S5654 Unexpected Harvest: Clinical Insights From Three Cases of Amanita Toxicity

Introduction: Unintended ingestion of amatoxin-containing mushrooms is a rare cause of acute liver failure (ALF). Here we present cases of 3 patients transferred to our academic tertiary care center 48 hours after suspected ingestion of Amanita phalloides. Case Description/Methods: Patient A was a 32-year-old healthy man. He reported nausea and diarrhea but was otherwise asymptomatic with normal physical exam and liver ultrasound. Liver enzymes peaked on admission. He was treated with NAC with improvement in liver enzymes and was discharged on hospital day (HD) 3. Patient B was a 32-year-old man with active alcohol and methamphetamine use. He presented with ALF (grade 2 encephalopathy, elevated international normalized ratio) and significant liver injury. Imaging confirmed heterogeneous liver enhancement consistent with acute hepatitis. He received NAC, octreotide, activated charcoal, penicillin G, and underwent placement of percutaneous cholecystostomy tube on HD 1. By HD 2 his transaminases and international normalized ratio were improving. Silibinin was started in lieu of penicillin for a 96-hour course. He was discharged on HD 13. Patient C was a 37-year-old healthy man who presented with nausea and normal physical exam, though significant liver injury that rapidly progressed to ALF by the end of HD 1. Imaging revealed diffuse hepatic hypoenhancement consistent with necrosis later confirmed on liver biopsy. He was treated similarly to Patient B, however developed several complications including hemoperitoneum following cholecystostomy, small bowel obstruction from activated charcoal, and amatoxin-mediated kidney failure. He ultimately recovered with supportive care and was discharged on dialysis on HD 32 with recovery of renal function by day 100. Discussion: Our cases demonstrate the spectrum of illness that may result from amatoxin poisoning, ranging from mild hepatitis to multi-organ failure. Treatment is multifaceted, targeting hepatocyte protection (NAC), reducing hepatocyte uptake of amatoxin (penicillin, silibinin), and disrupting enterohepatic recirculation of amatoxin (octreotide, charcoal). Biliary drainage via cholecystostomy is a potential novel method for amatoxin removal from the enterohepatic circuit and should be reserved for situations in which silibinin is unavailable or clinical progression is rapid. Although there is potential for complications, particularly in coagulopathic patients, it should be considered against the risk for progressive ALF requiring liver transplant.