Necrosis means the death of the tissue due to ischemia. Osteonecrosis means the death of the bone tissue and both the terms are used interchangeably though their historic usage was for different contexts.
Avascular necrosis of talus may occur following talar neck fractures or could occur due to atraumatic reasons.
Avascular necrosis of talus occurs in 40% of fractures of the neck.
The rate of occurrence of avascular necrosis talus is as follows in different types of talar neck fractures.
- Type I – 0% to 13%
- Type II – 20% to 50%
- Type III – 83% to 100%
Avascular necrosis of talus can involve the entire talar body or only a small part.
Relevant Anatomy of the Talus
The talus is the second largest of the tarsal bones and has a unique structure designed to channel and distribute body weight. Approximately 60% of its surface is covered by articular cartilage, and there are no muscular or tendinous attachments to this bone. Therefore, only a limited area of area of penetrable bone is available for vascular perforation.
Along with this, small nutrient vessels, variations in intraosseous anastomoses, and a lack of collateral circulation put talus at risk for avascular necrosis when its blood supply is disturbed.
Talus consists of body, neck, and head, articulating with the calcaneus inferiorly, the tibia and fibula supralaterally (proximally), and the navicular bone distally.
The body of the talus is wider anteriorly than posteriorly. It also includes two bone processes – a lateral process and a posterior process.
The posterior process is divided into medial and lateral tubercles by a groove for the flexor hallucis longus tendon.
The supralateral and, to a lesser extent, medial cartilaginous surface of the talus extend to articulate with the tibia and fibula.
The inferior surface articulates with the posterior facet of the calcaneus, forming a part of the subtalar joint.
The neck of the talus is narrow and cylindrical in shape.
Talar neck has many ligamentous insertion. In addition, the talar neck has both a paucity of cartilage. This gives it a rough appearance.
The head of the talus is a convex structure that articulates with the navicular bone anteriorly. Its inferomedial surface articulates with the anterior and middle facets of the calcaneus.
Three extraosseous arterial contributors branch to supply the bone: the posterior tibial artery, the dorsalis pedis artery, and the perforating peroneal artery.
Many variations are known to exist intraosseously and may help explain patterns of avascular necrosis and difference in the rate of avascular necrosis in patients with same Hawkins type fracture.
Posterior tubercle branches arise from the posterior tibial artery and in combination with branches of the perforating peroneal artery, supply both the medial and lateral tubercles.
Beyond this, about 1 cm proximal posterior tibial artery gives rise to the tarsal canal artery. This artery courses in a posteromedial to anterolateral direction through the tarsal canal into the tarsal sinus, where it anastomoses with the tarsal sinus artery which arises from the anastomotic loop between the perforating peroneal artery and the lateral tarsal artery. ‘The tarsal canal artery supplies the central and lateral two-thirds of the talar body.
Deltoid branches arising from this artery supply the remaining medial third of the talar body.
Branches of the anterior tibial artery supply the superomedial half of the talar head and neck.
The inferolateral half is supplied either directly by the tarsal sinus artery, from branches of the anastomotic “loop” between the tarsal sinus artery and the tarsal canal artery, or from the lateral tarsal artery (a branch of the dorsalis pedis artery).
Read more on talus anatomy
Read more on the blood supply of talus
Pathophysiology of Avascular Necrosis
Avascular Necrosis of talus occurs when there is an interruption in any part of the vascular network. That may be in arteries or capillaries, sinusoid, and veins.
The cause for this may be an obstruction within the vessel, compression of the vessel or trauma to the vessel. The resulting insufficient blood supply and subsequent oxygen deprivation lead to the osteonecrosis of the talus.
The repair response of the body attempts at reossification, revascularization, and resorption of necrotic bone.
This is the time when the avascular necrosis becomes apparent radiographically..
Initially, the avascular necrosis can be missed because the necrotic bone and surrounding bone are of equal radiopacity. With time, owing to increase in circulation of blood of the region, the surrounding normal bone decreases in radiopacity due to resorption [the dead bone remain of the same opacity because of lack of the blood supply and thus resorption].
At this point, radiographic evidence of talar osteonecrosis becomes apparent. Reossification occurs and new bone is laid down over necrotic trabeculae. This process accounts for the typical sclerotic picture seen in AVN of the talus.
Reossification of the necrotic bone and, revascularization and resorption of the normal bone leads to the formation of a radiolucent rim becomes apparent around the area of osteonecrosis.
Thus x-ray would detect the osteonecrosis quite late.
MRI, on the other hand, detects it in the early stages.
CT scan can be used to confirm radiographic findings and for viewing subtle depression, collapse, and fragmentation of the dome.
However, X-rays remain the mainstay of the diagnosis and temporal observation of talar AVN.
Classification of Osteonecrosis of Talus
Osteonecrosis of the talus can be classified on the basis of the traumatic and atraumatic processes that impair nutrient blood supply to the bone.
Atraumatic Avascular Necrosis of Talus
- Systemic lupus erythematosus
- Renal transplants
- Sickle cell anemia
- Inherited thrombophilias
- Tobacco abuse
- Gaucher’s disease
- Stress associated with exercise
Traumatic Avascular Necrosis of Talus
- Fracture and dislocation of the talar neck,
Diagnosis of Avascular Necrosis of Talus
In cases of patients following up after trauma, there may not be any symptom as the ankle is immobilized and the patient is nonweight bearing. The avascular changes would be only seen on x-rays 6-8 weeks after the injury. So a high index of suspicion needs to be maintained.
Atraumatic avascular necrosis may present with ankle pain, initially at weight bearing only and then increasing. There would be no changes in routine x-ray.
The patient then must be evaluated for the risk factors and if there is a high suspicion, more sensitive investigations like MRI and bone scans should be done.
Avascular necrosis is recognized on x-ray when the talar body shows increased radiodensity compared to the surrounding bone.
The partial or complete collapse of the subchondral bone, narrowing of joint space, and occasionally fragmentation of the talar body may occur as the revascularization advances.
Osteosclerotic changes in the posterolateral corner of the talus will persist for a long time since it has the poorest blood supply
Hawkins Sign on AP view
This suggests evidence of revascularization of talar body and is thought to indicate talar viability. It is indicated by
patchy subchondral osteoporosis at approx 6-8 weeks;
– resorption of subchondral bone
As in many cases, the blood supply that remains is from the medial side [by branches of deltoid artery], the Hawkin’s sign is often seen medially.
MRI shows low signal on T1-weighted images secondary to adipocyte death and a variable signal on T2-weighted images depending on contents of the avascular region. Pathognomonic “double line” sign uncommon.
It can pick the signs of osteonecrosis at the earliest.
Treatment of Avascular Necrosis of Talus
After trauma, the ankle is immobilized and kept nonweight bearing. This should be continued and the patient should keep the foot off the ground to not to load the weak talus and protect its integrity while it revascularizes and regains the strength to bear the load.
It may require up to 36 months of nonweight bearing as that is the period required for creeping substitution and the best results are obtained without nonweight bearing until revascularization is obtained.
If diagnosed before the collapse, the non-traumatic cases are treated in the same line.
Cases seen late and with collapse would require ankle arthrodesis with or without subtalar arthrodesis is required.
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