PULMONARY TUMOR EMBOLISM TO ARTERIAL VESSELS AND CARCINOMATOUS LYMPHANGITIS - A COMPARATIVE CLINICOPATHOLOGICAL STUDY

Citation
Fa. Soares et al., PULMONARY TUMOR EMBOLISM TO ARTERIAL VESSELS AND CARCINOMATOUS LYMPHANGITIS - A COMPARATIVE CLINICOPATHOLOGICAL STUDY, Archives of pathology and laboratory medicine, 117(8), 1993, pp. 827-831
Citations number
55
Categorie Soggetti
Pathology,"Medical Laboratory Technology","Medicine, Research & Experimental
Journal title
Archives of pathology and laboratory medicine
ISSN journal
00039985 → ACNP
Volume
117
Issue
8
Year of publication
1993
Pages
827 - 831
Database
ISI
SICI code
0003-9985(1993)117:8<827:PTETAV>2.0.ZU;2-E
Abstract
A prospective study of 222 consecutive autopsies of cancer cases was u ndertaken to investigate whether carcinomatous lymphangitis and pure a rterial tumor embolism of the lungs are different clinicopathological entities. The lungs were removed as a block and 15 sections (three fro m each lobe) were analyzed. A protocol containing clinical (ie, dyspne a, cyanosis, right ventricular failure, engorgement of jugular veins, and peripheral edema as main cause of death) and morphological (ie, ri ght ventricle thickness and dilatation, vascular sclerosis, pulmonary infarct) data were carefully recorded in each case. Arterial tumor emb olism was detected in 19 cases (8.5%) and carcinomatous lymphangitis i n 44 cases (19.8%). We found no differences in relation to signs and s ymptoms of arterial tumor embolism and carcinomatous lymphangitis, but respiratory distress as the main cause of death was significantly mor e frequent in the cases with arterial involvement by tumor emboli. Mor phologically, however, right ventricular hypertrophy-dilatation, histo logical signs of pulmonary hypertension, and hemorrhagic infarcts were more prevalent in the cases with arterial tumor embolism. This study permits us to conclude that although arterial tumor embolism and carci nomatous lymphangitis are clinically similar diseases, they are morpho logically different entities. Our results suggest that the most probab le pathogenesis of pulmonary endarteritis and subsequent pulmonary hyp ertension is the injury to the vascular endothelium caused by the arre st of tumor emboli.