Roentgenologic observations in hemorrhagic fever.

Abstract

Hemorrhagic fever was first encountered by western physicians when it appeared among the United Nations Forces in Korea in 1951. Osaka Army Hospital served as a center for the treatment of this disease at that time. A comprehensive study of 300 observed cases with 9 deaths has been reported by one of us (1, 2). The purpose of this paper is to present the roentgenologic observations in hemorrhagic fever. To our knowledge, roentgenograms of patients with this disease have not previously been published in the literature. Reviews of the Japanese and Russian literature (3, 4, 5) revealed reports of 491 cases of hemorrhagic fever from Manchuria and 125 cases from eastern Siberia between the years 1932 and 1944. No cases were reported after 1944 until the disease broke out in Korea during 1951. In that year, 1,016 cases were recorded among the United Nations Forces (6). During early Manchurian outbreaks, the Japanese called the disease Songo fever and other names, according to the region of occurrence, but in 1942 they officially adopted the name epidemic hemorrhagic fever (5). The Russians, on the other hand, referred to the same disease in Siberia as endemic hemorrhagic nephroso-nephritis (3, 4). Although the Japanese and Russians (3, 4, 5) claimed to have furnished experimental proof that the disease is due to a filtrable virus, American workers, in spite of intense effort, have been unable to identify the causative agent (7). Clinical Course The incubation period in hemorrhagic fever varies from seven to as long as forty-six days, with an average of two to three weeks. The course follows a common clinical pattern consisting of three fairly well defined phases, which one of us (1, 2) has termed the invasion, toxic, and convalescent stages. The invasion stage usually lasts from two to five days and is characterized by an acute onset with high fever, accompanied mainly by symptoms and signs common to acute febrile illness and laboratory studies which are generally within normal limits. The toxic stage usually begins from the third to the fifth day and lasts until the tenth to the fourteenth day of illness. Shock is common early in this stage and is followed by renal failure. A hemorrhagic diathesis, evidence of cerebral toxicity, and gastrointestinal disturbances occur throughout this entire period. The most significant laboratory findings are albuminuria, oliguria and hyposthenuria; azotemia with hyperpotassemia; leukocytosis, often with leukemoid reaction and atypical lymphocytes ; hemoconcentration; rapid sedimentation rate; thrombocytopenia; prolonged bleeding time; and increased capillary fragility. The convalescent stage usually begins between the tenth and fourteenth day and lasts for as long as four months. Polyuria and hyposthenuria with inability to concentrate urine normally are the most prominent and persistent findings during this phase. Pathology The pathological aspects have been completely covered elsewhere (2).