DOI: 10.1148/rg.252045709
RadioGraphics 2005;25:399-410
© RSNA, 2005
Avascular Necrosis of the Talus: A Pictorial Essay1
Dawn H. Pearce, MD, FRCPC,
Christopher N. Mongiardi, MD,
Victor L. Fornasier, MD, FRCPC and
Timothy R. Daniels, MD, FRCSC
1 From the Departments of Radiology (D.H.P., C.N.M.), Pathology (V.L.F.), and Orthopedic Surgery (T.R.D.), St Michael’s Hospital, University of Toronto, 30 Bond St, Toronto, Ontario, Canada M5B 1W8. Received April 29, 2004; revision requested June 3; final revision received August 18; accepted August 20. All authors have no financial relationships to disclose.
Address correspondence to D.H.P. (e-mail: pearced{at}smh.toronto.on.ca).
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Abstract
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The talus is predisposed to avascular necrosis (AVN), or bone death due to ischemia, owing to its unique structure, characteristic extraosseous arterial sources, and variable intraosseous blood supply. Both traumatic and atraumatic causes have been implicated in talar AVN. The risk of posttraumatic AVN can be predicted using the Hawkins classification system. In addition, the "Hawkins sign" can be used as a radiographic marker that excludes the development of AVN. At radiography, talar AVN typically manifests as an increase in talar dome opacity (sclerosis), followed by deformity and, in severe cases, articular collapse and bone fragmentation. At any stage of this sequence, the radiographic findings can vary depending on differences in the vascular status of the talus and the degree of bone repair. Magnetic resonance imaging is the most sensitive technique for detecting talar AVN and can be used when AVN is strongly suspected clinically despite normal radiographic findings. Computed tomography (CT) also demonstrates typical patterns and can be used to confirm radiographic findings. Coronal CT is required for viewing the articular surface of the talar dome to rule out subtle depression, collapse, and fragmentation. Nevertheless, radiography remains the mainstay of the diagnosis and temporal observation of talar AVN.
© RSNA, 2005
Abbreviations: AVN = avascular necrosis
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Introduction
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The word talus is derived from the Latin word taxillus, which refers to the ankle bone of a horse. These bones were used as playing dice by Roman soldiers (1). 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 (2,3). Consequently, only a limited area of penetrable bone is available for vascular perforation. This feature, combined with small nutrient vessels, variations in intraosseous anastomoses, and a lack of collateral circulation, predispose the talus to osteonecrosis when its vascular supply is disturbed (Figs 1, 2) (4).
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Figure 1. Lateral radiograph shows the normal skeletal anatomy of the foot and ankle. C = cuneiform bone, Cal = calcaneus, Cu = cuboid bone, F = fibula, M = metatarsal bones, N = navicular bone, Ph = phalanges, STJ = posterior facet of the subtalar joint, Tb = talar body, TD = talar dome, Th = talar head, Ti = tibia, Tn = talar neck.
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Figure 2a. Coronal computed tomographic (CT) scan (a) and sagittal T1-weighted magnetic resonance (MR) image (b) demonstrate the normal skeletal anatomy of the foot and ankle. AJ = ankle joint, C = medial cuneiform bone, Cal = calcaneus, Cu = cuboid bone, F = fibula, N = navicular bone, STJ = subtalar joint, T = talus, TD = talar dome, Ti = tibia, TN = talar neck.
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Figure 2b. Coronal computed tomographic (CT) scan (a) and sagittal T1-weighted magnetic resonance (MR) image (b) demonstrate the normal skeletal anatomy of the foot and ankle. AJ = ankle joint, C = medial cuneiform bone, Cal = calcaneus, Cu = cuboid bone, F = fibula, N = navicular bone, STJ = subtalar joint, T = talus, TD = talar dome, Ti = tibia, TN = talar neck.
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Avascular necrosis (AVN) is bone death due to ischemia. In the current literature, the term osteonecrosis is given this same definition. Historically, however, the term osteonecrosis has been used to describe ischemic bone death owing to sepsis, whereas the term avascular necrosis has been used to describe bone necrosis that was both avascular and aseptic in nature. Despite these differences, however, the terms AVN and osteonecrosis will be used interchangeably in this article. Other terms that have been used to describe aseptic bone necrosis include ischemic necrosis and bone infarction. Generally, the former term is used to describe necrosis of epiphyseal and subarticular bone, whereas the latter term refers to necrosis of metaphyseal or diaphyseal bone (5).
