[The curative effects of transmetil on Amanita verna poisoning].
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Abstract:
To observe the curative effects of transmetil on Amanita verna poisoning.Twelve cases with Amanita verna poisoning were reviewed. The patients were divided into 2 groups according to usage of transmetil: Group A was treated with traditional protocol (gastric lavage, catharsis, rehydration, diuresis, anti-infection and hemodialysis), Group B was treated with traditional protocol combined with transmetil. The liver function changes on the 1st, 3rd, 5th and 7th day after poisoning and the mortality were compared between 2 groups.Two cases in group A (6 patients) died. The mortality of group A was 33.3%. The AST levels continued to increase on the 3rd and 5th day, but decreased on the 7th day. TBIL continued to increased on the 1st, 3rd, 5th and 7th day. None in group B died. The TBIL level dropped at 7 d 5 patients showed an increase in ALT at 7 d and 3 patients showed a decrease in AST at 7 d.Transmetil may play an important role in reducing the mortality of Amanita verna poisoning.Keywords:
Amanita phalloides
Amanita
Mushroom poisoning
Gastric lavage
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The clinical and laboratory findings of 21 children with amitraz poisoning were evaluated retrospectively. Poisoning route, signs and symptoms of poisoning, duration of hospitalization and outcome were recorded. The mean age was 3.5 ± 1.9 years and the ratio of males to females was 1.63. In all cases poisoning was via the oral route. The time from ingestion to onset of symptoms was 30–180 min. Drowsiness (100%) and loss of consciousness (100%) were the most common clinical findings, followed by vomiting (61.9%). Hypotension was observed in 66.7% of cases, bradycardia in 61.9%, respiratory depression in 42.9%, hypothermia in 9.3%, and 14.3% had generalized seizures responsive to diazepam. Hyperglycaemia and glycosuria were detected in 47.6% and 38.1% of cases, respectively. Minimally elevated transaminases and alkaline phosphatase levels were detected in 23.8% of cases. All patients recovered completely and were discharged within 1.0–5.2 days (mean, 2.1 ± 1.1).
Abdominal distension
Amitraz
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Hemoperfusion
Amanita phalloides
Mushroom poisoning
Extracorporeal
Plasmapheresis
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Introduction
Mushroom poisoning is a rare problem. We report four concomitant cases of amatoxin intoxication, the most deadly cause of mushroom poisoning.Methods
Case Four women, living together in a convent, were admitted because of nausea, vomiting and diarrhoea. Symptoms started approximately 10 hours after eating wild mushrooms, self-picked in the forest. Laboratory data, 24 hours after ingestion, showed normal liver enzymes in 2 patients and normal INR and bilirubin in all 4 patients. Because of suspected amatoxin intoxication, a therapy with intravenous fluid, N-acetylcysteine and silibinin was started. 36 hours after intoxication, complaints of vomiting and diarrhoea improved in all 4 patients. Blood analysis however showed a dramatic increase of the liver enzymes in 3 of 4 patients (ALT-range 48 hours after ingestion: 558–1762 U/L), and an elevation of bilirubin and INR in all 4 patients. Two patients were transferred to a transplantcentre 48 hours after mushroom poisoning because they developed stage 2 hepatic encephalopathy. With maximal supportive therapy, all patients gradually improved from day 3 on. They were discharged from the hospital between 6 to 10 days after admission.Results
Discussion Our patients showed the typical clinical syndrome of an amatoxin intoxication. This syndrome can be divided into 3 phases. The gastrointestinal phase (starts 6–40 hours after consumption) is characterised by vomiting and diarrhoea and lasts 12–24 hours. In amatoxin intoxication, symptoms develop typically more than 6 hours after ingestion, while other toxic mushrooms cause symptoms earlier, after 0.5–3 hours. Blood analysis at this initial stage shows normal liver and kidney function. A careful history is very important, to avoid the risk that patients are discharged too early with a diagnosis of a common gastroenteritis. The second phase is characterised by an apparent recovery 36–48 hours after ingestion, while biochemistry shows a progressive increase of transaminases. In the third phase (2–6 days after ingestion), patients can develop hepatic failure, often complicated by renal failure. The therapy of amatoxin intoxication consists of supportive care and medical therapy with silibinin and N-acetylcysteine. Therapy with activated charcoal can be beneficial, if started early after the intoxication. We did not treat our patients with activated charcoal because of vomiting and presentation of the patients 24 hours after ingestion. Patients who develop liver failure should be transferred to a transplantcentre.Conclusion
Amatoxin intoxication is a rare cause of liver failure. When suspected, careful monitoring of the liver function and treatment with silibinin and N-acetylcysteine are mandatory.Disclosure of Interest
None Declared.Mushroom poisoning
Amanita phalloides
Concomitant
