What Is Deep Venous Thrombosis: Hypercoagulability of the Blood

Hypercoagulability of the Blood

The discovery of a number of prothrombotic conditions (known generally as thrombophilias) has led to the hypothesis that blood hypercoagulability is the major factor in thrombogenesis. In reality most patients with these conditions are at increased risk when a second thrombogenic factor is operating, e.g., injury, operation, pregnancy, or the contra-ceptive pill. The conditions that are now known to cause thrombophilia include antithrombin deficiency, protein C deficiency, protein S deficiency, activated protein C resistance (Factor V Leiden mutation), and antiphospholipid syndrome. Activated protein C resistance, for example, is present in 5% of the total population, but is found in 20% of those with deep vein thrombosis.
The process of thrombus initiation may be continually occurring on a daily basis as low levels of fibrin degradation products can be measured within all subjects’ blood throughout life. This process is probably overcome by the body’s own natural thrombolytic defenses.

What Is Deep Venous Thrombosis: Changes in the Vessel Wall

Changes in the Vessel Wall

Functional changes in the endothelial lining of the vessel wall are now being examined in greater detail. Abnormal platelet, leukocyte, and endothelial activation by cells may be an important factor in the genesis of a thrombus, but endothelial damage alone only produces cellular adhesion, not thrombus in an animal model.
Eddy currents within valve pockets may cause localized endothelial disturbance or activation, which promotes leukocyte and platelet adhesion. In animal studies leukocyte-mediated disturbance of endothelium occurs before platelet and red cell deposition are observed, and this has been proposed as an initiating mechanism.
Thrombus formation is reduced by substances that inhibit leukocyte adhesion and migration in animal models and in patients having hip replacements.No significant increase in the expression of adhesion receptors has, however, been found during thrombin-induced experimental thrombogenesis in man.Prolonged stasis does upregulate endothelial adhesive receptors in the rabbit external jugular vein, causing increased adhesion of leukocytes to the vessel wall, although this does not progress to endothelial damage and thrombus
generation.

Deep Venous Thrombosis And Pulmonary Embolism