Regardless of the terminology used, talar necrosis occurs when the vascular supply of the talus is disturbed and the bone is deprived of its oxygen source (6). Although no specific radiographic classification system exists, osteonecrosis of the talus exhibits a characteristic radiographic pattern. It usually appears as an area of increased opacity or sclerosis in the talar dome that may extend into the talar body (Figs 3–5), with possible collapse of the articular surface and, in severe cases, fragmentation of the talar dome and body. In this article, we review the normal anatomy and blood supply of the talus. We also discuss and illustrate the radiologic features as well as both traumatic and atraumatic causes of AVN. In addition, we describe articular collapse and the use of the "Hawkins sign" to help diagnose and evaluate talar AVN.
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Figure 3a. AVN of the talus. (3a) Lateral radiograph shows marked sclerosis of the talar dome and body (arrow). (3b) Radiograph (mortice view) shows marked sclerosis of the entire talar dome and throughout the lateral talar body (arrowheads).
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Figure 3b. AVN of the talus. (3a) Lateral radiograph shows marked sclerosis of the talar dome and body (arrow). (3b) Radiograph (mortice view) shows marked sclerosis of the entire talar dome and throughout the lateral talar body (arrowheads).
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Figure 4. Radiograph (mortice view) shows an area of increased opacity in the medial talar dome that extends laterally toward the lateral talar dome (arrowheads), a finding that represents an osteonecrotic segment.
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Figure 5. Radiograph (mortice view) shows a lobulated subchondral radiolucent area extending into the talar body. This area represents peripheral sclerosis, which outlines a necrotic segment (black arrows). The 1-mm-wide depression in the articular surface of the medial third of the talar dome (white arrow) represents talar collapse.
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Anatomy of the Talus
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Talar anatomy has been extensively studied. Ossification of the talus originates from a single primary center that induces elongation in an anteroposterior direction (7). The talar frame, consisting of the body, neck, and head, articulates with the calcaneus inferiorly, the tibia and fibula supralaterally (proximally), and the navicular bone distally (8,9).
The body of the talus is uniquely shaped, being 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. In approximately 50% of the general population, an os trigonum is present over the lateral tubercle (10). The supralateral and, to a lesser extent, medial cartilaginous surface of the talus extend to articulate with the tibia and fibula, whereas the inferior surface articulates with the posterior facet of the calcaneus, forming a portion of the subtalar joint (7,11).
The neck of the talus is narrowed superiorly, inferiorly, and laterally. In addition, the talar neck has both a paucity of cartilage and a roughened appearance due to its many ligamentous insertions. The head of the talus is a convex structure with numerous articulations. Its anterior cartilaginous surface articulates with the navicular bone, whereas its inferomedial surface articulates with the anterior and middle facets of the calcaneus, the spring ligament, and the deltoid ligament (7).
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Blood Supply of the Talus
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The intra- and extraosseous vascular network of the talus has been well documented in the literature (Fig 6) (2,4,12,13). Three extraosseous arterial contributors branch to supply the bone: the posterior tibial artery, the dorsalis pedis artery, and the perforating peroneal artery. Variations exist intraosseously, and these variations in intraosseous anastomoses may help explain patterns of AVN as well as differences in the rates of osteonecrosis in patients with the same Hawkins type fracture (4,14).
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Figure 6a. Drawings illustrate the blood supply of the talus. (a) Medial talar blood supply. The first branches of the posterior tibial artery are the posterior tubercle branches. More distally, the posterior tibial artery gives off the tarsal canal artery with its deltoid branches. This artery courses through the tarsal canal. (b) Lateral talar blood supply. The lateral tarsal artery connects the dorsalis pedis artery to the perforating peroneal artery. It also branches to form the tarsal sinus artery. (c) Inferior talar blood supply. The tarsal sinus artery and the tarsal canal artery form an anastomotic loop within the tarsal canal. (d) Posterior talar blood supply. The posterior tubercle branches of the posterior tibial artery and perforating peroneal artery supply the medial and lateral tubercles.
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Figure 6b. Drawings illustrate the blood supply of the talus. (a) Medial talar blood supply. The first branches of the posterior tibial artery are the posterior tubercle branches. More distally, the posterior tibial artery gives off the tarsal canal artery with its deltoid branches. This artery courses through the tarsal canal. (b) Lateral talar blood supply. The lateral tarsal artery connects the dorsalis pedis artery to the perforating peroneal artery. It also branches to form the tarsal sinus artery. (c) Inferior talar blood supply. The tarsal sinus artery and the tarsal canal artery form an anastomotic loop within the tarsal canal. (d) Posterior talar blood supply. The posterior tubercle branches of the posterior tibial artery and perforating peroneal artery supply the medial and lateral tubercles.
