After several descriptions by Hippocrates and a single possible medieval description by Gilles de Corbeil, a severe febrile illness accompanied by the passage of dark urine burst upon the medical scene in West Africa in 1819, described by an English surgeon named Tidlie.

Most of his patients died within a few days.

Further reports appeared from tropical regions until the turn of the century, J. Farrell Easmon having given the condition the name blackwater fever in 1884.

Controversy raged about its relationship to malaria, as well as over its treatment with cinchona bark and quinine.

Evidence evolved that it was a complication of falciparum malaria in which hemoglobinuria causing acute renal failure resulted from massive quinine-induced lysis of red blood cells. People with red cell abnormalities such as glucose-6-phosphate dehydrogenase deficiency proved particularly prone to developing it.

Its incidence fell as more mildly acting antimalarial drugs replaced quinine.

Several enigmatic issues bedeviled understanding of it, but a careful analysis of its historical development has enabled resolution of each of these.

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This clinical entity is characterized by acute intravascular hemolysis classically occuring after the re-introduction of quinine in long-term residents in Plasmodium falciparum endemic areas and repeatedly using the product.

This condition is also common in patients who have been subject to excessive fatigue, exhaustion, shock or injury , intercurrent infection, childbirth or alcoholic excess.

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

The cause of hemolytic crises in this disease is unknown. There is rapid and massive destruction of red blood cells with the production of hemoglobinemia, hemoglobunuria, intense jaundice, anuria, and finally death in the majority of cases.

The most probable explanation for blackwater fever is an autoimmune reaction.

Pathology: Macroscopically and microscopically the kidneys show features similar to those of hemoglobinuric or tubular nephrosis.

The severity of the clinical picture often requires initial management in intensive care unit. Nowadays, however, prognosis is good and the disease usually regresses without after effects.

Abstracts:

Haemolytic crisis of blackwater fever following artemether-lumefantrine intake].

A mild blackwater fever.Med Mal Infect. 2006 Jun;36(6):343-345. Epub 2006 Jun 27

Blackwater fever in children, Burundi.Emerg Infect Dis. 2005 ;11(7):1118-20

Epidemiological and clinical aspects of blackwater fever among African children suffering frequent malaria attacks.Trans R Soc Trop Med Hyg. 2003 Mar-Apr;97(2):193-7.

Blackwater fever.Presse Med. 2002 ;31(28):1329-34.

Blackwater fever in adults with sickle cell anemia. Two fatal cases.Med Trop (Mars). 2000;60(2):156-8

Recurrence of blackwater fever: triggering of relapses by different antimalarials.Trop Med Int Health. 1998 Aug;3(8):632-9

Blackwater fever and acute renal failure in expatriates in Africa.Ren Fail. 1996 May;18(3):525-31

Blackwater fever in southern Vietnam: a prospective descriptive study of 50 cases.Clin Infect Dis. 1996 Dec;23(6):1274-81

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