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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. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861§ionid=146057236.
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CONDITION/DISORDER SYNONYMS
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Deep vein thrombosis.
Thromboembolic disease.
Venous thrombosis.
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Increasing age.
History of VTE
Venous stasis.
Vascular injury.
Hypercoagulability.
Drug therapy.
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Alterations in any of three components can lead to pathologic clot formation (Virchow’s triad):
Vascular injury occurs with:
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.
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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%.
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PREVENTION AND SCREENING
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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.
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CLINICAL PRESENTATION
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