Surgical Management of Fractures of the Talus

John M. Tabit, DO

Lawrence X. Webb, MD, MBA

Dr. Webb or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of the Musculoskeletal Transplant Foundation; serves as a paid consultant to or is an employee of Biocomposites; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research-related funding (such as paid travel) from Kinetic Concepts, Doctors Group, Smith & Nephew, Stryker, and Synthes; and serves as a board member, owner, officer, or committee member of the Orthopaedic Trauma AssociationSoutheastern Fracture Consortium Foundation. Neither Dr. Tabit nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

INTRODUCTION

Anatomy

The talus consists of the head, neck, body, lateral process, and posterior process. The posterior process is divided into a medial tubercle and a lateral tubercle by the groove corresponding to the flexor hallucis longus (FHL) tendon. The talus and its constituent parts are illustrated in Figure 1. Sixty percent of the talus is covered by hyaline cartilage, and this feature is pivotal to its role as a major contributor to the motion of the midfoot, hindfoot, and ankle. There are no muscle or tendon attachments directly to the bone (Figure 2). The talus receives its blood supply from all three major arteries that supply the foot and ankle, including the peroneal, anterior tibial, and posterior tibial arteries.¹^,² Locally, the bone receives its blood supply from the arteries that derive from these three: the artery of the tarsal canal, the deltoid artery, and the artery of the sinus tarsi (Figure 3). Recent studies have shown that the talus has a rich and redundant intraosseous blood supply.³ This may help to explain why osteonecrosis is seldom associated with nondisplaced fractures of the talar neck. It also may explain the enhanced potential for vascular recovery in displaced fractures following open reduction and internal fixation (ORIF).³^,⁴^,⁵

FIGURE 1 Illustration depicts two views of the talus. FHL = flexor hallucis longus.

Mechanism of Injury

Talar neck fractures occur most commonly as a result of hyper-dorsiflexion of the foot. The low bone density and small cross-sectional area of the talar neck make it susceptible to fracture at the “giving way point,” as the stressed talus strikes the much denser anterior tibia. Based on laboratory studies and clinical data, it has been estimated that up to 26% of talar neck fractures have concomitant medial malleolar fractures, with hindfoot

supination playing a significant role in the mechanism of injury.⁶^,⁷ These fractures are often high-energy injuries, resulting in significant comminution and displacement and having a high incidence of associated fractures (64%) and disruptions of the soft-tissue envelope (21% are open injuries).⁶

FIGURE 2 Photographs show the lateral (A), inferior (B), medial (C), and cephalad (D) aspects of a fresh talus specimen from a right ankle.

FIGURE 3 Illustrations show anterior (A) and inferior (B) views of the talus with its blood supply. The blood supply is derived from an anastomotic ring with contributions from the posterior tibial artery by way of its deltoid artery branch and the artery of the tarsal canal. The dorsalis pedis artery and the perforating peroneal artery also contribute, by way of their branches, to the artery of the sinus tarsi and the lateral tarsal artery, respectively. (Adapted from Fortin P, Balazsy J: Talus fractures: Evaluation and treatment. J Am Acad Orthop Surg 2001;9[6]:114-127.)

Classification

The most widely used classification system for talar neck fractures is the one described by Hawkins in 1970.⁶ The Hawkins classification defines type I fractures as nondisplaced, type II fractures as displaced with subluxation or dislocation of the subtalar joint and an intact tibiotalar joint, and type III fractures as displaced with subluxation or dislocation of both the subtalar and tibiotalar joints. The rates of osteonecrosis of the talar body correlate with this classification, and the risk of vascular disruption increases with the extent of displacement. Osteonecrosis rates have been reported to be 0% to 13%, 20% to 50%, and 83% to 100% for Hawkins types I, II, and III fractures, respectively.⁶^,⁸ Improved techniques for open reduction and internal fixation of the talus have resulted in an overall diminution in the osteonecrosis rates for Hawkins type II and III fractures.⁵^,⁹^,¹⁰ Canale and Kelly⁸ later added a type IV talar neck fracture, characterized as a Hawkins type III injury with an accompanying dislocation of the talonavicular joint.

The Hawkins classification system is confined to fracture-of the dislocations of the neck of the talus alone; the AO/Orthopaedic Trauma Association (AO/OTA) classification is more encyclopedic. Although the AO/OTA system is used infrequently in common clinical orthopaedic parlance, it is of great value in research.¹¹

FIGURE 4 Photographs depict deformity associated with the dislocation of the subtalar joint. In this medial subtalar dislocation, the head of the talus is palpable on the dorsum of the foot (A), and the heel is displaced medially (B). C, In this lateral subtalar dislocation, the head of the talus is prominent medially, while the rest of the foot is dislocated laterally. (Reproduced with permission from Buckingham WW Jr, LeFlore I: Subtalar dislocation of the foot. J Trauma 1973;13[9]:753-765.)

PATIENT SELECTION

Indications

Truly nondisplaced fractures, as assessed on radiographs and CT scans as described below, can be managed nonsurgically in a short leg splint with conversion to a cast once the swelling has subsided. Non-weight bearing should be enforced for 8 to 12 weeks, with subsequent protected graduated weight bearing. Radiographic views obtained at office follow-up visits with the foot out of the cast should include an ankle mortise view, a lateral view, and a Canale view. At 8 weeks, the mortise radiographic view should be inspected for the presence of a Hawkins sign, which is a subchondral lucency of the talar body that indicates bone resorption and vascularity. A good prognostic Hawkins sign is seen in 95% of nondisplaced talar neck fractures. Tezval et al¹² studied the prognostic reliability of the Hawkins sign for osteonecrosis in patients with displaced fractures and demonstrated a sensitivity of 100% and a specificity of 58%.

Most talar fractures are displaced and require surgical management. Patients generally present with edema and ecchymosis of the ankle or foot. Gross deformity may be present in higher-grade fracture-dislocations (Figure 4). In the acute setting, closed reduction of dislocations of the peritalar joints should be attempted, especially if the soft-tissue envelope is compromised by the displacement. Immobilization can be accomplished with a posterior
splint or a bridging external fixator. Definitive management of the fracture with open reduction and internal fixation should proceed if closed reduction of the dislocation is unsuccessful. If closed reduction is satisfactory, an open reduction and internal fixation of the fracture should follow as soon as possible but is not emergent. In the recent past, controversy existed regarding the timing of reduction and fixation of talar fractures. A delay in reduction was thought to be related to a higher incidence of osteonecrosis. Several recent retrospective reviews, however, support the concept that the timing of reduction and fixation do not influence the incidence of osteonecrosis and posttraumatic arthritis.⁴^,¹³^,¹⁴

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