Dr KS Dhillon FRCS
Introduction
The talus is one of the largest bone of the foot. Fractures of the talus are uncommon and constitute less than 1% of all fractures and between 3 to 6% of foot fractures (1). About 60% of the talus is covered by cartilage and its blood supply is precarious. Hence injuries of the talus are associated with a high incidence of avascular necrosis (AVN) of the bone which can approach 100% in comminuted fracture of the body and type IV fractures of the neck. The outcome of treatment of AVN is generally poor with no definite consensus as to the best mode of treatment. To date the quality of evidence about the best method of treatment of AVN of the talus is very low.
Anatomy of the talus
The talus is the largest tarsal bone of the foot after the calcaneus. It is made up of three parts, the body, neck and the head. The head is covered with hyaline cartilage and it articulates inferiorly with the calcaneus (anterior subtalar joint) and anteriorly with the navicular bone (talonavicular joint). The body of the talus has two processes, the lateral and posterior processes. The posterior process forms the medial and lateral tubercle and in the groove between the two, passes the flexor hallucis longus tendon. The lateral process is large and it articulates superiorly with the fibula and inferiorly with the calcaneus to form the posterior subtalar joint. Inferior part of the body has a smaller middle articular facet which forms the middle subtalar joint with the calcaneus. Superiorly the body of the talus articulates with the tibia and fibula to form the tibiotalar joint. The part of the talus which forms the tibiotalar is also known as the dome or the trochlea. About 60% of the talus is covered with articular cartilage. The body of the talus is connected to the head by the neck of the talus which is non-articular and inferiorly it forms the tarsal tunnel (2). The talus has no tendinous or muscular attachments although it has ligamentous attachment.
The vascular supply to the talus is precarious due to the absences of any muscular attachment and the fact that a large portion of talus is covered with articular cartilage. The blood supply reaches the talus through the non-articular surface via the posterior tibial artery, the dorsalis pedis and the peroneal artery (2).
Fractures of the talus
Fractures of the talus may involve the head, neck or the body. Fractures of the body are the most common and constitute about 13 to 61% of talar fractures. Fractures of the neck constitute about 5% and fractures of the head constitute about 5 to 10% of talar fractures (3).
Fractures of the talus can often be associated with talar or peri-talar dislocations. When a talar fracture is suspected an AP, lateral and a mortise view x-ray of the ankle and an AP, lateral and oblique x-ray of the foot has to be done. For an accurate analysis of the talar injury a CT scan is usually needed. Undisplaced fractures can be treated conservatively but displaced fractures would require accurate open reduction and internal fixation (2).
In the past neck fractures were believed to be the most common fractures of the talus but now with clearer differentiation between neck and body fractures, neck fractures are believed to form only 5% of fractures of the talus(3).
Neck fractures were originally classified by Hawkins (4) in 1970 and later modified by Canale and Kelly (5). This classification has prognostic significance (5 and 6).
Type 1 – Nondisplaced fractures of the neck. Incidence of avascular necrosis (AVN) is between 0 to 15%.
Type 11 – Fractures of the neck with talocalcaneal dislocation. Incidence of AVN between 20 to 50%.
Type 111 – Fractures of the neck with talocalcaneal and tibiotalar dislocation. The incidence of AVN is 100%.
Type 1V – Fractures of the neck with disruption of all talar articulations. The incidence of AVN is 100%.
Talar body fractures are divided into 5 types according to a classification by Sneppen (2). The five categories of body fractures as suggested by Sneppen include:
Type A – Compression osteochondral fracture of the dome.
Type B - Coronal shear fractures
Type C – Sagittal shear fractures
Type D – Posterior tubercle fractures
Type E –Lateral process fracture
Type F – Crush comminuted fracture
The fractures are often associated with dislocation of the talocalcaneal, tibiotalar or both the joints. Coronal shear fractures are best seen in the lateral view x-rays and the sagittal shear fractures are best seen in the AP view x-rays. The crush comminuted fractures (type F), which usually result from high impact injuries, have the worse prognosis. They are often open and are associated with bone loss, inaccurate reduction and avascular necrosis (7).
