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KMID : 0357919730070010001
Korean Journal of Pathology
1973 Volume.7 No. 1 p.1 ~ p.11
A Pathologic Study on Tropical Malaria in South Vietnam-Analysis of Cause of Death in 7 Autopsy Cases-
±è¿ëÀÏ(ÑÑé¸ìé)/Yong Il Kim
±è±âÈ«(ÑÑÐñûó)/Ki Hong Kim
Abstract
The pathologic lesions in seven consecutive autopsy cases among 555 Korean army
personnel of falciparum malaria, during a period of November 1965 to July 1966,
performed at the Oth Evacuation Hospital, ROKA in South Vietnam, were presented and
correlated with cause of death.
1. All of the cases were heavily infected with P. falciparum, but one combined with P.
malariae as well. Their duration of illness ranged from 7 to 11 days.
2. Basic Pathologic changes in each organ and tissue were related with presence of
parasitized red blood cells and malaria pigments with subsequent development of tissue
hypoxia and advanced proliferative changes of reticuloendothelial system.
3. Direct cause of death in all of fatal cases was considered to be cerebral. malaria,
although cerebral lesions varied and presented no intimate relationship to clinical
manifestations ; their findings strongly indicated cerebral hypoxia secondary to capillary
blood stasis and plugging of parisitized red blood cells. None of cases demonstrated
actual thrombosis or Durck's glial nodes.
4. Renal lesions, both blackwater fever and malarial nephrosis, were inconspicuous,
and did not considered as a direct cause of death ; one case was featured with mild
hemoglobinuric nephrosis but giving no significant histologic differences from others.
Mesangial changes of renal glomeruli encountered in the others accompanied moderate
accentuation of glomerular lobulation, but evidence of malarial nephrosis remained
unclarified.
5. Myocardial changes occurred with relative frequency, revealing focal necrosis
together with interstitial edema, to result in acute myocardial insufficiency and
pulmonary edema in one.
6. Presence of fibrin thrombi, though rarely manifest, raised possibility of intravascular
coagulation as one of hemorrhagic diathetic mechanisms in fatal malarial infection.
KEYWORD
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