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Abstract. Mushroom poisoning leading to acute renal failure is extremely rare in North America. Cortinarius species and Amanita smithiana both can cause acute renal failure and inhabit the Pacific northwest. This article describes 4 patients who presented in acute renal failure and who ingested mushrooms described as resembling A. smithiana. Two patients (a 74‐year‐old Korean couple) described eating mushrooms with an approximately 6 × 0.5‐inch stipe with a white cap, 1.25‐1.5 inches in diameter. The other 2 patients (a 55‐year‐old male and a 30‐year‐old female) also described a white‐capped mushroom. All believed they were eating the matsutake (Tricho‐loma magnivalere) mushroom, which can be mistaken for A. smithiana. Onset of gastrointestinal symptoms ranged from 20 minutes to 12 hours, and presentation in acute renal failure ranged from 4 to 6 days postingestion (initial BUN and creatinine were 72–91 mg/dL and 12–13.9 mg/dL, respectively). One patient had underlying mild renal insufficiency and one had hypertension that was under control, while the others had no risk factors for renal disease. None had any other explanation for the episode of acute renal failure. All underwent acute hemodialysis for at least several weeks, eventually returning to baseline renal function.
Mushroom poisoning
Stipe (mycology)
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On December 5th of 2006 a 72 year old, otherwise healthy man from Asian descent, was admitted to the emergency department of a hospital in central Switzerland with symptoms of acute gastroenteritis. History revealed ingestion of a freshly picked mushroom 24 hours previously. Urine tested positive on α-amanitin. He was started on therapy with activated charcoal, N-acetylcysteine and silibinin. Due to imminent fulminant hepatic failure, he was transferred to a tertiary centre for assessment of emergency liver transplantation but fortunately, the liver function recovered after five days and he finally could be discharged home on day 7 in stable condition. To our knowledge, this is the first reported mushroom poisoning with Amanita phalloides in central Europe, caused by a freshly picked death cap in the month of December. Naturally death caps grow from May to October [1] in deciduous forests and parks. Accordingly, most cases of intoxication are noted in autumn, although occasionally poisoning with stored mushrooms has been reported in winter months [2]. Our case demonstrates that ‘off-season’intoxication with freshly picked death caps must be considered in patients with otherwise appropriate history of recent mushroom ingestion. It is possible that clima warming leads to more Amanita phalloides intoxication in atypical season.
Mushroom poisoning
Amanita phalloides
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Objective To study the effect of hemodialysis in patients of mushroom poisoning.Methods 10 mushroom poisoning pa- tients camplained with acute renal failure,toxic hepatitis or foxic myocarditis treated with hemodialysis and eonventional therapy.Results 10 patients received bemodialysis 2～8 times(mean 4 times).The results shew that the anaric stage last 2～15 days(mean 4.5 days).The pa- tient stayed in hospital last from 4～30 days(mean 16 days).9 patients were surviral except 1 patient was dead due to liver function fail- ure.Namy sequelae found inall patient with a half year follow-up.Conclusion Hemodialysis was an effective method to treat the mushroom poisoning patients.It needed to confirm either hemedialysis or peritoneal dialysis was a better method in patients with mushroom poisoning.
Mushroom poisoning
Toxic hepatitis
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Amanita phalloides
Mushroom poisoning
Transaminase
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Objective To investigate the factors influencing the incidence of acute pancreatitis (AP) in patients with organophosphorus poisoning and explore the effectiveness of measures for its prevention and treatment. Methods Clinical data of 50 patients with organophosphorus poisoning were reviewed retrospectively in our center between January 2001 and December 2006. Results The incidence of AP in patients with organophosphorus poisoning was 30% (15/50), and 14 patients suffered from MAP, while one patient occurred SAP. 13 of 15 AP patients underwent gastric lavage with cold normal saline; gastric tube was placed in 14 patients; toxic doses over 50 ml were observed in 10 patients; atropine overdose were observed in 11 patients. There were 35 cases of organophosphorus poisoning alone, and 2 of them underwent gastric lavage with cold normal saline; gastric tube was not placed in 1 patient; toxic doses over 50 ml were not observed in all the patients. The toxic dose, water temperature for gastric lavage, gastric tube placement, duration from poisoning to treatment between the two groups were significantly different (P＜0.01). All the patients with organophosphorus poisoning alone survived, while in these 15 patients with AP, 14 patients were cured, 1 patient died. Conclusions Organophosphorus poisoning can induce AP and development of AP was possibly related to organophosphorus poisoning and improper treatment.
