).
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.
Figure 3.6 Continued (D) Group IV Hawkins talar neck fracture. The dislocated talar body is associ-
ated 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. Categories
1. 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.
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. Add-
itionally, 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.
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.
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 reduc-
tions 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
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 anterome-
dial 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 con-
firmation 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. Unfortu-
nately, 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
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.
Extensor digitorum
longus retracted
Talar neck tracture
Extensor digitorum
longus
Incislon
Talonavicular joint
Superficial
peroneal nerve
Extensor digitorum
brevis
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 poster-
olateral 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.
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 limita-
tions. 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 re-
moval 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 treat-
ment 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
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.
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.
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 conse-
quence 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.
Figure 3.13 Continued (B1 and B2) Initial fixation was that of a tibiotalar pin fixation with accom-
panying 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]
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.)
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 Szyszko-
witz 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
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.
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.
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.
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% involve-
ment 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.
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 recom-
mended. 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 arthro-
plasty 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. 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 deform-
ity 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.
Figure 3.19 Continued (D) Postreduction radiograph displays the posterior-to-anterior screw place-
ment.
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 associ-
ation 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
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 arthrod-
esis 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
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.
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 poster-
omedial 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
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 arthro-
scopic procedures to confirm the Berndt and Harty classification scheme. Their four-part classifi-
cation 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 poster-
omedial 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 sub-
chondral 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.
Figure 3.23 (A and B) AP and lateral radiographs demonstrate a compression fracture of the ante-
rolateral 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 low-
resistance cycling are also encouraged. Grade III and IV lesions are treated with 6 weeks of
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. Debride-
ment 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 interpret-
ations 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. FRACTURES OF THE POSTERIOR PROCESS

A. Anatomy
The posterior process of the talus comprises two tubercles: the posterolateral and the poster-
omedial. 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 nonarti-
cular; 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
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 poster-
olateral 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
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.
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
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. 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 comminu-
tion, 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 devastat-
ing 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.
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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.
93
94 Juliano and Nguyen
I. 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 (calca-
neal 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].
Calcaneal Fractures 95
Right foot
Posterior articular Middle articular Anterior articular Articular surface
surface for talus surface for talus surface for talus for cuboid bone
Anterior articular
Body
surface for talus
Middle articular
surface for talus
Posterior
Articular surface
articularr
for cuboid bone
surface
for talus
Peroneal
Tuberosity Peroneal
Sustentaculum tali trochlea
trochlea
Lateral process Groove for peroneus
of tuberosity longus tendon Body
Lateral view
Anterior articular Middle articular surface for talus

Tuberosity
surface for talus Posterior articular
surface for talus
Superior view
Articular
Middle articular surface
surface
for cuboid Tuberosity Posterior
bone articular surface
Sustentaculum tali
Sustentaculum tali Medial Groove for flexor

Groove for flexor process of hallucis longus Peroneal
hallucis longus tendon tuberosity tendon trochlea
Medial view Medial
process of
Lateral
tuberosity
Fibula process of
Tibia tuberosity
Tuberosity
Interosseous membrane
Posterior Posterior view

tibiofibular
Talus
ligament
Posterior
40⬚
talofibular
Tube
33⬚ to
ligament r
angle
Deltoid
Calcaneofibular
ligament
ligament
Peroneal tendons in
Posterior inferior peroneal
talocalcaneal retinaculum
ligament
Critical
Posterior view angle
with ligaments 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
or minimally displaced fractures. High-energy injuries result in more comminuted and intra-
articular 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 ante-
romedial (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.)
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 entrap-
ment [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.)
IV. CLASSIFICATION
There have been many attempts to develop a universally accepted classification scheme for calca-
neus fractures. An ideal classification system would incorporate fracture anatomy and the mech-
anism 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. Not involving subtaloid joint
A. Tuberosity fracture
. Beak type
. Avulsion medial border
. Vertical
. Horizontal
B. Involving calcaneocuboid joint
. Parrot nose type
. Various
2. 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 compres-
sion 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 intra-
articular 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 articu-
lar 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.
Primary fracture
Lateral Superior
Two-part fracture
Shear Compression
Lateral Coronal Superior Coronal Lateral Coronal
T T
T
1 1 1
Joint depression 3
2 2
2
Extra-articular Intra-articular Tongue
Three-part fracture
Shear−compression
Lateral Coronal
Joint depression 1 3
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 three-
part 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.)
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
A C
B
Type IIA Type IIB Type IIC
B C
A C
A B
III AB III AC 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.)
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 recog-
nition 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).
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-
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].
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, compar-
isons 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
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 mech-
anism 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 Gissane’s angle. (Reprinted from Orthoped. Clin. North Am., 32, 47, 2001. With
permission.)
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 classifica-
tion. 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-to-
moderate workload.
Table 4.1 Results of Calcaneal Fracture Treatment*

Treatment and First Authory % Satisfactory % Unsatisfactory
Primary arthrodesis
Zayer65
Subtalar 0 100
Triple 50 50
Pennal40 76 24
Thompson60, 61
Triple 95 5
Noble37 56 44
Lindsay30 60 40
Hall20 74 26
No reduction
Zayer65 22 78
Pozo43 67 33
Bertelsen3 100 0
Lindsay30 76 24
Closed reduction
Omoto38 91 9
Herman24 73 27
Aitken1 75 25
Bertelsen3 100 0
Cotton12 50 50
Reuter14 45 55
Crosby (all types)13 13 47
Percutaneous reduction
Pescatori (llizarov)42 78 22
Essex-Lopresti15 60 40
Reuter (Essex-Lopresti)44 58 42
Open reduction
Zayer65 43 57
Harding21 75 25
Stephenson59 77 23
Stephenson58 86 14
Ross4
Tongue type 87 13
Joint depression 67 33
Romash45 70 30
Palmer39 96 4
Reuter44
Lateral approach 88 12
Medial approach 57 43
Beze4 85 15
Letronel29 90 10
Zwipp67 93 7
Sanders50
Type II 73 27
Type III 70 30
Type IV 11 89
Hutchinson25 76.6 22.4
Eberle14 73 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.
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 visualiza-
tion 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 no-
touch 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 frag-
ment, 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
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,
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.)
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 Trick: Use traction

lateral wall and valgus angulation
to access to restore hindfoot
posterior facet alignment
Pitfall: Failure
to correct varus
deformity
Figure 4.11 Continued Authors’ preferred method.

Trick: Thumb
pressure reduces Pitfall: Residual defect
lateral wall bulge 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 auto-

graft or allograft
Posterior facet fixed to

constant fragment
with .045 Kirschner wires
Body to posterior facet fixed with .062 Kirschner wires

Completed fixation
Calcaneal fracture fixed with calcaneal plate and screws
Pitfalls:
Trick: Fully threaded Forty cancellous lag screws
smaller cortical screws 1. Difficult removal due to
provide better bite no back cutting
(2.7 to 3.5 mm). Must 2. Large threads do not
lag with glide hole 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
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

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 arthrod-
esis 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
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.
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12. Stephenson, J.R., Displaced fractures of the os calcis involving the subtalar joint: the key role of the
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17. Sanders, R., Fortin, P., DiPasquale, T. et al., Operative treatment in 120 displaced intraarticular calcaneal
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19. Richman, J.D. and Barre, P.S., The plantar ecchymosis sign in fractures of the calcaneus, Clin. Orthopaed.,
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22. Myerson, M. and Manoli, A., Compartment syndromes of the foot after calcaneal fractures, Clin.
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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
117
118 Heady and Trevino
I. TARSOMETATARSAL (TMT) (LISFRANC) INJURIES

A. 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 long-
term 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]. Im-
provement in diagnostic evaluation, especially computed tomography (CT) and magnetic reson-
ance 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 preva-
lence 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 high-
lighted 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
Lisfranc Injuries and Midfoot Fractures 119
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.)
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.
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 cunei-
forms; 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 compart-
mentalization, 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
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 Dorsalis

deep peroneal pedis artery
nerve
Lateral tarsal 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 fre-
quent 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].
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
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
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 disloca-
tions, 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.)
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 particu-
larly 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 com-
pounded 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 ecchym-
osis 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
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.
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 spin-
echo (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].
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. Treatment
1. 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 Kirsch-
ner 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
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
Figure 5.15 CT scan through Lisfranc joint showing fracture of the second, third, and fourth meta-
tarsal bases.
stabilizes the soft tissue envelope, lessens the incidence of skin breakdown and vascular comprom-
ise, 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 interpos-
ition of the anterior tibialis tendon [7,13].
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. Alterna-
tively, 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 longitu-
dinal 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
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
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 frag-
ments, 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
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 inter-
space. 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
Inferior extensor retinaculum

Base of second metatarsal Inferior extensor retinaculum Medial cuneiform
Lateral cuneiform Lisfranc ligament (torn)

Base of Extensor
Base of Extensor hallucis brevis second metatarsal hallucis longus
third metatarsal
Dorsalis
pedis artery
Base of
first
metatarsal
Dorsalis
pedis artery
Extensor
digitorum longus Extensor
hallucis brevis
A B
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.
Figure 5.20 Continued Surgical photographs of the extensile dorsomedial approach to the midfoot.
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.
Figure 5.21 Continued Example of stabilization of a divergent Lisfranc injury. (C) The lateral meta-
tarsals 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].
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.
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. 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 abduc-
tion 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
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. 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 lower-
extremity 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 cunei-
forms 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
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 talona-
vicular 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.)
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 high-
performance 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 mid-
1990s 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).
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 lower-
extremity 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 weight-
bearing 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
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
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 rough-
ened 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-
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 immobil-
ization without weight-bearing.
Navicular body fractures. Conservative treatment of navicular body fractures almost invari-
ably 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 dissec-
tion 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
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
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.
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.
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 talona-
vicular 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-weight-
bearing 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 ad-
equate healing and symptom relief is achieved at 6 weeks, the patient may gradually begin weight-
bearing 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 man-
agement is similar to that for conservative treatment. Custom orthosis may be advisable if the
athlete returns to competitive training [75].
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 distin-
guished 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 surgi-
cally. 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-weight-
bearing 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 injur-
ies 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 immobiliza-
tion 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.
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.
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 H-
shaped 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
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 weight-
bearing 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
166 Hawkins
II. 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 displace-
ment 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 dis-
placement, 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 configur-
ation 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. FRACTURES OF THE LESSER METATARSALS

A. 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, espe-
cially 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 dis-
placement 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
168 Hawkins
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.
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.
170 Hawkins
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 suggest-
ing 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 dis-
placement, 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.)
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.
172 Hawkins
B. 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 approxi-
mately 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.)
(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 displace-
ment 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 radio-
graphic healing [6]. Quill [17] has suggested, based on his review of the literature, that approxi-
mately 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 non-
weight-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 recom-
mending 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.
174 Hawkins
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 intrame-
dullary 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.
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 progres-
sively 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-weight-
bearing 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 treat-
ment 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 recom-
mended 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 intra-
articular 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
176 Hawkins
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
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, Springer-
Verlag, 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.
178 Hawkins
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 wound-
healing 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
179
180 Pinzur
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 neur-
opathy 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 181
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 remem-
bered 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 weight-
bearing, 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 radio-
graphs.
182 Pinzur
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 low-
energy 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
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.
184 Pinzur
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.
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 popula-
tions, 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 life-
threatening 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 accommo-
dative 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
186 Pinzur
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.
Figure 7.5 Continued (C and D) Radiographs following tendon achilles lengthening and midfoot
stabilization
188 Pinzur
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 low-
energy 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).
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.
190 Pinzur
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.
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.
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prospective study, J. Clin. Endocrinol. Metab., 86, 32–38, 2001.
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diabetes, Am. J. Med. Sci., 309, 76–82, 1995.
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Ankle Int., 20, 564–567, 1999.
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treatment of Charcot foot, Foot Ankle Int., 21, 916–920, 2000.
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(Charcot) midfoot deformity, Foot Ankle Int., 14, 189–197, 1993.
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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
G. Long-Term Results and Prognosis............................................................................. 203
IV. Great Toe MTP Dislocation ............................................................................................. 203
G. Prognosis and Long-Term Outcome.......................................................................... 207
V. Conclusion ........................................................................................................................ 207
References .................................................................................................................................. 208
195
196 Porter and Arnold
I. 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 presenta-
tions and small series [1–12]. There are no articles on randomized treatment protocols or prospect-
ive 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 poster-
omedial 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 plantar-
flexed 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.
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 docu-
ment 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. 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 question-
able 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 surgi-
cal 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 poster-
omedial 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 muscu-
lotendinous 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 rehabili-
tation 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 intra-
articular 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. SUBTALAR JOINT DISLOCATION

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
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.

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.

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.
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.
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
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 concomi-
tant 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).
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
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 frac-
tures. 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. Forty-
four 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 non-
weight-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. 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. Heppen-
stall 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. GREAT TOE MTP DISLOCATION

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.

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. Low-
energy dislocations are commonly seen in tackling sports such as football and rugby.

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, sesa-
moids, 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.
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.
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
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.
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 neces-
sary 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).
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
Figure 8.6 (A) Lateral and (B) AP postreduction radiographs of the same foot demonstrating concen-
tric 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.
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
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.
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10. Wehner, J. and Lorenz, M., A case report and review of the literature. Lateral ankle dislocation without
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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
211
212 Carmichael
I. 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 lower-
extremity 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 adult-
like 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 malalign-
ment 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 213
B. 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 investi-
gation [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 ‘‘Classifi-
cation 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
214 Carmichael
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
II
Supination− Supination− Supination− Supination− Supination− Pronation

invertion(I) invertion(II) plantar plantar external eversion
flexion flexion rotation extermal
(AP view) (lateral view) rotation
Figure 9.1 Simplified diagram of the mechanistic Dias–Tachdjian classification system of pediatric
ankle fractures.
I 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 un-
necessary. 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 close-
reduced 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
216 Carmichael
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 triangu-
lar 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.
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.
218 Carmichael
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
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.
220 Carmichael
Figure 9.6 Continued (E) oblique, and (F) lateral views demonstrating good reduction of the metaphy-
sis 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 displace-
ment 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.
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.
222 Carmichael
Figure 9.7 Continued (E) oblique, and (F) lateral projections show the metaphyseal spike is well
reduced.
4. 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 inter-
vals 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
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.
224 Carmichael
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.
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.
226 Carmichael
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.
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.
228 Carmichael
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 dis-
placement 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, consid-
eration 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
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 weight-
bearing 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 ante-
rolateral 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
230 Carmichael
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.
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
232 Carmichael
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.
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.
234 Carmichael
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 non-
weight-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.
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.
236 Carmichael
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 non-
weight-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
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 underesti-
mated 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 metaphy-
seal spike are displaced medially (Figure 9.20) [28]. Another variant has been described in which the
238 Carmichael
Metaphyseal
fracture
Physeal fracture
Epiphyseal
fracture
Metaphyseal
fracture
Physeal fracture
Epiphyseal
fracture
B
A
Metaphyseal
fracture
Physeal fracture
Epiphyseal
fracture
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.)
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.
240 Carmichael
Figure 9.20 Diagram of medial triplane fracture (Marmor type). (From Karrholm, J., J. Pediatr.
remember is the fracture displacement of a medial triplane fracture occurs medially, the mechan-
isms 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 presen-
tation; 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
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 poster-
omedial 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 accom-
plished, 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].
242 Carmichael
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.
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.
Figure 9.22 Continued Postoperative radiographs: (C) AP and mortise, and (D) lateral views demon-
strate 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.
246 Carmichael
F. 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. Non-
unions 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 asym-
metric 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 consid-
erable 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 deform-
ities. 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 extra-
articular fractures, but does occur with intra-articular fractures. Up to 30% of patients with intra-
articular 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.
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 Frac-
tures’’ 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 suscep-
tible 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].
248 Carmichael
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 classifi-
cation systems.
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 non-
weight-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
250 Carmichael
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 Ortho-
paedic 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-weight-
bearing [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 malalign-
ment develops, as children are capable of remodeling some deformity [10]. Late osteotomies or
talectomies are used as salvage procedures.
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 trau-
matic 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
252 Carmichael
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 non-
weight-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 intra-
articular 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.
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 non-
weight-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 individual-
ized. In young children, these can often be managed conservatively but in older children it involves
accurate articular reduction and may require ORIF.
254 Carmichael
E. 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.
Figure 9.27 Continued (B) AP and oblique, and (C) lateral showing the reduction. The second meta-
tarsal 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
256 Carmichael
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.
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 interven-
tion [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 import-
ant, 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). Anti-
pseudomonal 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, ossifica-
tion 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; compari-
son 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.
258 Carmichael
Figure 9.29 Intra-articular fracture of the hallux proximal phalanx in a 16-year-old male. (A) Pre-
operative 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.
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 radio-
graphs 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
265
266 Johnson and Schmidt
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 weight-
bearing, 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 Size Foot sensation
Comorbid illness Depth Timing of surgery
Diabetes Location
Heart disease Weight-bearing
Obstructive Non-weight-bearing
Peripheral Mechanism
Vascular disease Ischemic
Venous disease Diabetic
Smoking history Traumatic
Soft Tissue Coverage of the Foot and Ankle 267
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. Elevation of the extremity
2. Reduction of edema using compression in patients with stasis ulcers
3. Mechanical or enzymatic debridement of all devitalized tissue
4. Control and treatment of any infection with appropriate antibiotic therapy
5. Presence or reestablishment of adequate arterial inflow
6. Control of medical illnesses such as diabetes mellitus and hypertension
VI. 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. Non-
operative 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, granu-
lation 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 reepithelia-
lization. This is achieved by keratinocyte migration. Keratinocytes migrate faster in a wet envir-
onment [9]. Large wounds require split thickness to allow reepithelialization.
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 per-
formed; 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 Ciar-
avino 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.
Table 10.2 Treatment Options

