Title: Killer Soup: A Case of Amanita Poisoning
Author(s): Mikayla Morrow, DO; Carrie Powell, DO; Adam Hackney, MD; Kalie Grargano-Murphy
Email: Mmorrow@mercy.com
Introduction: Foraging for mushrooms has become increasingly popular for a variety of reasons, however, confusing toxic mushrooms for edible ones is easy to do. a-amanitin is responsible for 90% of deaths related to mushroom ingestion and has an overall fatality rate of 10-30% even with appropriate management. Treating this toxicity remains a conundrum as there are no specific guidelines regarding care, meaning that current practices are largely based on speculation. With such a high mortality risk, providers must maintain amanita poisoning on their differential to offer available supportive care to ameliorate liver failure or death.
Case Report(s): We report the case of a 65-year-old Chinese female who presented to the emergency department with complaint of nausea, vomiting, and generalized abdominal pain that had been ongoing for approximately twelve hours prior to arrival. On arrival, she was hemodynamically stable, nontoxic appearing albeit uncomfortable on physical exam. She did not appear clinically dehydrated, she was afebrile, and she had generalized abdominal tenderness to palpation without rebound or guarding.
She arrived to the emergency room around 1240. On questioning, the patient and her husband noted that she had woken up from sleep with these symptoms between 2200-0000 the night prior. Her husband reported she had been foraging for mushrooms in her neighbor’s yard, had found one that she had thought looked safe and appetizing, and proceeded to make a soup out of it. Her husband had warned her against it but she ate all of it without sharing. Her husband had brought one of the mushrooms with him and the ED providers identified it to be an Amanita – specifically, a “destroying angel.” The case was discussed with clinical pharmacy and toxicology. The providers made the decision to not waste any time prior to starting treatment with N-acetylcysteine, continuous penicillin G, ocretotide, and scheduled activated charcoal in addition to symptomatic care medications. Patient was then accepted to two different toxicology centers with liver transplant capabilities, pending whichever transport was able to occur first.
Lab work in the emergency room resulted with an initial ALT of 40, AST of 51, alk phos 52, total bilirubin of 0.3, lactic acid of 2.1, lipase of 25, INR of 1.0, ammonia < 10, a BUN of 23 and a creatinine of 0.8. Labs were scheduled until transport arrived and hepatic function trended up to an ALT of 75 and an AST of 110 within eight hours.
At the accepting facility under gastroenterology and hepatology, they continued supportive care measures and added silibinin to the regimen as well as vitamins and cimetidine. Treatment continued for five days with hepatic function peaking at an AST of 1,299 and ALT of 1,697 roughly sixty-four hours post-ingestion. INR had increased to 1.4. Transaminitis trended down and she was discharged in good stable condition.
Discussion: This case demonstrates a critical diagnosis that has a high likelihood of severe consequences if not recognized. Amanita is easy to confuse with a simple diagnosis of gastroenteritis and the timeline following ingestion must be taken into consideration. Providers must maintain a broad differential and if indicated consult toxicology early to ensure appropriate recommendations and to not find false reassurance in initial hepatic function panels.
