Increased central venous pressure, which produces venous stasis in the extremities, may account for the high incidence of venous thrombosis in patients with heart failure. Stasis resulting from venous dilatation occurs in elderly patients, in patients with varicose veins, and in women who are pregnant or using supplemental estrogen, perhaps contributing to the increased incidence of thrombosis in these persons. Venous obstruction contributes to the risk of venous thrombosis in patients with pelvic tumors and to the risk of recurrent venous thrombosis in patients with persistent obstruction resulting from proximal vein thrombosis. Increased blood viscosity, which also causes stasis, may explain the risk of thrombosis in patients with polycythemia vera, hypergammaglobulinemia, or chronic inflammatory disorders. Direct venous damage may lead to venous thrombosis in patients undergoing hip surgery, knee surgery, or varicose vein stripping and in patients with severe burns or trauma to the lower extremities.
Blood coagulation is modulated by circulating inhibitors or by endothelial cell-bound inhibitors.
Some types of congenital dysfibrinogenemias can also predispose to thrombosis, as can a congenital deficiency of plasminogen. The risk of thrombosis in persons with APC resistance is increased by estrogen-containing oral contraceptives. Recent evidence also suggests that the administration of estrogens in the doses used for postmenopausal replacement may produce a small increase in the risk of thromboembolism. Estrogen replacement has several benefits and is not absolutely contraindicated in postmenopausal patients with a history of venous thrombosis. However, if estrogen replacement therapy is indicated in such patients, its risks and benefits of replacement should be discussed with the patient.