Nonoperative Operative
Dressing changes 18 closure

Enzymatic debridement + topical antibiotic Skin grafts
PDGF Pedicle flaps
Topical negative pressure Free flaps
HBO
A. 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 split-
and full-thickness skin grafts to provide adequate stable wound coverage to weight-bearing sur-
faces.
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 split-
and 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
Figure 10.1 (A) Preoperative lateral calcaneal flap. Patient has exposed hardware. (B) Postoperative
view.
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].
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.
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
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 independ-
ent 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 ampu-
tation. 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 consid-
ered 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].
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 sensa-
tion 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 micro-
surgery 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. Free-
muscle 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 subcuta-
neous 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
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 post-
operative radial forearm free flap.
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 myocu-
taneous [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) Seven-
month postoperative rectus free flap.
3. Latissimus Dorsi (LD)

Another workhorse flap is the LD muscle. Originally, this was the most common flap used in free-
tissue 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.
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 non-
weight-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.
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
Figure 10.8 (A) Severe frostbite injury with loss of plantar surface of the foot and all toes in a 15-year-
old 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.
Heel Small defect

Weight-bearing - 2 intent PDGF
Metatarsal - Medial plantar flap
Plantar
Large defect − exposed bone → free flap
Non-weight-bearing (instep)
Large defect − adequate soft tissue plantar fascia
2 intent PDGF intact → STSG
STSG
Exposed tendon Large area free flap

Plantar Small area
If no granulation
No tendon exposed STSG VAC
PDGF Free flap
Good granulation STSG
Lateral ankle − exposed bone → small area → lateral calcaneal artery flap
Large area → free flap
Small area or Granulation STSG

Posterior ankle poor surgical candidate − VAC
Achilles tendon PDGF
No granulation Free flap
(if reasonable surgical
Sural artery flap
Large area 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 phys-
ician on two of the cases mentioned in this chapter.
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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
288 Miller and Talarczyk
I. 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 patho-
physiology of the burn injury, initial wound management, definitive wound coverage, reconstruc-
tion 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. Fortu-
nately, 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 multi-
specialty 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 man-
agement 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 contribu-
tion 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
Burns to the Feet 289
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 bronchos-
copy. 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 associ-
ated 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
Figure 11.1 Burn depth of nonuniform burn.
are retained. With full-thickness burns, the entire epidermis and dermis and all of the skin append-
ages 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.

9%
1%
Adult body Percent of total BSA
Front
Part 18%
Arm 9 9% 9%
Back
Head 9 18%
Neck 1
18% 18%
Leg 18
Anterior trunk 18
Posterior trunk 18
18%
Child body Percent of total BSA
Front Part
9% 18% 9%
Back Arm 9
18%
Head and neck 18
Leg 14
14% 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
Age 0−1 1−4 5−9 10−14 15

A − ½ of head 9½% 8½% 6½% 5½% 4½%
B − ½ of one thigh 2¾% 3¼% 4% 4¼% 4½%
C − ½ of one leg 2½% 2½% 2¾% 3% 3¼%
A A
3½% 3½%
1%
1% Adult
2% 2% 2% 2%
13% 13%
1½% 1½% 1½% 1½%
2½% 2½%
1½% 1% 1½% 1½% 1½%
4¾% 4¾% 4¾% 4¾%

B B B B
C C C C
3½% 3½% 3½% 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 full-
thickness 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.
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 prob-
ably 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 twice-
daily 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 partial-
thickness 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.

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 Man-
agement, 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 cross-
species 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
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 reepitheliza-
tion 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 appear-
ance 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.

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
of ailments including frostbite injury, osteomyelitis, soft tissue infections, carbon monoxide poi-
soning, 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 approxi-
mately 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 impair-
ment 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
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, contrac-
tures 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 psycho-
social 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.

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 recur-
rence 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 inter-
phalangeal 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 dimin-
ished 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.

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.

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.

Figure 11.16 ExFix for leg elevation.
4. 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. SPECIAL ORTHOPEDIC ISSUES

A. 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.
C. 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. COMPLICATIONS
A. 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 regen-
eration, predisposing themselves to mutational malignant transformation. Other proposed etio-
logic 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.
Figure 11.17 Marjolin’s ulcer.

VIII. SPECIAL TYPES OF BURNS

A. 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 contrac-
tions 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 high-
voltage 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.
Figure 11.20 Electrical injury.
B. 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.

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 treat-
ment 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 educa-
tion and implementation of safety measures. Teaching employer health departments about on-the-
job burn injuries is extremely important. In the U.S., the Occupational Safety and Health Admin-
istration (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
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., Recon-
struction 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.
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foot contractures, J. Foot Ankle Surg., 35, 218–221, 1996.
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treatment of hypertrophic scars or keloids, Burns, 19, 17–21, 1993.
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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
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
4. Percutaneous Repair......................................................................................... 323
C. Chronic Rupture ..................................................................................................... 323
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
309
310 Schon and Herbst

IX.
Posterior Tibial Tendon.................................................................................................. 338
A. Etiology................................................................................................................... 338
D. Dislocation of the Posterior Tibial Tendon ............................................................ 340
X. Conclusion...................................................................................................................... 341
References .................................................................................................................................. 341
I. INTRODUCTION
Tendon ruptures and lacerations are common conditions affecting the foot and ankle. Understand-
ing 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 ten-
dons, 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, neo-
plasm, 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-
Tendon Ruptures and Lacerations 311
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 progres-
sive 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
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 outcome-
based 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. 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. Occasion-
ally, 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.
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.
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).
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.
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 surround-
ing 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.
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 applica-
tions 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 devel-
oped 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 meso-
tenon, 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 hypovascu-
larity (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].
A. Prerupture Conditions and Treatment

Spontaneous disruption of the Achilles tendon is associated with other disorders, including auto-
immune 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 degener-
ation to increase with age.
During the physical examination it is important to determine the point of maximum tender-
ness. 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. Nonoperative Treatment
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-inflamma-
tories 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 3/8-
in. 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.
II SPR is torn free from its anterior insertion on malleolus, and periosteum of tendons dissects
through at this level.
III SPR is avulsed from insertion on malleolus with avulsion of small fragment of bone.
IV SPR is torn from its posterior attachment as tendon dissects through, with SPR lying deep to
dislocating peroneal tendon.
Source: From Mann, R.A., Surgery of the Foot and Ankle, chap. 18, Table 18.2. With permission.
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, tendolipomato-
sis, 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
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 comorbid-
ities 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.
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 V-
Y 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
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. Immobil-
ization 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].
Conversely, Cetti and Christsen [47] (despite finding no significant difference between opera-
tive 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.
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 nonabsorb-
able 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 weight-
bearing. 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
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 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.
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.
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.
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
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 15̃8 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. PERONEALS
A. 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
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 conser-
vative 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’ prefer-
ence 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 condi-
tions that could arise:
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 radio-
graph demonstrates placement of the suture anchor.
1. Acute fracture of the os peroneum

2. Chronic nonunion or fibrous union of os peroneum fracture (Figure 12.14)
3. Attrition or partial tendon rupture proximal or distal to the os peroneum
4. Complete rupture proximal or distal to the os peroneum
5. Presence of a large peroneal tubercle, which entraps the longus or the os peroneum
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 com-
monly 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.
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.
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 re-
inforces 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 fibrocartila-
ginous 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.
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.
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.
VII. 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 compart-
ment 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.
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].
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.
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 intra-
venous sedation. This permits dynamic evaluation of the release intraoperatively. It can be other-
wise 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 lacer-
ations.
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
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. Post-
operative 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 inter-
osseous 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, longi-
tudinal 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
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.
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.
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 pre-
operative 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 intraopera-
tive 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 recom-
mend 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
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 Continued (C) Coronal MRI demonstrating the dislocation. (D) Intraoperative photo.
X. 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 dysfunc-
tional 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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13
Posttraumatic Infections in the Foot and Ankle
Maria Guidry
Department of Orthopaedics and Rehabilitation, University of Texas Medical Branch, Galveston,
Texas
Brian Hutchinson
Richard T. Laughlin
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
345
346 Guidry et al.
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
2. Treatment............................................................................................................ 361
C. Talus .......................................................................................................................... 362
2. Treatment............................................................................................................ 364
D. Calcaneus................................................................................................................... 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. Trau-
matic 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 man-
agement 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.
Posttraumatic Infections in the Foot and Ankle 347
A. 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 Crypto-
coccus neoformans, Aspergillus spp., Candida, Actinomycetes), Mycobacterium tuberculosis, and
atypical mycobacteria (M. avium-intracellulare, M. marinum) are rare, but are seen in immuno-
compromised 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 mycobac-
teria 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. mar-
inum. 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.
348 Guidry et al.
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. Palpat-
ing 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].
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, noninfec-
tious 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 leukocyte-
labeled 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 debride-
ment 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.
350 Guidry et al.
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 com-
patible 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 corner-
stone 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 (trovafloxa-
cin) cover anaerobes and Gram-positive organisms, including Streptococcus. Coagulase-negative
Staphylococcus may be treated with vancomycin, tetracyclines, clindamycin, Bactrim1 and rifam-
pin, 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, culture-
directed 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
Table 13.1 Gram-Positive Organisms: Initial Choice of Antibiotics for Therapy (Adult Doses)
Organism Antibiotics of first choice Alternative antibiotics
Methicillin-sensitive
Staphylococcus aureus Nafcillin 2 g every 4 h or Cefazolin, vancomycin
clindamycin 900 mg every 8 h
Coagulase-negative Nafcillin 2 g every 6 h or Cefazolin, vancomycin
Staphylococcus sp. clindamycin 900 mg every 8 h
Methicillin-resistant
Staphylococcus aureus Vancomycin 1 g every 12 h or SMZ–TMPa or minocycline +
linezolid 600 mg every 12 h rifampin
Coagulase-negative Vancomycin 1 g every 12 h or SMZ–TMPa or minocycline +
Staphylococcus sp. linezolid 600 mg every 12 h rifampin, clindamycinb
Group A Streptococcus Penicillin G 2Mu every 4 h or Clindamycin, cephalosporin,
Streptococcus pyogenes ampicillin 2 g every 6 h vancomycin
Group B Streptococcus Penicillin G 2Mu every 4 h or clindamycin, cephalosporin
Streptococcus agalactiae ampicillin 2 g every 6 h vancomycin
Sensitive
Streptococcus pneumoniae Penicillin G 2Mu every 4 h Clindamycin, erythromycin
Intermediate
Streptococcus pneumoniae Cefotaxime 1 g every 8 h Clindamycin, erythromycin
Resistant
Streptococcus pneumoniae Vancomycin 1 g every 12 h or Quinupristin–dalfopristin
levofloxacin 500 mg daily linezolid
Sensitive
Enterococcus sp. Ampicillin 1 g every 6 h,c or Ampicillin-–sulbactam,
vancomycin 1 g every 12 h linezolid
Resistant
Enterococcus faecium Quinupristin–dalfopristin linezolid Chloramphenicol þ rifampin
600 mg every 12 h
a
Sulfamethoxazole-trimethoprim.
b
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.
faecium (VRE) pose a problem in postoperative orthopedic patients, especially in diabetics. Pseu-
domonas resistance and Candidemia with residual bone seeding have also been observed. Treatment
regimens for VRE include prolonged treatment with linezolid or quinupristin/dalfopristin. Pre-
ferred 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
352 Guidry et al.
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 Ampicillin–sulbactam

daily or imipenem 500 mg every 6 h
Enterobacter sp. Cefotaxime 1 g every 6 h or imipenem Levofloxacin, mezlocillin,
500 mg every 6 h ticarcillin–clavulanate
Escherichia coli Ampicillin–sulbactam 3 g every 6 h Cefazolin, levofloxacin,
gentamicin, SMZ–TMPa
Haemophilus influenza Cefotaxime 1 g every 8 h or Levofloxacin, SMZ–TMPa
ampicillin–sulbactam 3 g every 6 h ampicillin,b azithromycin
Klebsiella sp. Cefotaxime 1 g every 6 h or Ampicillin–sulbactam,
levofloxacin 500 mg daily gentamicin
Proteus mirabilis Ampicillin 1 g every 6 h or Cefazolin, SMZ–TMP,a
levofloxacin 500 mg daily gentamicin
Proteus vulgaris, Cefotaxime 2 g every 8 h or Mezlocillin, gentamicin
Proteus rettgeri, imipenem 500 mg every ticarcillin–clavulanate
Morganella morganii 6 h or levofloxacin 500 mg daily
Neisseria gonorrhea Ceftriaxone 125 mg IM once þ Levofloxacin þ azithromycin
azithromycin 1 g oral once
Providencia sp. Cefotaxime 2 g IV every 8 h or SMZ–TMP,a amikacin,
levofloxacin 500 mg daily imipenem
Pseudomonas aeruginosa Cefepimec 2 g every 12 h or Ticarcillin–clavulanate,
piperacillin c 3 g every 6 h or tobramycin, amikacin,
imipenem 500 mg every 6 h ciprofloxacind
Serratia marcescens Cefotaxime 2 g every 6 h Levofloxacin, gentamicin,
imipenem
a
Sulfamethoxazole–trimethoprim.
b
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.
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 Ampicillin–sulbactam,

metronidazole 500 mg every 8 h ticarcillin–clavulanic acid
Prevotella sp. Clindamycin 900 mg every 8 h or Ampicillin–sulbactam, cefotetan
metronidazole 500 mg every 8 h
Peptostreptococcus sp. Penicillin G 2mu every 4 h or Clindamycin, metronidazole
clindamycin 900 mg every 8 h
Clostridium sp. Clindamycin 900 mg every 8 h or Ampicillin–sulbactam,
penicillin G 2mu every 4 h metronidazole
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 anti-
inflammatory 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
354 Guidry et al.
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 ceftazi-
dime 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 aer-
obes such as Streptococcus Pneumoniae and Staphylococcus spp. Infections involving lower extrem-
ities 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. 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 clin-
damycin 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; Staphylococ-
cus 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.
356 Guidry et al.
1. 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
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.
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 appropri-
ate antibiotics. Grading of infection based on the above classification may help to guide manage-
ment 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. FOOT AND ANKLE OSTEOMYELITIS

A. 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.
358 Guidry et al.
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 coa-

gulase-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]. Immunocom-
promised 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 Staphylococ-
cus 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 Strepto-
coccus usually cause postoperative osteomyelitis in uncompromised hosts. In the presence of
orthopedic implants, Coagulase-negative Staphylococcus, Staphylococcus aureus, and Propionibac-
terium 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.
Surgical management of postoperative osteomyelitis is similar to that of long bone osteomye-

litis and includes adequate debridement, culture-directed antibiotics, and insertion of antibiotic-
impregnated 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 re-
sponse 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, maintain-
ing 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: ad-
equate 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
360 Guidry et al.
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 mon-
itored. Sequential periodic debridements combined with antibiotics increase the chances for sup-
pression.
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 revascu-
larization 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 interven-
tion 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 infec-
tions 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
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
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
362 Guidry et al.
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
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, frac-
tures 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
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.
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.
364 Guidry et al.
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. Calcaneus
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 per-
formed 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 recom-
mended. 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 debride-
ment. If this is performed quickly, and there is adequate soft tissue coverage, then the surgeon can
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. Preopera-
tive care, timing of surgery, meticulous surgical techniques including adequate soft tissue coverage,
Figure 13.3 (A) Chronic open wound. (B) Sural artery-based rotational flap.
366 Guidry et al.
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
371
372 Vitello
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 sympathec-
tomy 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 hyper-
esthesia, 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 373
Table 14.1 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 dysfunc-
tion 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 stimu-
late 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 substan-
tial 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 inhib-
ition 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.
374 Vitello
A. 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 three-
phase 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 demineraliza-
tion, 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,
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 cor-
rect 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 radionucleo-
tide 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 infor-
mation 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].
376 Vitello
C. 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 administra-
tion 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 laser-
Doppler velocimetry. Lower extremities with RSD manifest consistently abnormal thermoregula-
tory 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 pharmaco-
logic 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-
ing necessitating sympathetic blockade with local anesthetics, sympathetic blocking drugs, or
vasodilating drugs. A myofascial pain component is common in RSD so a nonsteroidal anti-
inflammatory 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]. Amitrip-
tyline 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.
378 Vitello
D. 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. The patient should experience pain relief from sympathetic block on several occasions.
2. Pain relief should last at least as long as the vascular effects of the sympathetic block last.
3. 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.
4. Possible secondary gain motives and significant psychopathology should be ruled out as
possible causes of pain complaints.
E. 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.
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, Orthopaed-
ics, 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 auto-
mobile 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.
381
382 Perry and Manoli
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. Radio-
graphs and careful clinical evaluation [15] are the foundation of surgical intervention. Weight-
bearing 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 hemo-
stasis [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.
Late Reconstruction 383
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 naviculocunei-
form 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. SPECIFIC INJURIES

A. Talus Fractures
Nondisplaced talar neck fractures should be stabilized acutely. In this circumstance, two cannu-
lated 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 contraindi-
cated 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
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
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.

