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 a challenging entity to treat. Poor outcomes remain all too common. Even though most osteonecrosis of the talus are traumatic, up to 25% of cases have atraumatic etiologies, including corticosteroid use, alcoholism, hyperlipidemia, irradiation, thrombophilia, and idiopathic etiologies. Treatment strategies for osteonecrosis of the talus can be divided into three categories: nonsurgical, joint-sparing surgery, and joint-sacrificing surgery. Before the collapse of the articular surface, nonsurgical treatment designed to protect the joint along with limited weight-bearing should be used until revascularization. For a patient who has undergone unsuccessful nonsurgical treatment or has articular collapse of the talar dome, the treatment options may include core decompression and bone grafting. A joint-sacrificing surgery should be considered as a last resort or for a patient with end-stage arthritic changes.
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.
Symptoms and Diagnosis
Pain is the most common symptom of talar osteonecrosis and is strongly associated with a loss of articular integrity.17 Before the collapse of the articular surface, a patient may be asymptomatic. With osteonecrosis of the subchondral bone, subchondral collapse can occur owing to a lack of structural support against pressure from body weight on the articular surface. This sequence is regarded as subchondral fracture and can cause pain as well as mechanical symptoms.1
Although MRI and bone scanning are useful for early detection of talar osteonecrosis, evaluation should begin with plain radiography of the ankle. Early sclerotic changes, cystic changes, and advanced changes related to subchondral collapse can be seen on plain radiographs. The Hawkins sign may provide evidence of revascularization and is thought to be a reliable early indicator of vascular viability, with few false-negative results1 (Figure 3). The Hawkins sign is a subchondral radiolucent band in the dome of the talus that can be seen on AP radiographs of the ankle at 6 to 8 weeks after fracture, and on lateral radiographs at 10 to 12 weeks after fracture. Subchondral collapse often has no symptoms, and it is rare to detect lesions on plain radiographs during the early stage of talar osteonecrosis. MRI is considered a key diagnostic tool during the early stage.4 It is used to diagnose and quantify the extent of osteonecrosis because of its sensitivity to altered fat cell signals. Bone marrow is predominantly composed of fat components responsible for strong T1-weighted images, and bone marrow necrosis with subsequent edema is an early indication of osteonecrosis.1 The necrotized materials show the density of water, which is revealed with high signal intensity on T2-weighted images. Chen et al studied the prognostic value of the Hawkins sign and diagnostic value of MRI after talar neck fractures. They concluded that a positive Hawkins sign has no predictive value regarding ankle function in low-energy fractures and may predict better ankle function in high-energy fractures, and recommended that Hawkins-sign-negative patients should undergo MRI examination at 12 weeks after fracture, especially in high-energy trauma cases.18
MRI can also be used to examine advanced stages of talar osteonecrosis. Titanium screws should be used for fixation of a talar fracture to minimize signal interference. Titanium implants are preferable to stainless-steel implants because of their nonmagnetic properties. Technetium Tc 99m bone scanning is also helpful for diagnosing early stage talar osteonecrosis; it is usually performed at 6 to 12 weeks after internal fixation of the talar fracture and shows decreased uptake in the talar body. Radiographic findings are commonly used with the Ficat and Arlet classification system to determine the extent of talar osteonecrosis (Table 1).17
Treatment options for talar osteonecrosis can be grouped into four categories: nonsurgical, surgical joint-sparing, surgical salvage, and joint-sacrificing treatment. Nonsurgical treatment includes restricted weight-bearing, patellar tendon-bearing braces, and extracorporeal shockwave therapy. Surgical joint-sparing treatment includes internal implantation of a bone stimulator,19 vascularized autograft, and core decompression. Joint-sacrificing procedures include talar replacement (partial or total). Salvage treatment includes arthrodesis.
TABLE 1 The Ficat and Arlet Classification of the Radiographic Appearance of Talar Osteonecrosis
Cystic and sclerotic lesions. Normal talar contour
Crescent sign. Subchondral collapse
Narrowing of the joint space. Secondary changes in the tibia
Adapted with permission from Delanois RE, Mont MA, Yoon TR, Mizell M, Hungerford DS: Atraumatic osteonecrosis of the talus. J Bone Joint Surg Am 1998;80(4):529-536.
Many treatments for talar osteonecrosis have been described, but few long-term or critical-outcome studies have been published, and there is currently no consensus as to the best form of treatment. Nonsurgical treatment is preferred for talar osteonecrosis at Ficat and Arlet stage I, II, or III. Some early studies found benefit in avoiding weight-bearing until revascularization was complete.20,21,22 A study of 23 patients with posttraumatic osteonecrosis found that patients who were non-weight-bearing on crutches for an average of 8 months had a fair-to-excellent result.8 Those who were partially weight-bearing in a patellar tendon brace or short leg brace with limited ankle motion had a poor-to-good result. Most of those who received no treatment (defined as non-weight-bearing for less than 3 months) had a poor result. Other investigators reported that protected weight-bearing using a patellar tendon brace had a favorable outcome and that delayed weight-bearing had no benefit.23,24 The amount and duration of weight-bearing should be determined for each individual patient based on the location of the lesion and its symptoms. No need to restrict weight-bearing ambulation exists if sufficient bony structures remain to support weight-bearing.24 Regardless of the extent of weight-bearing, it is important to preserve ankle motion, especially flexion and extension, and to protect the ankle from varus and valgus stress by using a patellar tendon brace or a cam boot walker (Figure 4).
Oral or intravenous bisphosphonates can be used for patients with talar osteonecrosis.25 Bisphosphonates are antiresorptive agents that inhibit the action of mature osteoclasts on bone, thereby changing the balance between resorption and deposition of bone to allow greater deposition. Bisphosphonates appear to transiently stimulate the proliferation of pro-osteoblast cells, increase their differentiation, increase the production of antiresorptive protein osteoprotegerin by osteoblasts, and decrease edema at the site of osteonecrosis.26 Although bisphosphonates have been used widely for patients with osteonecrosis of the femoral head, their use for talar osteonecrosis is off-label and controversial.
Ultrasound bone stimulators can also be used for bone regeneration.25 Low-intensity pulsed ultrasound was found to enhance the osteogenic differentiation of mesenchymal stem cells, stimulate the differentiation and proliferation of osteoblasts, inhibit the activities of osteoclasts, improve local blood perfusion and angiogenesis, and accelerate stress fracture healing.27 Extracorporeal shockwave therapy was found to be an effective treatment for osteonecrosis of the femoral head but is a controversial off-label treatment for talar osteonecrosis.28