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Partial exchange transfusion prior to treating cerebral malaria in an African child with glucose‐6‐phosphate dehydrogenase deficiency

Partial exchange transfusion prior to treating cerebral malaria in an African child with glucose6-phosphate dehydrogenase deficiency When cerebral malaria occurs in a patient who has glucose6-phosphate dehydrogenase (G6PD) deficiency, management is difficult, because the recommended treatment, intravenous quinine,' may induce intravascular hemolysis.2 However, partial exchange transfusion could permit the use of quinine by reducing the number of circulating enzymedeficient red cells. We report the case of an 8-year-old boy, known to have a G6PD deficiency and a history of drug-induced hemolysis, who was successfully treated for cerebral malaria with quinine after partial exchange transfusion. The child was admitted in deep coma after a convulsion. He had a 3-day history of headache, vomiting, fever (>40°C), and drowsiness. Initial treatment with chloroquine and paracetamol was unsuccessful. On admission, the blood glucose was 6.6 mmol per L (119 mg/dL), hemoglobin was 8.2 g per dL, and peripheral blood smears showed 1.08 x lo6 Plasmodium falciparum asexual parasites per pL (i.e., >30% parasitemia). Despite intramuscular injections of chloroquine (5 mg chloroquine baselkg every 6 hours), his clinical status deteriorated during the subsequent 24 hours. Other causes of deep coma and status epilepticus were excluded. Peripheral parasitemia increased to over 56 percent b1.3 x lo6 asexual parasiteslwl), and the hemoglobin concentration decreased to 6.2 g per dL. Partial exchange transfusion was initiated (removal of 45 mLlkg of venous blood and transfusion of 70 mLlbg ofwhole blood).The transfused volume was greater than the extracted volume to compensate for the initial anemia. The exchange was followed by an intravenous infusion of quinine (15 mg/kg twice a day).This therapy lead to a dramatic clinical improvement within 36 hours and decreased intravenous hemolysis (monitored and judged by urine color). There was a transient rise in the G6PD level. The child recovered fully without neurologic sequelae and was discharged 5 days after the partial exchange transfusion (Table 1). The use of exchange transfusion in severe malaria was first described by Gyr et aL3 Possible advantages of exchange transfusion include more rapid reduction of the parasite load than is seen with chemotherapy alone, safer correction of anemia in volume-overloaded patients, and removal of putative circulating toxic factors. In this case, the goal of partial exchange transfusion was to allow the use of quinine in a patient with known G6PD deficiency. G6PD deficiency is an X-linked defect. Males are hemizygous and therefore at greater risk for hemolysis than are heterozygous females. The A-G6PD variant common in Africans is less susceptible to hemolysis than Mediterranean variants, although the hemolytic crisis may be severe, depending on the nature of the offending agent. We recognize that a randomized clinical trial would be required to establish the benefit of exchange transfusion in preventing mortality in severe malaria. Our case report provides evidence that exchange transfusion might benefit patients with severe malaria and very high parasite counts. This approach could be useful in other instances when there is a risk of drug-induced hemolysis due to a concomitant disposition.