Pulmonary tumor embolism.

Abstract

Among the various causes of morbidity and mortality in patients with cancer, perhaps the least well described is tumor embolism. This condition was first documented in 1897 by Schmidt (1), but since then most information on this topic has been in the form of case reports or autopsy series. The paucity of information is due in part to the failure to recognize this condition antemortem. A significant proportion of such patients are diagnosed as having pulmonary thromboembolism and are treated with anticoagulation. Although recent studies have attempted to diagnose and differentiate malignant embolism from thromboembolism, lung biopsy remains the procedure of choice. These studies as well as the clinical manifestations of tumor embolism are the focus of this report. Although the specific cellular and molecular mechanisms of tumor embolism are not yet well understood, our onderstanding of the phenomenon has improved substantially in the last decade. Tumor cells access the systemic circulation via active invasion of small veins, venules, or the tumor's own microvasculature (2). The pulmonary vascular bed receives the entire cardiac output and filters any cell with a diameter of 10 μm or greater (3). Most tumor cells in the circulation are destroyed either by mechanical and shear forces of the microcirculation or by the various effector cells of the immune system. In fact, less than 1% of tumor cells that enter the circulation survive the passage through the lungs (4-6). The surviving tumor cells have a wide spectrum of biological fates and clinical manifestations: (1) Tumor cells may remain asymptomatic. In fact, autopsy review studies have shown that 18% to 68% of tumor emboli are discovered as incidental findings (7, 8). (2) Tumor cells may present a clinical picture similar to thromboembolic disease (9-12). (3) Finally, neoplastic cells that reach the capillaries may traverse the endothelium and form a potential focus of metastasis (4, 13). Current evidence has shown that the simple entrapment of cells in the pulmonary vasculature is insufficient for metastasis. Tumor cells must (1) adhere to lung-specific adhesion molecules such as laminin and fibronectin located on the vascular endothelium and basement membrane, (2) produce enzymes that degrade elastin, a molecule which is preferentially located in the lung extracellular matrix, and (3) be able to grow in association with lung-specific growth factors. The subject of metastasis formation is beyond the scope of this report but has been reviewed elsewhere (14). This article will review the clinical and pathological manifestations of pulmonary tumor embolism, focusing mainly on the patient with cancer presenting with dyspnea and no obvi-