Venous Thromboembolism

Blood clotting within the venous circulatory system, in contrast to arterial thrombosis, occurs at a relatively slow pace in response to stagnation of flow (stasis) and activation of coagulation. As with arterial thrombosis, vascular injury, either direct in the setting of trauma or indirect as a diffuse, systemic inflammatory response (that ultimately causes endothelial cell damage), represents an important stimulus. Venous thrombi are intravascular deposits composed predominantly of erythrocytes and fibrin, with a variable contribution of platelets and leukocytes. In a majority of cases, thrombosis begins in areas of slow flow within the venous sinuses of valve cusp pockets either in the deep veins of the calf or upper thigh or at sites of direct injury following trauma (Kakkar et al., 1969; Nicolaides et al., 1971). Stasis predisposes to thrombosis most profoundly in the setting of inflammatory states and activated coagulation factors. Slowed blood flow impairs the clearance of coagulation proteases, which through bioamplification increases the local concentration of thrombin substrate. If local thromboresistance is impaired, as may be the case with inherited or acquired thrombophilias (see Chapter 24), thrombosis occurs. Blood flow velocity is reduced by indwelling catheters, which also causes focal endothelial injury, peripheral edema, pregnancy, and valve cusp damage from prior venous thrombosis and/or chronic venous insufficiency (Trottier et al., 1995). Although venous thrombosis can occur in a variety of sites, the most common encountered in clinical practice is within the deep veins of the lower extremity. Thrombi developing within the veins of the calf or thigh can serve as a nidus for growth (propagation), which may cause complete venous obstruction, or embolize to the lungs (pulmonary embolism).