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Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third most common acute cardiovascular syndrome and a leading preventable cause of in-hospital mortality. Annual incidence is approximately 1-2 per 1000 person-years.
Virchow's triad describes the three predisposing factors: venous stasis, endothelial injury, and hypercoagulability. Thrombosis begins with platelet activation at sites of endothelial disruption, followed by activation of the coagulation cascade generating thrombin and fibrin. Inherited thrombophilias (Factor V Leiden, prothrombin gene mutation) and acquired states (malignancy, antiphospholipid syndrome, immobility, surgery) amplify thrombotic risk.
Clinical reasoning begins with pretest probability (Wells DVT score for DVT; Wells PE score or Geneva score for PE). D-dimer has high negative predictive value in low-probability patients. Compression ultrasound diagnoses DVT; CTPA diagnoses PE. Anticoagulation (LMWH, DOAC) is the cornerstone of treatment. Duration depends on provoked vs. unprovoked VTE and thrombophilia status. Massive PE with hemodynamic compromise warrants thrombolysis. First unprovoked VTE in a young patient warrants thrombophilia evaluation and consideration of extended anticoagulation.