Abstract Introduction Cerebral malaria is a severe complication of malaria with a high mortality rate and neurological sequelae. Here, we present a case of severe malaria that led to cerebral edema and herniation in the setting of starting continuous renal replacement therapy (CRRT). Case A 51-year-old Caucasian female with recent travel to Uganda not on malaria prophylaxis was admitted due to headache, lethargy, and fever. Her labs were notable for a leukocytosis of 30,000/uL, hemoglobin of 11.0 g/dL, platelets of 35,000/uL, lactate of 17 mmol/L, total bilirubin of 15 mg/dL, D-Dimer of 10.15 ug/mL, BUN of 124 mg/dL, and creatinine of 6.2 mg/dL. Initial chest and abdominal x-rays, abdominal ultrasound, and CT head were unremarkable. She had a positive malaria screen and smears showing 5% parasitemia with dual infection of Plasmodium falciparum and Plasmodium malariae. Vasopressors were started for shock as well as intravenous artesunate for severe malaria with an improvement in parasite load to 0.6% within 36 hours. On day 2, she had an electrographically confirmed seizure. MRI brain showed bilateral subcortical white matter hyperintensities, leptomeningeal enhancement, and diffuse symmetric petechial microhemorrhages, consistent with cerebral malaria. There was no mass effect or midline shift. She was started on CRRT with net even fluid balance and 4K baths to minimize cerebral perfusion changes. Within 5 hours, her vitals became labile, and she developed fixed pupils several hours later. 23.4% saline and mannitol were given. CTA of the head and neck showed diffuse cerebral edema with tonsillar herniation, and the patient was transitioned to comfort care. Discussion Cerebral malaria occurs mostly in children, pregnant women, and immunocompromised adults and its pathogenesis is incompletely understood. Mortality is between 15-25% and many survivors have persistent neurologic sequelae. Generally, CRRT is known to have a lower risk of cerebral edema compared to hemodialysis, but it can still occur with rapid osmolar shifts. Our patient had neurologic symptoms on admission but a negative initial head CT. It remains unclear whether the cerebral edema and subsequent herniation were a consequence of CRRT or simply a sequela of severe malaria. Conclusion We report a case of severe malaria with complications of cerebral edema and herniation that occurred shortly after initiation of CRRT. While there is scant evidence of the effect of osmolar shifts due to CRRT in patients with cerebral malaria, close neurologic monitoring is critical, and further research is needed on management in these cases. This abstract is funded by: None
Shyu et al. (2026) studied this question.