Clinical Pathology of Yellow Fever

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Abstract
Clinicopathologic studies on 11 yellow fever patients who died in Panama from November, 1948, to February, 1952, and on 149 patients who recovered and 57 who died in Costa Rica between July 1951 and March 1953 established that the basic pathologic processes are(l) histologically typical hepatitis, (2) prothrombin deficiency, (3) hemorrhagic diathesis, and (4) lower nephron (hemoglobinuric) nephrosis. These processess are manifested clinically by: (1) hyperbilirubinemia due mainly to an increase in the 1-minute direct bilirubin, more intense in the fatal cases, and occasionally paradoxically present secondarily during convalescence; (2) profound prothrombin deficit during period of greatest liver damage; (3) marked retention of nonprotein nitrogenous metabolites (mainly urea) in fatal cases. Eosino-penia and leukopenia were noted early in many severe cases. Albuminuria, constant in all terminating fatally, was absent in 35% of the severe cases terminating in recovery.
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