Dysbaric osteonecrosis: a consequence of intravascular bubble formation, endothelial damage, and platelet thrombosis.

Survival and turnover of platelets, fibrinogen, and plasminogen were measured in association with hyperbaric exposure in man. In addition, kinetic and vascular studies were carried out in a hyperbaric swine model to assess the role of vascular injury and thrombosis in the pathogenesis of dysbaric osteonecrosis. In man, significant increases in platelet and fibrinogen consumption were directly associated with dive depth and with repetitive exposure at lesser depths. The increased destruction of platelets and fibrinogen was not accompanied by reduced blood levels because of compensatory shifts in production rats and distribution between circulating and storage compartments. Platelet consumption was substantially greater than fibrinogen destruction with respect to both severity and duration. Platelet function inhibitors decreased platelet consumption. Increased fibrinogen consumption was sometimes associated with reduced plasminogen survival, but levels of fibrinogen/fibrin degradation products were never measurably altered from normal values. The relationships among platelet and fibrinogen consumption, vascular changes, and dysbaric osteonecrosis were studied in hyperbaric swine. Consumption of hemostatic factors was most severe with rapid, uncontrolled decompression, low oxygen concentrations, and deeper or repetitive dives. Platelet consumption induced by hyperbaric exposure resolved spontaneously with time, suggesting a repair process after the simulated diving conditions were discontinued. Interruption of increased platelet and fibrinogen consumption in the swine model required either moderation of the dive profile or a combination of drugs that inhibit platelet function (dipyridamole or sudoxicam) together with an anticoagulant (warfarin or heparin). Repeated hyperbaric exposure under conditions that uniformly produced femoral osteonecrosis and consumption of platelets and fibrinogen was associated with detectable endothelial injury and arterial intimal lesion formation. Since the diving characteristics of increasing depth and inadequate decompression were associated with both the most severe consumption and the highest frequency of intravascular bubble formation, we postulate that intravascular bubbles, formed during hyperbaria, produce osteonecrosis, perhaps through the following sequence: (1) bubble-related endothelial cell damage; (2) platelet thrombus formation with secondary fibrin deposition; (3) microvascular occlusion; and (4) platelet-dependent arterial narrowing through intimal lesion formation. The role of antithrombotic therapy in the prevention of dysbaric osteonecrosis remains to be determined.