Chapter 58. Severe Malaria

• Consider the diagnosis of malaria in any acutely febrile patient with a history of recent travel to a malarious area or who might have been infected through blood transfusion, needlestick, or other nosocomial parenteral exposure.
• Transfer severely ill patients to an ICU and make a rapid clinical assessment, including spot measurement of blood glucose.
• If the diagnosis of severe falciparum malaria is proved or suspected, initiate antimalarial chemotherapy using optimal doses of an appropriate agent (licensed quinine or quinidine or an artemisinin derivative such as artesunate on a named-patient basis) administered intravenously, using a loading dose. Monitor the clinical and parasitologic responses.
• Prevent, or detect early and treat, the numerous complications (especially generalized convulsions, hypoglycemia, hyperpyrexia, and secondary bacterial infections).
• Ensure correct fluid, electrolyte, and acid-base balance. Control fluid replacement to prevent circulatory overload and pulmonary edema. Anticipate renal and respiratory failure.
• Expert nursing care of the unconscious patient is essential.
• Avoid the use of potentially harmful ancillary treatments of unproven benefit, such as corticosteroids, heparin, and epinephrine.

Malaria is a mosquito-borne protozoal infection caused in humans by four species of Plasmodium: P. falciparum, P. vivax, P. malariae, or P. ovale.1 Only P. falciparum causes life-threatening malaria, but other species can cause severe illness in debilitated individuals. Plasmodium sporozoites, inoculated by female Anopheles mosquitoes during their blood meal, invade hepatocytes where they mature into schizonts, and after 6 to 16 days rupture to release merozoites into the bloodstream. In the cases of P. vivax and P. ovale, some sporozoites remain dormant in the liver for months or years in the form of hypnozoites, and can give rise to relapsing infections months or even years later. Plasmodium falciparum and P. malariae may persist as inapparent low-grade parasitemias to cause symptomatic recrudescences. However, these species do not persist in the liver. The erythrocytic cycle consists of invasion, development from rings to mature pigmented multinucleated schizonts, and rupture with release of 4 to 32 merozoites, depending on the species. These invade erythrocytes to produce repeated cycles of infection, or develop into male and female gametocytes. Merozoites cannot reinvade the liver from the blood. Erythrocytes containing mature trophozoites and schizonts of P. falciparum are sequestered in the tissues. Gametocytes taken up by mosquitoes complete a sexual cycle producing sporozoites which are injected with the mosquito's saliva during a blood meal. The usual intervals between the mosquito bite and the appearance of parasitemia are 10 days for P. falciparum, 8 to 13 days for P. vivax, 9 to 14 days for P. ovale, and 15 to 16 days for P. malariae. Minimal intervals between the bite and first symptom (incubation period) are a few days longer.

Epidemiology

Malaria is endemic throughout tropical countries except in Pacific Islands east of Vanuatu (Fig. 58-1). P. falciparum is the most common cause of malaria in Africa, Haiti, some parts of South America, Southeast Asia, and New Guinea, but is now absent ...