Venous thromboembolism (VTE) is a significant cause of morbidity and mortality in the United States. Each year approximately 2 million people develop VTE and 60,000 of these are fatal.1 The economic burden to the health-care system is roughly $1.5 billion/year.2 VTE encompasses both deep venous thrombosis (DVT) and pulmonary embolism (PE). The mainstay of treatment for VTE is anticoagulant agents. Anticoagulants are also used short and long term to prevent thromboembolic events, including those associated with cardiac valve replacement and myocardial infarction, thromboembolic stroke related to atrial fibrillation, high-risk hospitalized patients, and high-risk patients undergoing surgery.
Hemostasis, or termination of bleeding, is a fundamental bodily process. However, the balance between hemostasis and pathogenic thrombus formation is sensitive and depends on the stability and collaboration of three primary components known as Virchow's triad: venous stasis, vascular wall injury, or hypercoagulability.3 A disruption in any of these components can result in thrombosis.
Patients presenting with VTE often have one or more risk factors for thromboembolism (Table 6-1).4 Classic symptoms of a DVT include unilateral pain, swelling, erythema, and tenderness usually of the lower extremity; although some patients may be symptom free. Ultrasound (duplex ultrasonography) is typically used to diagnose a DVT. The symptoms of a PE are nonspecific and may include chest pain, shortness of breath, tachypnea, dyspnea, and hemoptysis. Most PEs originate from a DVT. The diagnosis of a PE is made by the presence of symptoms in conjunction with findings on ventilation-perfusion (V/Q) and computerized tomography scans. Medical work-up of patients presenting with VTE include determination of risk factors for VTE. Certain risk factors are reversible (eg, estrogen use, recent orthopedic surgery, prolonged immobility) and may be eliminated over time. The presence of irreversible or continuing risk factors (eg, cancer, thrombophilia, previous history of VTE) requires longer or indefinite duration of therapy. Short- and long-term sequelae of VTE include recurring thromboembolic events, death, and postphlebitic syndrome.
TABLE 6-1 Risk Factors for Venous Thromboembolism4 |Favorite Table|Download (.pdf)
TABLE 6-1 Risk Factors for Venous Thromboembolism4
|History of previous VTE|
|Selective estrogen receptor modulators (eg, Raloxifene)|
|Factor V Leiden|
|Prothrombin gene mutation|
|Protein C deficiency|
|Protein S deficiency|
|Anticoagulation—the process of preventing blood clot formation|
|Deep venous thrombosis (DVT)—blood clot formation in a deep vein,
usually in the leg (eg, iliac vein)|
|Postphlebitic syndrome—chronic condition occurring after DVT
characterized by venous insuffi ciency, pain, edema, stasis dermatitis,
varicose veins, and ulceration|
|Pulmonary embolism (PE)—blockage of a pulmonary artery, usually
from a thrombus that has traveled from another site, such as the leg|
|Thromboembolism—occlusion of a blood vessel due to a blood clot
that has broken away and traveled from its place of ...|
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