Sixty percent of the bone is covered by articular cartilage, significantly limiting extraosseous perfusion to the bone.

Disruption of circulation to the talus correlates with open or comminuted talus fractures, leading to an increased risk of avascular necrosis. The blood supply to the talar body enters through the inferior talar neck via the artery of the tarsal canal. This key vessel originates from the posterior tibial artery. Secondary blood supply to the body is derived from the deltoid branch of the posterior tibial artery, entering the talar body along its medial surface. Circulation to the neck, head, and lateral body is supplied via the dorsalis pedis, tarsal sinus, and lateral tarsal sinus arteries. This last artery is an anastomosis between the peroneal and dorsalis pedis arteries.³

Peroneal artery contributed 17% talar perfusion.

Anterior tibial artery contributed 36% talar perfusion.

Posterior tibial artery contributed 47% of talar perfusion.

Three main surfaces articulate with the plafond and lateral malleolus, whereas three surfaces articulate with the calcaneus.

The final articulation of the talar head with the tarsal navicular represents an important articulation for midfoot motion.

These fractures constitute up to 10% of all fractures of the talus.

They are uncommon but must be looked for in the event of an isolated subtalar dislocation.

After completion of the neck fracture, continued hyper-dorsiflexion and axial load to the body of the talus may force dislocation of the talar body posteriorly, disrupting significant extraosseous circulation.

Fracture patterns of the body of the talus include coronal, sagittal, horizontal shear, and crush fractures of the weight-bearing surface.

Lateral and posterior process fractures are sustained by inversion and eversion mechanisms of the ankle, respectively. These fractures are often missed on plain film radiographs of the ankle and diagnosed as ankle sprains.

Posteromedial and posterolateral process fractures lie to each side of the flexor hallucis longus (FHL) tendon. These are commonly intra-articular fractures of the inferior surface of the posterior talus.

Fractures of the head of the talus are commonly nondisplaced because of powerful capsular and talonavicular ligamentous attachments.

Displaced fractures of the talar head have a 10% incidence of osteonecrosis and can lead to secondary posttraumatic arthrosis.

The type I fracture is nondisplaced. Disruption of blood flow is limited to the anterolateral region of the bone. I recommend a computed tomography (CT) scan to confirm no displacement of the fracture before diagnosing a type I fracture. Historically, Hawkins reported a 13% incidence of osteonecrosis in type I injuries (FIG 1A).

In the type II talar neck fracture, there is displacement of the talar dome fragment, which is routinely posterior, often depicting clear subluxation of the talar body. Blood flow to the medial body and head is preserved. The type II talar neck fracture has a 20% to 50% risk of avascular necrosis (FIG 1B).

In the type III injury, the transverse fracture of the talar neck is associated with dislocation of the talar body. The incidence of osteonecrosis of the talar body is 50% to 100%. All major perfusion to the body of the talus is damaged (FIG 1C).

A type IV injury of the talar neck has been documented; it is a type III fracture-dislocation with associated talonavicular dislocation.² All extraosseous blood flow to the talus is considered disrupted. The value of the Hawkins classification is that it allows the orthopaedic surgeon to predict what to expect with a specific talar neck injury. Open reduction and rigid internal fixation is the recommended treatment (FIG 1D).²

The relationship of severe lower extremity trauma and airbags is well known. After airbag deployment, the torso and lower extremities are directed toward the floor panel of the car.

I believe that the incidence of high-energy hindfoot trauma will increase over time. Globally, transport-related injuries remain the leading cause of disability from injury. By 2020, traffic injuries will increase from a current ninth position to third disability-adjusted life-years lost.¹

On the initial examination, the physician should note pain, motion, crepitus, deformity, soft tissue swelling, open fractures, and associated fractures of adjacent bones to the foot and ankle and should perform a complete neurovascular evaluation of the extremity.

Soft tissue local pressure phenomenon, commonly found anterolaterally in closed type III fractures of the talar neck, may precipitate full-thickness pressure necrosis of the skin if not decompressed early.

Severe swelling of the ankle is common in the acute fracture of the talus and may progress to fracture blister formation, precluding safe execution of operative incisions.