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Figure 6c. Drawings illustrate the blood supply of the talus. (a) Medial talar blood supply. The first branches of the posterior tibial artery are the posterior tubercle branches. More distally, the posterior tibial artery gives off the tarsal canal artery with its deltoid branches. This artery courses through the tarsal canal. (b) Lateral talar blood supply. The lateral tarsal artery connects the dorsalis pedis artery to the perforating peroneal artery. It also branches to form the tarsal sinus artery. (c) Inferior talar blood supply. The tarsal sinus artery and the tarsal canal artery form an anastomotic loop within the tarsal canal. (d) Posterior talar blood supply. The posterior tubercle branches of the posterior tibial artery and perforating peroneal artery supply the medial and lateral tubercles.
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Figure 6d. Drawings illustrate the blood supply of the talus. (a) Medial talar blood supply. The first branches of the posterior tibial artery are the posterior tubercle branches. More distally, the posterior tibial artery gives off the tarsal canal artery with its deltoid branches. This artery courses through the tarsal canal. (b) Lateral talar blood supply. The lateral tarsal artery connects the dorsalis pedis artery to the perforating peroneal artery. It also branches to form the tarsal sinus artery. (c) Inferior talar blood supply. The tarsal sinus artery and the tarsal canal artery form an anastomotic loop within the tarsal canal. (d) Posterior talar blood supply. The posterior tubercle branches of the posterior tibial artery and perforating peroneal artery supply the medial and lateral tubercles.
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The first branches supplying the talar body arise from the posterior tibial artery. These are the posterior tubercle branches, which, in combination with branches of the perforating peroneal artery, supply both the medial and lateral tubercles. Beyond this branching point, about 1 cm proximal to its division into the medial and lateral plantar arteries, the posterior tibial artery gives rise to the tarsal canal artery (4). 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. The tarsal sinus artery 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 (12).
Branches of the anterior tibial artery supply the superomedial half of the talar head and neck. In addition, 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) (4).
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Radiologic Appearance of Talar AVN
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AVN (osteonecrosis) of the talus occurs with an interruption in any part of the vascular network, including arteries, capillaries, sinusoids, and veins. This interruption can be classified as obstruction, compression, or physical disruption (trauma) of vessels (5). In all cases, ischemic necrosis of bone occurs due to an insufficient blood supply and subsequent oxygen deprivation (6). The body’s response to AVN is an attempt at repair by means of reossification, revascularization, and resorption of necrotic bone (15). It is when these processes occur that AVN becomes apparent radiographically.
At initial radiography, necrotic bone and the surrounding viable bone are equal in opacity, and early AVN can be missed. As time passes and hyperemia results, healthy bone is resorbed and subsequently becomes osteopenic. However, necrotic bone cannot undergo resorption because it lacks a vascular supply; therefore, it eventually appears more radiopaque than the surrounding osteopenic bone. At this point, radiographic evidence of talar AVN becomes apparent. The opacity of necrotic bone continues to increase as 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 (Figs 7, 8). In addition to reossification, revascularization and resorption also tend to occur around necrotic bone. When these processes take place, a radiolucent rim becomes apparent around the area of osteonecrosis (Fig 9) (5,6,15).
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Figure 7a. AVN of the talus in a 42-year-old man who was involved in a serious motor vehicle accident. (a) Axial CT scan through the talus shows diffuse sclerosis involving the majority of the talus (white arrows), with focal sparing of the lateral talar dome (black arrow). (b) Axial fat-saturated T2-weighted MR image shows diffuse high signal intensity in the majority of the talus. The lateral talar dome demonstrates normal bone marrow signal intensity (arrowheads), a finding that corresponds to the normal region seen at CT.
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Figure 7b. AVN of the talus in a 42-year-old man who was involved in a serious motor vehicle accident. (a) Axial CT scan through the talus shows diffuse sclerosis involving the majority of the talus (white arrows), with focal sparing of the lateral talar dome (black arrow). (b) Axial fat-saturated T2-weighted MR image shows diffuse high signal intensity in the majority of the talus. The lateral talar dome demonstrates normal bone marrow signal intensity (arrowheads), a finding that corresponds to the normal region seen at CT.
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Figure 8a. Osteonecrosis of the talus in a 51-year-old woman who had received a short course of prednisone. Axial (a) and coronal (b) CT scans through the right talus show a mixed hypoattenuating-sclerotic pattern along the medial half of the talar dome that is outlined by a serpiginous sclerotic line (arrows). The mixed imaging pattern is consistent with osteonecrosis.
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Figure 8b. Osteonecrosis of the talus in a 51-year-old woman who had received a short course of prednisone. Axial (a) and coronal (b) CT scans through the right talus show a mixed hypoattenuating-sclerotic pattern along the medial half of the talar dome that is outlined by a serpiginous sclerotic line (arrows). The mixed imaging pattern is consistent with osteonecrosis.
