Abstract

Blackwater fever is a complication of malaria infection in which red blood cells burst in the bloodstream (hemolysis), releasing hemoglobin directly into the blood vessels and into the urine, frequently leading to kidney failure. The disease was first linked to malaria by the Sierra Leonean physician Dr John Farrell Easmon in his 1884 pamphlet entitled "The Nature and Treatment of Blackwater Fever." Easmon coined the name "blackwater fever" and was the first to successfully treat such cases following the publication of his pamphlet.

Signs and symptoms

Within a few days of onset there are chills, with rigor, high fever, jaundice, vomiting, rapidly progressive anemia, and dark red or black urine.

Causes

The cause of hemolytic crises in this disease is unknown (mainly due to intravascular haemolysis). There is rapid and massive destruction of red blood cells resulting in hemoglobinemia (hemoglobin in the blood, but outside the red blood cells), hemoglobinuria (hemoglobin in urine), intense jaundice, anuria (passing less than 50 milliliters of urine in a day), and finally death in the majority of cases.

The most probable explanation for blackwater fever is an autoimmune reaction apparently caused by the interaction of the malaria parasite and the use of quinine. Blackwater fever is caused by heavy parasitization of red blood cells with "Plasmodium falciparum". There has been at least one case, however, attributed to "Plasmodium vivax".

Blackwater fever is a serious complication of malaria, but cerebral malaria has a higher mortality rate. Blackwater fever is much less common today than it was before 1950. It may be that quinine plays a role in triggering the condition, and this drug is no longer commonly used for malaria prophylaxis. Quinine remains important for treatment of malaria.

Treatment

The treatment is antimalarial chemotherapy, intravenous fluid and sometimes supportive care such as intensive care and dialysis.