Background: Amanita pantherina ingestions may cause a myriad of effects, including sedation, hallucinations, agitation, and seizures, but fatal exposures are rare. Symptoms typically occur within 2 hours of ingestion but may be delayed for up to 6 hours. We report a case of A. pantherina ingestion resulting in refractory status epilepticus and death.
Case Report: A 68 year-old woman with a history of diabetes mellitus, hypertension, and chronic kidney disease (CKD) with baseline creatinine (Cr) 2.5 mg/dL presented to an Emergency Department with status epilepticus after consuming a mushroom she had foraged. The mushroom was later identified as A. pantherina by a mycologist. She was markedly hypertensive upon arrival with systolic BPs between 230 and 240 mm Hg. Endotracheal intubation was performed and a propofol infusion started. Her initial labs were: sodium 140 mEq/L, bicarbonate 21 mEq/L, anion gap 8, glucose 84 mg/dL, and Cr 3.14 mg/dL. Her head CT was negative for acute pathology. Due to persistent hypertension, a nitroprusside drip was started. Electroencephalogram (EEG) monitoring confirmed continuous seizure activity. Her hypertension resolved and norepinephrine was required for persistent hypotension after hospital day (HD) 1. Despite administration of lorazepam, a therapeutic phenytoin concentration (14.7 mcg/mL), a therapeutic levetiracetam concentration (46.9 mcg/mL), and a slightly sub-therapeutic phenobarbital concentration (14.6 mcg/mL), the patient's seizures persisted for 6 days, and life support was withdrawn on hospital day (HD) 7. She had no prior seizure history.
Case Discussion: A. pantherina does not contain amatoxin or other cyclopeptide toxins; rather it contains ibotenic acid and muscimol. Ibotenic acid has neurologic effects analogous to those of glutamate and may cause agitation, seizures, and delirium via N -methyl D -aspartate (NMDA) receptor agonism. Muscimol, a selective GABA A agonist, may produce somnolence, ataxia, confusion, and hallucinations. In light of these opposing effects, patients ingesting A. pantherina exhibit variable CNS toxicity. Ibotenic acid is renally excreted; therefore, the severity of this patient's symptoms and protracted clinical course may have been exacerbated by her CKD, resulting in a prolonged elimination half-life and sustained toxicity. This case is unique because most A. pantherina ingestions produce a self-limited illness without permanent sequelae.
Conclusion: This case highlights the potential for serious, even fatal, toxicity following Amanita pantherina ingestion. Renal impairment may contribute to or exacerbate toxicity.