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Upon completion of the chapter, the reader will be able to:

  1. Identify risk factors and signs and symptoms of deep vein thrombosis (DVT) and pulmonary embolism (PE).

  2. Describe the processes of hemostasis and thrombosis.

  3. Determine a patient’s relative risk of developing venous thrombosis.

  4. Formulate an appropriate prevention strategy for a patient at risk for DVT.

  5. Select and interpret laboratory test(s) to monitor antithrombotic drugs.

  6. Identify factors that place a patient at high risk of bleeding while receiving antithrombotic drugs.

  7. State at least two potential advantages of newer anticoagulants (ie, low molecular weight heparins [LMWHs], fondaparinux, oral direct thrombin inhibitors [DTIs], and oral direct factor Xa inhibitors) over traditional anticoagulants (ie, unfractionated heparin and warfarin).

  8. Manage a patient with toxicity secondary to warfarin (elevated international normalized ratio [INR] with or without bleeding).

  9. Identify anticoagulant drug–drug and drug–food interactions.

  10. Formulate an appropriate treatment plan for a patient who develops a DVT or PE.


Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT; ie, thrombus causing obstruction of a deep vein in the leg, pelvis, or abdomen) and pulmonary embolism (PE; ie, thrombus causing obstruction of a pulmonary artery or one of its branches and resulting in pulmonary infarction) (Figure 10–1).1,2 A thrombus is a blood clot attached to the vessel wall composed of platelets, fibrin, and clotting factors that may partially or completely occlude the lumen of a blood vessel and compromise blood flow and oxygen delivery to distal tissue. It is often provoked by prolonged immobility and vascular injury and most frequently seen in patients hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder.

FIGURE 10–1.

Venous circulation. (From Witt DM, Clark NP, Vazquez SR. Venous thromboembolism. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 10th ed. New York, NY: McGraw-Hill; 2017:232.)

Although VTE may initially cause few or no symptoms, the first overt manifestation of the disease may be sudden death from PE, which can occur within minutes, before effective treatment can be given.2,3 A history of VTE is a significant risk factor for recurrent thromboembolic events.4-7 Postthrombotic syndrome (PTS) is a complication of VTE that occurs due to damage to the vein caused by a blood clot and leads to development of symptomatic venous insufficiency such as chronic lower extremity swelling, pain, tenderness, skin discoloration, and ulceration.

The treatment of VTE is fraught with substantial risks.8 image Antithrombotic therapies (thrombolytics and anticoagulants) ...

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