Pathophysiology of Thrombosis Virchow's original triad formulated in 1846 still explains the primary mechanism of the development of DVT. It describes the initiation of thrombosis as a complex interaction between venous stasis, vessel wall injury, and a hypercoagulable state. The relative importance of each factor is still debated. DVT most often originates in the deep veins of the major calf muscles. This anatomic site with its plexus of multiple branching veins seems to be predisposing to venous stasis in patients with prolonged immobility. In the triad model for thrombogenesis, stasis allows for more time of clotting and an increased blood viscosity. Also, small thrombi are not so easily washed away. Other factors contributing to stasis are e.g. obesity, varicose veins, and cardiac dysfunction. Major predisposing conditions to DVT are any type of trauma including surgery and childbirth. These can be possible causes of vessel wall injury, which can lead to a disturbed balance between thrombogenesis and fibrinolysis. For surgical patients, the risk of DVT is also related to the procedure itself, including the operation site, technique, and duration of the procedure, the type of anesthetic, indwelling central lines, the presence of infection, and the degree of postoperative immobilization.