Osteonecrosis in the Foot

Imaging of Postoperative Avascular Necrosis of the Ankle and Foot

“…Bone marrow edema correlates with histological findings of ischemic death of hematopoietic cells, capillary endothelial cells, and lipocytes with subsequent increase in extracellular fluid in the bone, present by the second week after infarction. 3 In the traumatic or postoperative setting, marrow edema and hemorrhage also occurs due to disruption of the trabeculae and leakage of fluid and blood products into the extracellular space. 15 Congestive marrow edema, proposed as a mechanism of AVN in patients with marrow packing disorders or on corticosteroids and predominantly involving the femoral head and proximal humerus, is likely secondary to vascular occlusion or thrombosis and is probably less important in the postoperative ankle and foot.…”

“…10,31 The risk of AVN increases in talar neck fractures that extend to involve the body, increasingly comminuted and displaced talar body fractures, and with talar head fractures. 3,32,33 A commonality of higher grade injuries is the increased disruption to the extraosseous blood supply and soft tissue attachments that occurs with dislocations.…”

“…There are no tendinous attachments or muscle origins and $60% of the talar surface is covered by articular cartilage, leaving little area for vascular perforation. 3,7 Major extraosseous arterial supply comes from branches of the posterior tibial artery, anterior tibial artery, dorsalis pedis artery, and perforating peroneal artery with a key anastomosis in the sinus tarsi between the artery of the tarsal canal and tarsal sinus artery.…”

“…A further complicating factor in assessing pathogenesis and determining the clinical prevalence is the observation that although most cases of posttraumatic AVN of the foot manifest clinically within the first 10 months after injury, cases in the distal tibial metaphysis may remain clinically asymptomatic. 3 Our discussion is limited to include the characteristic patterns of bone necrosis observed in the postoperative setting. Purported so-called idiopathic or stress-related AVN of the foot bones including the sesamoid bones, Mueller-Weiss disease of the lateral navicular bone, and Freiberg's disease of the metatarsal heads are beyond the scope of this review article.…”

“…2,3,7 Systemic causes including sickle cell disease, SLE, corticosteroids, and ischemia due to diabetes may cause multifocal infarctions of the foot and ankle and have a predilection for the talus and calcaneus. 8 Some authors limit the definition of AVN to include only systemic causes, arguing that bone necrosis is a histological end point of many disease processes including severe osteoarthritis, fractures, infections, and tumors.…”