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.
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
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.
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 accommo-
dative 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 Foot compartment Other compartment Arterial
symptoms syndromes syndromes occlusion Neuropraxia
Pressure increase þ þ
Pain with stretch þ þ
Paresthesia þ þ þ
Paresis or paralysis þ þ þ
Pulse intact þ þ þ
Source: From Perry, M.D. and Manoli, A., II, Orthoped. Clin. North Am., 32, 103–111, 2001. With permission.
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 well-
known 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 appreci-
ation of the injury and the anatomy, along with realistic goals, provide the patient with the most
optimal results.
REFERENCES
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602, 1997.
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, high-
energy 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,
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.,
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 osteoar-
throsis 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.
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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
C. Lesser Toe Amputation ............................................................................................. 406
1. Technique ............................................................................................................ 406
2. Complications ..................................................................................................... 406
D. Ray Resections .......................................................................................................... 407
1. Technique ............................................................................................................ 408
2. Complications ..................................................................................................... 408
E. Transmetatarsal Amputations ................................................................................... 410
1. Technique ............................................................................................................ 410
2. Complications ..................................................................................................... 413
393
394 Pleimann et al.
F.Lisfranc’s Amputation ............................................................................................... 413

G.Chopart’s Amputation............................................................................................... 413
1. Technique............................................................................................................ 414
2. Complications ..................................................................................................... 415
H. Syme’s Amputation ................................................................................................... 417
1. Technique............................................................................................................ 417
2. Complications ..................................................................................................... 418
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 recon-
structive techniques, including free-tissue transfer, skeletal fixation, hyperbaric medicine, and
A B
Figure 16.1 (A) Clinical appearance and (B) radiograph of a severe lawn mower injury to the foot.
Traumatic Amputations of the Foot and Ankle 395
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 ampu-
tation, 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 indica-
tions, 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 contral-
ateral 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].
396 Pleimann et al.
Figure 16.2 (A) Partial foot amputation and (B) custom-molded orthotic device.
B. 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
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).
398 Pleimann et al.
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
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]. Transcuta-
neous 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.
400 Pleimann et al.
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 character-
istics 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-weight-
bearing 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 Concentrations
Hemoglobin >11 g/dl
Hematocrit >32%
Total lymphocyte count >1500/ml
Total protein >6.2 g/dl
Albumin >3.5 g/dl
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. CHRONIC MANAGEMENT

A. 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
402 Pleimann et al.
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 limb-
specific 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 prom-
inences 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
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 osteo-
myelitis, while cast immobilization is the mainstay of treatment for acute Charcot neuroarthro-
pathy (Figure 16.10).
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.
404 Pleimann et al.
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 pain-
management 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 understand-
ing 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.

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.
406 Pleimann et al.
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.

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 import-
ant 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 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 hyperexten-
sion of the MP joint. When symptomatic, this is treated with revision amputation at the MP joint
level or extensor tenotomy and MP joint release.

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.
408 Pleimann et al.
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 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.
410 Pleimann et al.
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.

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 proximal-
level 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

412 Pleimann et al.
Figure 16.19 Continued Technique of transmetatarsal amputation: (B) level and direction of bony
resections, (C) tension-free closure.
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.

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, max-
imum 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 lengthen-
ing 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.
414 Pleimann et al.
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.

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.
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,
416 Pleimann et al.
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.

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 Orthosis used for Chopart’s amputation, consisting of an AFO with a custom-molded
insole.
H. 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 ampu-
tation, 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.

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
418 Pleimann et al.
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 subper-
iosteally 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 post-
operative heel pad migration.
Wound closure is performed over a drain, utilizing inverted absorbable sutures in the subcuta-
neous 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 mainten-
ance of the blood supply to the heel pad.
Figure 16.25 Technique of Syme’s amputation: (A) incision, (B) dissection of the talus and calcaneus
and closure.
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.

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.
420 Pleimann et al.
Figure 16.26 Syme’s amputation prosthesis with distal window to accommodate entry of bulbous
stump.
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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17
Orthotic Management of Foot and Ankle Fractures
Géza F. Kogler
Department of Rehabilitation, School of Health Sciences, Jönköping University, Jönköping, 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
423
424 Kogler
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 short-
term, 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. Prefabri-
cated 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, deform-
ity, 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 incorpor-
ated 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,
Orthotic Management of Foot and Ankle Fractures 425
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 transmis-
sion 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 accom-
plish 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 com-
pression 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 circum-
ferential 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
426 Kogler
(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 double-
limb 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
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.
428 Kogler
3. 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 asso-
ciated 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 total-
contact 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, compres-
sion 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.
described by Campbell and Inman [11] for the University of California Berkeley Laboratory, UC-
BL 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.

430 Kogler
B. 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 load-
bearing 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 custom-
molded 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 shock-
absorbing 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
Figure 17.5 A right-foot orthosis designed to decrease loading to fractured sesamoids during weight-
bearing. 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 meta-
tarsal 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 meta-
tarsal 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 custom-
molded 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.
432 Kogler
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 inflam-
mation 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.
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 non-
contoured flat interfaces. Custom-molded arch supports provide additional control in prefabri-
cated 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 UC-
BL 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,
434 Kogler
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 incorp-
orated 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
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).
436 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 manage-
ment within orthopedics. The scope of orthotic intervention is broad, encompassing the full
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 know-
ledge 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.
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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.
439
440 Thompson and Calhoun
and include malunion, nonunion, and infection. Many deformities, such as congenital malforma-
tions, 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 consider-
ation. 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. SIMPLE DEFORMITIES

A. 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 neurovas-
cular 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 con-
nected 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 compres-
sion 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.
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 comfort-
ably, 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. Theoret-
ically, 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.
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
history studies to guide treatment, but there are biomechanical studies that can help guide treat-
ment. 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 multi-
planar 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 nomo-
grams (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 osteo-
tomies 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
‘‘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.

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 weight-
bearing.
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 fix-
ation 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
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 regard-
less 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.
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 preferen-
tially 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 compres-
sion 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 hyper-
trophic 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 non-
union site and the use of autogenous bone graft.
After application of the frame, the proximal and distal ring blocks are compressed intraopera-
tively. 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
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.
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. Al-
though 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 com-
promised 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 fix-
ation, 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
Figure 18.8 (A) Radiograph of a 29-year-old man 3 years after a pilon fracture with severe posttrau-
matic 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 contrac-
ture (burns) but has been more commonly seen at the authors’ institution as the result of over-
correction of the forefoot during equinus correction. Rocker-bottom feet have been treated
Figure 18.9 (A) Preoperative view of severe equinocavus deformity secondary to burns in an 11-year-
old 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.
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 mid-
foot 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 nonosteot-
omy 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.
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 compres-
sion 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. 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, amputa-
tion 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 lengthen-
ing through a metaphyseal corticotomy. (B) Clinical demonstration of the frame before lengthening.
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 neuromus-
cular 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 post-
operative 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.
Figure 18.12 (A) Severe equinocavovarus deformity in a 42-year-old woman with a history of polio-
myelitis 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
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 deform-
ities, 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.
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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
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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
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New York: Marcel Dekker, 2004.
Calhoun: Fractures of the foot and ankle DK2448_index Final Proof page 459 18.2.2005 5:54pm
Index
A Aeromonas spp., 347

Abduction Agent(s)
forefoot, 121, 126, 143, 156 antihypertensive, 377
midfoot, 126 ganglionic blocking, 377
Abduction III, pronation (PAB), 9 vasoconstricting, 289
Abductor Algodystrophy, 373
digiti, 400 mineures, 373
hallucis, 400 reflexes, 373
hallucis fascia, 109 Alloderm, 294
Ablative surgery Allodynia, 372, 374, 404
digital and ray resection, 359 Allograft, 71, 82, 109, 294
midfoot disarticulation, 359 cadaveric, 294
Syme amputation, 359 American Orthopaedic Foot and Ankle Society
transmetatarsal amputation, 359 (AOFAS), 312, 387
Abnormalities Amikacin, 350
gait, 275 Aminoglycosides, 350
hormone, 180 Amitriptyline, 377
Abscess, foot, 180, 349 Amoxicillin, 350
Accident(s), motor vehicle, 123, 200, 381 Amputation
Acetabulum pedis, 51, 146 Chopart’s, 410, 413–417
Achilles tendon, 310, 317–328; see also Tendon foot and ankle, 394–421; see also Foot and ankle
chronic rupture, 323–328 forefoot, 143
operative treatment, 325–328 great toe, 405–406
prerupture conditions and treatment, 318–321 lesser toe, 406–408
nonoperative treatment, 318 Lisfranc’s, 413
operative treatment, 319 nonstandard, 395
rupture, 321–323 Syme’s, 414–417
conservative treatment, 322 transmetatarsal, 410–414
comparison of operative and nonoperative Amputee, transtibial, 46
treatment, 322 Analgesia, 377
operative treatment, 323 aggressive, 378
percutaneous repair, 323 Analgesics, narcotic, 377
Aching, 109 Anastomosis, 247, 274–275, 327–328
Acid microvascular, 267
hydrofluoric, 307 Anesthesiology (ASA), 275
polyglycolic, 18 Angiogenesis, 267, 297, 353
Acinetobacter sp., 352 Angiogram, radionuclide, 375
Acticoat, 293–294 Angiography, 267
Actinomycetes, 347 Angle
Activities of daily living (ADL), 199 Bohler’s, 94, 97, 101–103, 108; see also Bohler’s
Activity, afferent, 373 angle
Adduction, 239 Gissane’s, 97, 101–103, 105; see also Gissane’s
Adduction I, supination (SAD), 9 angle
Adductor hallucis, 206 talocrural, 6, 10
Adductus metatarsus, 212 talometatarsal, 132
Adjunctive therapy, 353 tuber, 94
hyperbaric oxygen therapy (HBO), 353 Angle bone of Gissane, 94
459
460 Index
Ankle Anteversion excessive femoral, 212

anatomy, 2, 212 Antibiotics, topical
arthrodesis, 14, 77–78 antimicrobial therapy, 352
arthroplasty, 21 foot and ankle infections, 352
diastasis, 12 mafamide, 293
dorsiflexion, 4, 434 sulfamylon, 293
equines, 58 transcyte, 293
equinus, 374 xeroform, 293
fracture, 1–23; see Ankle fractures Antidepressants, 377
fracture classification Apligraf, 294
Danis–Weber, 4 integra, 294
Lauge–Hansen, 4 Aponeurosis plantar, 254, 271, 317
injuries, 3, 213 Approach
ipsilateral, 82, 246 anteromedial, 62, 249
joint, 3, 6, 14, 38, 41, 57 dorsomedial extensile, 136
lesser saphenous vein, 14 surgical, calcaneal fractures, 108
saphenous nerve, 14 lateral approach, 108
ligaments, 2 medial approach, 108
sprain, 89 Arbeits-gemeinschaft fur Osteosynthesefragen-
stability, 11 Orthopaedic Trauma Association
stiffness, 434 (AO-OTA), 4
stirrup-style brace, 339 Arch plantar arterial, 121
subluxation, 12 Arizona bracevarus, 76
syndesmosis, 21 Arrhythmias, cardiac, 307
Ankle–foot motion, 424 Artery(ies)
Ankle–foot orthosis (AFO), 325, 416, 424 anastomotic loop of, 247
Ankle fractures, 1–23, 361 anterior tibial, 5, 269, 316
anatomy, 2–4 arcuate, 121
classification of ankle fractures, 4–5 dorsalis pedis, 54, 121, 132, 143–146, 247
dislocation, 21–22 lateral calcaneal, 269
examination (physical, radiographic), 5–7 lateral plantar, 143
incidence and risk, 361 peroneal, 54
osteoporosis, 19–21 posterior tibial, 5, 54–55, 143, 146
postoperative infections, 360–367 sinus tarsi, 54
results (operative, nonoperative, operative thoracodorsal, 279
intervention), 8–9 Arthritis, 8–9, 21, 50, 77, 246
subtypes and treatment, 9–13 ankle, 76, 87
closed reduction and care, 13 degenerative, 145
isolated lateral malleolus, 9–10 inflammatory, 311
medial malleolar, 11 injuries talar, 50
open fractures, 12 osteo-, 70
osteochondral injury, 12 posttraumatic, 9, 45, 55, 69, 89, 246, 383
posterior malleolar, 10–11 septic, 349
syndesmosis involvement, 11–12 subtalar, 59, 62, 87, 114, 383, 385
talar shift, 12 Arthrodesis, 12, 76, 108, 151, 382, 403,
surgical techniques, 13 450
bimalleolar, 15–19 ankle, 77–78
lateral malleolus, 13 Blair type, 65
medial malleolus, 14–15 hindfoot, 76
trimalleolar, 19 pantalar, 65
treatment, 361 primary subtalar, 94
Anorthosis, 430 primary, 106
Antalgia, 139 talonavicular, 155
Anterior colliculus, 2 tibiotalocalcaneal, 384
Anterior inferior tibiofibular ligament (AITFL), triple, 114
4, 9, 197; see also Ligament(s) Arthropathy
Anterior talofibular ligament (ATFL), 2, Charcot foot, 180, 183, 185, 188
197 acute, 181
Anterior tibial tendon (ATT), 64, 310 osteo-, 190
Anterograde flap, 277 Arthroplasty, 14
Anterolateral tibial tubercle, 33 abrasion, 251
Index 461
ankle, 21, 76 Blister(s), 6, 101, 109

