Epidemiology and pathogenesis of venous thrombosis

Abstract

Venous thrombi are intravascular deposits composed predominantly of fibrin and red blood cells with a variable platelet and leukocyte component. They frequently arise in large venous sinuses in the calf, in valve cusp pockets either in the deep veins of the calf or thigh or in venous segments that have been exposed to direct trauma. Venous thrombosis can be produced experimentally by a combination of stasis and systemic hypercoagulability or by stasis and endothelial damage. Thrombosis is augmented if the fibrinolytic mechanism is inhibited or defective. A number of clinical conditions and laboratory abnormalities are associated with and predispose to venous thrombosis and, in many of these, it is possible to identify one or more of the thrombogenic factors discussed. Venous thromboembolism (venous thrombosis and pulmonary embolism) is a serious and potentially fatal disorder that usually complicates the course of sick hospitalized patients, but occasionally affects ambulant and otherwise healthy individuals. Screening studies with iodine-125 fibrinogen leg scanning, impedance plethysmography and perfusion lung scanning have shown that the majority of venous thrombi and pulmonary emboli that occur in hospitalized patients are small and asymptomatic, and it is likely that most are clinically insignificant. In bedridden patients, most thrombi commence in the calf and are asymptomatic. When a calf vein thrombus extends into the proximal venous segment, the risk of clinically significant pulmonary embolism increases. Less is known about the incidence and clinical significance in a nonhospital population; although asymptomatic disease occurs, its frequency is unknown. In contrast to the patients with asymptomatic venous thrombosis, symptomatic patients with venous thrombosis usually have large occulsive thrombi localized in their proximal veins.