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Source: Witt DM, Clark NP, Vazquez SR. Venous thromboembolism. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017.




  • Deep vein thrombosis.

  • Thromboembolic disease.

  • Venous thrombosis.




  • Venous thromboembolism (VTE) involves clot formation in venous circulation, manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE).




  • Increasing age.

  • History of VTE

  • Venous stasis.

  • Vascular injury.

  • Hypercoagulability.

  • Drug therapy.




  • Alterations in any of three components can lead to pathologic clot formation (Virchow’s triad):

    • Blood vessels.

    • Circulating elements in blood.

    • Speed of blood flow.

  • Vascular injury occurs with:

    • Trauma.

    • Surgery.

    • Indwelling venous catheters.

  • Hypercoagulable states occur with many medical conditions (see Risk Factors).

  • Venous stasis favors thrombogenesis through reduced clearance of clotting factors, damage to venous valves, vessel obstruction, prolonged immobility, or increased blood viscosity (see Risk Factors).

  • Thrombi can form in any part of venous circulation, but most begin in lower extremities. Once formed, venous thrombus may:

    • Remain asymptomatic.

    • Lyse spontaneously.

    • Obstruct venous circulation.

    • Propagate into more proximal veins.

    • Embolize.

    • Act in combination of these ways.




  • Venous thromboembolism is associated with major global disease burden.

  • Incidence rate of symptomatic first VTE is estimated at 1.32 per 1000 patient-years and occurs more frequently in women (55.6%).

  • After accounting for age, Blacks have the highest VTE incidence (2.03 per 1000 patient-years) followed by Whites (1.91 per 1000 patient-years), and Asians (1.22 per 1000 patient-years).

  • Reoccurrence of VTE is highest in the first 180 days following the initial event and declines slowly over the next 4–10 years.

  • The 10-year cumulative risk of recurrent VTE is approximately 25.0%.




  • Prevention based on identifying and modifying or removing risk factors when possible (see below).




  • Venous stasis.

    • Acute illness requiring hospitalization.

    • Paralysis or immobility (eg, stroke, spinal cord injury)

    • Polycythemia vera.

    • Obesity.

  • Vascular injury.

    • Major orthopedic surgery.

    • Trauma (especially pelvic, hip, or leg fractures)

    • Indwelling venous catheters.

  • Hypercoagulable states.

    • Malignancy.

    • Activated protein C resistance/factor V Leiden (homozygous >> heterozygous)

    • Prothrombin (G20210A) gene mutation.

    • Protein C deficiency.

    • Protein S deficiency.

    • Antithrombin deficiency.

    • Factor VIII excess (>90th percentile)

    • Factor XI excess (>90th percentile)

    • Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies, anti–β2-glycoprotein I antibodies)

    • Inflammatory bowel disease.

    • Nephrotic syndrome.

    • Paroxysmal nocturnal hemoglobinuria.

    • Pregnancy/postpartum.

  • Drug therapy.

    • Estrogen and selective estrogen receptor modulators (tamoxifen, raloxifene)

    • Cancer chemotherapy.

    • Heparin-induced thrombocytopenia.




  • Many patients with VTE remain asymptomatic.

  • Symptoms of DVT include:

    • Unilateral leg swelling.

    • Pain.

    • Tenderness.

    • Erythema.

    • Warmth.

  • Physical signs may include:

    • Palpable cord.

    • Positive Homan’s sign.

  • Post-thrombotic syndrome may produce:

    • Chronic lower extremity swelling.

    • Pain.


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