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Figure 9a. AVN of the talus in a 42-year-old man who was receiving prednisone for inflammatory bowel disease. (a) Lateral radiograph of the ankle shows a large, curvilinear radiolucent cleft extending from the talar dome into the talar body (arrowheads). In addition, there is serpiginous sclerosis within the distal tibia, calcaneus, and navicular bone (arrows). (b) Corresponding sagittal reconstructed image of the ankle from CT data shows a hypoattenuating area (arrowheads) surrounding a collapsed fragment of the talar dome. Areas of serpiginous sclerosis within the distal tibia, calcaneus, navicular bone, and base of the first metatarsal bone are again evident (arrows), findings that are consistent with medullary infarcts.
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Figure 9b. AVN of the talus in a 42-year-old man who was receiving prednisone for inflammatory bowel disease. (a) Lateral radiograph of the ankle shows a large, curvilinear radiolucent cleft extending from the talar dome into the talar body (arrowheads). In addition, there is serpiginous sclerosis within the distal tibia, calcaneus, and navicular bone (arrows). (b) Corresponding sagittal reconstructed image of the ankle from CT data shows a hypoattenuating area (arrowheads) surrounding a collapsed fragment of the talar dome. Areas of serpiginous sclerosis within the distal tibia, calcaneus, navicular bone, and base of the first metatarsal bone are again evident (arrows), findings that are consistent with medullary infarcts.
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MR imaging is the most sensitive technique for detecting osteonecrosis of the talus, especially in the early stages. In addition, MR imaging can be used when there is a high clinical suspicion for AVN in the setting of normal radiographic findings (Fig 10 ). CT scans also reveal characteristic talar AVN patterns and can be used to confirm radiographic findings. Coronal CT of the talus is required for viewing the articular surface of the talar dome to rule out subtle depression, collapse, and fragmentation, especially at preoperative assessment. Despite the availability of cross-sectional imaging, however, conventional radiography remains the mainstay of the diagnosis and temporal observation of talar AVN.
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Figure 10a. Posttraumatic osteonecrosis of the talus in a 42-year-old man who subsequently underwent below-the-knee amputation. (a) Sagittal T1-weighted MR image through the ankle demonstrates a serpiginous low-signal-intensity line in the talar dome (arrows). (b) Corresponding sagittal fat-saturated T2-weighted MR image shows a high-signal-intensity line in the talar dome (arrow) that outlines an avascular segment. (c) Low-power photomicrograph (original magnification, x25; WHO stain [hematoxylin, phloxine, saffron, alcian green]) helps confirm AVN of the talus. The cartilage is thinned and is stained green by the alcian green dye, which helps identify mucopolysaccharides. Note the paler than expected green staining of the articular cartilage of the talar dome (white arrow). Near the ankle joint, a curvilinear band of fibrous tissue (black arrows) appears as a pale pink band outlining the area of necrosis; trabeculae are preserved in this area. On the external aspect of the arch of fibrosis, there are coarser, thicker trabeculae, indicating that this area of the bone is viable and is capable of reaction. (d) High-power photomicrograph (original magnification, x250; WHO stain) of a decalcified section shows viable tibia (Ti) on one side of the joint and necrotic talus (Ta) on the other. The bone trabeculae on the viable (tibial) side show smooth endosteal contours (white arrows); the adipose tissue of the bone marrow shows a fine filiform pattern (white arrowheads). These findings contrast with the necrotic (talar) side of the joint: Here, the cartilage shows a more homogeneous pattern with loss of all cellular detail, the subjacent bone contains irregular and partly fragmented trabeculae (black arrows), and the bone marrow shows patchy eosinophilia (black arrowheads), which indicate that the fat has undergone degenerative change with saponification.
