Hunter also stressed the role of inflammation and infection as causes of thrombi, although this association is now considered unimportant as it is rarely seen today.
In 1856 Virchow’s detailed pathological studies led him to postulate that thrombosis may be caused by a slowing or cessation of blood flow (stasis), increased thrombotic potential of the blood (hypercoagulability) and abnormalities in the vessel wall (endothelial lining). These etiological factors, known as Virchow’s triad, are still accepted.
In 1866 John Gay recognized clot and thrombi in the deep veins of many of the limbs he dissected with venous ulcers, and he was also the first person to recognize the importance of the calf-perforating veins and lipodermatosclerosis.
Oschner and DeBakey reported that deep vein thrombosis was common after surgical operations and advocated its avoidance and treatment by vein ligation or anticoagulants to prevent pulmonary embolism. Homans had previously advocated vein ligation to prevent pulmonary embolism as a consequence of deep vein thrombosis. He also recognized that the postthrombotic leg was an important cause of venous ulceration.
Homans, Bauer, and Linton advocated ligation of the deep veins in patients with post-thrombotic limbs to
prevent venous reflux and reduce the risk of recurrent venous ulceration. The advent of the coumarin anticoagulants, heparin, and recently the low molecular weight heparins has focused attention away from the avoidance of postthrombotic sequelae; protection against the lethal complications of pulmonary embolism has now taken center stage.
The development of vena caval filters by Mobin-Uddin and Greenfield has added a further therapeutic option to pulmonary embolism prevention. There is little evidence that any of the present treatments including thrombolysis and thrombectomy reduce the incidence of postthrombotic limb.
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