Cases reported "Mushroom Poisoning"

Filter by keywords:

Retrieving documents. Please wait...

1/102. Poisoning by amanita phalloides ("deathcap") mushrooms in the Australian Capital Territory.

    amanita phalloides ("deathcap") mushrooms are widespread in south-eastern Australia. Seven patients presented to hospital in the australian capital territory with poisoning by this mushroom between 1988 and 1998. Three developed hepatoxicity and one died. Because A. phalloides is becoming more widespread, increased community and medical awareness is needed to reduce the frequency and morbidity of poisoning. ( info)

2/102. Use of acetylcysteine as the life-saving antidote in amanita phalloides (death cap) poisoning. Case report on 11 patients.

    alpha-amanitin is an amatoxin known to produce deleterious effects on the liver and the kidneys, when circulating in the blood. It is produced by a particular kind of mushroom called amanita phalloides. Therapeutic options employed to treat mushroom intoxication, such as haemodiaperfusion on activated charcoal, high dosages of penicillin g, oral charcoal, etc., very often failed to act properly and liver transplantation (when a graft is available) appeared to be the only solution. In recent years, as suggest by some authors, it has been postulated that the oxidant effects of alpha-amanitin could be counteracted by the use of antioxidants such as silibinin. High dosages of N-acetyl-cysteine (CAS 616-91-1, NAC), already used as antioxidant in paracetamol poisoning, were successfully used in our intensive care Unit (ICU) in the treatment of amanita phalloides poisoning. In the last two years, 11 patients (mean age of 5-72 = 38.5) were treated for amanita phalloides poisoning of various degrees, with a protocol (haemodiaperfusion on activated charcoal, high dosages of penicillin g, etc.) further comprehending NAC (fluimucil). All the patients recovered successfully but one (bearing precedent liver disease) needed liver transplantation. Daily monitoring of liver enzymes, creatinine, coagulation, LDH, blood and urinary alpha-amanitin were used to screen the progresses of the patients. ( info)

3/102. Fatal mushroom poisoning caused by amanita virosa in thailand.

    Consumption of toxic mushrooms belonging to the genus amanita frequently leads to severe gastrointestinal distress followed by acute hepatic failure with a fatal outcome. In thailand, valuable information as to the locally prevalent poisonous species, the preferred habitat and the management of suspected victims of intoxication is basically non-existent. We report here 5 cases of fatal poisoning with amanita virosa having occurred in a family residing in the northeast of thailand who as countless others had enjoyed mushroom gathering as a pasttime. Within 4 to 6 days after ingestion of the mushrooms, all had succumbed to acute hepatic failure with subsequent hepatoencephalopathy. Treatment modalities exist in the form of penicillin and silibinin, or thioctic acid administration followed by plasmapheresis. In cases taking a lethal course apparent from the results of liver biochemistry, liver transplantation is clearly indicated. In order to prevent mushroom poisoning altogether, educating the general population to that end certainly presents the method of choice. ( info)

4/102. The futility of hemoperfusion and hemodialysis in amanita phalloides poisoning.

    amanita phalloides mushrooms are extremely toxic. A variety of treatments have been proposed based as often on anecdotal experience as on firm evidence. General consensus exists regarding some treatments, such as the use of silibinin, penicillin, and activated charcoal. The most polarized debate concerns the value of extracorporeal elimination. We describe a case of 2 adults with confirmed amanita phalloides poisoning treated with hemodialysis (HD) immediately after arrival at our tertiary care hospital (23 h after ingestion) and later with hemoperfusion (HP); a series blood samples were taken to determine the clearance of the toxin by each method. No amatoxin was detected before treatment, after treatment, or in the HD/HP circuits. Neither HD nor HP contributed to the clearance of amatoxin. ( info)

5/102. Continuous renal replacement therapy and charcoal plasmaperfusion in treatment of amanita mushroom poisoning.

    hemoperfusion has been used in the treatment of mushroom poisoning for many years. The aim of this study was to study the efficacy of charcoal plasmaperfusion (CPP) and continuous renal replacement therapy (CRRT) in 2 patients severely poisoned by the amanita mushroom. Both patients arrived at the ICU from another hospital with a diagnosis of amanita phalloides mushroom poisoning. The patients were precociously treated with CRRT for 20 h and CPP for 3 h every day. The treatments were effected for 3 and 5 days, respectively. Both patients recovered completely and were discharged asyntomatic after 7 and 10 days. ( info)

6/102. amanita virosa induced toxic hepatitis: report of three cases.

