Technically, cerebral malaria is unrousable coma without fits in the preceding 30 min with no cause except for malaria. Hypoglycemia should always be excluded. Mortality from cerebral malaria can be up to 30 per cent even with ideal treatment. Despite this, patients who survive seldom have significant neurological sequelae.
Trials have shown that prophylactic intramuscular phenobarbital (phenobarbitone) improves outcome in cerebral malaria; where this is not available it is likely that other anticonvulsants given prophylactically help. Fits occur commonly in cerebral malaria and should be treated conventionally. There is no contraindication to using benzodiazepines. The role of cerebral edema in the pathology of cerebral malaria is unclear, but it has been clearly demonstrated that steroids and mannitol have no place in the management of adult cases of cerebral malaria.
In practice, any reduction in conscious level or neurological signs in the context of malaria are significant, and patients should ideally be nursed in a high-dependency unit. There is no indication for routine lumbar puncture or CT scanning in cerebral malaria, except where coexisting meningitis is suspected.
Renal failure is one of the common causes of death in severe falciparum malaria. This can occur acutely or after the patient seems to have begun to recover. Hemofiltration and dialysis should be started early in renal impairment due to malaria as this probably improves outcome, although there are currently no good trials to prove this. Extreme care should be taken to avoid overhydration.
Quinine and quinidine are metabolized in the liver, and so dosage seldom has to be adjusted for at least the first 3 days of treatment when patients are in renal failure.
Where facilities to monitor drug levels are not available, it is conventional to reduce dosage by a third on day 3. Dialysis marginally reduces quinine levels. Certain antimalarial second-line drugs, particularly Fansidar, are best avoided in renal failure. Doxycycline is probably the second-line drug of choice, at a reduced dose of 100 mg/day.
'Blackwater fever', an old term mainly used for patients with black urine secondary to intravascular hemolysis, should be treated like any other malaria. It is sometimes triggered by antimalarial drugs, particularly in cases of glucose-6-phosphate dehydrogenase deficiency, but the risks of stopping treatment are almost always greater than those of the hemolysis itself.
Pulmonary involvement in malaria is very serious, with a high mortality even with intensive care. Fluid excess should be excluded with the help of a pulmonary artery catheter, and if present corrected with diuretics. In severe cases, however, it may be caused by a form of acute respiratory distress syndrome. Apart from optimizing the fluid balance and standard intensive care support for acute respiratory distress syndrome, no specific treatment has been shown to help.
The exact role of exchange blood transfusion where high parasite loads are present is controversial ( Wilkinson §L§.L 1994). Exchange transfusion involves substituting unparasitized donated blood for the heavily parasitized blood of the patient. It is not indicated for parasitemias of less than 5 per cent. At parasitemias of greater than 10 per cent it has a place in certain cases where complications are present. At confirmed parasitemias of over 20 per cent it is very likely to be indicated. It should never be performed without close nursing and medical supervision to balance blood coming out with blood going in. Laboratory errors in estimation of parasitemias (by up to a factor of 10) are not uncommon, with overestimation more likely than underestimation. Therefore it is advisable to have high parasitemias checked by a reference laboratory.
Profound anemia is common in severe malaria, particularly where there has been a prolonged history. Parasitized cells are broken down and the parasite suppresses hemopoiesis, so that there is seldom a reticulocytosis. Transfusion is usually indicated at a hemoglobin concentration below 5 g/dl. Low platelets are almost invariable in malaria and require no specific treatment unless bleeding occurs. There is no association between platelet count and severity.
DIC is a rare but serious complication of severe malaria. It can present with profuse bleeding into the gut. Since almost all patients with DIC and malaria will already be anemic, blood transfusion is usually indicated. The role of heparin, fresh frozen plasma, and other treatments is no more clearly worked out than in other causes of DIC.
Shock (algid malaria)
Shock in malaria is often associated with coexisting sepsis, and all patients with this complication should receive broad-spectrum antibiotics with good Gram-negative cover. Otherwise treatment is supportive. Malaria has surprisingly little effect on cardiac function in most cases.
Pregnant women who contract malaria are at increased risk. Quinine remains the antimalarial drug of choice. Doxycycline is contraindicated. Fansidar should be used with caution, and always given with a folate supplement. Pregnant women should have their quinine treatment extended for at least 48 h beyond the point where they become parasite free on blood film, and treated for a minimum of a week if no second-line agent is used. Recrudescence can occur more than a month after adequate treatment of pregnant women.
Anemia and hypoglycemia are common in pregnancy. Risk of abortion is increased, and congenital malaria is well recognized when malaria occurs near term, although it is more common in P. vivax cases. Low-birth-weight babies are common after malaria in pregnancy.
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