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What is VTE?

Thrombosis, or clot formation, is the underlying mechanism in a number of serious, potentially fatal medical conditions. Venous thromboembolism (VTE) comprises deep vein thrombosis (DVT), or clots usually occurring in the lower limbs, and pulmonary embolism (PE), a sudden blockage of the pulmonary artery usually due to a clot that has traveled to the lung from a leg DVT, and occurs in an estimated 200,000 US patients each year. VTE is commonly associated with surgery, including orthopedic surgery such as hip or knee replacement and abdominal surgery such as gastric bypass surgery for the morbidly obese. VTE can also occur in hospitalized medical patients due to prolonged immobility or as a result of their underlying illnesses.1 While VTE is associated with many types of hospitalization, the risk of VTE is especially high in patients with major trauma or spinal cord injury, and in acutely ill patients admitted to critical care units. Major trauma patients who do not receive prophylactic treatment for VTE have a greater than 50% risk of DVT, and PE is the third most common cause of death among these patients if they survive beyond the first day.2, 3

Diagnosis of VTE can be difficult, since most cases of hospital-acquired DVT and PE are clinically silent. In some cases, the first sign of VTE is a fatal PE. DVT is a common complication of hospitalization but difficult to recognize early due to a lack of specific signs and symptoms. Asymptomatic DVT can be detected with tests such as contrast venography and venous doppler ultrasonography, but routine screening of all patients is logistically difficult, expensive, and ineffective at preventing clinically important thromboembolic events. Thus, many guidelines on VTE recommend prophylactic treatment using pharmacologic agents, physical methods such as graduated compression stockings or intermittent pneumatic compression devices, or a combination of both.4

Thrombosis occurs when the delicate balance between blood coagulation and anticoagulation is disturbed, leading to unwanted clot formation. Thromboprophylactic therapy aims to restore this balance by inhibiting one or both of the two major components of the clotting system: platelet activation and thrombus formation via the proteins of the clotting cascade.5 Until recently, only a few relatively nonspecific agents such as aspirin, unfractionated heparin (UFH) and warfarin were available to carry out this task. Aspirin alone is no longer recommended for thromboprophylactic therapy due to limited efficacy and a small but significant risk of major bleeding.4  UFH therapy has low bioavailability and unpredictable anticoagulation activity, necessitating close monitoring of patients. UFH is also associated with a potentially serious complication known as heparin-induced thrombocytopenia (HIT), an immune-mediated reaction that causes low platelet counts with a paradoxic high risk of potentially life-threatening thromboembolic events.6 Warfarin is an oral therapy used in 2 million US patients a year, but attaining the correct dosage takes time and over-treatment can lead to potentially devastating bleeding complications.7

Recent advances in our understanding of the coagulation process have led to the development of newer thromboprophylactic therapies, including low-molecular-weight heparins (LMWH), such as enoxaparin, dalteparin, and tinzaparin, and agents targeted at specific factors in the clotting cascade, such as fondaparinux and bivalirudin. These agents have begun to change recommended practices in many types of clinical situations that require thromboprophylaxis.8 The newer, targeted agents that are unrelated to heparin are particularly useful in the treatment of HIT, where nonheparin therapy is a necessity to prevent clot formation.9 These agents have created an educational need for health care providers in the area of thromboprophylaxis.

  1. Blann AD, Lip GY. Venous thromboembolism. BMJ. 2006;332(7535):215-219.
  2. Geerts WH. Prevention of venous thromboembolism in high-risk patients. Hematology Am Soc Hematol Educ Program. 2006:462-466.
  3. Knudson MM, Ikossi DG. Venous thromboembolism after trauma. Curr Opin Crit Care. 2004;10(6):539-548.
  4. Geerts WH, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 Suppl):338S-400S.
  5. Chakrabarti R, Das SK. Advances in antithrombotic agents. Cardiovasc Hematol Agents Med Chem. 2007;5(3):175-185.
  6. Dager WE, Dougherty JA, Nguyen PH, Militello MA, Smythe MA. Heparin-induced thrombocytopenia: treatment options and special considerations. Pharmacotherapy. 2007;27(4):564-587.
  7. Hirsh J, O'Donnell M, Eikelboom JW. Beyond unfractionated heparin and warfarin: current and future advances. Circulation. 2007;116(5):552-560.
  8. Bauer KA. New anticoagulants. Hematology Am Soc Hematol Educ Program. 2006:450-456.
  9. Warkentin TE. Think of HIT. Hematology Am Soc Hematol Educ Program. 2006:408-414.