Pathophysiology

The pathophysiology of DVT involves abnormalities in venous blood flow, the vessel wall, and the coagulation system, collectively termed Virchow’s triad. This triad of factors promotes thrombus formation in hospitalized patients.

·         Venous stasis: Immobility and critical illness lead to sluggish venous blood flow and stasis in the lower extremities, increasing risk of thrombus formation.

·         Endothelial injury: Damage to the venous intimal lining in the lower extremities exposes subendothelial collagen and promotes clotting through platelet activation and accumulation. Lower extremity trauma, surgery, central venous catheters, or inflammation can cause injury.

·         Hypercoagulability: Critical illness, malignancy, pregnancy, oral contraceptives, and inherited thrombophilias increase procoagulant factors like fibrinogen. This creates a prothrombotic state.

In hospitalized patients, the factors of Virchow’s triad combine to increase risk of DVT formation. Thrombi often initially develop in the deep calf veins, propagating proximally to femoral and iliac veins if untreated.

Key impacts of DVT:

·         Obstructs venous blood flow and damages venous valves

·         Causes distal venous hypertension

·         Promotes edema and post-thrombotic syndrome

·         Break-off of thrombus can lead to deadly pulmonary embolism

·         Strains right heart if pulmonary embolism occurs

In summary, the interplay between venous stasis, endothelial injury, and hypercoagulability promotes DVT formation in hospitalized patients. Prompt prophylaxis and treatment are crucial to prevent morbidity and mortality from DVT and resultant pulmonary embolism.