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Figure 10b. Posttraumatic osteonecrosis of the talus in a 42-year-old man who subsequently underwent below-the-knee amputation. (a) Sagittal T1-weighted MR image through the ankle demonstrates a serpiginous low-signal-intensity line in the talar dome (arrows). (b) Corresponding sagittal fat-saturated T2-weighted MR image shows a high-signal-intensity line in the talar dome (arrow) that outlines an avascular segment. (c) Low-power photomicrograph (original magnification, x25; WHO stain [hematoxylin, phloxine, saffron, alcian green]) helps confirm AVN of the talus. The cartilage is thinned and is stained green by the alcian green dye, which helps identify mucopolysaccharides. Note the paler than expected green staining of the articular cartilage of the talar dome (white arrow). Near the ankle joint, a curvilinear band of fibrous tissue (black arrows) appears as a pale pink band outlining the area of necrosis; trabeculae are preserved in this area. On the external aspect of the arch of fibrosis, there are coarser, thicker trabeculae, indicating that this area of the bone is viable and is capable of reaction. (d) High-power photomicrograph (original magnification, x250; WHO stain) of a decalcified section shows viable tibia (Ti) on one side of the joint and necrotic talus (Ta) on the other. The bone trabeculae on the viable (tibial) side show smooth endosteal contours (white arrows); the adipose tissue of the bone marrow shows a fine filiform pattern (white arrowheads). These findings contrast with the necrotic (talar) side of the joint: Here, the cartilage shows a more homogeneous pattern with loss of all cellular detail, the subjacent bone contains irregular and partly fragmented trabeculae (black arrows), and the bone marrow shows patchy eosinophilia (black arrowheads), which indicate that the fat has undergone degenerative change with saponification.
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Figure 10c. Posttraumatic osteonecrosis of the talus in a 42-year-old man who subsequently underwent below-the-knee amputation. (a) Sagittal T1-weighted MR image through the ankle demonstrates a serpiginous low-signal-intensity line in the talar dome (arrows). (b) Corresponding sagittal fat-saturated T2-weighted MR image shows a high-signal-intensity line in the talar dome (arrow) that outlines an avascular segment. (c) Low-power photomicrograph (original magnification, x25; WHO stain [hematoxylin, phloxine, saffron, alcian green]) helps confirm AVN of the talus. The cartilage is thinned and is stained green by the alcian green dye, which helps identify mucopolysaccharides. Note the paler than expected green staining of the articular cartilage of the talar dome (white arrow). Near the ankle joint, a curvilinear band of fibrous tissue (black arrows) appears as a pale pink band outlining the area of necrosis; trabeculae are preserved in this area. On the external aspect of the arch of fibrosis, there are coarser, thicker trabeculae, indicating that this area of the bone is viable and is capable of reaction. (d) High-power photomicrograph (original magnification, x250; WHO stain) of a decalcified section shows viable tibia (Ti) on one side of the joint and necrotic talus (Ta) on the other. The bone trabeculae on the viable (tibial) side show smooth endosteal contours (white arrows); the adipose tissue of the bone marrow shows a fine filiform pattern (white arrowheads). These findings contrast with the necrotic (talar) side of the joint: Here, the cartilage shows a more homogeneous pattern with loss of all cellular detail, the subjacent bone contains irregular and partly fragmented trabeculae (black arrows), and the bone marrow shows patchy eosinophilia (black arrowheads), which indicate that the fat has undergone degenerative change with saponification.
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Figure 10d. Posttraumatic osteonecrosis of the talus in a 42-year-old man who subsequently underwent below-the-knee amputation. (a) Sagittal T1-weighted MR image through the ankle demonstrates a serpiginous low-signal-intensity line in the talar dome (arrows). (b) Corresponding sagittal fat-saturated T2-weighted MR image shows a high-signal-intensity line in the talar dome (arrow) that outlines an avascular segment. (c) Low-power photomicrograph (original magnification, x25; WHO stain [hematoxylin, phloxine, saffron, alcian green]) helps confirm AVN of the talus. The cartilage is thinned and is stained green by the alcian green dye, which helps identify mucopolysaccharides. Note the paler than expected green staining of the articular cartilage of the talar dome (white arrow). Near the ankle joint, a curvilinear band of fibrous tissue (black arrows) appears as a pale pink band outlining the area of necrosis; trabeculae are preserved in this area. On the external aspect of the arch of fibrosis, there are coarser, thicker trabeculae, indicating that this area of the bone is viable and is capable of reaction. (d) High-power photomicrograph (original magnification, x250; WHO stain) of a decalcified section shows viable tibia (Ti) on one side of the joint and necrotic talus (Ta) on the other. The bone trabeculae on the viable (tibial) side show smooth endosteal contours (white arrows); the adipose tissue of the bone marrow shows a fine filiform pattern (white arrowheads). These findings contrast with the necrotic (talar) side of the joint: Here, the cartilage shows a more homogeneous pattern with loss of all cellular detail, the subjacent bone contains irregular and partly fragmented trabeculae (black arrows), and the bone marrow shows patchy eosinophilia (black arrowheads), which indicate that the fat has undergone degenerative change with saponification.
