Fat embolism, intravascular coagulation, and osteonecrosis.

A triad of intraosseous fat embolism, intravascular coagulation (both thrombosis and hemorrhage), and osteonecrosis was pathologically demonstrated to coexist for the first time in humans. Specimens were evaluated from the earliest nontraumatic (18 hours) and traumatic (29 hours) femoral head lesions yet reported, and the cause and early pathogenesis were confirmed in a third case. An absolute overload of subchondral fat emboli, with hypercoagulability, stasis, and endothelial damage by free fatty acids, appears to cause end-organ death by triggering intravascular coagulation. This intermediary pathway appears to be capable of producing osteonecrosis by progressive fibrin platelet thromboses, which begin in vulnerable subchondral capillaries and sinusoids, especially when associated with arteriolar vasoconstriction and impaired secondary fibrinolysis (reperfusion of necrotic vessels with peripheral marrow hemorrhages). A relative overload of subperiosteal and subchondral fat emboli, which is below the ischemic/anoxic threshold but insufficient for intravascular coagulation, may cause osteopenia.