joint, 14 clear fluid-filled, 5
interpositional, 159 fracture, 45
Arthroscope, 81 Blockade
Arthroscopy, 12 differential neural, 375
subtalar, 76 sympathetic, 375–377
Arthrosis, 7, 45, 84, 166, 175, 196 Blocker calcium channel, 377
pseudo-, 65, 78 Blocks
posttraumatic, 13, 15, 139, 145, 155 intravenous regional, 377
subtalar, 251, 385 nerve, 377
talonavicular, 147, 152 sympathetic, 378
Arthrotomies, 151 Blood sugar, 180
Arthrotomy, 15, 158 Bohler’s angle, 94, 97, 101–103, 108, 252
anterolateral, 231, 241 Bone
anteromedial, 222 absorption, 257
Articulation acute atrophy of, 373
Lisfranc’s, 122 cancellous, 15, 34, 97, 382
talonavicular, 50 cement, 73
TMT, 121 chondroosseus, 247
Aspergittus spp., 347 contusions of tibia/talus, 198
Asplenia, 347 cuboid, 105, 108
Astragalus, 50 density, 19
Athlete(s), 140, 149, 256 elastic, 212
Atrophy, 109 graft, 35, 65, 109, 158
muscular, 374 grafting, 15, 175, 246
subcutaneous, 374 autogenous, 448
Sudeck’s, 373, 375 healing, 44
Autogenous graft, 79 loss, 50, 73, 180, 383, 387
Autograft, 288, 295, 313, 387 metaphyseal, 215
osteochondral, 82 navicular, 105, 147
Autoimmune disorders, 5 necrotic, 84
Autologous grafting, 325 osteochondral, 212
Avascular necrosis (AVN), 55, 70, 75, 207, osteopenic, 185
249–250 osteoporotic, 15
of distal tibia/talus, 198 scan, 82, 375, 403–404
of talar body, 80 subchondral, 82, 84, 153, 159, 383
of talar head, 67 transport, 38–39
Avulsion fracture, 2 triple arthrodesiscuboid, 94
Axial weak, 19
compression injuries, 214 Bone marrow edema, 82
loading, 147 Bony stability, 2
load mechanism, 27 Boot(s)
brace or cast, 337
B flexible arthrodesis, 436
Bacillus, 347 silicone, 300
Bacteroides fragilis, 352 soft-shelled, 88
Bacteroides spp., 358 walker, 13
Bactrim, 350 Box within a box alignment, 197
Bandage Brace stirrup, 13
Ace, 150 Bracing, 325, 402
Esmarch, 397 functional, 322–323
Bent bone type fracture, 213 Bronchoscopy, 289
Bier block technique, 377 Buckle fracture pattern, 213
Biking, 84 Buddy taping, 177, 257
Bimalleolar fracture fixation, 8 Bunk bed injury, 253
Biobrane, 294 Bupivacaine, 377
Bites, dog and cat, 348 Burn(s), 394, 404
Blair fusion, 384 management, 297
Blair type arthrodesis, 79 plantar, 274
Blindness, 179 wounds, 269
462 Index
Burns, to the feet, 288–307 fractures, 364

complications, 303–304 ankle, 2
dystrophic calcification, 303 incidence and risk factors, 364
Marjolin’s ulcers, 303–304 pilon, 30–31, 37–38
osteoporosis, 303 treatment, 364
pigmentation, 303 midfoot fractures, 158
initial evaluation, 289 paediatric foot, 247, 252
inhalation injury and associated injuries, 289 talar, 78
of burn wound, 289–292 Lisfranc (TMT) injuries complications,
pathophysiology of burn injury, 289–290 143
modern burn care, burn team concept, 288–289 Syme’s amputations complications, 418
prevention, 307 well, 103
reconstruction and rehabilitation, hypertrophic Calcification dystrophic, 303
scars, and contractures, 297–302 Caliper patella-bearing, 75
classification of contractures, 299–300 Cancellous, 94, 153
treatment, 300–302 Cancellous bone, 143
special orthopedic issues, 302–303 Candida, 347
bone and Achilles tendon exposure, 302 Cannulated cancellous screws, 175
fractures, 302 Cantilever effect, 56
involved joints, 303 Capsule joint, 33
special types of burns, 305 Capsulotomy, 153
chemical burns, 306–307 talonavicular, 153
electrical burns, 305–306 Carbonic anhydrase inhibitor, 293
treatment, 291–297 Carboxyhemoglobin, 297
definitive wound coverage, 294–296 Carcinoma
escharotomy, 292 basal cell, 303
hyperbaric oxygen, 296–297 squamous cell, 303
initial wound care, 292–294 Cast(ing)
resuscitation, 291–292 acrylic, 300
immobilization, 229, 322, 434, 436
C mallet, 94
Cadaveric feet, 56 long leg, 216, 222, 231
Caisson disease, 297 serial, 298
Calandruccio clamp, 79 short leg, 105, 151, 155, 216, 252–255
Calcaneal, 99 walking, 150, 156, 254
anatomy, 94–95 total-contact, 185, 188, 191
classification, 98–101 Causalgia, 372–374
Essex-Lopresti system, 98 Cavus, 301
Soeur and Remy system, 98 Cedell’s fracture, 85
Warrick and Bremner system (modified), 98 Cefazolin, 397
complications, 109, 114 Cefoxitin, 73
definitive management, 104 Cells, white blood, 180, 347, 403
extra-articular fractures, 104–106 Cellular injury
intra-articular fractures, 106–108 by acids, 307
fractures, 56, 93–115 by alkali agents, 307
groove, 94 lipid saponification, 307
initial presentation, 101 liquefaction necrosis, 307
management, 101 protein denaturation, 307
mechanism of injury, 95–97 Coagulation necrosis, 307
open calcaneal fractures, 114 Cellulites, 349–350
postoperative management, 109 Center(s)
preferred method of treatment, 108–113 accessory ossification, 229, 254
radiographic examination, 101–103 distal fibula ossification, 212
salvage procedures, 114 epiphyseal ossification, 212
sulcus, 96 Cephalosporin, 350, 397
surgical approach, 108 Cerclage wire, 23
lateral/medial, 108 Cervical ligaments, 56
tuberosity, 33 Charnley compression device, 79
Calcaneofibular ligament (CFL), 2, 197 Checkreins, 2
Calcaneus, 302, 317, 328 Chondrocyte autologous, 89
distraction, 440 Chopart’s amputation, 410, 413–417
Index 463
Chronic Complications in fractures

hypoxia, 358 amputation, 27
lymphedema, 358 infection, 27
Ciprofloxacin, 350, 354 nonunion, 27, 45
Circulation malunion, 45
extraosseous, 54–55 osteoarthritis, 45
interosseous, 54–55 Soft tissue, 73
Clamp(s), 94 Compression
bone reduction, 241 arthrosis, 130
percutaneous bone, 228 fracture of cuboid, 134
reduction, 231 Computed axial tomography (CAT) scan, 332
Weber, 153 Computer tomography, 33
Clarithromycin, 350 Configuration Ilizarov, 41
Classification Congruency joint, 130
AO comprehensive, 29 Contact forces, 2
Hawkins, 70 Continuous passive motion (CPM), 298
of periarticular fractures Contracture(s), 297–302, 389
AO, subtypes, 28 burn, 297
complete articular, 28 classification, 299–300
Claw toes, 299, 389 dorsiflexion, 299
Clawing of lesser toes, 109 equinus, 41, 410
Clindamycin, 350, 352 plantar flexion, 425
Closed reduction, 8; see also Reduction rigid
Clostridium sp., 347, 352, 358 causes of, 439
Closure treatment, 300–302
single-layered, 109 external fixators, 300
tension-free, 43 garments, 301
vacuum-assisted wound (VAC), 71 limb suspension, 301–302
Coalition calcaneonavicular, 155 orthotics, 302
Coccidioides imitis, 347 Corrective orthotics, 318
Cold Corticotomy
intolerance, 376 percutaneous, 446
stress, 376 proximal, 36
Collagen Cosmesis, 78
deposition, 297 Cranioplast, 228, 246
fibers, 301 Crash(es)
Collapse, 89 motorcycle, 394
Colliculus motor vehicle, 43
anterior, 54 C-reactive protein (CRP), 348
posterior, 52, 54 Crepitans, peritendinitis, 311
Comminution, 28, 41, 89, 147, 176, 243 Crepitus
central, 38 audible and palpable, 319
degree of, 62 sensation of, 311
Comorbidities, 5, 274, 313, 320–322, 382 Crescents, tibial and talar, 6
Compartment syndrome, 101, 257 Crest
Complete transverse fractures, 213 anterior tibial, 33
Complex iliac, 65, 155, 158
ankle joint, 19 metaphysis, 34
gastrocnemius–soleus, 410 proximal tibiailiac, 143
lateral subtalar ligamentous, 200 Chronic regional pain syndrome (CRPS), 402
Complex Crush(ing)
Lisfranc, 121, 126–128, 132, 145 injuries, 394
joint, 143 ipsilateral, 46
ligament, 134 Cryptococcus neoformans, 347
midfoot–forefoot, 200 Cuboid, 118, 127–128
sesamoid, 196, 203, 205, 400, 406 Cuff, pressure, 6
TMT, 156, 159 Cuneiform(s), 41, 118–121, 127–128
TMT-Lisfranc joint, 118 medial, 167
Complex plantar plate-sesamoid (CPPS), 205 Roman arch configuration of, 119
Complex regional pain syndrome (CRPS), Curettes, 143
371–378 Cuts axial, 33
464 Index
Cycling low-resistance, 83 loss of height, 385

Cysts subchondral, 84 lateral impingement, 385
midfoot dorsiflexion, 442
D neuromuscular, 456
Damage neuropathic (Charcot) foot, 180
articular, 45 osteomyelitis, 180
bone and ligamentous, 5 persistent, 220
cartilage, 27 planus foot, 121
contusional, 30 planovalgus, 145
iatrogenic, 220 progressive, 246
neurovascular, 274 flatfoot, 311
soft tissue, 9, 45, 123, 167 residual, 220, 243
Danis–Weber classification, 5 rotational, 246
Deafferentation, 373 simple, 440
Debridement, 65, 134, 257 arthrodesis, 450
surgical, 353 distal tibial angular deformity, 443–444
Debulking, 275 equinus contracture, correction, 440–443
Defect(s) external fixation technique, 446
calcaneal, 271 osteotomy with internal fixation, 444
cancellous, 35 simple nonunion, 448
metaphyseal, 35–36, 39 techniques to address, 440
osteochondral, 79 tibial, 359
Definitive toe, 312
fixation, 114, 131, 152 varus, 36, 155, 185
reduction, 131 Degeneration
wound coverage, 294–296 collagen, 318
Deformation cavus, 123 mucoid, 319
Deforming forces tendon, 339
abduction, 4 Deltoid ligament, 2, 61
adduction, 4 complex, 2
external rotation, 4 Denervation, 143
Deformit(y)ies Depression, 376
angulatory, 428, 431 Destruction Charcot type, 123
bony, 439–440 Devascularization, 143
burn, 301 Device(s)
cavus, 450 bridging, 36
Charcot midfoot, 189 buttress, 36
chronic nail, 404 Doppler, 450
classification Diabetes, 5, 115, 274, 288, 311
simple/complex, 440 mellitus, 375, 395
complex Diaphysis, 172
bony nonunions, 440 Diabetic foot osteomyelitis, 358
contractures, 301, 440 Diabetic patients, foot and ankle fractures, 179–191
equinocavus, 440, 452 Diastasis, 98, 126, 131, 140, 121
equinus, 450 ankle joint, 214
rocker-bottom deformity, 440, 451–453 distal tibiofibular, 212
congenital recurrent, 136
malformations, 440 residual, 132
planovalgus, 339 subtle, 126–127
donor site, 279 tibia–fibula, 231
equines, 425, 428 Diffuse osteopenia, 374
fibrous, 390 Direct-force injury, 157
foot, 101, 143, 179, 311 Disc herniation, 310
flat foot, 338 Discharge sympathetic, 373
foot and ankle, 439 Disease(s)
forefoot, 109 autoimmune, 318
hallux, 176 cast, 15
hallux valgus, 145 cerebrovascular, 348
heel varus, 385 ischemic peripheral vascular, 180
hindfoot, 76, 339 peripheral arterial, 348
interphalangeal joint, 338 peripheral vascular, 5, 132, 374, 394–395, 399
Index 465
posttraumatic degenerative, 403 joint, 126

vascular, 274 Lisfranc’s ligament, 126, 131, 147, 139
Disimpaction with mallet casting, 94 naviculocuneiform, 155
Dislocation, 3, 42 posterior tibial tendon, 127–128
ankle, 196–199, 243 synchondrosis, 149
clinical findings, 197–198 syndesmosis, 231, 237
epidemiology and anatomy, 197 Dissecans, 156
pathogenesis and history, 197 Dissection subperiosteal, 133
prognosis and long-term follow-up, 199 Distal joint, 2
radiographic findings, 198 Distal reverse flow flap, 277
treatment options, 199 Distal tibial, 8
dorsal or plantar, 123 metaphyseal region, 213
great toe MTP dislocation, 203–207 physis, 212–213
clinical findings, 204 Distraction, 241
epidemiology and anatomy, 203 Distractor, 384–385, 389
pathogenesis and history, 203–204 AO, 33
prognosis and long-term outcome, 207 external, 152
radiographic findings, 205–206 Divers ‘‘bends,’’ 297
treatment options, 205–207 Dog ears, 405
hindfoot (talus, navicular), 185 Doppler
Lisfranc fracture, 134, 170, 203, 382, 390 device, 450
midfoot (tarsometatarsal), 188 examination, 6
MTP, 127–128, 130, 207 laser flowmetry, 317
peroneal, 333 studies, 267
peroneus brevis, 331 Dorsalis pedis artery, 54, 136, 143
plantar, 124 Dorsiflexion, 121, 126, 166, 197, 331, 337
posterior tibialis, 340 ankle, 11, 18, 413–414
stalonavicular, 153 force, 56
subluxation or frank, 59 of ankle, 88
subtalar, 60, 252 forced, 248
clinical findings, 200–201 metatarsal, 440
epidemiology and anatomy, 200 Dorsiflexor, 310
joint, 199–203 Drainage, 45
long-term results and prognosis, 203 Dressing
pathogenesis and history, 200 biosynthetic, 294
radiographic findings, 200–201 alloderm, 294
treatment options, 201–202 apligraf, 294
subtalar, 340 apligraf integra, 294
subtle Lisfranc, 127–128 biobrane, 294
talar, 50–89 compression, 45
head, 58 Jones, 101
talonavicular, 56, 87 postoperative, 44
talus, 68 topical, 294
tarsometatarsal joint, 183 Drift
toe, 301 valgus, 400
Displacement(s), 2, 10, 28, 59, 231 varus, 400, 406
articular, 222 Drilling transmalleolar, 84
initial, 9 Dry skin, 180
intra-articular, 6 Dynamic compression plates (DCPs),
physeal, 243 382
posterior tibiofibular joints, 40 Dysfunction, 121
residual, 11, 132 leukocyte, 185
risks of, 13 progressive posterior tibial, 126
rotatory, 173, 176 sympathetic nervous system, 373
sagittal plane, 167 vasomotor, 372
subtalar, 68 Dysrhythmias, 305
ankle dislocation, 56 Dystrophy
congruous ankle, 56 posttraumatic, 373
TMT joints, 139 reflex neurovascular, 373
Disruption, 21 reflex sympathetic, 145, 371–378,
deltoid ligament, 6, 9 247
466 Index
E Fentanyl, 377
Ecchymosis, 56, 148 Fibers, soleus, 317
plantar, 126, 204 Fibrosarcoma, 303
Edema, chronic traumatic, 373 Fibula, 2–23, 28, 30–41, 50
Edwardsietta tarda, 347 displacement, 2
Effect, medial buttressing, 44 distal, 15, 21
Enterobacter sp., 352 fracture, 5
Enterococcus sp., 347, 350–351, 358 periosteum, 14
E. faecium, 351 shortening fixation of, 32
Entrapment Fixation, 9, 11, 17, 23
nerve, 143 absorbable pin, 224
sural nerve, 323 antegrade, 62
Epiphyseodesis, 228, 246 anatomic reduction, 118
Equines, 31 AO Association for the Study of Internal Fixation
resting, 323 (ASIF), 9
Equinocavus, 311 arthroscope-assisted, 85
Equinovarus, 413–415 bimalleolar, 12
Equinus, 59, 85, 301 circular, 34
subtle, 413 definitive, 30–31, 37, 152, 249
Erysipelothrix sp., 347 delay of, 30
E. rhusiopathiae, 347 delayed, 12
Erythema, 289 extensive, 15
Erythrocyte sedimentation rate (ESR), 348 external, 73, 346, 398
Eschar burn wound, 288 in Lisfranc injuries, 132, 143
Escharotomy, 292 in midfoot fracture, 153
Escherichia coli, 352 in pilon fracture, 35–45
Ethambutol, 350 fibular, 22–21, 33
Eversion, 241 half-pin, 39
passive, 132 hybrid, 39
stresses, 2 initial, 34, 69
Examination interfragmentary screw, 170
Doppler, 6 internal, 94, 241, 346, 382
neurovascular, 6 arthroscope-assisted, 89
radiographic, 6 in ankle fracure, 12–13
Excision early wound, 288 in Lisfranc injuries, 132, 144
Exostectomy, 177 in metatarsal and phalanges fracture, 167, 173
calcaneal, 385 in midfoot fracture, 150, 153, 156
Exostosis, 329 in pilon fracture, 32–44
painful bony, 145 in talar fractures and dislocations, 50, 59, 78, 83
Exposure bone and Achilles tendon, 302 intramedullary screw, 174
Extended steel shank, 136 Kirschner wire, 249, 252
Extensile dorsomedial approach to midfoot, 137–138 in Lisfranc injuries, 140, 153
Extensive scarring, 358 metatarsal and phalanges fracture, 167, 170, 175
Extensor lag screw, 36–39, 151
digitorum brevis, 62, 313, 400 medial, 15
digitorum longus (EDL), 62, 64, 310, 414 multiple-plane, 41
hallucis brevis, 136, 313, 400 open reduction, 106
hallucis longus (EHL), 136, 310 open reduction and internal (ORIF), 360–361, 434
Extensors, long toe, 312 in ankle fracture, 10, 12, 19, 21
External fixator, 101 in calcaneal fracture, 106, 114
Extremes of age, 358 in pediatric foot and ankle fracture, 229–243,
Extremity contralateral, 246 249–253
in talus fracture, 62, 76, 85, 87, 89
F operative, 94
Falls from heights, 147, 253 percutaneous
Fascia, 136 pin, 170
Fascia plantar, 406 screw, 59
Fasciocutaneous flap, 280 pin, 59, 143
Fasciotomy, 109 plaster, 131
Feet neuropathic, 126, 288 plate, 33–36, 77
Femur, distal, 34 plate and screw, 170
Index 467
primary, 115 tertius flaps, 269

