Venous thromboembolism encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE). Virchow's triad—venous stasis, endothelial injury, hypercoagulability—drives pathogenesis. Risk factors include immobility, surgery, malignancy, and thrombophilia.
Understand why PE mortality is high: acute right ventricular strain from sudden increase in afterload. Study Wells criteria and D-dimer for diagnostic stratification. Review thrombophilia screening and when to recommend.
Not all elevated D-dimer indicates thrombosis—infection, malignancy, and trauma elevate it. Negative compression ultrasound does not exclude PE; PE can occur without DVT. Anticoagulation duration depends on provocation (transient vs. unprovoked).
From your study of thrombosis pathophysiology, you know that clot formation requires at least one element of Virchow's triad: venous stasis, endothelial injury, or hypercoagulability. Venous thromboembolism is the clinical outcome when thrombosis occurs in the deep venous system and the formed clot dislodges. VTE is best understood as a two-event disease: the first event (DVT formation) and the second event (PE, when that thrombus travels to the pulmonary arterial tree).
Deep venous thrombosis most commonly begins in the valve pockets of calf veins — regions where blood pools and flow is slowest, creating the stasis element. Red cell-fibrin thrombus propagates proximally toward the popliteal, femoral, and iliac veins. Below-knee DVT carries modest embolism risk; proximal DVT (above the knee) carries substantially higher risk. The endothelial injury element dominates after surgery — especially orthopedic hip and knee replacement, which both traumatizes vessels and immobilizes patients. Hypercoagulability drives DVT in patients with inherited thrombophilias (factor V Leiden, prothrombin G20210A) or acquired states (antiphospholipid syndrome, malignancy). Malignancy deserves emphasis: tumors release tissue factor and other procoagulant mediators that chronically activate coagulation — unprovoked DVT is the presenting sign of occult malignancy in roughly 10% of cases and warrants cancer screening.
Pulmonary embolism occurs when a thrombus fragment breaks free and lodges in the pulmonary arterial tree. The physiological consequence scales with embolus size and the patient's cardiopulmonary reserve. Small peripheral emboli may cause pleuritis — chest pain and hemoptysis from pulmonary infarction in the lung tissue — without hemodynamic compromise. Large central emboli obstruct main pulmonary arteries, creating sudden right ventricular (RV) pressure overload. The normal RV is a thin-walled, low-pressure chamber adapted to the low-resistance pulmonary circulation. When resistance suddenly doubles or triples, the RV cannot generate enough pressure to push blood through, dilates, and fails. The dilating RV shifts the interventricular septum leftward (visible on echocardiography as the "D-sign"), compromising LV filling and producing systemic hypotension — the picture of obstructive cardiogenic shock. Stretched RV myocardium releases troponin and BNP. Massive PE carries 30-day mortality exceeding 30% precisely because this RV failure cascade is rapid.
Risk stratification drives clinical decision-making. The Wells score formalizes clinical probability by assigning points for signs of DVT, PE as the most likely diagnosis, immobilization, cancer, prior VTE, hemoptysis, and tachycardia. In low-probability patients, a negative D-dimer (a fibrin degradation product) safely excludes VTE without imaging — because D-dimer sensitivity exceeds 97%, so a negative result reliably rules out active thrombosis. However, D-dimer has poor specificity: infection, trauma, surgery, and malignancy all elevate it, making a positive result nearly meaningless in hospitalized patients. The asymmetry is the key rule: D-dimer is for ruling out, not ruling in. Once VTE is confirmed, anticoagulation duration depends critically on whether the episode was provoked by a transient reversible risk factor (surgery, immobilization, estrogen therapy — typically 3 months of anticoagulation) or unprovoked (idiopathic — high recurrence risk favoring extended therapy), a distinction that requires explicit assessment at every VTE diagnosis.
No topics depend on this one yet.