Dislocation of the talus.
Dislocation of the talus can be of two types namely, a subtalar (peritalar) or a pantalar dislocation. Subtalar dislocations can be medial (more common) or lateral (less common). Anterior and posterior dislocation may occur but is very rare. In subtalar dislocation the tibiotalar and the calcaneocuboid joints remain intact while the subtalar and talonavicular joints are disrupted. Lateral dislocations are less common but more serious being associated with higher incidence of AVN and posttraumatic subtalar OA (8).
Pantalar dislocations are very rare. The talus usually dislocates anterolaterally. It may be an open or a close injury and the talus may or may not have soft tissue attachment. Open injuries are often associated with osteomyelitis and AVN. Traditionally pantalar dislocations have been treated by excision of the talus and arthrodesis but there are calls for relocation of the talus whenever possible (9).
Outcome of treatment of talar injuries
Frawley et al (10) studied the long-term outcome of treatment of major talus fractures which excluded isolated fractures of the dome and the posterior tubercle. They studied 26 patients, 15 of whom were treated by open reduction and internal fixation and 11 were treated by nonsurgical means. They found the incidence of AVN to be 15% (4 out of 26 patients) and only in 1 patients the AVN was severe enough to require fusion. Subtalar OA was seen in 61% of the patients. Only 3 patients did not return to work at an average follow-up of 6 years. Forty-two percent of the patients were not able to return to their premorbid activity level.
Ebraheim et al (11)and there were two associated neck fractures. At an average of 26 (18-43) months the AOFAS (American Orthopedic Foot and Ankle Society) scores were excellent in 4, good in 6, fair in 4 and poor in 5 patients. There was AVN in 7, deep infection in 1 and malunion in 1 patient.
Vallier et al (12) in a level IV study reported a 38% incidence of AVN, 65% incidence of tibiotalar OA and 34% incidence of subtalar OA, in 26 talar body fractures at minimal follow-up of 1 year.
Vallier et al (13) in another retrospective review of 100 patients with talar neck fractures who were treated surgically, sixty were available for review at an average of 36 months follow-up. Of these 39 had complete radiographic data. The incidence of AVN was 49%. In 37% of these patients with AVN revascularization occurred with no collapse of the dome. The overall incidence of collapse of the dome was 31%. The incidence of AVN was 39% in the Hawkins II fractures and 64% in Hawkins III fractures. Fifty-four percent of the patients developed post-traumatic OA and it was more common in patients with comminuted and open fractures.
Pajenda et al (14) reviewed the clinical outcome of 50 patients with talar neck fractures. Thirty-two percent were type I, 28% type II, 18% type III and 22% type IV (Hawkins) fractures. Mild ankle OA developed in 28% of patients and severe OA was seen in 20% of the patients. Fifty percent of patients with severe OA needed ankle arthrodesis. Subtalar OA was seen in 8% of the patients and AVN with dome collapse was seen in8% of the patients. Functional scores according to Weber was good to excellent in 95% of patients with type I and II fractures. Good results were seen in 70% of patients with type III and 10% of type IV fractures.
Sneppen et al (15) in a review of 51 patients with fracture of the body of the talus found that the severity of the initial injury determines the long-term outcome. Severe compression fractures of the body are associated with about 50% incidence of OA of the ankle. Shearing pattern fractures are associated with about 41% incidence of ankle and subtalar OA.
Canale and Kelly published the outcome of 71 fractures of the talar neck at an average follow-up of 12.7 years. They reported a 59% good to excellent results in their patients. The incidence of AVN was 52% in their study.They found that ‘triple arthrodesis, tibiocalcaneal fusion, and dorsal beak resection of the talar neck all resulted in a high percentage of satisfactory results, but talectomy did not’ (16).
Post-traumatic avascular necrosis
Seventy-five percent of talar AVN is post-traumatic in origin which results from fracture\dislocations of the talus (17). Non-traumatic causes include steroid use, alcoholism, hyperuricemia, hyperlipidemia, occlusive vascular disease, SLE and sickle cell disease (18).
