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Introduction: The majority of cases of mushroom poisoning in children involve benign gastrointestinal irritants, but critical poisonings are due to Amanita phalloides[1]. The relative rarity of liver transplantation in children due to Amanita phalloides poisoning and the multiple organ toxicity led us to describe its clinical evolution and the anaesthetic management.
Case report: A 2-year-old girl weighing 12 kg and with clinical symptomatology of fulminant hepatic failure was admitted to the emergency room 15 h after ingestion of wild mushrooms presenting somnolence, pallor, vomiting, diarrhoea, prostration and liver 2 cm palpable. The laboratory findings showed increased hepatic cytolysis enzymes and abnormal coagulation tests 25 h after ingestion. Therapeutic support included penicillin, siblibinin, activated charcoal, vitamin K, sucralfate, lactulose and neomycin. Her clinical situation rapidly progressed with renal failure, haematuria, grade III encephalopathy and haemodynamic instability (tachycardia and hyptotension); 81 h after ingestion, she was submitted to a split-liver orthotopic transplantation. Immediate preoperative data include prothrombin time 570% above control, 7720 U L−1 of TGP and 267 μmol L−1 of total bilirubin. Fentanyl (2 μg kg−1) and thiopental (6 mg kg−1) were used for induction, succinylcholine (1 mg kg−1) and vecuronium (0.1 mg kg−1) as muscle relaxants, isoflurane and fentanyl for maintenance. Diuresis varied from 1 to 2 mL kg−1 h−1 under furosemide, mannitol and aminophylline therapy. During the immediate postoperative period there occurred cardiac insufficiency and some haemodynamic instability. Perfusion of fentanyl (2 μg kg−1 h−1) was used for postoperative analgesia and sedation. Renal failure improved with haemofiltration and peritoneal dialysis. Now, 3 years after the transplant the child is alive, the graft functioning and she has quite a normal life.
Discussion: Severe Amanita phalloides mushroom poisoning is a potentially lethal problem for which liver transplantation can offer definitive therapy [2]. The amatoxins interfere with DNA transcription; the synthesis of mRNA and protein are interrupted, resulting in cell death. Rapid progression of the hepatic injury result in increased prothrombin time, rising aminotransferase levels coagulopathy, jaundice, acidosis, hepatic encephalopathy and renal failure. Without treatment, death from fulminant hepatic failure occurs 6 to 16 days after ingestion [3]. Therefore this is a great challenge to the anaesthesiologist.
