Venous Thromboembolism

SOURCE

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&sectionid=146057236.

CONDITION/DISORDER SYNONYMS

• Deep vein thrombosis.

• Thromboembolic disease.

• Venous thrombosis.

DEFINITION

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

ETIOLOGY

• Increasing age.

• History of VTE

• Venous stasis.

• Vascular injury.

• Hypercoagulability.

• Drug therapy.

PATHOPHYSIOLOGY

• 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.

EPIDEMIOLOGY

• 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 AND SCREENING

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

RISK FACTORS

• 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.

CLINICAL PRESENTATION

SIGNS AND SYMPTOMS

• 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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