Abstract
Current evidence suggests that intravascular coagulation (IC), an intermediary mechanism, is the most likely final common pathway by which intraosseous fat embolism causes nontraumatic osteonecrosis (ON). Stage 1A lesions (fatty osteocytic necrosis) appear to progress to classic Stage 1B lesions (ischemic degeneration of necrotic osteocytes and adipocytes) when the ischemic threshold is exceeded by absolute subchondral fat overload with insufficient local clearance of procoagulants, especially tissue thromboplastin. The result is vascular stasis, hypercoagulability, endothelial damage (by free fatty acids) and IC, especially if there is coexistent subchondral vasoconstriction and impaired secondary fibrinolysis. Osteonecrosis can be produced in animals by IC, which begins in the vulnerable subchondral microcirculation (Arthus phenomenon). Cartography (embolic scintimetry with superselective angiography) indicates early complete devascularization of the femoral head, suggesting progressive venous and retrograde arterial thrombosis. Increased plasma fibrinopeptide A and direct histologic evidence of intraosseous thromboses and peripheral hemorrhages further indicate that IC is the final pathway. Best evidence are 51 ON lesions complicating disseminated IC in eight children (Shwartzman phenomenon), with collateral histologic evidence of intraosseous thrombosis and ON.
Published Version
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