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Traumatic and Atraumatic AVN
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Osteonecrosis of the talus can be classified on the basis of the traumatic and atraumatic processes that impair nutrient blood supply to the bone. Many possible causes of atraumatic AVN have been well documented (16–19), including (but not limited to) corticosteroids, alcoholism, systemic lupus erythematosus, renal transplants, sickle cell anemia, hyperlipidemia, irradiation, and inherited thrombophilias. Traumatic causes of osteonecrosis generally involve fracture and dislocation of the talar neck, one of the areas of the talus most at risk for injury (20). In fact, the risk of posttraumatic AVN can be approximated by determining the degree of injury using the Hawkins classification system.
In 1970, Leland Hawkins (20) described three primary patterns of talar neck injury; later, Canale and Kelly (9) added a fourth pattern (Fig 11). The risk of vascular disruption and subsequent osteonecrosis is commensurate with the magnitude of displacement and dislocation in these injuries. A Hawkins type I fracture is a nondisplaced talar neck fracture associated with a 0%–15% prevalence of AVN. Type II fractures are displaced fractures with dislocation or subluxation of the subtalar joint and have an associated risk of AVN of 20%–50%. Hawkins type III fractures are displaced fractures with dislocation or subluxation of both the ankle joint and the subtalar joint. The risk of AVN in Hawkins type III fractures approaches 100%. Finally, type IV fractures are displaced fractures with dislocation or subluxation of the subtalar, tibiotalar, and talonavicular joints. Type IV fractures have an associated risk of AVN of 100% (Figs 12 , 13).
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Figure 11a. Drawings illustrate the Hawkins classification system for talar neck fractures. (a) Hawkins type I fracture is a nondisplaced fracture of the talar neck without dislocation. (b) Hawkins type II fracture is a displaced fracture through the talar neck with subluxation or dislocation of the subtalar joint. (c) Hawkins type III fracture is a displaced fracture through the talar neck with dislocation of the talar body from the subtalar and ankle joints. (d) Hawkins type IV fracture is a fracture through the talar neck with displacement of the talar head as well as subluxation or dislocation of the subtalar, tibiotalar, and talonavicular joints.
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Figure 11b. Drawings illustrate the Hawkins classification system for talar neck fractures. (a) Hawkins type I fracture is a nondisplaced fracture of the talar neck without dislocation. (b) Hawkins type II fracture is a displaced fracture through the talar neck with subluxation or dislocation of the subtalar joint. (c) Hawkins type III fracture is a displaced fracture through the talar neck with dislocation of the talar body from the subtalar and ankle joints. (d) Hawkins type IV fracture is a fracture through the talar neck with displacement of the talar head as well as subluxation or dislocation of the subtalar, tibiotalar, and talonavicular joints.
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Figure 11c. Drawings illustrate the Hawkins classification system for talar neck fractures. (a) Hawkins type I fracture is a nondisplaced fracture of the talar neck without dislocation. (b) Hawkins type II fracture is a displaced fracture through the talar neck with subluxation or dislocation of the subtalar joint. (c) Hawkins type III fracture is a displaced fracture through the talar neck with dislocation of the talar body from the subtalar and ankle joints. (d) Hawkins type IV fracture is a fracture through the talar neck with displacement of the talar head as well as subluxation or dislocation of the subtalar, tibiotalar, and talonavicular joints.
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Figure 11d. Drawings illustrate the Hawkins classification system for talar neck fractures. (a) Hawkins type I fracture is a nondisplaced fracture of the talar neck without dislocation. (b) Hawkins type II fracture is a displaced fracture through the talar neck with subluxation or dislocation of the subtalar joint. (c) Hawkins type III fracture is a displaced fracture through the talar neck with dislocation of the talar body from the subtalar and ankle joints. (d) Hawkins type IV fracture is a fracture through the talar neck with displacement of the talar head as well as subluxation or dislocation of the subtalar, tibiotalar, and talonavicular joints.
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Figure 12a. AVN of the talus in a 33-year-old man with a talar neck fracture. (a) Coronal CT scan through the talar dome shows an irregular, approximately 1-cm-thick region of subchondral sclerosis spanning the entire width of the dome (arrows). (b) Corresponding coronal fat-saturated T2-weighted MR image through the talus shows normal subchondral signal intensity across the talar dome (arrows) and high signal intensity throughout the talar body. (c) Coronal follow-up CT scan obtained 5 months later shows a region of subchondral sclerosis (arrows) that is unchanged from the corresponding area seen in a.
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Figure 12b. AVN of the talus in a 33-year-old man with a talar neck fracture. (a) Coronal CT scan through the talar dome shows an irregular, approximately 1-cm-thick region of subchondral sclerosis spanning the entire width of the dome (arrows). (b) Corresponding coronal fat-saturated T2-weighted MR image through the talus shows normal subchondral signal intensity across the talar dome (arrows) and high signal intensity throughout the talar body. (c) Coronal follow-up CT scan obtained 5 months later shows a region of subchondral sclerosis (arrows) that is unchanged from the corresponding area seen in a.
