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ESSENTIALS OF DIAGNOSIS

  • Predisposition to venous thrombosis, usually of the lower extremities.

  • One or more of the following: dyspnea, chest pain, hemoptysis, syncope.

  • Tachypnea and a widened alveolar-arterial PO2 difference.

  • Elevated rapid D-dimer and characteristic defects on CT pulmonary angiography, ventilation-perfusion lung scan, or pulmonary angiogram.

GENERAL CONSIDERATIONS

Pulmonary venous thromboembolism, often referred to as pulmonary embolism (PE), is a common, serious, and potentially fatal complication of thrombus formation within the deep venous circulation. PE is the third leading cause of death among hospitalized patients. Despite this prevalence, most cases are not recognized antemortem, and less than 10% of patients with fatal emboli have received specific treatment for the condition. Management demands a vigilant systematic approach to diagnosis and an understanding of risk factors so that appropriate preventive therapy can be given.

Many substances can embolize to the pulmonary circulation, including air (during neurosurgery, from central venous catheters), amniotic fluid (during active labor), fat (long bone fractures), foreign bodies (talc in injection drug users), parasite eggs (schistosomiasis), septic emboli (acute infective endocarditis), and tumor cells (renal cell carcinoma). The most common embolus is thrombus, which may arise anywhere in the venous circulation or heart but most often originates in the deep veins of the lower extremities. Thrombi confined to the calf rarely embolize to the pulmonary circulation. However, about 20% of calf vein thrombi propagate proximally to the popliteal and iliofemoral veins, at which point they may break off and embolize to the pulmonary circulation. Pulmonary emboli will develop in 50–60% of patients with proximal deep venous thrombosis (DVT); half of these embolic events will be asymptomatic. Approximately 50–70% of patients who have symptomatic pulmonary emboli will have lower extremity DVT when evaluated.

PE and DVT are two manifestations of the same disease. The risk factors for PE are the risk factors for thrombus formation within the venous circulation: venous stasis, injury to the vessel wall, and hypercoagulability (Virchow triad). Venous stasis increases with immobility (bed rest—especially postoperative—obesity, stroke), hyperviscosity (polycythemia), and increased central venous pressures (low cardiac output states, pregnancy). Vessels may be damaged by prior episodes of thrombosis, orthopedic surgery, or trauma. Hypercoagulability can be caused by medications (oral contraceptives, hormonal replacement therapy) or disease (malignancy, surgery) or may be the result of inherited gene defects. The most common inherited cause in white populations is resistance to activated protein C, also known as factor V Leiden. The trait is present in approximately 3% of healthy American men and in 20–40% of patients with idiopathic venous thrombosis. Other major risks for hypercoagulability include the following: deficiencies or dysfunction of protein C, protein S, and antithrombin; prothrombin gene mutation; hyperhomocysteinemia and the presence of antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibody).

PE has multiple physiologic effects. Physical obstruction of the vascular bed and vasoconstriction from neurohumoral reflexes both increase pulmonary vascular resistance. Massive thrombus may cause right ventricular failure. ...

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