In type III fractures of the neck the incidence of AVN can approach 83% to 100%. In type IV fractures of the neck and comminuted fractures of the body the incidence of AVN can reach 100% (18). In AVN the amount of bone involved may be small as in osteochondral lesions, partial or complete with total involvement of the body of the talus (19).
The diagnosis of AVN can be made on an AP mortise view of the ankle where the avascular bone will appear dense compared to the surrounding vascular bone. These changes may not be visible till about 3 months or more after the injury to the talus. The earliest sign of revascularization of the talus can be seen as early as 6 to 8 weeks post-trauma and it manifests as the Hawkin’s sign which is a line of subchondral radiolucency due osteoporosis in vascular zone seen in the AP mortise view of the ankle. A partial Hawkin’s line is a sign of partial revascularization most often seen on the medial side where vascularity is better. The presences of Hawkin’s sign is highly predictive of absences of AVN. Though it is highly sensitive (100%), it is not very specific(57.7%) since the absence of the sign does not predict the presences of AVN (19). The posterolateral corner of the body has the poorest blood supply and hence AVN changes are most common at that site. Later as revascularization occurs a partial or complete collapse of subchondral bone will occur. Occasionally fragmentation of the whole talar body can occur (19). An MRI is useful in determining the extent of AVN. The more extensive the AVN the greater the chance of collapse and fragmentation.
The primary goal in the treatment of talus fracture is to achieve an accurate stable reduction and union. Bony union is possible even in the presence of AVN (20). Weight bearing should be avoided till fracture union has occurred. After fracture union in the presence of AVN (absent Hawkin’s sign) the aim of treatment is prevention of late collapse. The process of creeping substitution of the avascular segment can take up to 36 months (21).
From the point of view of treatment it is useful to divide talar AVN into the early and the late stage categories. In the late stage the options for treatment are limited to a talectomy or an arthrodesis (21).
The treatment of early stage AVN is controversial. The question is what to do while revascularization is occurring? Some believe that the patient should be non-weight bearing till revascularization is complete (22-24) while others believe that patients should be partial weight bearing on a patella tendon brace (25-27). There are others who believe that it is not possible to be non-weight bearing or partial weight bearing for long periods of time when we know that revascularization can take up to 36 months. They believe that it is better to deal with the symptoms as and when they arise (28-30). Poor results in patients with AVN of the talus does not apparently correlate with the method of treatment and the time the patient has been non-weight bearing (31).
In patients who have pain due AVN in the pre-collapse stage, core decompression to reduce intraosseous pressure and promote revascularization has been recommended by some surgeons. In patients who continue to have pain after decompression various types of bone grafting has been proposed. This include non-vascularised auto or allografts or vascularized bone grafts (21).
In the late stage when talar collapse and post-traumatic OA has set in the treatment options in symptomatic patients is talectomy or an arthrodesis. Traditionally talectomy has not been associated with good results but Gunal et al (32) has developed a new technique which apparently gives excellent to good results. More often arthrodesis of the ankle, subtalar joints or a triple arthrodesis is carried out depending on the joints affected by post-traumatic OA and the AVN (19).
Although there are many published treatment options for post-traumatic talar AVN, ‘critical outcome studies are still lacking’ (33). Gross et al (34) did a systematic review of treatments for AVN of the talus. They were able to identify 19 suitable studies with 321 ankles at final follow-up. The modalities of treatment included conservative measures such as protective weight bearing, core decompression, bone grafting, vascularized bone grafting, hindfoot fusion and talar replacement. The quality of evidence was ‘very low’ and all the studies were level IV studies. In the early stages protected weight bearing appears to be the treatment of choice and if it fails core decompression may be an option. Arthrodesis would be the salvage operation of choice when all else have failed.
Conclusion
Injuries to the talus are fortunately uncommon.The major part of the talus is covered with cartilage and there is no muscle attachment to the talus.Hence the blood supply to the talus is precarious and it makes it vulnerable to avascular necrosis, the incidence of which can reach 100% in some types of fractures and dislocation of the talus. The outcome of treatment of AVN is generally poor and there is no consensus as to best method of treatment of patients with AVN. The quality of evidence to support any particular form of treatment of patient with AVN remains poor.
References
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