Key words:
Pancreatitis; Pesticides; Poisoning
Gastric lavage
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To analyze the clinical manifestation and therapeutic method in patients with acute mushroom poisoning.A retrospective study was conducted. The clinical data of 48 patients with acute mushroom poisoning admitted to Department of Poisoning Treatment of the 307th Hospital of PLA from January 2016 to May 2017 were analyzed. The clinical data including gender, age, clinical symptoms, onset season, initial symptoms, incubation time, the length of hospital stay, treatment, and prognosis. In addition to the conventional treatment, the patients with severe liver damage were treated with continuous blood purification (CBP). The changes in routine blood test, biochemical parameters, blood ammonia and coagulation function before and 1, 3 and 7 days after CBP were observed.There were 29 of male (60.4%) and 19 of female (39.6%) in 48 patients with acute mushroom poisoning, with an average age of (48.10±13.14) years. There were 9 patients suffering from gastroenteritis type, 26 suffering from liver damage type, 8 suffering from neuro-psychosis type, 2 suffering from hemolytic type, and 3 suffering from renal damage type. All of the poisoned patients had evident seasonal characteristic, mainly concentrated in the autumn, especially in August, according for 66.7% (32/48). The initial symptoms of poisoning patients were mainly manifested as nausea and vomiting (50.0%). In five kinds of poisoned patients, the incubation time [(1.44±1.15) hours] and the length of hospital stay [(3.50±2.33) days] of neuro-psychosis type was the shortest, and the incubation time of liver-damaged type [(10.63±3.50) hours] and the length of hospital stay of renal damage type [(20.67±0.58) days] was the longest. Patients received symptomatic treatment according to different types, among whom 12 patients with severe liver damage received additional treatment for CBP. After the treatment, alanine aminotransferase (ALT), aspartate aminotransferase (AST), MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH), and prothrombin activity (PTA) were significantly improved as compared with those before CBP treatment, with significant differences between 7 days after CBP and before CBP [ALT (U/L): 213.08±127.30 vs. 2 766.83±1 909.66, AST (U/L): 50.00 (41.00, 85.00) vs. 2 142.00 (1 225.00, 3 126.00), CK-MB (U/L): 24.09±8.87 vs. 44.75±22.09, LDH (μmol×s-1×L-1): 3.70±1.46 vs. 13.03±12.77, PTA: (79.08±24.29)% vs. (35.25±19.85)%, all P < 0.01]. Among 48 patients, 47 were cured and discharged, and 1 patient with liver failure died due to aggravation of liver dysfunction, abnormal coagulation and bleeding, and massive hemorrhage of gastrointestinal tract.Acute mushroom poisoning patients demonstrated obvious seasonal characteristics, mostly liver-damaged type, and its initial symptoms were mainly presented as nausea, vomiting and other gastrointestinal manifestations. Early clarification of diagnosis, timely treatment, as well as providence with CBP treatment in severe patients should be carried out as soon as possible. In such a way the curative effect can be enhanced, the mortality can be reduced, and the prognosis of the patients could be improved.
Mushroom poisoning
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Twenty-two patients who ate mushrooms containing hepatotoxic amatoxins were treated during the fall and winter seasons of 1982 and 1983. All patients were treated with intensive supportive care and repeated oral doses of activated charcoal. In two patients fulminant hepatic failure developed and they died. One patient in whom encephalopathy developed had an orthotopic liver transplant and survived. Liver biopsy specimens obtained from five patients during the acute illness showed centrilobular hemorrhagic necrosis. The hepatic histopathology in a biopsy specimen from a 5-year-old boy eight weeks after mushrooms were eaten showed bands of fibrosis and islands of hepatocytes suggestive of early cirrhosis. Radioimmunoassay for amanitins, done on the serum from all patients, detected the toxins in only three, probably because most of the specimens were obtained 24 hours or more after the ingestion. This series, with a mortality rate of 9%, illustrates the outcome in patients who receive intensive supportive care and provides a background on which success of specific treatments should be judged.
Histopathology
Fulminant hepatic failure
Hepatic Encephalopathy
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