Abstracts

Rationale: Primary amoebic encephalitis is a rare condition caused by CNS infection with Naegleria fowleri.  It is commonly contracted by contact of warm stagnant water with the nasal mucosa with subsequent cerebral invasion of the organisms via the olfactory tracts.  Clinical course is a fulminant febrile illness with encephalopathy due to progressive cerebral edema and necrosis leading rapidly to death.  There is little information about the EEG findings in this condition. Methods: A retrospective chart review was performed of two pediatric patients treated for primary amoebic encephalitis in our institution in 2015, and a review of the medical literature was performed.  Results: Patient #1 was a 4-year-old previously healthy boy who presented with a 5-day history of headache and fever. 3 days prior to onset of symptoms he was camping and swam in a lake. On the day of admission he was lethargic with confused speech and had an event of generalized convulsion.  In the ER, he had right eye deviation and nystagmus. CSF findings were consistent with meningitis.  Initial EEG showed focal left temporal slowing; subsequent EEG and cEEG monitoring showed progressive background slowing, multifocal subclinical seizures, multifocal epileptiform discharges, and regional right frontotemporal voltage suppression progressing to generalized burst suppression and finally to generalized suppression.  He was treated with lorazepam, fosphenytoin, midazolam infusion, ceftriaxone, vancomycin, and acyclovir.  Amoebas were seen on CSF wet mount on HD#2, confirmed to be N. fowleri by PCR, and he was subsequently treated with amphotericin, rifampin, azithromycin, fluconazole, dexamethasone, and miltefosine, but developed cerebral edema with loss of brainstem reflexes and died on HD#3.Patient #2 was a 14-year-old boy who presented with a 2-day history of headache, fever, myalgias and emesis, and confusion on the day of admission.  He swam in a lake 6 days prior to onset of symptoms.  CSF was consistent with meningitis; wet mount revealed amoebas, confirmed N. fowleri by PCR.  CT showed cerebral edema, treated with mannitol and hypertonic saline. Seizures developed during transfer and were treated with lorazepam and levetiracetam; midazolam was used for sedation. Initial EEG showed background slowing. Pentobarbital was used for 1 day therapeutically, and cEEG showed progression to burst suppression and then to generalized suppression which persisted after discontinuation of pentobarbital.  He was treated with ceftriaxone and vancomycin, amphotericin B IV and via EVD, fluconazole, rifampin, azithromycin, miltefosine, dexamethasone, chlorpromazine, and hypothermia, but developed cerebral edema and herniation with loss of brainstem reflexes, and died on HD#9.  Conclusions: Primary amoebic encephalitis shows an EEG progression from background slowing with or without epileptiform features, to burst suppression and then generalized suppression, corresponding to clinical course of progressive cerebral edema leading to brain death. Funding: None