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Approximately 100,000 patients in the United States die each year directly as a consequence of acute pulmonary embolism (PE), with another 100,000 deaths occurring in patients with concomitant disease in whom PE contributes significantly to their demise.1,2 Three-month mortality in unselected patients with acute PE is as high as 15%.3 Although a number of patients die of comorbidities that predispose them to the thromboembolic event, a substantial number of patients die from PE within 1 hour of presentation, often before the diagnosis can be confirmed and therapy initiated, or because the diagnosis was overlooked.4 Autopsy studies have repeatedly documented the high frequency with which PE has gone unsuspected and undetected.5 Despite advances in diagnostic imaging tests and therapeutic interventions, PE remains underdiagnosed and prophylaxis continues to be dramatically underused.


Over the past decade, a number of valuable insights into the natural history of venous thrombosis and PE have enhanced our diagnostic and therapeutic approaches. One such insight is the awareness that patients hospitalized for medical problems face a thromboembolic risk similar to that of their surgical counterparts. Another is an understanding of the substantial thromboembolic recurrence risk among patients with idiopathic or unprovoked venous thrombosis.6 Yet another insight is the awareness that the presence of right ventricular (RV) dysfunction in the setting of PE may be associated with an increased risk of adverse consequences, including subsequent cardiovascular collapse and death.7 Anticoagulation with heparin as a "bridge" to warfarin is still considered the standard treatment for PE. The spectrum of anticoagulant drugs has been expanded recently. Low-molecular-weight heparins (LMWHs) have been shown to be effective and safe for both treatment and for prevention of venous thromboembolism (VTE), particularly in hospitalized medical patients. Fondaparinux, a new pentasaccharide, is very effective in a fixed low dose in preventing VTE after orthopedic and abdominal surgery and has been demonstrated in clinical trials to be as effective as LMWH and unfractionated heparin (UFH) for the initial treatment of patients with deep venous thrombosis (DVT) and PE. A new generation of oral direct thrombin inhibitors and factor Xa inhibitors appears to be on the horizon.


In 1856, Virchow proposed his triad of factors leading to intravascular coagulation, including stasis, vessel wall injury, and hypercoagulability. Risk factors for DVT are based on these processes (Table 72–1). The overwhelming majority of emboli originate from the deep veins of the lower extremities, although any venous bed can be involved. Although thrombi may form at any point along the vein wall, most originate in valve pockets. The veins of the calf are the most common site of origin, with subsequent extension of the clot prior to embolization.8 Eventually, the thrombus may expand to fill the vessel entirely, with both retrograde and proximal extension. If embolization does not occur, the thrombosis can partially or completely resolve via three mechanisms: recanalization, organization, and lysis. Postthrombotic syndrome occurs in 20% to 50% of patients ...

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