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Figure 12c. AVN of the talus in a 33-year-old man with a talar neck fracture. (a) Coronal CT scan through the talar dome shows an irregular, approximately 1-cm-thick region of subchondral sclerosis spanning the entire width of the dome (arrows). (b) Corresponding coronal fat-saturated T2-weighted MR image through the talus shows normal subchondral signal intensity across the talar dome (arrows) and high signal intensity throughout the talar body. (c) Coronal follow-up CT scan obtained 5 months later shows a region of subchondral sclerosis (arrows) that is unchanged from the corresponding area seen in a.
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Figure 13a. AVN of the anterior talus in a 33-year-old man injured in a motor vehicle accident. (a) Axial CT scan through the talar dome reveals focal sclerosis in the anterior part of the dome (arrows), a finding that corresponds to an osteonecrotic segment. The posterior two-thirds of the dome shows normal bone marrow attenuation, which correlates with normal attenuation in the fibula. (b) Corresponding fat-saturated T2-weighted MR image shows diffuse increased signal intensity in the posterior two-thirds of the dome and normal bone marrow signal intensity in the anterior third. A serpiginous line separates these two regions (arrows).
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Figure 13b. AVN of the anterior talus in a 33-year-old man injured in a motor vehicle accident. (a) Axial CT scan through the talar dome reveals focal sclerosis in the anterior part of the dome (arrows), a finding that corresponds to an osteonecrotic segment. The posterior two-thirds of the dome shows normal bone marrow attenuation, which correlates with normal attenuation in the fibula. (b) Corresponding fat-saturated T2-weighted MR image shows diffuse increased signal intensity in the posterior two-thirds of the dome and normal bone marrow signal intensity in the anterior third. A serpiginous line separates these two regions (arrows).
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More recently, Inokuchi et al (21) reviewed the radiographs, MR images, and CT scans of 195 major fractures of the talus. Of these fractures, 112 (57.4%) involved only the talar neck and 22 (11.3%) involved only the talar body; the remaining 61 fractures (31.3%) involved portions of both the talar neck and body. The authors defined a talar neck fracture as being present when the lateral fracture line started extraarticularly at the lateral entrance to the tarsal sinus, regardless of whether the fracture extended into the anteromedial portion of the talar dome (trochlea). With use of this definition, the 61 fractures that involved both the talar neck and body were further subdivided into 28 talar neck fractures and 33 talar body fractures. The authors found that the location of the inferior fracture line was the most accurate criterion for determining whether the fracture was a talar neck or body fracture: If the inferior fracture line involved the posterior facet of the talus, the fracture was defined as a talar body fracture. This definition has significant clinical implications because fractures involving the talar body have a higher prevalence of AVN and a worse prognosis (Fig 14) (21).
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Figure 14a. Collapse and fragmentation of the talus in a 61-year-old man who had sustained minor trauma. (a) Coronal CT scan of the right ankle shows collapse of the articular surface of the talar dome (white arrows) and a vertical split fracture extending from the talar dome into the subtalar joint (black arrow). In addition, there is a curvilinear sclerotic line within the talar body (arrowheads) that represents necrotic bone. (b) Corresponding axial CT scan through the talar dome shows linear fractures through the posterior aspect of the dome (black arrows). The bone attenuation of the talar dome looks diffusely increased compared with that of the distal tibia and fibula. In addition, there is a small, ossific hyperattenuating area at the lateral aspect of the talus (white arrow), likely due to prior trauma.
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Figure 14b. Collapse and fragmentation of the talus in a 61-year-old man who had sustained minor trauma. (a) Coronal CT scan of the right ankle shows collapse of the articular surface of the talar dome (white arrows) and a vertical split fracture extending from the talar dome into the subtalar joint (black arrow). In addition, there is a curvilinear sclerotic line within the talar body (arrowheads) that represents necrotic bone. (b) Corresponding axial CT scan through the talar dome shows linear fractures through the posterior aspect of the dome (black arrows). The bone attenuation of the talar dome looks diffusely increased compared with that of the distal tibia and fibula. In addition, there is a small, ossific hyperattenuating area at the lateral aspect of the talus (white arrow), likely due to prior trauma.
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Articular Collapse
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The images in Figures 15–17 demonstrate AVN of the talus in which severe necrosis along with resorption around necrotic bone has led to the collapse of articular surfaces. In severe AVN, the talar dome is a typical location for articular collapse. However, collapse may also occur at the inferior articular surface of the talus (subtalar joint).
