Osteonecrosis of the Talus

Osteonecrosis of the Talus

Young Koo Lee, MD, PhD

Hyuk Jegal, MD

Keun-Bae Lee, MD, PhD

Thomas H. Lee, MD

Dr. Thomas H. Lee or an immediate family member has received royalties from Bledsoe Corporation, Stryker, and Wright Medical Technology, Inc.; has stock or stock options held in GLW Medical Innovations; and serves as a board member, owner, officer, or committee member of the American Orthopaedic Foot and Ankle Society. None of the following authors or 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: Dr. Young Koo Lee, Dr. Jegal, and Dr. Keun-Bae Lee.

This chapter is adapted from Lee KB, Byun JW, Lee TH: Osteonecrosis of the Talus in Chou LB, ed: Orthopaedic Knowledge Update: Foot and Ankle 5. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2014, pp 283-293.


Osteonecrosis of the talus is difficult to diagnose and treat because of the anatomic location of the talus and because its blood supply is precarious.1 Osteonecrosis of the talus is not always clinically symptomatic, and patients should be followed until revascularization and consolidation are complete. No consensus exists as to the pathophysiology or natural course of the disease. Many treatments and surgical techniques have been attempted, but few long-term outcome reports have been published.

The incidence of talar osteonecrosis is rising, along with an increasing incidence of high-energy trauma.1 Although previous studies cite an incidence of 0.1 to 2.5% for all fractures, the true incidence is unknown.2 Injury to the talus requires extreme force; falls from a substantial height and motor vehicle crashes are the primary causes of this condition.3 Survivors of a high-speed motor vehicle crash often incur injuries to the distal extremities. The use of highly developed imaging techniques has led to an increase in the number of patients diagnosed with an early talar lesion.

Anatomy and Vascular Supply

An understanding of the unique anatomy of the talus and its blood supply is crucial for comprehending diagnosis of talar osteonecrosis. The orientation of the talar neck differs from that of the body of the talus in both the horizontal and sagittal planes. In the horizontal plane, the neck shifts medially with deviation. In the sagittal plane, the neck deviates downward. This complex shape can lead to difficulty in determining the accuracy of reduction on radiographs. The talus has seven articular surfaces that make up almost 60% of its surface, and screw fixation using the anteromedial approach is complicated1 (Figure 1). The talus is most stable in the mortise at dorsiflexion because it is much wider anteriorly than posteriorly. The bone is recessed for dorsiflexion at the neck of the talus, which is the common site of talar fracture, especially during hyper-dorsiflexion with axial loading.

The talus has no tendinous attachments or muscular origins. The entire blood supply comes from several direct vascular insertions; understanding the contribution of each of these is important to avoid iatrogenic vascular
injury. The posterior tibial, dorsalis pedis, and perforating peroneal arteries are the three main extraosseous arteries that supply the talus4 (Figure 2). The posterior tibial artery constitutes the principal blood supply of the talar body through the artery of the tarsal canal and deltoid artery.5 The artery of the tarsal canal arises from the posterior tibial artery within the deltoid ligament below the medial malleolus and passes between the sheath of the flexor digitorum longus and flexor hallucis longus to enter the tarsal canal. The deltoid artery, which travels between the deep and superficial deltoid ligament and arises near the origin of the artery of the tarsal canal, is an important source of extraosseous circulation to the body of the talus. Preservation of the deltoid artery is therefore critical during stabilization or reduction of the talar neck and body. The artery of the tarsal sinus is formed from the anatomic loop between the dorsalis pedis and perforating peroneal arteries and merges with the artery of the tarsal canal. Together, these arteries feed most of the talar neck and head.1,4,5

FIGURE 1 Schematic drawings showing the important anatomic features of the talus. A, Posterior view; B, inferior view; C, lateral view; D, superior view; and E, medial surface of the talus.

FIGURE 2 Schematic drawings showing the blood supply of the talus. A, The medial talar blood supply. The first branches of the posterior tibial artery are the posterior tubercle branches. More distally, the posterior tibial artery comes off the tarsal canal artery with its deltoid branches. This artery courses through the tarsal canal. B, The lateral talar blood supply. The lateral tarsal artery connects the dorsalis pedis artery to the perforating peroneal artery and branches to form the tarsal sinus artery. C, The inferior talar blood supply. The tarsal sinus artery and the tarsal canal artery form an anastomotic loop within the tarsal canal. D, The posterior talar blood supply. The posterior tubercle branches of the posterior tibial artery and perforating peroneal artery supply the medial and lateral tubercles.

Etiology and Incidence

Osteonecrosis of the talus has three primary causes. Approximately 75% of patients have a history of trauma including talar neck or body fracture. The incidence of osteonecrosis after talar neck fracture increases with greater initial fracture displacement.6 Fifteen percent of patients have a nontraumatic medical condition as well as a history of steroid use (regardless of dosage or duration of use).1 Some of these patients have alcoholism, sickle cell disease, dialysis, hemophilia, hyperuricemia, or lymphoma.5,7,8,9,10

The remaining 10% of patients have idiopathic talar necrosis without a determined traumatic or medical cause.11 The Hawkins12 classification system for talar neck fractures stratifies the future risk of osteonecrosis based on fracture displacement and joint congruency. The risk after a type I talar fracture is 10%; after a type II fracture, almost 40%; and after a type III fracture, approximately 90%. Type IV implies the development of talar osteonecrosis to an even greater extent than type III.5,13 Talar body and neck fractures do not differ significantly in terms of the risk of developing osteonecrosis.14 Vallier et al15 introduced the possibility of dividing the Hawkins type II classification into subluxated (type IIA) and dislocated (type IIB) subtalar joint subtypes in terms of predicting the development of osteonecrosis of the talus. They concluded that following talar neck fracture, osteonecrosis of the talar body is associated with the size of the initial displacement. Osteonecrosis did not occur when the subtalar joint was not dislocated.

The death of hematopoietic cells, capillary endothelial cells, and lipocytes can usually be confirmed microscopically after 1 to 2 weeks of circulatory compromise. Lipocytes release lysosomes that acidify the tissue, causing osteocytes to shrink and the water content of bone to increase. As a consequence of bone collapse, saponification of fat or creeping substitution occurs, which means the gradual replacement of necrotic tissue with new osteogenic tissue followed by bone formation. Without the ability to repair itself, the dysvascular bone eventually collapses, appearing fragmented and sclerotic. This process accelerates with additive microtrauma, which can occur during unprotected weight-bearing with ambulation.5,16

FIGURE 3 The Hawkins sign in a woman who had undergone external and internal fixation of a complex pilon fracture. Mortise view (A) and lateral (B) radiographs of the ankle reveal striking subchondral radiolucency (arrows), indicating talar viability.

Feb 27, 2020 | Posted by in ORTHOPEDIC | Comments Off on Osteonecrosis of the Talus

Full access? Get Clinical Tree

Get Clinical Tree app for offline access