Cerebral Malaria

September 14, 2005
Hesham Taha, MD

,
Gamil Kostandy, MD

,
David Dosik, MD

A 20-year-old woman, who had been confused and delirious for 2 days, was brought to the emergency department (ED). She had no significant past medical history and was taking no medication but had recently returned from a trip to Southeast Asia. In the ED, the patient had several convulsions and rapidly became comatose. She was unresponsive; her temperature was 37.9°C (100.3°F), and her blood pressure measured 80/50 mm Hg. The neurologic examination showed no signs of meningeal irritation. Cranial nerve examination was normal and showed mild, bilateral, symmetric increase in deep tendon reflexes. All other physical examination findings were normal.

A 20-year-old woman, who had been confused and delirious for 2 days, was brought to the emergency department (ED). She had no significant past medical history and was taking no medication but had recently returned from a trip to Southeast Asia. In the ED, the patient had several convulsions and rapidly became comatose. She was unresponsive; her temperature was 37.9°C (100.3°F), and her blood pressure measured 80/50 mm Hg. The neurologic examination showed no signs of meningeal irritation. Cranial nerve examination was normal and showed mild, bilateral, symmetric increase in deep tendon reflexes. All other physical examination findings were normal.

Laboratory results included white blood cell count, 6,500/µL; platelet count, 450,000/µL; hemoglobin, 7 g/dL; and hematocrit, 20%. Total serum bilirubin measured 5 mg/dL, and direct bilirubin was 1 mg/dL. The urine was dark red and positive for hemoglobin. A CT scan of the brain was negative for bleeding and infarction. The peripheral blood smear, seen here, shows normochromic, normocytic anemia, with Plasmodium falciparum trophozoites and schizonts involving erythrocytes (arrows). The diagnosis of cerebral malaria was made.

Drs Hesham Taha, Gamil Kostandy, and David Dosik of Brooklyn, NY, point out that cerebral malaria usually is caused by infection with P falciparum transmitted by the bite of an infected anopheles mosquito. Coma, a characteristic feature of this condition, is associated with a 20% mortality rate and is caused by the sequestration of parasitized red blood cells in the cerebral microvasculature.1The onset of coma may be sudden or gradual following a period of obtundation, delirium, or abnormal behavior.

Cerebral malaria is a diffuse symmetric encephalopathy, and focal neurologic signs are unusual. Associated conditions include hypotension, anemia, jaundice, hypoglycemia, and renal failure.2 Cerebral malaria is an acute emergency. The mainstay of treatment is cinchona alkaloids (quinidine and quinine), which act against chloroquine-resistant strains of P falciparum. This patient responded to intravenous quinidine gluconate and had an uncomplicated recovery.

REFERENCES:1. Marsh K, English M, Crawley J, Peshu N. The pathogenesis of severe malaria in African children. Ann Trop Med Parasitol. 1996;90:395-402.
2. Turner Gj. Cerebral malaria. Brain Pathol. 1997;7:569-582.