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Figure 15a. Severe AVN of the talus with collapse of the talar dome. (a) Coronal CT scan through the talus shows a large hypoattenuating area surrounding an osteonecrotic segment of the medial talar dome, with a 1-mm articular step-off due to collapse of the medial articular surface (arrows). (b) Axial CT scan through the talar dome clearly depicts the large osteonecrotic segment (arrows), a finding that corresponds to the collapsed fragment seen in a.
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Figure 15b. Severe AVN of the talus with collapse of the talar dome. (a) Coronal CT scan through the talus shows a large hypoattenuating area surrounding an osteonecrotic segment of the medial talar dome, with a 1-mm articular step-off due to collapse of the medial articular surface (arrows). (b) Axial CT scan through the talar dome clearly depicts the large osteonecrotic segment (arrows), a finding that corresponds to the collapsed fragment seen in a.
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Figure 16. Bilateral AVN of the talus in an 18-year-old man who had undergone renal transplantation. Coronal CT scan of both ankles shows collapse of the articular surface of the lateral talar domes bilaterally (arrows), with underlying mixed hypoattenuating-sclerotic regions of necrotic subchondral bone.
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Figure 17a. AVN of the talus in a female patient who had undergone renal transplantation. (a) Lateral radiograph of the right ankle shows diffuse sclerosis of the entire talus due to AVN, with sparing of the superior aspect of the talar head (white arrow). The inferior aspect of the talus shows irregular radiolucency (black arrows), with severe narrowing and anterior subluxation of the subtalar joint. (b) Coronal CT scan through the ankle shows sclerosis of the talar dome due to necrosis, along with multiple cystic hypoattenuating areas and fragmentation of the inferior articular surface of the talus (arrows). Note also the severe narrowing of the subtalar joint.
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Figure 17b. AVN of the talus in a female patient who had undergone renal transplantation. (a) Lateral radiograph of the right ankle shows diffuse sclerosis of the entire talus due to AVN, with sparing of the superior aspect of the talar head (white arrow). The inferior aspect of the talus shows irregular radiolucency (black arrows), with severe narrowing and anterior subluxation of the subtalar joint. (b) Coronal CT scan through the ankle shows sclerosis of the talar dome due to necrosis, along with multiple cystic hypoattenuating areas and fragmentation of the inferior articular surface of the talus (arrows). Note also the severe narrowing of the subtalar joint.
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Hawkins Sign
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The Hawkins sign, which becomes evident 6–8 weeks after injury, is an area of disuse osteopenia caused by resorption of the subchondral bone and is visualized as a thin subchondral radiolucent line along all or part of the talar dome (Figs 18, 19).
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Figure 18a. Hawkins sign in a female patient who had undergone external and internal fixation of a complex pilon fracture. Mortice-view (a) and lateral (b) radiographs of the ankle reveal striking subchondral radiolucency (arrowheads in a, arrows in b), a finding that indicates talar viability.
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Figure 18b. Hawkins sign in a female patient who had undergone external and internal fixation of a complex pilon fracture. Mortice-view (a) and lateral (b) radiographs of the ankle reveal striking subchondral radiolucency (arrowheads in a, arrows in b), a finding that indicates talar viability.
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Figure 19. Hawkins sign in a 27-year-old man who had undergone open reduction internal fixation for injuries sustained in a motorcycle accident. Radiograph (mortice view) shows a thin subchondral area of radiolucency involving the entire talar dome and lateral talar gutter (arrowheads), a finding that signifies talar viability and excludes future development of AVN.
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The Hawkins sign is most evident on anteroposterior radiographs and can be missed on lateral radiographs (20). When present, this sign indicates an adequate blood supply to the relevant portion of the talar body. Furthermore, a partial Hawkins sign can be an indicator of incomplete (partial) AVN (22). Incomplete AVN has a reported predilection for the lateral region of the talus, which has been attributed to the fact that the talus has a rich medial blood supply and protection of medial vessels by surrounding structures (23).
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Conclusions
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AVN of the talus is a rare but real complication of both traumatic and atraumatic processes. Regardless of the cause, however, the underlying mechanism remains the same: interruption in the vascular supply leading to ischemic bone death. Osteonecrosis of the talus follows a characteristic radiographic sequence that generally begins with an increase in talar dome opacity (sclerosis), then advances to deformity and, in severe cases, to articular collapse and bone fragmentation. At any stage of this sequence, the radiographic appearance of talar AVN can vary considerably. This variability depends on differences in both the vascular status of the talus and the degree of bone repair (revascularization, reossification, resorption) that is induced in response to osteonecrosis.
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Acknowledgments
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We thank Tim Dowdell, MD, FRCPC for his contribution to our collection of images.
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References
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Abstract
Introduction
