Amanita phalloides poisoning is an uncommon cause of acute liver failure, although it is associated with high mortality in the absence of urgent liver transplantation. We report the case of a 53-year-old man who developed fulminant amatoxin-induced acute liver failure complicated by refractory shock, severe hyperlactatemia, and acute kidney injury requiring continuous renal replacement therapy and therapeutic plasma exchange. Despite rapid progression of coagulopathy and multiorgan failure, the patient remained free of hepatic encephalopathy throughout the pre-transplant period. Progressive clinical deterioration and fulfillment of specific prognostic criteria led to urgent liver transplantation. After a prolonged and complex ICU stay, the patient achieved graft recovery and survived to hospital discharge. This case highlights that the absence of encephalopathy does not exclude a fulminant course in Amanita phalloides poisoning and underscores the importance of early multiorgan support and timely transplant evaluation.