As the initial recipient of the venous circulation, the pulmonary vascular bed is uniquely positioned to filter diverse particulates within the venous circulatory system. The etiology of these circulating particles may be thrombotic, as seen in pulmonary thromboembolism, or nonthrombotic, as encountered in a number of uncommon syndromes including embolism from air, amniotic fluid, fat, tumors, septic foci, and other miscellaneous sources. The pathophysiologic sequelae of these emboli are related to both mechanical occlusion of the pulmonary vasculature and inflammatory mediated damage to the pulmonary microvasculature resulting in capillary leak and pulmonary edema. The intent of this chapter is to describe the incidence, pathophysiology, and clinical features of these varied embolic phenomena and to provide a rational approach to the diagnosis and treatment of these disorders.
Pulmonary embolism (PE) is a commonly occurring condition associated with significant morbidity and mortality. Although there is a well-established and decreased incidence of PE with appropriate prophylaxis and a significant improvement in patient outcome associated with the prompt institution of appropriate therapy, prophylaxis and therapy for venous thromboembolic disease continue to be underused, thereby contributing to the morbidity, mortality, and high costs associated with the condition. In the United States, it is estimated that more than 500 000 cases of PE occur each year1 with a mortality rate of greater than 15% in the first 3 months after diagnosis.2 Despite our increased knowledge about the condition and ever-increasing technological sophistication, mortality rates associated with PE remain high and relatively unchanged over the past half century.3 Additionally, autopsy studies continue to demonstrate that the diagnosis of PE is made less than 50% of the time prior to death.4 While specific risk factors have been identified for the occurrence of PE and numerous effective prophylactic regimens have been demonstrated, recent studies show that appropriate prophylactic regimens continue to be significantly underused.5
PE results from the detachment and migration of thrombi fragments, which lodge within and obstruct blood flow to a single or multiple areas of the pulmonary vascular bed (Figure 45-1). Pulmonary emboli generally detach from deep venous thromboses (DVTs) of the proximal lower extremities.6 Less commonly, deep pelvic veins or proximal upper extremity DVTs associated with central venous catheters can be the source of pulmonary emboli.7 PE is, therefore, a part of the continuum of venothromboembolism (VTE). Thrombi, from which pulmonary emboli may arise, occur, in the majority of cases, when one or more components of Virchow's classic triad is/are present: Venous stasis, hypercoagulability, and/or intimal injury.
Endarterectomy specimen demonstrating obstruction of pulmonary vascular bed.
Reproduced, with permission, from Jamieson SW, Kapelanski DP, Sakakibara N, et al. Pulmonary endarterectomy: experience and lessons learned in 1500 cases. Ann Thorac Surg. 2003;76:1457-1464.
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