Letters to the Editor

Lumbar puncture in cerebral malaria

Cerebral malaria is the most severe neurological complication of Plasmodium falciparum malaria. Even though this type of malaria is most common in children living in sub-Saharan Africa, it should be considered in anybody with impaired consciousness that has recently travelled in a malaria-endemic area. Cerebral malaria has few specific features, but there are differences in clinical presentation between African children and non-immune adults. Subsequent neurological impairments are also most common and severe in children. Sequestration of infected erythrocytes within cerebral blood vessels seems to be an essential component of the pathogenesis. However, other factors such as convulsions, acidosis, or hypoglycaemia can impair consciousness. In this review, we describe the clinical features and epidemiology of cerebral malaria. We highlight recent insights provided by ex-vivo work on sequestration and examination of pathological specimens. We also summarise recent studies of persisting neurocognitive impairments in children who survive cerebral malaria and suggest areas for further research.

Severe falciparum malaria is one of the most lethal parasitic infections in the world and is responsible for more than one million deaths in African children per year. Changes to management over the last 40 years have not improved survival. A reduction in the mortality and morbidity may only come about by a better understanding of the pathophysiological processes that are responsible for severe disease and that determine the outcome before antimalarials have had time to work. This review discusses potential adjunctive therapies for severe malaria that are under development following such detailed clinical and pathophysiological studies.

Serial clinical and metabolic changes were monitored in 115 Gambian children (1·5–12 years old) with severe malaria. Fifty-three children (46%) had cerebral malaria (coma score </2) and 21 (18%) died. Admission geometric mean venous blood lactate concentrations were almost twice as high in fatal cases as in survivors (7·1 mmol/L vs. 3·6 mmol/L; P < 0·001) and were correlated with levels of tumour necrosis factor (r = 0·42, n = 79; P < 0·0001) and interleukin 1-α (r = 0·6, n = 34; P < 0·0001). Admission blood venous glucose concentrations were lower in fatal cases than survivors (3·2 mmol/L, vs. 5·8 mmol/L; P < 0·0001). Treatment with quinine was associated with significantly more episodes of post-admission hypoglycaemia when compared with artemether or chloroquine. After treatment, lactate concentrations fell rapidly in survivors but fell only slightly, or rose, in fatal cases. Plasma cytokine levels fluctuated widely after admission. Sustained hyperlactataemia (raised lactate concentrations, 4 h after admission) proved to be the best overall prognostic indicator of outcome in this series. Lactic acidosis is an important cause of death in severe malaria.