rigid internal, 50, 106, 151, 188 tibialis anterior, 269
ring, 41 radial forearm, 276
screw, 77, 152 sensate fascial, 275
smooth-wire, 217 skin, 414
stable, 15 suitability for a free, 275
surgical, 155 sural artery, 271
syndesmotic, 19–21 thrombosed, 275
temporary, 30 walking tube, 274
tibiotalar pin, 69 Fleck sign, 128
Fixator(s) Flexion
external, 106, 167, 301 interphalangeal (IP), 337
arthrodesis external, 12 neutral, 102
hybrid external, 42–44 planta, 84, 147, 239
in Lisfranc injuries, 132–134 Flexor
in midfoot fracture, 152–153, 157 ankle, 336
in pilon fracture, 30, 31, 38–39, 42 digitorum brevis, 269, 271, 400
in talar dislocation, 77 digitorum longus (FDL) tendon, 310
medial external, 30, 33 hallucis longus (FHL) tendon, 52, 94, 310
medial spanning external, 32, 34 Flowmetry laser, Doppler, 317
ring external, 43–44 Fluid
Ilizarov, 39, 246, 301 requirements, 291
internal, 157 synovial, 228
lateral, 132 Fluoroquinolone, 318
Flap(s) Fluoroscopy, 132
cross leg, 274 intraoperative, 109
free, 276–281 Fools, 2, 23
gracilis, 279–280, 400 Foot
lateral arm flap, 280–281 abscess, 180
latissimus dorsi, 278–279, 400 burns, 292
paxascapulax, 279–280 cavovarus, 155
radial forearm flap, 276–277 Charcot, 185, 190–191
reconstruction, 273–276; see also compartment syndrome, 396
Reconstruction contralateral, 6
rectus abdominis, 277, 400 crushed, 133
serratus anterior, 279, 281 deformity, 179
lateral arm, 280 dorsiflexed, 311
rectus femoris, 280 dorsiflexion of, 85
scapular, 280 dorsum of, 6
temporal parietal fascia, 280 dysvascular, 198
tensor fascia lata, 280 equinovarus deformity of, 77
lateral calcaneal, 270 eversion of, 148
latissimus, 402 fractures, 50, 165–177, 213
local (pedicle), 269–273 fractures of I metatarsal, 167–169
dorsalis pedis artery, 273 fractures of lesser metatarsals, 167, 170–175
lateral calcaneal artery, 269–271 metatarsals, 167–175
medial plantar, 271–272 phalanges, 175–177
sural fasciocutaneous, 271, 273 injured, 126
muscle, 400 injury, 148
abductor digiti minimi, 269, 400 insensate, 274
abductor hallucis brevis, 269, 400 inversion, 310
extensor digitorum brevis, 271, 400 ischemic, 143
extensor hallucis brevis, 400 narrowing, 407
flexor digitorum brevis, 269, 271, 400 orthoses, 185
intrinsic muscle, 269 orthosis, 432
pedicle muscle, 269 plantar, 399
neurosensory fasciocutaneous, 275 plantargrade, 143, 185, 191, 384
osteocutaneous, 280 position (supination or pronation), 145
pedicle muscle, 269 pronation of, 145
peroneus brevis, 269 pump, 101
soleus, 269 residual, 395, 399–400
468 Index
Foot (continued) articular, 114

socket, 51 avulsion, 85, 105, 156, 215, 254
supination of, 94, 99, 145 displaced, 106
truss action, 425 dorsal, 146–148
ulcers, 179, 348 of metatarsal, 128
varus hind, 250 midfoot, 147–151
with varus inclination, 76 tuberosity, 146, 148
Foot and ankle type, 10
fractures in diabetic patients, 179–191 blisters, 5, 45
calcaneus, 185–188 fluid-filled and blood-filled, 5
Charcot foot, 185 Boyd’s classification of talar body, 70
displaced or unstable, 182, 184 calcaneal, 93–115, 384–385, 433
forefoot, 188 in children, 252
hindfoot, 185, 188–189 incidence and risk factors, 364
midfoot (tarsometatarsal), 188 treatment, 364
susceptibility, 180–181 closed, 30, 42
undisplaced, 180–183 grades 0, I, II, and III, 29
wound healing, 179–180 coding and classification of
fractures, orthotic management, 423–437 OTA committee for, 28
determination of pain reduction potential, 426 common signs
mechanical function and control mechanisms, distortion of the normal anatomy, 101
424 ecchymosis, 101
negative impression technique considerations, swelling, 101
428 tenderness, 101
orthotic principles and biomechanical complications after calcaneus
considerations, 425 early and late, 109
orthotic treatment of fractures, 429 compression, 105, 156–157
prefabricated vs custom-molded, 424 coronal, 70
infections, 352 cuboid, 127–128, 253, 387, 389
antimicrobial therapy, 352 compression, 156–157
posttraumatic infections, 346–365 cuneiform, 127–128, 156
soft tissue coverage, 266–282 diaphysisintra-articular, 28
mechanism, 267 posterior, anterolateral and anteromedial, 28
nonoperative coverage of wounds, 268 dislocation, 9
nonoperative treatment, 267–268 displaced, 216, 249
operative treatment, 268–282 foot or ankle, 183
patient evaluation, 266–267 minimally displaced, 96
reconstruction, 267 distal fibula, 18, 21, 23
wound evaluation, 266 isolated, 13
wound management principles, 267 supination-external rotation, 13
trauma, 346 distal tibial pilon, 13, 15
traumatic amputations, 394–421 dorsal avulsion, 147–148, 150
assessment and acute treatment, 395–399 extra-articular, 104
chronic management, 401–404 extremities, 190
specific amputation levels, 404–420 fibula, 17, 20, 197, 212, 241
subacute management, 398–402 long spiral, 229
Football, 203 transverse, 216
Footwear, therapeutic/protective, 184–185, 191 foot, 50, 213, 247
Force(s) foot and ankle, 381
avulsion, 147 in diabetic patients, 179–191
compressive, 97 orthotic management, 423–437
crushing, 123 pediatric, 212–257; see also Pediatric foot and
external rotation, 236 ankle
Forefoot, 126, 165, 191, 364–365 forefoot, 126, 191, 364–365
Fracture growth plate, 241
ankle, 1–23 Hawkins III, 65
incidence and risk factors, 361 impact, 9
operative/nonoperative treatment, 8 intra-articular, 96, 98, 104, 106
outcome, 7 ipsilateral tibia, 237
poor fixation, 7 ipsilateral tibial shaft, 243
Weber classification, 9 joint depression type, 97
Index 469
juvenile Tillaux, 229, 241 tongue type, 97, 99, 252

Lisfranc, 183 transitional, 222, 229
malalignment, 2 transverse, 241
malleolar, 23, 436 triplane, 214, 229, 236–237, 241
bimalleolar, 8, 10, 15, 22–23 tuberosity, 252
medial, 12, 15 undisplaced, 106, 180–181
multi, 9 Weber types
trimalleolar, 3, 11 B, 9, 21, 197
unimalleolar, 9 C, 9, 12 14, 83, 197
malleolus, 9–10, 13 Fragment(s)
posterior, 19 anterolateral epiphyseal, 229, 237, 241
metaphyseal, 39, 237 anteromedial (sustentaculum or constant), 96
metatarsal [MT], 156, 167–175, 203, 430 avulsed, 106
metatarsals and phalanges, 165–177 larger avulsion, 150
anatomy, 166 depression of, 98
mechanism of injury, 166 metaphyseal, 217, 224, 237
phalangeal fractures, 167, 175–177 osteochondral, 134
radiographic evaluation, 166–167 posterolateral (tuberosity), 96
midfoot, 126, 364–365 superomedial, 99
navicular, 56, 133, 156 sustentacular, 108
nondisplaced, 11, 96, 151, 173 talonavicular, 153
nutcracker type, 156, 253 thalamic, 97
open, 29, 56, 257, 346 Thurston-Holland, 216
ankle, 5, 12 tuberosity, 96, 99, 108
calcaneal, 114 unreconstructable, 153
pilon, 35 Fragmentation, 89
osteochondral, 83, 251 Frame(s)
pattern, 2, 28 cavus frame, 452
Essex-Lopresti, 96 equinus, 452
fibular, 28 Galveston equines, 440
phalanges, 175–177 Ilizarov, 78
hallucal fractures, 175 shalf-pin, 132
lesser toe fractures, 176 Taylor spatial, 42
pilon type, 10, 27–46, 243, 360; see also Pilon Frostbite, 394, 404
fractures Frustrum, 50, 52
plafond Fulcrum, Achilles tendon, 97
incidence and risk factors, 360 Fusion
treatment, 360–361 Blair-type, 70, 384
postoperative infections, 360–367 delayed, 65
pronation-external rotation simulated, 12 interpositional, 159
reduction, 423 primary
rigidly fixed fibular, 9 subtalar, 65, 89, 114
sagittal plane, 36, 70 tibiotalar, 65
Salter-Harris types talonavicular, 152
I and II, 213, 215 tibiocalcaneal, 65, 70, 78
III and IV, 222, 224 tibiotalocalcaneal, 80
sesamoid, 430
spine, 190 G
stabilization and maintenance, 423 Gait, 94, 145
plaster of Paris, fiber resin tape, metals, and abnormalities, 145, 275
plastics, 423 analysis, 8, 139
stress, 180, 183, 185, 255–257, 374, 430 biomechanics of, 50
subtle compression, 127–128 cycle, 166
talar, 50–89 dysfunction, 400
talar neck, 56, 248 impairing, 156
talus, 42, 383 stance phase of, 159
tarsal bone, 93, 125 velocity, 420
tarsometatarsal joint, 387 Gastroc slide, 413
tibial, 28, 197 Gastrocnemius, 201, 317, 390
shaft, 9, 311 Gentamycin, 397
tillaux type, 214, 222, 236, 241 Gissane, angle of, 97
470 Index
Gissane, boneangle of, 94 Hyperbaric oxygen (HBO), 267–268, 296–297

Gissane’s angle, 101–103, 105 therapy, 353
Glycocalyx, 358 Hyperdysfunction sympathetic, 376
Gracilis, 279, 400 Hyperemia, 404
Graft(ing) Hyperesthesia, 372
autogenous, 78 Hyperflexion, 156, 302
cancellous, 158 plantar of forefoot, 123, 124
interpositional arthroplasty, 143 Hyperglycemia, 179–180, 288, 305, 307
keratinocytes, 295 Hypermobility heel pad, 419
local bone, 76 Hyperparathyroidism, 180
polytetrafluoroethylene, 274 Hyperpathia, 372, 374
skin, 257, 402 Hypersensitivity, 374
sliding tendon, 313 Hypertension, 348
tendon, 316 Hyperthermia, 374
tibial, 78 Hypertrichosis, 374
tricortical, 158–159 Hypertrophic pseudarthrosis, 448
iliac crest, 387 Hypertrophic scars, 297–302
Gram-negative organisms, 347 Hypertrophysynovial, 337
Gram-positive cocci, 347 Hypesthesia, 372
Greenstick (bent bones) fracture, 213 Hypocalcemia, 307
Groove, calcaneal, 94 Hypochondriasis, 376
Growth disturbance, 228 Hypoplasia, 197
Growth factor, platelet-derived (PDGF), 267–268 Hypothermia, 374
Growth plate Hypothesis vicious cycle, 372
crush (Salter-Harris type V), 214 Hypovolemia, 289
injuries, 213 Hypoxia, 180
Guanethidine, 377 Hysteria, 376
Guidewire, 19, 84, 134, 224
I
H Ilizarov construct, 42
Haemophilus influenza, 352 Images, plain stress, 128
Hallux, 175, 313–317, 336–337, 400 Imaging, magnetic resonance (MRI), 311, 348,
rigidus, 207 403
valgus, 406–408 in ankle dislocation, 198
Hardcastle’s classification, Lisfranc disruptions, in ankle fracture, 11, 213
125 in talar fracture, 58
types A, B, C, 125 Lisfranc injuries, 118
Hawkins classification scheme, 248 Imipenem, 350
types I, II, III, 89 Immobilization
Hawkins classification cast, 255
Heel postoperative, 299
lifts, 425, 432 Immune deficiency, 185, 358
pad plantar, 417, 419 Immune disease, 358
varus-valgus alignment, 109 Immunosuppression, 358
Hematoma(s), 14, 30, 109, 134, 323 Impaction, 28
subungual, 176 degrees of, 27
Hemoglobin glycosylated, 348 Impaired immune response, 180
Hemoglobin, 305 Implants, 36
Hemostasis, 382, 397 artificial tendon, 323
Hernia, transverse rectus abdominis myocutaneous carbon fiber, 323
[TRAM], 277 collagen tendon, 323
Hindfoot, 57, 139, 201, 338, 430 Marlex mesh, 323
calcaneus, navicular, 200 prosthesis, 323
dislocations of the (talus, navicular), 185 bioabsorbable, 89
eversion, 2 Incision(s), 65
varus, 374 dual, 76
Hockey players, 310 fishmouth type, 406, 414, 417
Human immunodeficiency virus (HIV), 347 Oilier, 66, 77, 88
Humerus, 280 tibial, 33
Hydrocholecalciferol, 180 Incisura fibularis, 6
Hydrotherapy, 303 Incongruity articular, 222, 231, 241, 246
Index 471
Index lawn mower, 394

ankle-brachial (ABI), 348, 399 Lisfranc, 123
high body mass, 109 talus, 70
toe-brachial (TBI), 348 cuboid, 156
Infection(s), 29, 50, 55 deep deltoid, 10
erythema, 357 deltoid ligament, 12
foot and ankle direct, 123–124
abscess, 347 displaced Lisfranc, 123, 139
bacterial, 347 distracting, 126
bone infections, 346 divergent, 126
cellulitis, 347 dorsiflexion, 50
classification, 347 pronated, 85
constitutional symptoms, 347 electrical, 302, 305
diabetic, 347 extensor hallucis longus, 205
diagnosis, 347 external rotation, 12, 241
fractures, 347 extra-articular, 44
fungal, 347 falls from ground level/height, 123
host factors, 346 fibula, 12
immunocompromised, 347 flexor hallucis longus, 205
necrotizing fasciitis, 347 foot, 46
osteomyelitis, 347 foot and ankle, 45, 381
postoperative, 347 frostbite, 297, 394, 398
posttraumatic, 346–365 Gustilo type, 114
septic arthritis, 347 gunshot, 394
soft tissue infections, 346 Hawkins type IV, 67
trauma, 347 head and thoracic, 381
pin track, 39, 45, 355 high-energy, 126, 394
postoperative infections, 190, 360 calcaneal, 96
pseudomonal, 257 midfoot, 148, 156
soft tissue, 297 talar body, 70
Inferior retinaculum, 310 indirect-force, 123–124
Inflammation, 45 industrial setting, 394
nonspecific markers of, 348 inhalation, 289
Inflow, vascular, 183, 185 intra-articular growth plate, 257
Influenza, haemophilus, 352 ipsilateral, 205
Injury(ies) ischemiavascular, 143
acid, 307 lacerating trauma, 394
acute lawn mower, 257, 394, 407
neglected, 126 ligamentous, 9, 197, 199, 214, 387
sprain, 125 Lisfranc, 118, 124, 156, 159
ankle neuropathic, 132
extent, 5 pediatric foot, 253
pattern, 5 mechanism of, 5, 229, 394
associated injuries, 5 midfoot, 213
alkali, 307 hindfoot/midfoot bones, 126–128
athletic, 126 low-energy, 95
avulsion, 274 lower leg, 45
axial load mechanism of, 27 maisonneuve, 213
primary articular cartilage damage, 27 medial
blast, 395 diastasis, 144
blunt, 311 malleolar, 11
burn motorcycle, 197, 394
pathophysiology, 289–290 nerve, 372
calcaneocuboid, 155 neuropathic, 123
calcaneus, 198 neurovascular, 199
associated, 101 occult tendon, 127, 198
chronic neuropathic, 125 open, 30, 139
chronic repetitive, 147 os trigonum, 198
crush, 213, 228, 257 osteochondral, 9, 12, 213, 251
pilon, 44 overuse, 311
industrial setting, 394 pattern, 139
472 Index
Injury(ies) (continued ) ankle and subtalar, 55, 76

