Treatment of severe malaria

Warrell, D. A.
July 1989
Journal of the Royal Society of Medicine (Supplement);Jul1989, Vol. 82 Issue 17, p44
Academic Journal
In the treatment of severe Plasmodium falciparum infection antimalarial drugs should, ideally, be given by controlled rate intravenous infusion until the patient is able to swallow tablets. In cases where infection has been acquired in a chloroquine resistant area, and where it has broken through chloroquine prophylaxis or where the geographical origin or species are uncertain, quinine is the treatment of choice. When access to parenteral quinine is likely to be delayed, parenteral quinidine is an effective alternative. A loading dose of quinine is recommended in order to achieve therapeutic plasma concentrations as quickly as possible. In the case of chloroquine sensitive P. falciparum infection, chloroquine, which can be given safely by slow intravenous infusion, may be more rapidly effective and has fewer toxic effects than quinine. There is limited experience with parenteral administration of pyrimethamine sulphonamide combinations such as Fansidar, and resistance to these drugs has developed in South East Asia and elsewhere. Mefloquine and halofantrine cannot be given parenterally. Qinghaosu derivatives are not readily available and have not been adequately tested outside China. Supportive treatment includes the prevention or early detection and treatment of complications, strict attention to fluid balance, provision of adequate nursing for unconscious patients and avoidance of harmful ancillary treatments. Anaemia is inevitable and out of proportion to detectable parasitaemia. Hypotension and shock ('algid malaria') are often attributable to secondary gram-negative septicaemia requiring appropriate antimicrobial therapy and haemodynamic resuscitation. Many patients with severe falciparum malaria are hypovolaemic on admission to hospital and require cautious fluid replacement. Failure to rehydrate these patients may lead to circulatory collapse, lactic acidosis, renal failure and severe hyponatraemia. However, pulmonary oedema may be precipitated by excessive fluid replacement. Hypoglycaemia can result from quinineor quinidine-induced hyperinsulinaemia or may be associated with appropriately low plasma insulin concentrations in patients who have not yet started antimalarial chemotherapy. Young children, pregnant women and patients with severe manifestations, such as hyperparasitaemia, are at particular risk of developing hypoglycaemia. Disseminated intravascular coagulation is a relatively uncommon complication and treatable by transfusion of fresh blood or concentrates. Dexamethasone, once fashionable for the treatment of cerebral malaria, did not improve mortality when when used in a total dose of 2 mg/kg in 48 h in Thailand or 11.4 mg/kg in 48 h in Irian Jaya. In Thailand, dexamethasone treated patients remained unconscious for longer and had an increased risk of infections and gastrointestinal bleeding. Established renal failure requires peritoneal dialysis or haemodialysis which should be started early. From published evidence on 30 selected cases, it seems likely that exchange blood transfusion may lower parasitaemia more rapidly than optimal chemotherapy alone. However, the potential advantages of exchange transfusion must be balanced against the dangers, especially in the malaria endemic area. There is currently great interest in the possibility of reversing cytoadherence of parasitized erythrocytes in deep vascular beds by the use of hyperimmune serum.



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