A closed injury with mild or moderate swelling (bony landmarks palpable) indicates talar neck type I and II fractures and process fractures.

A closed injury with severe swelling indicates talar neck type III and IV fractures and body fractures.

The AP and mortise views of the ankle demonstrate alignment of the talar body in the ankle mortise. The lateral view depicts the sagittal outline of the talus.

High-energy injury mechanisms that cause talus fractures precipitate fracture displacement and joint surface incongruity.

These injuries are treated acutely in well-padded, compressive dressings with posterior splints and non-weight bearing. Swelling and immediate pain in the ankle improve significantly by 7 to 10 days. The patient is subsequently converted to a short-leg, non-weight-bearing cast for 6 weeks followed by progressive range of ankle and subtalar motion and return to weight bearing in a removable fracture boot.

If the process fracture is severely comminuted, precluding surgical reconstruction, the same initial and definitive nonoperative management is employed.

Acutely, an isolated, nondisplaced talar head fracture is splinted for 7 to 10 days with subsequent short-leg casting
in neutral plantarflexion with non-weight bearing for 4 weeks. Intermittent daily ankle and subtalar motion with Achilles tendon stretching should follow with application of a removable fracture boot. The patient remains non-weight bearing until 6 to 8 weeks after injury. Next, progressive weight bearing, range of motion, stretching, and strengthening of the entire lower extremity are recommended.

A subgroup of these injuries may present with displacement of the talar neck on initial injury plain radiographs. After closed manipulation of the fracture in plantarflexion, the talar neck fracture may reduce. A true Hawkins type I talar neck fracture will not displace even with gentle dorsiflexion. The type I fracture strongly warrants a CT scan with sagittal reconstruction to confirm anatomic alignment of the talar neck.

Truly nondisplaced fractures of neck of the talus can be treated nonoperatively in a short-leg, non-weight-bearing cast for 6 to 8 weeks. Close follow-up is recommended to watch for any displacement of the neck fracture. At 6 to 8 weeks after the injury, progressive weight bearing, range of motion, stretching, and strengthening are initiated.

One recent study indicates that orthopaedic trauma surgeons do not believe that a displaced fracture of the neck of the talus is an orthopaedic emergency.

However, it is important to differentiate the potential of vascular injury to the talar body from soft tissue and neurovascular compromise of the foot because of injury to the talus. In particular, fracture-dislocation of the body of the talus is associated with compromised blood flow to the bone, the threat of pressure phenomenon to the skin, and possible tibial nerve dysfunction.

The acute severity of soft tissue swelling or the impact of an open hindfoot wound may preclude safe, immediate reconstruction of the talus fracture after reduction of the dislocation.

Any open talus fracture must be treated as an orthopaedic emergency.

Preoperative antibiotics may be selected on the basis of wound contamination. These include a cephalosporin and possibly gentamicin. Penicillin is added if gross or farm contamination is present. All patients should receive a tetanus toxoid booster.

The patient is taken to the operating room, and after soft tissue débridement, the wound receives at least 3 to 9 L of normal saline using pulsed lavage.

At this time, in addition to partial or complete fixation of the talus fracture, provisional foot and ankle external fixation may be used to provide soft tissue and osseous stabilization before delayed closure.

Recent studies indicate that displacement or malalignment will have a negative impact on foot function. Two millimeters of fracture displacement has been shown to affect subtalar joint mechanics.

There is less agreement regarding surgical indications for process fractures of the talus. Acute, displaced fractures with large fragments showing extension into the subtalar joint by CT imaging are best treated with open reduction and internal fixation.

There are two common types of neck fractures: an extraarticular pattern and an intra-articular type that extends into the subtalar joint.

The goals of temporary external fixation are to maintain the length of the talus for reconstruction, facilitate soft tissue management, and restore general alignment. External fixation is a temporary form of management for talus fractures until internal fixation can be safely performed.

Displaced, open or closed, fractures benefit most from rigid internal fixation for bone healing and early motion. However, a recent report evaluating results of the extruded talus identified definitive external fixation as an option to manage the purely dislocated talus. This is an excellent treatment option to stabilize the ankle and subtalar and talonavicular articulations of the talus.