Pathophysiological mechanisms of thromboembolism.

Abstract

The first section of this review describes the hemostatic balance as it is regulated at the blood-tissue interface. Endothelial cells have a nonthrombogenic surface during resting conditions. In diseased states, such as trauma or infection, the endothelial cells become perturbated and the anticoagulant activity is transformed into a procoagulant activity. Recent data have demonstrated that endothelial cells have surface receptors and the capacity for initiating coagulation and propagating the coagulation cascade. The second part of this review discusses the role of the fibrinolytic system in thromboembolism. Defects in the system have been found to be pathogenetic factors in postoperative deep vein thrombosis. Several studies have indicated that this surgical sequela does not occur in patients with an active fibrinolytic system. These results suggest that screening patients for fibrinolytic abnormalities may identify those persons at high risk for the development of postoperative deep vein thrombosis.