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Acute deep vein thrombosis (DVT) and its complications, including pulmonary embolism (PE), recurrent venous thromboembolism (VTE), and the postthrombotic syndrome (PTS), are important not only as the most common preventable cause of hospital death but also as a cause of substantial long-term morbidity. The early natural history of acute DVT is characterized by a balance between factors favoring restoration of the venous lumen and recurrent thrombosis. The balance between these competing events is also related to development of PTS, the most important late complication of DVT.
DVT is fundamentally a disease of coagulation localized to the lower extremity veins. Most of the risk factors for acute DVT are associated with some degree of hypercoagulability as a congenital, acquired, or situational risk factor ( Box 1 ). However, most thrombi arise from multiple risk factors acting together in a synergistic fashion. Lower extremity venous thrombi originate in areas where imbalanced coagulation is localized by stasis, such as in the soleal sinuses, behind venous valve pockets, and at venous confluences. The calf veins are the most common site of origin, although 40% of proximal thrombi arise primarily in the femoral or iliac veins.
Factor V Leiden
Prothrombin G20210A
Protein C
Protein S
Antithrombin
Factor XI excess
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