pediatric burn, 302 anterolateral, 229
pronation-external rotation (PER), 9 aviculocuneiform, 152
renal, 305 calcaneal cuboid (CCJ), 62, 97, 103, 109, 425
Salter-Harris type, 214, 228 midfoot, 145–147, 156–159
Sanders classification types, 114 calcaneus, 147
severe degloving, 399 subluxation of, 147
sites of, 200 capsule, 2
soft tissue, 196, 252 Chopart’s, 145, 156
Lisfranc, 127–128, 139 contractures of the toes and ankles, 268
pilon, 27–30, 35, 41–42 debri, 196
sports, 123 dislocation tarsometatarsal, 183
subtle, 126 dislocation
subtle joint, 140 ankle, 196–199
supination-adduction, 10 great toe metatarsal-phalangeal (MTP),
supination-external rotation (SER), 9–10, 214 203–207
supination-inversion (SI), 214 subtalar, 199–203
syndesmosis, 6, 11, 212, 241, 389 hallux MTP, 313
talar, 67, 80 inter cuneiform, 145, 151
talar neck, 50–51 interphalangeal (IP), 175, 299, 338, 406
tarsometatarsal, 253 Lisfranc, 131, 430
tendon, 9 metatarsocuboid, 172
thermal, 394 metatarsocunieform, 118
turf toe, 203 metatarsophalangeal (MTP), 166, 175, 299, 317,
types, 214, 228 338
calcaneal, 114 great toe, 205, 406
great tow, 205, 207 lesser toe, 407
talar, 76 orthotic treatment, 429
venous, 199 paediatric foot, 254
Insertion metatarsophalangeal-interphalangeal, 257
Achilles tendon, 97, 252 midfoot or forefoot TMT, 126
extensor hallucis longus, 405 naviculo cuneiform, 139, 145, 153, 155
tibialis anterior, 121 subtalar, 200–201, 384, 424
tendinosis, 325 ankle, 61
Instability calcaneal, 94, 99, 108
ankle syndesmotic, 18, 20 midfoot, 155
chronic, 199 surgical treatment, 78
hindfoot, 203 talar, 84, 88–89
midfoot, 126 talar neck, 50, 59
MTP joint, 207 subtaloid, 98
Insulin, 180 talocalcaneal, 200
Integrity plantar plate, 205 talocrural, 197, 424, 434
Interobserver reliability, 5 talofibular, 89
Interposition soft tissue, 131 talonavicular, 50, 62, 67, 200–201
Intervention midfoot, 145, 147, 151–155
operative, 13, 241 orthotic treatment, 432
orthotic, 430 tarsometatarsal (TMT), 130, 140, 156–159,
surgical, 21, 109 413
aggressive surgical, 13 tibiofibular, displacement, 40
Intraepiphyseal, 224 tibiotalar, 50, 78, 383–384, 417
Inversion transverse tarsal
passive, 132 talonavicular and calcaneocuboid, 413
plantar, 239 transverse tarsal, 145
Iontophoresis, 318 Jones
Irrigation, copious, 14 dressing, 101
Irritation posterior tibial tendon, 13 fractures, 172
Ischemia, 46 Junction
metaphyseal-diaphyseal, 45, 255
J musculotendinous, 317
Joint naviculocuneiform, 134
ankle, 52, 316, 383 Juvenile osteonecrosis, 79
Index 473
K posterior talocalcaneal, 52
Keratinocytes, 267–268, 294 posterior talofibular (PFL), 52, 84, 197
Keratosis, 175 posterior tibiofibular, 19, 40
Kirschner wire remodeling of the ruptured, 131
in ankle fracture, 15, 17, 22 sprains, 213
in calcaneal fracture, 108–109 spring, 200
in metatarsal fracture, 167, 173 superomedial calcaneal navicular, 51
in midfoot fracture, 136, 152–153 syndesmotic, 11
in pediatric fracture talocalcaneal, 94
ankle, 217, 220, 228, 231 talofibular, 328
foot, 249, 254 talonavicular, 146, 147
in talar fracture, 84 tarsometatarsal, 140
in treatment of Lisfranc injury, 132 tibiafibula, 328
Klebsiella sp., 352 tibionavicular, 146, 147
Ligation, 134
L Limb
Lacerating trauma, 394 contralateral, 246
Laceration(s), 83, 323 vascular status of, 185
acute indirect, 311 Line sagittal fracture, 237
tendon, 339 Linked toe, 128, 130
Latissimus dorsi, 279, 400 Liposarcoma, 303
Leg distal, 30 Lisfranc disruptions types
Lesions divergent injuries, 125
anterolateral, 251 partially incongruent injuries, 125
grade III and IV, 83 totally incongruent injuries, 125
of talus Lisfranc injuries classification
chondral, 80 displacement in the coronal plane, 125
osteochondral, 80 divergent dislocations, 125
osteochondral, 198, 375 homolateral dislocations, 125
posteromedial, 251 partial dislocations, 125
stage III and IV, 84 Loss
tibial, 84 of bone, 383, 387
transchondral, 82 of eversion, 76
Levofloxacin, 350 of fixation, 155
Lidocaine, 337, 377 of motion, 146
Ligament(s) of protective sensation, 180–181, 185, 190
ankle, 21 of supination, 156
anterior inferior tibiofibular (AITFL), 3, 197, of soft tissue, 274
229 Low contact dynamic compression plate (LC-DCP),
anterior talofibular (ATFL), 87, 105, 197, 200 14
bifurcate, 87 Lower extremity trauma, 374
calcaneofibular (CFL), 108, 197, 200, 328 Lucency subchondral, 249
calcaneonavicular (spring), 146 Lund-Browder chart, 290
calcaneus talocalcaneal, 52
cervical, 52–53, 87, 200 M
deltoid, 146, 197, 200, 247 Madura foot, 347
in ankle, 6, 11, 13, 15, 21 Mafamide, 293
in talar, 52, 54 Major vessel compromise, 358
intercuneiform, 118 Malalignment, 50
intermetatarsal, 118–119 forefoot, 151
interosseous, 94–96, 167, 200 hindfoot, 382
talar, 52–56 lower-extremity, 212
tibiofibular, 3 rotational, 66
intersesamoid, 203, 205 sagittal, 65
lancinate, 338 talar neck, 65
Lisfranc, 118–120, 134, 136, 139–140 varus, 250
medial subtalar talonavicular, 200 Malignancy, 358
naviculocuneiform, 147 Malleolar
otaxis, 33, 152 medial, 17, 56, 62, 83, 231
posterior inferior tibiofibular (PITFL), 3, 9, medial osteotomies, 70
197 osteotomy, 64, 73
474 Index
Malleoli (growth plates), 27, 78, 213 tibial, 15

instability Metatarsal(s), 165
residual, 10 base, 31
rotational, 10 forefoot, 118
translational, 10 Metatarsalgia, 143, 167, 390, 400, 430
medial and lateral, 9 Metatarsophalangeal (MTP) joint, 310, 336
medial and posterior, 20 Methadone, 377
Malleolus, 102, 108, 271, 328–331 Methicillin, 350
ankle, 18 Metronidazole, 352
lateral, 94, 229, 269 Microorganisms, invading, 346
ankle, 9, 11, 13 Midfoot, 139
medial, 338, 340, 383 anatomy, 145
ankle, 13–15, 18, 22, 197 bone, 118
midfoot, 152 dislocation (tarsometatarsal), 188
paediatric foot and ankle, 212, 222, 237, 248 fractures, 145–159
pilon, 33, 41 postoperative infections, 364–365
talar, 50, 55, 62, 78 navicular fractures, 146
pilon, 34 classification and mechanism of injury,
posterior, 33 146
talar, 85 diagnosis, 148
Malnutrition, 358, 395 treatment, 150–159
Malreduction, 383 Migration, keratinocyte, 267–268
degenerative joint disease, 2 Minimum inhibitory concentration (MIC),
Malunion(s), 45, 55, 59, 80, 250 350
calcaneal, 385 Minnesota Multiphasic Personality Inventory
equinus, 246 (MMPI), 376
progressive, 246 Model, cadaveric fibular malunion, 10
sagittal plane, 246 Molding, closed manual, 94
talar neck, 76 Mood elevation, 377
valgus, 45 Morbidit(y)ies, 175, 177, 185, 297
varus, 45 donor-site, 276
Management fracture-associated, 190
nonsurgical, 228 Morganella morganii, 352
orthotic, 404, 76 Morphine, 377
Mangled extremity severity score (MESS), 395 Mortise, 118
Mannitol, 305 ankle, 197, 200, 201
Mapping of physeal bars, 213 ankle fractures, 2–4, 11, 13, 20–23
Marjolin’s ulcers, 303–304 pilon fractures, 33, 38
Maturity, skeletal, 258 Mosaicplasty, 82
Mechanism(s) Motion
axial load, 27 sagittal, 121
calcaneal locking, 430 subtalar, 145
flexor and extensor, 175 Motor vehicle accidents, 101
gastrocnemius–soleus, 94 Mubarak chart, 389
plantar flexion, 85 Mucosa tracheobronchial, 289
soft tissue coverage of foot and ankle, 267 Muscles
Mechanism of injury, calcaneal fracture, 96 gastrocnemius, 305
displacement with the sustentaculum tail, 96 interosseous, 127–128, 130
joint depression, 96 Musculotendinous junction, 310
tongue type, 96 Mycobacterium tuberculosis, 347
Melanoma, malignant, 303 M. avium-intracettulare, 347
Menopause, 19 M. fortuitum, 347, 350
Meropenem, 350 M. marinum, 347
Mesotendon, 310, 317, 319 Myofibroblasts, 297
Metabolic acidosis, 293 Myoglobin, 305
Metadiaphysis, 38 Myonecrosis, 305
Metaphyses, 172, 215, 241 Myonecrosis bacterial, 305
comminution of, 35
distal tibial, 27, 237 N
in pilon, 35–36, 38 Nafcillin, 350
supra-articular, 27 Nails brittle, 374
Index 475
Navicular, 2, 118 Night walker fracture, 166

fractures Nocardia spp., 347
basic types of, 146–148 Nociceptors, 373
body, and stress, 146 Nondisplaced fractures, 56
dorsal avulsion, 146 Nonoperative treatment, 267–268
tuberosity avulsion, 146 Nonunion, 173, 185, 359, 382
sustentaculum tali, 432 midfoot fractures, 145 147, 150–151
Naviculum, 58 of V metatarsal, 175
Necrosis pediatric foot and ankle fractures, 213, 246
avascular, 50, 247, 375 pilon fractures, 44–45
in midfoot fracture, 145–146, 151, 155 talar fractures and dislocations, 55, 76, 85
pressure, 70 Norepinephrine, 373, 377
skin, 106, 132 Nutcracker type fractures, 253
talar avascular, 384
tissue, 69 O
toe-tip, 404 Obes(e)ity, 185, 338, 424
wound-edge, 45 Occlusion arterial, 389
Necrotizing fascitis, 354 Open fracture dislocation, 5
clinical presentation, 354 Open reduction and internal fixation (ORIF),
radiographic evaluation, 354 360–361, 434
diagnosis, 354 in ankle fracture, 10, 12, 19, 21
treatment, 355 in calcaneal fracture, 106, 114
HBO, 355 in pediatric fracture
parenteral antibiotics, 355 ankle, 231, 241, 243
surgical debridement, 355 foot, 249, 252, 253
Neisseria gonorrhea, 352 in talus fracture, 76, 85, 87
Neocortex, 373 Orthopaedic Trauma Association, 5
Neoplasm, 310 Orthoses, 423
Nerve(s) custom-fitted, 424
conduction disease, 180 custom-molded, 424, 428
entrapment, 143 nonmolded, 424
of foot and ankle, 6 Orthosis, 136, 155, 416
plantar, 6 aircast ankle stirrup, 434
saphenous medial and lateral, 6 ankle-foot, 140, 414
sural, 6 patella tendon bearing (PTB), 75
medial plantar, 327 total-contact, 140
peroneal, 6, 313, 316–317 Orthotic(s), 302
Lisfranc, 121, 123, 132–133, 136, 143 foot, 276
saphenous, 121 intention, 433
superficial peroneal, 14 management, 404, 433
sural, 85, 108, 121, 271, 389 of ankle fractures, 434
midfoot, 157 sheel wedge, 329
tibial, 336 Os
Neuralgia, tibial, 340 calcis, 93
Neuritis, sural, 109, 389 naviculare, 147, 149
Neuroarthropathy, Charcot, 403 peroneum, 329
Neurodystrophy, 373 subtibiale, 212
Neuroma, 132, 398, 402, 404, 419 trigonum, 52, 84–85, 252, 337
sural, 389 vesalianum, 254
Neuropathy(ies), 132, 358 Ossicles, 84
autonomic vasomotor, 180 Ossification pattern, 247
compressive, 375 Osteoarthritis, 45, 70
diabetic, 274 Osteoarthropathy, 190
motor peripheral, 188 Charcot osteoarthropathy, 349
peripheral, 180, 183, 185, 188, 191 Osteochondral lesions (OCLs), 79
vasomotor, 185 Osteochondritis, 156, 354
vasomotor and motor, 180 dissecans, 79
vasomotor autonomic, 183 Osteochondroma, 329
Neuropraxia, 198, 389 Osteomyelitis
Neurovascular dysfunction, 101 ankle dislocation, 199
Nifedipine, oral, 377 burnt feet reconstruction, 297
476 Index
Osteomyelitis (continued ) supramalleolar, 246

