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Deep vein thrombosis (DVT) and pulmonary embolism (PE) represent a spectrum of venous thromboembolism, where blood clots form in deep veins and can travel to pulmonary circulation. DVT most commonly occurs in lower extremity veins, while PE results from embolic migration of thrombi to pulmonary arteries, potentially causing life-threatening respiratory and cardiovascular compromise.
Venous thromboembolism develops through Virchow's triad: venous stasis, endothelial injury, and hypercoagulability, leading to fibrin-rich clot formation in deep veins. When thrombi dislodge from their origin (commonly lower extremity or pelvic veins), they travel through venous circulation to pulmonary arteries, causing mechanical obstruction and release of vasoactive mediators that increase pulmonary vascular resistance and right heart strain.
DVT presents with unilateral leg swelling, pain, warmth, and erythema, while PE manifests with acute dyspnea, chest pain, tachycardia, and potential hemodynamic instability depending on clot burden. Risk stratification using clinical prediction rules (Wells score), D-dimer testing, and imaging studies (ultrasound for DVT, CT pulmonary angiography for PE) guide diagnostic approach and anticoagulation decisions to prevent clot extension and recurrence.
Key imaging focus: Filling defects in pulmonary arteries, RV strain signs, Hampton hump, Westermark sign on CXR