Case Presentation: A 13-year-old male with a history of Graves’ disease was admitted with 24 hours of vomiting and diarrhea. The patient awoke at 4:30 AM on the day prior to admission with non-bloody, non-bilious vomiting. He vomited hourly for 10 hours and developed watery, non-bloody diarrhea, accompanied by sharp, intermittent bilateral lower quadrant pain. He had subjective fever and chills. For dinner the previous evening, the patient and his father had eaten mushrooms foraged from the neighborhood and his father also became ill. The patient was a first-generation American whose parents had immigrated from China. He denied drug or alcohol use. Methimazole was his only home medication. He presented to an OSH ED where he was afebrile but tachycardic to 115 with a normal BP. His exam was non-focal except for dry mucous membranes and mild bilateral LQ tenderness. Labs were significant for AST 154 and ALT 186, raising concern for hepatitis due to Amanita mushroom toxicity. Toxicology was consulted and the patient received 40cc/kg normal saline, an N-acetylcysteine (NAC) bolus, and a NAC infusion. He arrived at our institution 36 hours after the ingestion, at which point the vomiting had resolved, though he continued to have watery diarrhea. Repeat labs showed AST 606 and ALT 870 with INR 1.34, PTT 41.3 and normal ammonia. The patient was transferred to the PICU. He was kept NPO on 2x maintenance fluids, octreotide infusion, NAC infusion, and q4h activated charcoal. LFTs peaked at ALT 1209/AST 692 with peak INR 1.45. LFTs and INR began to downtrend 60 hours after ingestion. The patient tolerated PO and was discharged home 96 hours after the ingestion with plan for GI follow up.
Discussion: Amatoxin poisoning is the most common mushroom toxidrome and accounts for > 90% of mushroom-associated fatalities. Amatoxin is found in several mushroom species, but the majority of fatal cases are caused by Amanita phalloides (“death cap”). Amatoxin causes cell apoptosis by inhibiting DNA-dependent RNA polymerase-II and thereby impairing protein synthesis. The liver is differentially affected because it is the first organ to make contact with the blood after the amatoxin has been absorbed via the intestinal epithelium and liver exposure to the toxin is prolonged by enterohepatic recirculation. Patients are also at risk for nephrotoxicity because the toxin is renally cleared. Patients are asymptomatic for 6-24 hours after ingestion, then develop vomiting and profuse watery diarrhea. Patients may then appear to recover but hepatic and renal dysfunction can develop after 24-72 hours. Treatment includes gastrointestinal decontamination if ingestion is recognized early, supportive care with aggressive hydration to promote renal clearance, and reduction of intestinal absorption and recirculation with repeated doses of activated charcoal. Several chemotherapy options exist to reduce hepatocyte uptake and damage, including IV silibinin (milk thistle extract), penicillin, NAC, and octreotide, though evidence to support their use is weak. Fulminant hepatic failure is the most feared complication and emergent liver transplantation is required in severe cases.
Conclusions: Delayed onset of gastrointestinal symptoms six or more hours after ingestion of a foraged mushroom should prompt concern for Amanita mushroom toxicity and evaluation for liver and kidney injury.
To cite this abstract:Stewart M, Wedin T. Foraging for Trouble. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 779. Journal of Hospital Medicine. 2015; 10 (suppl 2). https://www.shmabstracts.com/abstract/foraging-for-trouble/. Accessed November 22, 2019.