    We report here three cases of amanita virosa induced toxic hepatitis. Two of the three cases recovered but the other died 10 days after mushroom ingestion. Since the mortality of amanita mushroom induced toxic hepatitis is very high, prompt diagnosis and aggressive therapeutic measures should be initiated as soon as possible. Our cases showed that the initial serum aminotransferase levels might not predict the clinical outcome of the patient, but that the prothrombin time (PT) seemed to be a more useful prognostic marker. Close monitoring of aminotransferase levels and PT as well as appropriate therapy are recommended. All three cases showed signs of proteinuria and we were able to characterize mixed tubular and glomerular type proteinuria at 3 or 4 days after ingestion in two cases. Among the previously reported Korean cases of suspected amanita induced toxic hepatitis, most species could not be identified except for four cases of amanita virosa. No cases of amanita phalloides induced toxic hepatitis have been identified in korea so far. ( info)

7/102. Main features of cortinarius spp. poisoning: a literature review.

    Introduction: cortinarius spp. poisoning is characterized by a delayed acute renal failure. The main features of this severe poisoning are still poorly known and often overlooked. The aim of this literature review is a better description of cortinarius spp. poisoning.Materials and methods: The main medical databases were searched: abstracts of mycology, Current Contents, medline, Pascal, Micromedex Poisindex, toxicology abstracts, Toxline. All case reports that included a description of the clinical features of cortinarius spp. poisoning were studied.Results: 245 cases were collected and 90 cases could be analyzed in details. Gastrointestinal disorders are the main symptoms of the prerenal phase of the poisoning. They appear a few days after the ingestion of the mushrooms (median 3 days). The renal phase is delayed (median 8.5 days). Moderate and transient hepatic abnormalities have been reported. A severe hepatic failure can be ruled out. Muscular lesions are highly questionable. Treatment is supportive. No specific treatment can be recommended. Acute renal failure progressed towards chronic renal failure in half of the cases; intermittent hemodialysis or kidney transplantations were necessary in 70% of those cases.Conclusion: cortinarius spp. poisoning is severe. Ingestion of cortinarius species must be systematically suspected whenever tubulo-interstitial nephritis is diagnosed, especially as mushrooms may have been ingested 1-2 weeks before. ( info)

8/102. Management of maternal amanita phalloides poisoning during the first trimester of pregnancy: a case report and review of the literature.

    BACKGROUND: amanita phalloides poisoning produces acute liver failure and often death. Maternal poisonings are rare, and medical decisions of abortion or liver transplantation in this critical situation frequently are based on laboratory data. We report here the case of a 22-year-old-woman in the 11th week of pregnancy, who ingested mushrooms. CASE REPORT: The patient's clinical symptoms (e.g., vomiting and diarrhea) and blood chemistry data (persistent increases of aspartate aminotransferase and alanine aminotransferase and severe decreases in prothrombin, factor V, factor II, factor vii, and factor x) indicated poisoning of medium severity. The management consisted of intravenous hydration, and administration of silymarine and N-acetylcysteine. No fetal damage was observed, and birth and development of the infant (now 2 years of age) proceeded without incident. CONCLUSION: Abortion is not necessarily indicated in maternal poisoning by A. phalloides, even in the first trimester of pregnancy. ( info)

9/102. erythromelalgia and mushroom poisoning.

    OBJECTIVE: To report the first European observations of erythromelalgia due to mushroom poisoning. methods: Clinical features of erythromelalgia were observed in 7 cases seen over 3 years. All patients had eaten the same mushrooms species, gathered in the same French alpine valley. erythromelalgia was first described in japan after Clitocybe acromelalga ingestion. Clitocybe amoenolens was identified as the possible cause of poisoning in our cases. ( info)

10/102. Amatoxin poisoning from ingestion of Japanese Galerina mushrooms.

    BACKGROUND: Although some Japanese Galerina species poisonings manifest as gastrointestinal symptoms followed by late-onset hepatorenal failure (phalloides syndrome), the toxin responsible for this has not been determined. CASE REPORT: We report a 6-year-old boy who developed characteristic cholera-like diarrhea and late-onset severe hepatic deterioration after eating mushrooms, later identified as a Galerina species, most likely Galerina fasciculata. A residual mushroom revealed alpha-amanitin. This account is the first known reported case of poisoning by Japanese Galerina species where an amatoxin was demonstrated to be responsible for the toxicity. ( info)
| Next ->

Leave a message about 'Mushroom Poisoning'

We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.