calcaneal fracture complications, 114 talar, 383
chronic, 359 talar neck, 66
Cierny-Mader classification system, 357–358 OTA Committee for Coding and Classification of
diffuse, 358 fractures, 28
localized, 358 Overdistraction, 45
medullary, 358 Overgrowth bony, 402–403, 413
superficial, 358 Overlap
contiguous focus, 358 tibia–fibula, 213
diabetic patients, 180 tibiofibular, 6
diagnostic techniques, 349 Oxygen
computerized axial tomography scan, 349 hyperbaric (HBO), 30, 267–268, 296, 297
gallium scan, 349 molecular, 267
hemethylpropylamine oxime (HMPAO) scan, tension arterial (PAO2), 297
349 tension tissue (PTO2), 297
magnetic resonance imaging, 349 transcutaneous, 267–268
radionuclide scan, 349
technetium (Tc) bone scan, 349 P
etiology, 357 Pain
foot and ankle aching midfoot, 143
deformities treatment, 448, 453–454 burning, 372, 374
operative treatment of soft tissue coverage, 269 chronic disabling, 147
posttraumatic infections, 346–348, 350, 353–358 myofascial, 377
traumatic amputations, 403–404 palmaris longus, 276
hematogenous, 357 pancytopenia, 293
in subtalar dislocation, 203 pantalar arthrodesis, 65
in talar complications, 71 paralysis, 389
management, 359–360 complete, 305
postoperative, 358 phantom limb, 402
posttraumatic, 359 sympathetically maintained (SMP),
Osteonecrosis, 89 372–374
talar neck, 54–59, 61, 248 Paratendinitis, 319
Osteopenia, 155, 181, 185, 348 Paratenon, 317, 323
calcaneal fracture, 106 Paresis, 389
diffuse, 375, 404 Paresthesia, 305, 389
Osteophyte, 311, 383 Parkland Formula, 291
Osteoporosis, 372, 374–375 Pasteurella multocida, 347
ankle fracture, 19, 22 Patella, 42
calcaneal fracture, 94 Pathogens, skin, 6
diabetic patients, 180 Pathognomonic for calcaneal fractures, 101
feet burns, 303 Patient(s)
in talar complications, 75 burn, 289
posttraumatic, 373 diabetic, 267–268, 418
Osteosynthesis, bifocal, 454 dysvascular, 400, 418
Osteotomes, 143 evaluation, 266–267
Osteotomy(ies), 62, 78, 79, 83, 220, 246, 298, 333, 390, ischemic, 185
440 neuropathic, 185
banana, 445 Pediatric foot and ankle fractures
calcaneal, 339 ankle fractures, 212–247
closing dome, 445 anatomy of distal tibia and fibula, 212
closing wedge, 76, 444 classification systems, 214–215
corrective, 185 complications, 246–247
derotational, 80 etiology, prevalence, diagnosis, and natural
fibular, 19, 61–62, 64, 79, 83 history, 213
in fibula, 383 transitional fractures, 229, 231, 235–245
late, 250 treatments, 215–234
malleolar, 61–64, 73, 78, 83 foot fractures, 247–258
medial malleolar, 61–62 anatomy, 247–248
oblique, 444 calcaneus fractures, 252–253
opening wedge, 76, 444 lesser tarsal fractures and tarsometatarsal
relatively transverse, 444 injuries, 253
Index 477
metatarsal fractures, 254–257 intramedullary (of metatarsal shaft), 170

phalanx fractures, 257–258 technique, antegrade–retrograde, 170–171
talus fractures, 247–252 Plafond, 27
Pedorthotists, 302 tibial, 7, 383
Penicillin G, 350 Plane(s)
Peptostreptococcus sp., 352 coronal, 99, 147
Perfusion, 6 dorsoplantar, 132
Periosteum, 302, 331 frontal, sagittal, transverse, 424
ankle, 14 navicular, 150
fibular, 333 sagittal, 97, 143, 147
pediatric ankle, 212, 217 sagittal and transverse, 65
pilon, 33 sagittal and coronal, 72
Peripheral vascular disease, 347 transverse, 143
Peritendinitis, 311, 318 Plantar
Peritenon, 323 ecchymosis, 101
Peroneal, 6, 247, 385 flexion, 126
longus brevis, 329 ligaments, 119
nerve palsy, 310 plates, 203
tendons, 2, 310 Planum, pes, 338
Peroneus Planus, pes, 143
brevis, 254, 325 Plaster, 300
longus, 331 Plate(s)
teritus, 62, 64, 316 buttress, 37
PGA pins, 84 cloverleaf, 36
Phalangeal fractures dynamic compression (DCPs), 382
fractures of the lesser toes, 175 locking, 36
hallucal fractures, 175 plantar, 203
Phalanges, 165, 257, 429 surgical reconstruction, 207
Phalanx, 166, 400, 406 posterior buttress, 41
Phalanxdistal, 336 spanning, 167
Phentolamine, 376 Platelet-derived growth factor (PDGF), 267–268
Phonophoresis, 318 Plethysmography, 348
Physeal injuries, 213 Poisoning carbon monoxide, 297
Physis distal tibial, 246 Polymicrobial infection, 347, 358
Pigmentation abnormal, 303 Position
Pilon fractures, 27–46 decubitus, 108
classification, 28 lateral decubitus, 65
soft tissue classification, 28–29 plantigrade, 41
complications, 45–46 valgus, 338
fixation, 30–37 Posterior
external, 37 colliculus, 2
methods, 35 inferior tibiofibular ligament (PITFL), 9, 197
of tibial articular surface, 33–36 malleolar, 2
plate, 36 fixation, 3
temporary, 30–32 fragment, 6
postoperative care, 43–44 subluxation, 3
treatment results, 44–45 talofibular ligament (PFL), 2, 197
Pin(s) tibial
bioabsorbable, 83, 153 nerve, 374
calcaneal, 61 tendons, 6
guide, 132 tuberosity, 109
infection, 39 Posterolateral tubercle, 52
talar or the calcaneal, 39 Posttraumatic infections, 50
track infections, 355 in foot and ankle, 346–365
clinical presentation, 356 Pressures, joint-contact, 10
diagnosis, 357 Prevotella sp., 352
management, 357 Procedure(s)
skin and soft tissue, 355–357 anchovy, 143
traction, 94 modified Kidner, 339
transfixion, 30–31, 37 salvage, 143
Pinning Process, anterolateral, 97
478 Index
Pronation passive, of midfoot and forefoot, 126 synthetic options, 325

Propionibacterium spp., 358 collagen tendon prosthesis, 325
Proteus dacron vascular graft, 325
P. mirabilis, 352 Marlex mesh, 325
P. rettgeri, 352 polyglycol threads, 325
P. vulgaris, 352 polymer and carbon fiber, 325
Providencia sp., 352 tendon, 325
Pseudohernia, 277 Achilles turndown, 325
Pseudomonas sp., 347, 358 fascia lata, 325
P. aeruginosa, 352 plantaris tendon, 325
Pulsed electromagnetic fields, 175 V–Y advancement, 325
Pulses Reconstruction and rehabilitation, 297–302
nonpalpable pedal, 399 Recovery, soft tissue, 37
palpable pedal, 268 Rectus abdominis, 277, 400
palpation of, 6 Reduction, 33
pedal, 185 anatomic, 167, 251, 387
Pump foot, 101 in ankle fractures, 15, 23, 228
Puncture wounds, 353 Lisfranc injuries, 118, 132, 136, 139
clinical evaluation, 353 anatomic bone, 15
treatment, 353 closed, 106, 167, 170
anatomic, 9, 131, 150
R in ankle fractures, 12, 222
Radiation fibrosis, 358 in pilon fractures, 33
Radiograph(s), 353 in talar fractures and dislocations, 59, 61, 69,
anteroposterior (AP), 6 76
positive stress, 10 definitive, 198
Radiography, image intensifier, 33 Essex-Lopresti, 252
Rami communicans fibular external rotation reduction of talus, 10
gray, 373 initial open, 12
white, 373 nonanatomic, 139
Range-of-motion (ROM), 199, 268 open, 173, 228
Ray resections, 407–411 in calcaneous fractures, 94
Raynaud’s phenomenon, 377 in Lisfranc injuries, 131–132
Receptors in pilon fractures, 32–35, 44
alpha-adrenergic, 373 in talar fractures and dislocations, 59
mechano, 373 operative, 9
Recognition, compartment syndrome, 101 Reepithelialization, 267, 289, 293–294
Reconstruction, 34 Reflex sympathetic dystrophy (RSD), 145, 247,
deltoid, 9 371–378
free-flap, 273–276; see also Flaps definitions, 372
diabetes and free-tissue transfer, 274 diagnosis, clinical, 374–375
failures and revisions, 275 diagnostic testing, 375–376
free flaps and the elderly, 275 psychological evaluation, 376
gait, 275–276 radiographs, 375
long-term results of free-flap foot reconstruction, sympathetic blockade, 376
275 thermo regulatory testing, 376
sensitivity and foot and ankle reconstruction, three-phase radionuclide bone scan, 375
274–275 pathophysiology, 372–373
vascular disease and free-tissue transfer, stages, 373–374
274 stage I (acute), 374
lateral ankle ligament, 5 stage II (dystrophic), 374
soft tissue coverage of foot and ankle, 267 stage III (atrophic), 374
specific injuries, late, 383–390 treatments, 376–378
calcaneus, 384–386 intravenous regional blocks, 377
compartment syndrome, 389–390 nerve blocks, 377
cuboid, 387–389 pharmacological treatment, 376–377
flexion contractures, 390 physical therapy, 378
midfoot, 387 surgical sympathectomy, 378
talus fractures, 383–384 Regranex, 268
syndesmotic injuries, 389 Relative avascularity, 320
syndesmotic, late, 389 Remodeling, 220
Index 479
Renal failure, Salter–Harris type

hepatic, 358 fractures
myoglobinuria-induced, 305 I and II, 215
Repair III and IV, 222, 224
calcaneus, 325 injuries
medial malleolus, 6 V, 228
tendon repair, 325 Sanders classification, 108
Rerupture Scan
rates, 322 bone, 404
sural nerve, 323 computed axial tomography (CAT), 19, 34, 98, 383
Resection(s) computed tomography (CT), 58, 202, 213, 348
metatarsal, 399 hemethylpropylamine oxime (HMPAO), 349
physeal bar, 228, 246 radionuclide, 348–349
Ray, 407–411 technetium (Tc) bone, 349
Residual Scaphoid, 54
diastasis, 132 Scar
displacements, 132 epiphyseal, 34
foot, 407 hypertrophic, 297–302
forefoot, 410 Scarring, 44
functional deficits, 7 Score(s)
hindfoot, 108 American Orthopaedic Foot and Ankle Society
metatarsal, 413 (AOFAS), 8, 387
toes, 410 Mangled Extremity Severity (MESS), 395
Response, inflammatory, 180 Olerud and Molander ankle, 8
Resuscitation, 291–292 syndesmosis outcome, 9
Retinaculum, 328, 331, 333, 336, 339 Screw(s)
extensor, 52 antegrade compression, 62
flexor, 338, 340 bioresorbable, 15
inferior, 317, 329 syndesmotic, 17
stenotic, 328 breakage, 174
superior, 317, 329 cancellous, 86, 130, 152
superior peroneal (SPR), 328 cannulated, 382, 383
Retinopathy, diabetic, 179–180 in ankle fractures, 15, 19
Rifampin, 350 in Lisfranc injuries, 132, 139
Rigid internal fixation, 2 in paediatric foot and ankle fractures, 224, 228,
Rocker bottom, 301 235
ROM, 328; see also Range-of-motion cannulated pediatric hip, 78
walker boot, 339 compression, 76, 150, 173
Rotation cortical, 152, 382, 387
external, 13, 229, 241 countersunk, 62, 83
pronation-eversion-external (PEER), 214 fixation, 79
pronation-external (PER) injuries, 9 lag, 150
supination and external, 14 headless, 62, 83
Rugby, 203 Herbert, 83
Rule of Nines, 290 intramedullary, 174
Running long-distance, 147 lag, 19, 35, 78
Rupture cortical, 132
deltoid ligament, 12–13, 15 in Lisfranc injuries, 130, 152, 155
frank nerve, 198 in paediatric foot and ankle fractures, 229
neglected, 311 malleolar, 15, 174
peroneus longus, 329 noncompression, 76
spontaneous, 311 Steinmann, 108
spring ligament, 127–128 syndesmotic, 21
syndesmosis, 13, 197 titanium, 58
cancellous, 153
S Sedation, 377
SAD type fibula fracture (Weber type A), 9 Semitendinosis, 313
Sagittal Sensory changes, 109
alignment, 59 Sepsis, 180, 346
malalignment, 65 Seroma, 296
480 Index
Serotonin, 377 Spinal cord, 317

Serratia marcescens, 352 Splint stirrup, 13
Serratus anterior, 279 Splinting, 45
Sesamoidectomy, 207 Sporothrix schenkii, 347
Sesamoids, 203, 205–206, 257, 336 superior peroneal retinaculum (SPR), 328,
Shaft 333
ipsilateral tibia, 236, 241 Sprain, 212, 328
metatarsal, 133 ankle, 105, 148, 156
tibial, 7, 35, 39 midfoot, 126, 140
Shear fractures of talar body, 70 syndesmotic, 13
Sheath Springiness, 328
synovial, 317 Stability, midfoot, 408
tenosynovial, 328 Stabilization, syndesmotic, 12
Shell, metaphyseal, 41 Stance phase, gait, 2
Shenton’s line of ankle, 389 Staphylococcus sp., 347, 351, 358
Shock burn wound, 288–289 S. aureus, 347, 350–351, 357–358
Shoe S. epidermidis, 350
extended steel shank, 140, 143 Status
rigid-soled, 433 altered mental, 126
Short leg cast (SLC), 13–14, 59, 85 fibula, 35
Shortening neurovascualar, 198, 202, 237
fibular, 10 nutritional, 400
lateral shift, 2 vascular, 6
skeletal, 400 Steida’s process, 52, 84
Shunt, arteriovenous, 185 Steinmann pin, 108
Shunting, arteriovenous, 183 Stenosis, 337
Silver sulfadiazine cream (SSD), 293 of tendons, 385
Sinus tarsi, 84, 103 Steroids, 381
Skate blade, 310 injection, 311, 340
Skin Stiffness, 101, 109, 166, 175
blistering, 101 ankle and foot, 44
grafting, 202, 289, 297, 400 in ankle dislocation, 196
in paediatric foot and ankle fractures, 257 in great toe MTP dislocation, 203
Lisfranc injuries, 145 in subtalar joint dislocation, 199
soft tissue coverage of foot and ankle, 269, 274 Strain, 328
ischemia, 200 Streptococcus spp., 347, 350, 358
lacerations, 310 S. agalactiae, 351
loss, 400 S. epidermidis, 357
necrosi, 56, 71, 145 S. pneumoniae, 351
slough, 56 S. pyogenes, 351
Skin-tenting, 145 Stress(es)
Sleeve periosteal, 11 advanced age, 320
Slide gastrocnemius, 390 chronic steroid use, 320
Slough, 45, 56 contact, 10
Sloughing, 106 diabetes, 320
Small vessel disease, 358 external rotation, 12, 19
Smok(ers)ing, 109, 115, 382 fracture, 339, 374
Snowboarding, 87, 251 hindfoot, 166
fracture, 251 midfoot, 147, 149–150, 155
Soft tissue inflammatory arthopathy, 320
coverage, 266 inversion, 222
foot and ankle, 266–282; see also Foot and ankle lateral translation, 12
paucity, 346 test, 126
injury, 114 valgus, 205
Space varus, 205
fibulocalcaneal, 97 views, 12, 213
intercuneiform, 126 Study(ies)
intermetatarsal, 126 Doppler, 267
medial clear, 6, 10, 13, 18, 20 labeled leukocyte, 403
syndesmotic, 6 Subluxation, 150, 157
tibiofibular clear, 6 dorsolateral peritalar, 185
Index 481
midtarsal, 150 terminal, 404–405

peroneal, 333 Sympathalgia, 373
peroneus brevis, 331 Sympathectomy, 378
posterior, 19 surgical, 372
subtalar, 200 in RSD, 378
talonavicular, 56 Sympathetically maintained pain (SMP),
Suboptimal operative fixation, 8 373–374
Subtalar joint, 109, 433, 652 cardinal signs, 374
Subtalar valgus, 425 edema, 374
Sudeck’s atrophy, 373, 375 pain, 374
Sulcus, 84, 99, 197, 328 stiffness, 374
calcaneal, 96, 247 secondary signs
interosseous, 94 demineralization, 374
support, 429 palmar fibromatosis, 374
talus, 247 pseudomotor changes, 374
Sulfamylon, 293 thermoregulatory changes, 374
Superior extensor retinaculum, 310 trophic changes, 374
Supination, 239, 241, 248 vasomotor instability, 374
foot, 94 Symptoms
injuries, 213 of pain, 376
Supination-plantar flexion (SPF), 214 cold intolerance, 376
Supine position, 14 peroneal paratendinitis, 329
Sural nerve, 85, 108, 121, 271, 323, 389 Synchondrosis, 85
Surgery Syndesmosis, 197, 389
ablative in ankle fractures, 3, 5, 9, 11–12, 18, 20
digital and ray resection, 359 in pilon fractures, 33
midfoot disarticulation, 359 involvement, 9, 11
Syme amputation, 359 level of the Weber B or C, 10
transmetatarsal amputation, 359 rupture, 197
Surgical tibiotalar, 197
debridement, 353 widening, 12
techniques, 84 Syndesmotic ligament complex, 3
intervention, 109 Syndrome
ligation, 199 chronic regional pain (CRPS), 395
reapproximation, 2 compartment, 389–390, 396
techniques, 310 in Lysfranc injuries, 127–128, 143–144
debridement, 310 complex regional pain, 371–378
repairs, 310 impingement, 375
reconstructions, 310 lateral, 109
tendon transfers, 310 ostrigonum, 85
treatment pain-dysfunction, 373
posttraumatic infections in foot and ankle, posttraumatic pain, 373
351 shoulder–hand, 373
treatment, complications sympathetic overdrive, 37
delayed union, 174 Synovitis, 81, 385
failure of intramedullary fixation, 174 chronic posttraumatic, 374
refracture, 174 Synovium, 385
Surgical site infections (SSIs), 355 Synthesis collagen, 267
diagonosis, 355 System
Sustentaculum, 336–337 Ruedi and Allgower, 28
Sustentaculum tali, 52, 94, 98, 103, 434 Shin, 237
Suture(s)
Allgower-Donati, 109, 385 T
Bunnell, 323 Talar body, shear fractures, 70
Ethibond, 327 type I (coronal/sagittal fracture)
Kessler, 323 displacement at the trochlea, 70
Kessler–Tajima, 313 simple nondisplaced, 70
Krackow, 313, 323 trochlear fracture with dislocations of subtalar
Swimming, 83–84 and tibiotalar joint, 70
Syme’s type II (horizontal), 70
amputation, 414, 417–419 Talar dome, 75, 81–83
482 Index
Talar head, 147, 153, 155, 200 surgical techniques, 62–65

