Talar Avascular Necrosis

Talar Avascular Necrosis

Christopher F. Hyer

William T. DeCarbo

Avascular necrosis (AVN) or osteonecrosis is defined as a disease resulting from temporary or permanent loss of the blood supply to bone (1). Bone without blood supply and nourishment will necrose, causing the bone to collapse (1). This process is often very painful and debilitating, particularly in the case of the talus since it supports both the ankle and subtalar joints (STJs) (Fig. 115.1A).

There are many causes of AVN to bone, including include idiopathic, alcoholism, corticosteroid use, caisson disease (decompression sickness), vascular compression, hypertension, vasculitis, thrombosis, bisphosphonates, sickle cell anemia, and rheumatoid arthritis. The most common cause in the foot and ankle is posttraumatic talar fracture (2,3,4,5,6,7,8,9,10 and 11) (Fig. 115.1B).


The unique anatomy and tenuous blood supply of the talus makes it susceptible to AVN. The talus comprises a body, head, and neck. The talus articulates with the tibia, the malleoli, the navicular, and the calcaneus. Due to the multiple articulations, the talus is covered with approximately 60% of hyaline cartilage (12). This high percentage of hyaline cartilage coverage leads to a precarious blood supply since there are limited nonarticular surfaces for the vessels to penetrate.

The arterial supply of the talus is made up of both extraosseous and intraosseous circulation. The three main branches that supply the talus are the posterior tibial artery, the dorsalis pedis artery, and the perforating peroneal artery. The posterior tibial artery gives off the artery of the tarsal canal. This branch enters the canalis tarsi and anastomoses with the artery of the sinus tarsi. This anastomosis helps to supply the talar head and neck. The artery of the tarsal canal gives off a branch deep to the deltoid ligament called the deltoid artery. This artery supplies the talar body. Laterally, the artery of the sinus tarsi is formed by the anastomosis of the perforating peroneal artery and the lateral tarsal artery. The lateral tarsal artery is a branch of the dorsalis pedis artery (13,14,15,16,17 and 18). The intraosseous blood supply of the talus is made up of various vascular foramina. The talar head is supplied primarily by the anterior tibial artery. The deltoid artery contributes significantly to the intraosseous circulation in the medial and proximal portions of the talar body. The anterolateral talar body and the posterior tubercles are relatively avascular (12) (Fig. 115.2).


The true pathomechanism of AVN remains unknown. The three broad causes are idiopathic, medication induced, and traumatically induced. It appears that an acute injury comprising vascular disruption, along with a delayed form of microvessel thrombosis and fibrosis in acute traumatic events, leads to AVN (19).

Glucocorticoid administration is the most common cause of nontraumatic AVN (20,21) (Fig. 115.3). There are many theories to describe this etiology. One theory suggests that fat embolism from the liver, the marrow fat cell, or from destabilization and coalescence of plasma lipoproteins could be responsible. Another theory states that the associated insulin resistance favors the development of hypertension and arteriosclerosis. Suggestions have also been made that steroidinduced osteoporosis can cause microfractures in susceptible bone (22). Another factor that seems to contribute to the development of AVN is the inhibition of angiogenesis. This inhibition is apparently caused by reduction in proteolytic activity by the synthesis of plasminogen activator inhibitor (20,23).

Another potential cause of AVN is alcoholism. It has been reported that patients who consume up to 320 g of ethanol per week had a 2.8 increase in the relative odds of developing AVN (24). As mentioned above, several other case reports have been made in regards to the development of AVN; however, the majority of causes for the talus remains trauma.


In regards to the talus, it is generally accepted that the incidence of AVN is dependent on the severity of the fracture and the degree of displacement (25,26). There are many classifications for talar fractures, depending on the anatomic location of the fracture (27,28,29,30,31,32 and 33). The most accepted classification system, that also serves as a prognostic indicator, is that described by Hawkins and later modified by Canale and Kelly (27,28) (Fig. 115.4).

This classification system comprises four types, with percent incidences of developing talar AVN. The incidence of AVN with talar neck fractures is reported as 0% to 100%, depending on severity and the amount of dislocation. More than half of all talar fractures are talar neck fractures, and this accounts for 90% of all traumatic AVN (12,27,28,34,35 and 36) (Fig. 115.5).

Hawkins type I fractures are nondisplaced vertical neck fractures. The reported incidence of AVN is 10%. Hawkins type II fractures consist of a vertical talar neck fracture with either subluxation or displacement of the STJ. The reported incidence of AVN is 42%. Hawkins type III fractures are characterized by a vertical talar neck fracture with subluxation or dislocation of both the ankle and STJs. The AVN incidence in this type is reported at 91%. Hawkins type IV fractures, as
modified by Canale and Kelly, consist of a vertical talar neck fracture with subluxation or dislocation of the ankle, STJ, and the talonavicular joint. Type IV fractures had a reported incidence of AVN at 100% (27,28,37).

Figure 115.1 A: Lateral radiograph left ankle: talar body AVN with collapse. B: Lateral radiograph right ankle: suspicious talar body sclerosis after ORIF of talar body fracture.


Patients with AVN of the talus usually present with pain and swelling. The degree of symptoms usually is determined by the integrity of the articular surface involvement (1). Patients typically have a history of previous injury or trauma. Initially, patients may complain of stiffness in the ankle and “soreness” with extended weight-bearing activities. Occasionally in the early stages, patients may be asymptomatic and without radiographic changes, suggesting AVN. As the AVN and collapse progress, the articular incongruity increases. Pain and mechanical symptoms such as clicking, locking, and grinding are the typical presenting complaints. Often, pain progresses from a predominately weight-bearing pain to more persistent and constant pain. Sequelae such as anterior ankle impingement and arthritis of the ankle, the STJ, and less commonly, the talonavicular joint, occur. As the process continues, collapse of the talar body can present as shortening of the affected limb.

Figure 115.2 Schematic of talar blood supply.

Figure 115.3 A: Lateral radiograph right ankle: systemic steroid-related talar body AVN with associated degenerative joint disease (DJD). B: Lateral radiograph left ankle: systemic steroid-related talar body AVN with associated DJD.

Jul 26, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Talar Avascular Necrosis

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