Prevention

Given that VTE is often clinically silent and potentially fatal, prevention strategies have the greatest potential to improve patient outcomes. To rely on the early diagnosis and treatment of VTE is unacceptable because many patients will die before treatment can be initiated. Furthermore, even clinically silent disease is associated with long-term morbidity from the PTS and predisposes the patient to future thromboem-bolic events. Despite an immense body of literature that overwhelmingly supports the widespread use of pharmacologic and nonpharmacologic strategies to prevent VTE, prophylaxis is underutilized in most hospitals. Even when prophylaxis is given, many patients receive prophylaxis that is less than optimal. Educational programs and computerized clinical decision support systems have been shown to improve the appropriate use of VTE prevention methods.2

The goal of an effective VTE prophylaxis program is to identify all patients at risk, determine each patient's level of risk, and select and implement regimens that provide sufficient protection for the level of risk.20 At the time of hospital admission, all patients should be evaluated for their risk of VTE, and strategies to prevent VTE appropriate for each patient's level of risk should be routinely employed. Prophylaxis should be continued throughout the period of risk. The risk classification criteria and recommended prophylaxis strategies published by the American College of Chest Physicians (ACCP) Conference on Antithrombotic Therapy are widely used in North America (Table 10-2). Several pharmacologic and nonpharmacologic methods are effective for preventing VTE, and these can be used alone or in combination. Nonpharmacologic methods improve venous blood flow by mechanical means, while drug therapy prevents thrombus formation by inhibiting the coagulation cascade.

FIGURE 10-4. Coagulation cascade. (AT, antithrombin; HCII, heparin cofactor II; TFPI, tissue factor pathway inhibitor.) (From Haines ST, Witt DM, Nutescu EA. Venous thromboembolism. In: Di Piro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th eel. New York: McGraw-Hill; 2008:336.)

FIGURE 10-4. Coagulation cascade. (AT, antithrombin; HCII, heparin cofactor II; TFPI, tissue factor pathway inhibitor.) (From Haines ST, Witt DM, Nutescu EA. Venous thromboembolism. In: Di Piro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th eel. New York: McGraw-Hill; 2008:336.)

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