depressed, 185 surgical treatment, 76–79
Talar injuries, 50 principles of arthrodesis, 76–78
Talar neck, 2, 152, 247, 383–384 talectomy and tibiocalcaneal fusion, 78–79
fracture, 33, 56–57 tibiotalar fusion with partial talectomy, 78
displacement, 57 Tarsal bones, 133
Hawkins talar neck fracture, 57–58 lesser, 253
joint sub talar subluxation, 57 midfoot, 118
malalignment of, 65 navicular, the cuboid cuneiforms, 253
Lisfranc injury, 133 Tarsal tunnel, 374
impaction or breakage, 56 Tarsals occult fractures of, 247
osteotomy of, 66 Tarsometatarsal (TMT/Lisfranc) injuries, 118–145
Talar anatomy, 118–121
shift, 2, 6, 10, 12 articular complex, 120, 124
tilt, 6–7 biomechanics, 121–122
Talectomy(ies), 65–70, 73, 250 classification, 124–126
canis, 50 complications, 143–145
limping, 78 devascularization, 143
residual pain, 78 other complications, 145
shortness, 78 skin compromise, 145
Talotibial joint, 2 diagnosis, 126–129
Talus, 146, 197, 247, 424 disruption, 133
anatomy, 51–55 type III, 133
blood supply, 52–55 history, 118
body, 52 mechanism of injury, 122–124
head, 51 midfoot sprains in athletes, 140
neck, 51–52 postoperative care, 135–136
complications, 70–76 prognosis, 136, 139
avascular necrosis (AVN), 75 salvage procedures, 143
malunions of talar neck, 76 treatment, 129–135, 137–142
nonunion, 75 closed reduction and casting, 131
osteomyelitis, 71–75 closed reduction and percutaneous fixation,
posttraumatic arthritis, 76 131
skin problems, 70–71 extensile dorsomedial approach to the midfoot,
dislocation, 68–70 132
fractures of talar neck, 55–62 external fixation, 132
categories, 58–62 open reduction and internal fixation, 132
classification, 56 principles, 129
clinical features, 56 timing of surgery, 130
imaging studies, 56–58 Taxillus, 50
fractures of the lateral process, 87–89 Tear periosteal, 216
clinical evaluation, 87–89 Tears peroneus brevis, 329
mechanism of injury, 87 Technique(s), 406, 408, 414, 417
treatment, 89 Bier block, 377
fracture of the medial tubercle (Cedel’s fracture), Bunnell, 323
85–87 closed reduction, 94
fractures of the posterior process, 84–85 end-to-end repair, 323
anatomy, 84 external fixation technique, 446–448
clinical features, 85 fluoroscopic dye, 84
mechanism of injury, 84–85 free-flap, 45
treatment, 85 Kessler-style suture, 323
Hawkins III open fractures, 65–67 Krackow, 323
Hawkins type IV injuries, 67 Ilizarov, 440, 448
in ankle fractures, 2–7, 10–15, 19, 21 imaging, 348
osteochondral lesions (OCLS) of talus, 79–84 nonstandard amputation, 400
prognosis, 84 olive wire, 448–449
treatment, 82–84 osteotomy, 62
postoperative infections, 362–364 reconstruction, 382, 394–396; see also
incidence and risk factors, 362 Reconstruction
treatment, 364 free-tissue transfer, 394
shear fractures of talar body, 70 hyperbaric medicine, 394
Index 483
skeletal fixation, 394 peroneal tenosynovitis, attritional tears, and

vascular reconstruction, 395 rupture, 328–329
replacement, 89 posterior tibial tendon, 15, 121, 147–148, 150
splinting, 300 dislocation of the posterior tibial tendon, 340
surgical, 13 etiology, 338–339
corticocancellous inlay grafts, 175 nonoperative treatment, 339
reversed trapezoid grafting, 175 operative treatment, 339–340
sliding local grafting, 175 ruptures and lacerations, 310–341
Tendinitis, 337 Achilles tendon, 317–328
peroneal, 385 anterior tibial tendon, 310–315
Tendinopathy, calcifying, 319 extensor digitorum longus tendon, 317
Tendinosis, 319, 323, 329 extensor hallucis longus tendon, 313,
asymptomatic, 318 316
Tendolipomatosis, 319 spontaneous disruption of, 318, 336
Tendon autoimmune disease, 318
Achilles, 185, 302, 413–414, 418 cavovarus, 318
in calcaneal fractures, 106 collagen abnormalities, 318
in free flaps, 249, 279 corticosteroid use, 318
in talar fractures and dislocations, 65, 85 fluoroquinolone usage, 318
rupture and lacerations, 317–328 infectious disease, 318
allograft interposition, 313 neurological abnormalities, 318
anterior tibialis, 62, 74, 121, 131, 316, 410 pronation, 318
etiology of rupture, 311 weakness and stiffness of gastrocsoleus
nonoperative treatment, 311–312 complex, 318
operative treatment, 313–315 stenosing tenosynovitis, 310–311
autograft interposition, 313 transfers, 403
degeneration, 310 vincular system, 310
extensor digitorum longus, 62, 64, 310, 317, Tendonitis, 322, 336, 339, 374
414 FHL, 336
ruptures of the EDL, 317 insertional, 339
extensor hallucis brevis, 133 Achilles, 390
extensor hallucis longus, 133, 205, 249, 313, Tendonosis, 339
316 Tenectomy, 385, 389
etiology of rupture, 313 Achilles, 413–416
nonoperative treatment, 313 extensor, 407
operative treatment, 316 Tenodesis, 313, 327
flexor carpi radialis, 276 Tenosis, 329
flexor digitorum longus, 87, 310, 336 Tenosynovectomy, 329, 339–340
flexor hallucis longus (FHL), 52, 65, 94, 205, Tenosynovitis, 328–329, 338–339
418 FHL, 336–337
etiology, 337 stenosing, 310–311
nonoperative treatment, 337 Tenotomies, 403
operative treatment, 337–338 Tension
function, 6 cutaneous oxygen, 348
healing, 322 transcutaneous oxygen, 348, 399
integrity, 325 Tenting skin, 106
laceration, 310 Tertius, peroneus, 317
lengthenings, 403 Tetanus
loss, 316 immune, 353
of continuity, 323 toxoid, 353
malleolus of, 318 Tetracycline, 350
nodularity, 337 Theory, neurotraumatic, 185
periosteum of, 318 Therapy(ies)
peroneal, 97, 328–335 adjunctive, 353
anatomy, 328 antimicrobial, 348, 350
chronic repairs, 333–335 cytokine, 274
os perineum and peroneus longus tears, hyperbaric oxygen (HBO), 353, 400
329–332 leech, 275
peroneus brevis subluxation or dislocation, nonoperative, 267
331–332 physical, 297, 377–378
peroneus brevis tears, 172–173, 329–330 in RSD, 378
484 Index
Tibia, 30–37, 41, 78, 94 Traumatic injuries

ankle fracture, 2, 6, 11–12, 15, 19, 21, 27 burns, 346
distal, 15 fractures, 346
proximal, 34 nail punctures, 346
Tibial tendon injury, 318
graft, 79 Treatment
incisura, 6 calcaneal fracture, 107
nerve, 337 modalities, soft tissue (unroofing, aspirating,
damage, 85 leaving intact), 5
plafond, 83, 85 orthotic, 185
plateau, 42 plafond fracture
Ticarcillin-clavulanic acid, 352 open reduction and internal fixation (ORIF),
Tilt, talar, 6–7 360–361
Tobramycin, 73 RSD, 376–378
Toe(s), 180 intravenous regional blocks, 377
active motion of, 6 nerve blocks, 377
contracture or rotation of, 269 pharmacological treatment, 376–377
dislocation, 301 surgical, 351
distal phalanx, 166 surgical sympathectomy, 378
lesser, 400 Trochlea, 50
middle phalanx, 166 Trovafloxacin, 350
pressures, 348 Truss medial, 430
proximal phalanx, 166 Tuber angle, 94
stubbing, 176 Tubercle
Tomography, 81 Chaput, 33–34
computed (CT), 7, 30, 58, 98 Gerdy’s, 62, 70
Tourniquet, 84 hypertrophic peroneal, 329
Tourniquet calf, 382 peroneal, 328
Trabeculae Tuberosity, 103–106, 252
compression, 94 calcaneal, 153
pattern of, 94 medial, 147
sparse, 94 navicular, 146, 149, 151
Tract, afferent spinothalamic, 373 V metatarsal, 172
Traction, 94 Tunnel
axial, 61 cuboid, 329
calcaneal, 33 FHL fibroosseous, 337
skeletal, 300 tarsal, 15
Transchondral fractures, 79
Transcyte, 293–294 U
Transfer UC-BL shoe, 432
abductor hallucis tendon, 207 Ulceration, 289
free-tissue, 30, 269, 274, 400 Ulcers, 185
peroneus brevis tendons, 415 foot, 179
tendons, 313, 316, 389, 403 Marjolin’s, 303–304
anterior tibialis, 415 stasis, 269
Transformation, malignant, 303 trophic, 275
Transitional fractures of ankle Union, delayed, 246
Tillaux and triplane fractures, 258 of V metatarsal, 175
Transplant, renal, 274 Ustentaculum, 100
Transverse fibula fractures, 213
Traps, sterile finger, 132 V
Trauma, 394 Valgus, 30, 37, 96, 301, 339
blunt, 328 alignment, 32, 114
direct-blow, 156 of heel, 109
distal, 382 drift, 33, 400
high-energy, 123, 203 forefoot wedge, 430
inner, 311 genu, 212
lower energy, 203 malunions, 45
lower extremity, 372 orientation, 33
mechanical, 328 wedge, 432
motor vehicle, 197 Vancomycin, 73, 350
Index 485
Variant intramalleolar, 241 Widening, physeal, 217

Varus Wire(s)
alignment of heel, 109 calcaneal, 41
angulation, 44, 62, 76 cerclage, 23
collapse, 35, 38, 44 guide, 15, 19, 139
deformity, 36, 155, 185 Kirschner, 333, 387
drift, 400 ankle, 217, 220, 228, 231
fractures B type (partial articular), 35 foot, 249, 254
genu, 212 in ankle fracture, 15, 17, 22
heel, 385 in calcaneal fracture, 108–109
hindfoot, 250 in metatarsal fracture, 167, 173
malalignment, 59, 76–77, 108, 250, 301 in midfoot fracture, 136, 152–153
malunions, 45, 51 in talar fracture, 84
shift, 147 in treatment of Lisfranc injury,
Vascular disease, 180 132
Vasculogenesis, 297 percutaneous Kirschner, 252
Vasomotor abnormalities, 374 tensioned, 39
Vasospasm traumatic, 373 transfixion, 34, 43
Velocimetry, laser-Doppler, 376 Wound(s), 44–45
Venae comitantes, 271, 274 breakdown, 35, 402
Venous engorgement care, 69, 292–294
pallor, or cyanosis, 6 compression, 150
Venous stasis, 358 coverage, 400
Venus, 50 dehiscence, 14, 109
Vessels delayed closure, 12
calcific, 399 edge necrosis, 45
intramedullary, 172 failure, 185
metaphyseal, 172 foot, 274
Vibrio vulnificus, 347 foot and ankle
View(s) management principles, 267
anteroposterior (AP) ankle, 75 nonoperative coverage of, 268
Broden (s), 59, 62, 102–103, 109 gunshot, 372, 394, 407
Canale, 58, 62, 248 healing, 45, 180, 399
Canale pronation, 59 high-velocity gunshot, 394
coned-down, 149 infection, 109, 185
Kelly, 248 clostridial infection, 397
mortise, 103, 109, 213 management, 183
stress, 213 open, complications, 5, 34, 199
abduction-pronation, 126 abrasions, 29
transverse, 77 contusions, 29
weight-bearing, 126 necrosis, 29
slough, 74
W puncture, 353
Walker boot surgical management, 199
range-of-motion (ROM), 318
Walking boot, 136, 156, 183, 236 X
aircast, 199 Xenograft, 294
Walking cycle, 166 Xeroform, 293
Weakened warrior, 321 gauze, 294
Weakness, 109
Web space, 6 Z
Weber fracture classification, 13, 197 Zone of
Wedge(s), 425 hyperemia, 289
heel, 318 hypovascularity, 317
valgus, 424–425 necrosis, 289
forefoot, 431 stasis, 289
varus, 424–425 Z-plasties, 299
Weight-bearing capacity, 2

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DK2448_Discl Page 1 Friday, February 11, 2005 2:54 PM

© 2005 by Taylor & Francis Group, LLC

No claim to original U.S. Government works

International Standard Book Number-10: 0-8247-5916-8 (Hardcover)

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About the Editors

Robert B. Anderson, M.D. Steven A. Herbst, M.D.

Jason H. Calhoun, M.D. R. Michael Johnson, M.D.

Sidney F. Miller, M.D., F.A.C.S. David A. Porter, M.D., Ph.D.

Michael S. Pinzur, M.D. Saul G. Trevino, M.D.

Jason H. Pleimann, M.D. William A. Vitello, M.D.

1. Ankle Fractures .................................................................................................................... 1

17. Orthotic Management of Foot and Ankle Fractures ......................................................... 423

2 Miller and Herbst

4 Miller and Herbst

III. CLASSIFICATION OF ANKLE FRACTURES

Figure 1.2 Ankle fracture classification systems.

IV. PHYSICAL EXAMINATION

6 Miller and Herbst

Table 1.1 Radiographic criteria

VI. OUTCOME OF ANKLE FRACTURES

8 Miller and Herbst

VII. COMPARISON OF OPERATIVE AND NONOPERATIVE RESULTS

VIII. RESULTS OF OPERATIVE INTERVENTION

IX. HISTORICAL AND RESEARCH CONSIDERATIONS FOR TREATMENT

10 Miller and Herbst

B. Posterior Malleolar Fracture

Figure 1.6 Posterior malleolus fracture with minimal displacement.

C. Medial Malleolar Fracture

12 Miller and Herbst

E. Talar Shift without Fracture

H. Techniques of Closed Reduction and Subsequent Care

14 Miller and Herbst

16 Miller and Herbst

The issue of syndesmosis fixation remains controversial, as discussed previously. We prefer to

18 Miller and Herbst

XI. OSTEOPOROSIS AND ANKLE FRACTURES

20 Miller and Herbst

XII. ANKLE DISLOCATION OR LIGAMENTOUS DISRUPTION

22 Miller and Herbst

24 Miller and Herbst

26 Miller and Herbst

Lateral Anteroposterior Axial

Figure 2.1 Ruedi–Allgöwer classification of pilon fractures [4,5].

II. FRACTURE CLASSIFICATION

III. SOFT TISSUE CLASSIFICATION

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

Figure 2.3 Tscherne [11] classification of soft tissue injury.

IV. TEMPORARY FIXATION

V. FIXATION OF THE TIBIAL ARTICULAR SURFACE

Table 2.1 Fixation Methods for Pilon Fractures

VI. PLATE FIXATION

VII. EXTERNAL FIXATION

VIII. POSTOPERATIVE CARE

50 Trevino and Panchbhavi

B. Tibiotalar Fusion with Partial Talectomy................................................................ 78

Talar Fractures and Dislocations 51

A. The Head of the Talus

B. The Neck of the Talus

52 Trevino and Panchbhavi

C. The Body of the Talus