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A large majority of pulmonary emboli are thrombotic in origin. Therefore, unless otherwise specified, the term "pulmonary embolus" typically refers to pulmonary thromboembolus. Pulmonary thromboembolism is involved in approximately 10% of hospital deaths. In more than 95% of cases, the source of pulmonary thromboemboli is a thrombus in a deep vein of the lower extremity (Chap. 27). Risk factors for venous thrombosis and pulmonary thromboembolus include prolonged bed rest (especially in the setting of lower extremity immobilization), severe trauma, burns, congestive heart failure, and hypercoagulable states (Table 26.1).
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When a venous thrombus embolizes, it travels in progressively larger systemic veins toward the right heart. Upon ejection from the right ventricle, fragments of the embolism move into progressively smaller branches of the pulmonary artery until they reach vessels too small to allow passage. At that point the thromboemboli occlude a pulmonary artery or arteriole and increase pulmonary vascular resistance and can induce vasospasm. When a major vessel is occluded, the resulting pulmonary hypertension can reduce cardiac output and induce cor pulmonale and death. If death does not result, pulmonary thromboembolism results in hypoxemia due to ventilation-perfusion mismatch with increased dead space ventilation (Chap. 8). The ischemia may also reduce surfactant release and cause pleuritic pain that add to the work of breathing (Chaps. 5 and 6). Despite the lung's systemic blood supply (Chap. 2), pulmonary thromboembolism can result in lung parenchymal ischemia and pulmonary infarction. In patients with patent foramen ovale (~30% of all people), pulmonary arterial thrombotic occlusion can cause right-to-left shunting and subsequent paradoxic embolism, in which a venous thrombus enters and embolizes systemic arteries and cause distal ischemia.
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Grossly, a pulmonary thromboembolus is a serpentine blood clot impacted in a pulmonary arterial branch [Fig. 26.3 (a)]. A very large thromboembolus occluding the main pulmonary arteries is typically referred to as a "saddle embolus." Microscopically, the thromboembolus is characterized by alternating layers of fibrin (eosinophilic) and erythrocytes. Ischemic lung damage is characterized by intra-alveolar hemorrhage [Fig. 26.3 (b)]. A pulmonary infarct will be conical (or, on cut section, wedge-shaped) and hemorrhagic [Fig. 26.4 (a)]. Initially, the infarct is red-blue. It becomes paler and later red-brown as erythrocytes lyse and hemoglobin is degraded to hemosiderin. Next, as fibroblasts progressively replace necrotic tissue with scar, the infarct shows a gray-white peripheral zone. Microscopically, infarcted lung tissue shows coagulative necrosis with loss of nuclear basophilia, although alveolar hemorrhage often dominates the microscopic appearance [Fig. 26.4 (b), (c)]. In cases of sudden death due to saddle embolus, there are typically no gross or microscopic changes to the lung.
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Clinically, 60%-80% of pulmonary thromboemboli are asymptomatic; approximately 5% cause acute cor pulmonale, shock, or sudden death; and 10%-15% affect medium-sized arteries and, through an unknown mechanism, cause dyspnea. In the presence of an underlying risk factor, a patient who has had pulmonary thromboembolism has a 30% chance of recurrent pulmonary thromboembolism. A minority (<3% of patients with recurrent pulmonary thromboembolism develop pulmonary hypertension (see below), chronic cor pulmonale, vascular sclerosis, and worsening dyspnea. Treatment of pulmonary thromboembolism involves thrombolysis and anticoagulation. If anticoagulation is contraindicated or not sufficient, a filter (Greenfield filter, umbrella) can be placed in the inferior vena cava; thromboemboli caught in the filter will undergo fibrinolysis.
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In addition to venous thrombi, the student should remember that embolism of the lung can be caused by air, bone marrow, fat, foreign bodies, and amniotic fluid. In most instances, the hemodynamic effects from such materials resemble those caused by thrombi (Chap. 27). However, the duration of such effects and the severity of pulmonary compromise they cause may be transient (as for the nitrogen in air), or may persist (as has been noted for crystals of talcum used to "cut" certain drugs before their intravenous abuse). Amniotic fluid embolism is a devastating event, often resulting in maternal death in the peripartum period.