Letters to the Editor

Indian Pediatrics 2000;37: 1028-1029

Amanita Poisoning in a Child Treated with Plasma Exchange

Widespread usage of mushrooms as food results in serious poisonings especially due to Amanita species. Here, we describe a case with amanita poisoning (AP) and a role of plasma exchang (PE) in treatment is proposed.

An 11-year-old boy who ate wild mushroom for dinner, presented to our hospital with complaints of nausea, vomiting, watery diarrhea and abdominal pain 28 h after ingestion. Activated charcoal and intravenous fluids that were administered at 8 h after ingestion by local emergency department were continued. Physical examination and initial biochemical tests were normal. Then the transaminases (AST and ALT) rose to 153 IU/L and 132 IU/L, respectively. Diagnosis of acute viral hepatitis, Wilson’s disease and alpha-1 antitrypsin deficiency were excluded by appropriate tests and AP was diagnosed clinically. High dose of penicillin G (5,00,000 IU/kg/day), ascorbic acid, cimetidine, fresh frozen plasma (FFP) and vitamin K were started for AP and lactulose, gentamicin and L-Dopa for heptatic precoma. AST and ALT levels reached peak values (1900 IU/L and 14100 IU/L, respectively) within 54 h. Prothrombin time was prolonged (62.5 sec vs control 13 sec), total bilrubin level was 5.9 mg/dl and serum ammonia level was 198 hmol/L (normal 11-32). He developed hepatic encephalopathy, while renal functions remained normal. Mannitol and fluid restriction was started for cerebral edema. On fourth and fifth days, as the clinical condition deteriorated, PE was performed. After catheterization of the femoral vein, 60 ml FEP per kilogram body weight were exchanged at each time. He was considered to be a candidate for liver transplantation, but no suitable donor was available. Seven days after ingestion, mental status and hepatic function started to improve. He was discharged from the hospital 15 days after the ingestion.

Amanita species have two types of oligo-peptide toxins. Amatoxins bind with a subunit of RNA polymerase II and interfere with mRNA synthesis and cause clinical symptoms(1). Although, isolation of amatoxin could not be done, presentation of the patient resembled AP. The mother had also eaten the mushrooms but was in good condition. This might be due to the fact that amongst the singly fried mushrooms, the nonpoisonous ones were eaten by the mother. Beside the standard therapy with penicillin G(2), drugs that are of no proven benefit including ascrobic acid and cimeti-dine(1) were also tried. Charcoal hemoperfusion, hemodialysis and exchange transfusions are recommended in case of renal failure(2). Mortality rate of 84% was also reported with these therapies(3). Although, our patient did not experience renal failure, we performed PE at late period. PE appears to be effective in patients with acute hepatic failure. Increased inflammatory mediators could be removed from the patient's plasma(4). Mercuriali and Sirchia(5) and Valbonesi(3) reported their experience with PE in AP cases. Their mortality rates were 12% and 15% respectively. It is proposed that in case of amanita poisoning with acute hepatic failure and heptaic encephalopathy, beside the standard therapy, PE may be a good therapeutic approach.

1. O'Brien BL, Khuu L. A fatal Sunday brunch: Amanita mushroom poisoning in a gulf coast family. Am J Gastroenterol 1996; 91: 581-583.

2. Vesconi S, Langer M, Iapichino G, Costantino D, Busi C, Fiume L. Therapy of cytotoxic mushroom intoxiciation, Crit Care Med 1985; 13: 402-406.

3. Valbonesi M. Apheresis in acute liver failure. In: Therapeutic Hemapheresis: Valbenesi M, Pineda AA, Biggs JC edn. Milano Wichting Editore, 1986; pp 119-126.

4. Iwai H, Nagaki M, Naito T. Removal of endotoxin and cytokines by plasma exchange in patients with acute hepatic failture. Crit Cae Med 1998; 26: 873-876.

5. Mercuriali F, Sirchia G. Plasma exchange for mushroom poisoning. Transfusion 1977; 17: 644-646.