The pathology of thirty-nine fatal cases of epidemic hemorrhagic fever

Abstract

The pathologic changes observed in thirtynine fatal cases of hemorrhagic fever in 1952 have been studied in the light of the significant clinical data. The cases have been grouped according to the clinical phase in which death occurred in an attempt to determine the sequential development of the pathologic changes and to evaluate the role of shock in their pathogenesis. Several conclusions resulting from this correlation of clinical and pathologic data seem clearly evident. The almost constant occurrence of hemorrhage in the right atrium of the heart, of severe congestion of the renal medulla, and of congestion and infarct-like necrosis in the anterior lobe of the pituitary gland, in association with the pattern of the vascular changes, supports the contention proposed in the Japanese literature and by Steer and Hullinghorst 1,2 that capillary damage is the basic process. Retroperitoneal edema, observed only once in secondary shock, is the striking pathologic feature when the patient dies during shock in early phases of the disease. It is rarely encountered after the eighth day when the initial shock usually terminates, suggesting that vascular damage has subsided. Recurrent shock in the later phases of the disease is due to other contributing factors. The abrupt increase in incidence of pulmonary edema in the oliguric phase, particularly after the eighth day of the disease when retroperitoneal edema is rare, supports the clinically suspected role of redistribution of fluid and electrolytes coincident with resorption of the abnormal interstitial fluid. The frequent coexistence of pulmonary edema and bronchopneumonia in the oliguric and diuretic groups and the high incidence of pulmonary abscess formation support the concept of Moon that pulmonary edema of the albuminous type is conducive to the development of pulmonary infections. The almost constant presence of necrosis of the anterior lobe of the pituitary gland in cases of more than nine days' duration, irrespective of occurrence, type or duration of preceding shock, strongly suggests that shock is not the only major factor in the pathogenesis of pituitary necrosis in hemorrhagic fever. Anoxemia from severe congestion and stasis resulting from vascular damage is also an important factor and probably is the major cause of necrosis in the absence of shock.