Venous thrombogenesis.

Venous thrombosis develops when stasis in the deep veins of the legs occurs at times of increased coagulability of the blood. This combination leads to the local generation of thrombin, which is the crucial event in the pathogenesis of this disease. Impaired fibrinolysis allows a small platelet-fibrin nidus to grow into an occluding thrombus. Demonstrable damage to the vessel wall does not appear to play a major role in the development of most cases of venous thrombosis. While the biochemical definition of hypercoagulability remains elusive, immunoregulatory cytokines have been shown to impair the normal non-thrombogenicity of the endothelial wall. This leads to local expression of procoagulant activity and resultant fibrin deposition. In the presence of stasis, the stage is then set for the development of clinically significant thrombi. Although hereditary absence of natural anticoagulants has been found in many patients with venous thrombosis, most patients have no detectable abnormality of their blood.