05), elderly individuals, obesity, prior history of DVT, venous stasis, local compression on the veins, and acute factors like severe dehydration (Guirguis, 2000). DVT also can occur from iatrogenic injury of the femoral veins (Wood, 2000. Joynt, 2000), malignancy (pancreas, lung, ovary, testes, urinary tract, breast and stomach), after major surgery (orthopedic, thoracic, abdominal and genitourinary procedures), following trauma (fractures of spine, pelvis, femur, tibia and spinal cord), burns, pregnancy and the postpartum period, estrogen use, hypercoagulable states (deficiencies of protein C, protein S, fibrinogen, factor V, factor VIII, factor IX, factor XI, prothrombin, and antiphospholipid antibodies), venulitis (thromboangitis obliterans, Behcets disease, and homocystinuria) (Creager &amp. Dzau, 1998), end-stage renal disease and congestive cardiac failure (Casserly, 2000).
Thrombogenesis is a finely balanced process between coagulation and fibrinolytic pathways. The interaction between plasminogen activators (e.g. tissue plasminogen activator) and inhibitors that modulate this activity (e.g. plasminogen activator inhibitor, PAI-1) influences the fibrinolytic system. Plasma fibrinogen determines plasma viscosity, blood flow, affects platelet aggregation, blood viscosity, interacts with plasminogen binding and along with thrombi, mediates the final steps in clot formation. The levels of fibrinogen associates directly with age, obesity, smoking, diabetes and LDL-C and inversely with HDL-C, alcohol use, physical activity and exercise level. Increased fibrinogen is also associated with many different forms of vascular and inflammatory disease.
Impaired fibrinolysis, as demonstrated by the elevated levels of plasminogen activator, is seen in obese patients, and explains the increased risk of thrombosis and other vascular disease in the obese (Chung &amp. Lip, 2004).
Virchow’s classical triad of factors that lead to the development of thrombosis (thrombogenesis)

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