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Source: Witt DM, Nutescu EA. Venous Thromboembolism. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://accesspharmacy.com/content.aspx?aid=7973333. Accessed July 5, 2012.

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  • Deep vein thrombosis
  • Thromboembolic disease
  • Venous thrombosis

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

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  • Increasing age
  • History of VTE
  • Venous stasis
  • Vascular injury
  • Drug therapy

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  • Alterations in any of 3 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

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  • Incidence unknown, because at least half of patients have clinically silent disease.
  • Approximately 350,000–600,000 people in United States develop VTE each year and more than 100,000 die.
  • Incidence nearly doubles in each decade of life over age 50 and is slightly higher in men.
  • African Americans are at higher risk than Americans of European ancestry; Hispanic Americans may be at slightly lower risk than Americans of European ancestry.

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

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  • Venous stasis
    • Acute illness requiring hospitalization
    • Paralysis or immobility (e.g., stroke, spinal cord injury)
    • Polycythemia vera
    • Obesity
    • Varicose veins
  • 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
    • Protein C deficiency
    • Protein S deficiency
    • Antithrombin deficiency
    • Factor VIII excess
    • Factor XI excess
    • Antiphospholipid antibodies
    • Dysfibrinogenemia
    • Hyperhomocysteinemia
    • 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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Signs and Symptoms

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  • 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
  • Postthrombotic syndrome may produce:
    • Chronic lower extremity swelling
    • Pain
    • Tenderness
    • Skin discoloration
    • Ulceration
  • Symptoms of PE include:
    • Dyspnea
    • Tachypnea
    • Pleuritic chest pain
    • Tachycardia
    • Palpitations
    • Cough
    • Diaphoresis
    • Hemoptysis
    • Cardiovascular collapse with cyanosis, shock, and oliguria may occur.

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Means of Confirmation and Diagnosis

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  • Signs and symptoms of DVT are nonspecific; objective tests required to confirm or exclude diagnosis.

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Laboratory Tests

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  • Elevated D-dimer blood level is sensitive marker of clot formation but can occur with other conditions (e.g., recent surgery or trauma, pregnancy, cancer).

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Imaging

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  • Ultrasonography
  • Computed tomography
  • Ventilation-perfusion scan
  • Contrast venography
  • Pulmonary angiography

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Differential Diagnosis

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