sible. Despite optimal care, between 10 and 30 percent of children with cerebral malaria die, and a similar proportion suffer neurological damage (Molyneux et al., 1989a). In most cases, the actual cause of death is unknown (World Health Organization, 1990).
Hypoglycemia Many illnesses cause hypoglycemia, a condition which requires immediate, specific treatment to prevent permanent brain damage and death (Kawo et al., 1990). Because its clinical presentation (confusion, coma, and convulsions) closely mimics that of cerebral malaria, the coexistence of hypoglycemia in some patients with severe malaria was not suspected until quite recently (White et al., 1983b). As a result, an unknown number of patients may have died or suffered brain damage from what is an eminently recognizable and easily treated condition. The emergency treatment of hypoglycemia is an intravenous bolus of a very concentrated sugar solution, followed by a continuous intravenous supply of glucose until the patient can take food and fluids by mouth.
Hypoglycemia is an especially common finding in pediatric malaria. In two recent studies, 23 and 32 percent of pediatric patients, respectively, were admitted with hypoglycemia (blood glucose levels less than 2.2 millimoles per liter, or 40 milligrams per deciliter) (White et al., 1983b; Taylor et al., 1988). The prognosis is particularly poor for such patients. In the Malawi study, 37 percent of those with hypoglycemia died and 26 percent were discharged with neurological sequelae (Taylor et al., 1988). These rates are six to nine times higher than those for cerebral malaria patients with normal blood sugar levels.
Studies on hypoglycemia in children suggest that the condition develops through one or more of several mechanisms. One theory suggests that malaria infection may impair the liver's capacity to produce glucose from circulating precursors. It may also be that the sequestration of parasitized red blood cells in tissue capillaries slows the circulation enough to cause a change in tissue metabolism, thereby enhancing glucose consumption.
Malarial Anemia Red blood cells infected with malaria parasites either are destroyed outright when schizonts mature and merozoites burst from the cell or are cleared from the circulation by the spleen. In acute malarial infections, splenomegaly is often associated with mechanical destruction of normal red blood cells, perhaps because the cell architecture becomes distorted. Several studies of patients with acute malaria have shown that there is also a decrease in the bone marrow production of new red blood cells (Marchiafava and Bignami, 1894; Abdalla et al., 1980; Phillips et al., 1986a). Cytokines such as TNF may be involved in this marrow suppression and dyserythropoiesis (abnormal red blood cell production). In addition, red blood cells coated with low levels of immunoglobulin G may be