Virchow's triad includes all of the following, EXCEPT-

Virchow's triad refers to three primary influences that predispose to thrombus formation. Endothelial injury (or vascular injury) Stasis or turbulence of blood flow Blood hypercoagulability Virchow's triad should be the cornerstone for assessment of risk factors for deep venous thrombosis. Stasis can occur with venous insufficiency, severe heart failure, or prolonged bed rest or immobility of an extremity following coma, pelvic or limb fracture, paralysis, extended aeroplane travel, or a lengthy operation. Endothelial injury can result from direct trauma (severed vein, venous cannulation, or transvenous pacing) or local irritation secondary to the infusion of chemotherapy, previous DVT, or phlebitis. Damaged endothelium leads to platelet aggregation, degranulation and formation of thrombosis as well as vasoconstriction ad activation of the coagulation cascade. The hypercoagulable state can be inherited or acquired. These are def. of antithrombin III, protein C or S increased homocysteine factor V Leiden mutation prothrombin gene mutation antiphospholipid syndrome paroxysmal nocturnal hemoglobinuria malignancy (lung cancer - most commonly pancreas, prostate, breast, ovary etc...) nephrotic syndrome pregnancy, high dose estrogen therapy or OCPs. Some important questions on deep vein thrombosis Homan's sign → Calf tenderness on forced ankle dorsiflexion. Phlegmasia alba dolens → Painful white leg Phlegmasia cerulea dolens → Painful blue leg Moses Sign → Calf tenderness on direct pressure on the calf Pratt's Sign → Calf tenderness on squeezing the calf from the sides. Duplex ultrasound is the diagnostic modality of choice in deep vein thrombosis.