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MORE ABOUT More About Acute Poisoning MORE ABOUT More about Acute poisoning MUSHROOM POISONING (death cap, duiwelsbrood, slangkos) similar mushroom should be is found throughout southern Africa. obtained. As an initial procedure, Only 100 of the thousands of mush- After summer and autumn rains the activated charcoal is recommended room species are poisonous. Among fruit bodies develop under oaks, if it can be administered within 4 the potentially poisonous mush- pines and poplars. The species is hours of ingestion. The time inter- rooms, a small number may cause readily recognisable by the oliva- val between ingestion and the onset serious intoxication and even fatali- ceous yellow-green colours of the of symptoms is important for differ- ties. Although South African mush- cap surface, the white lamellae ential diagnostic purposes rooms are well described, informa- (gills) and stem, the membranous (described above and in Table I). If tion with regard to the poisonous ring, and the white, sac-like volva the ingested mushroom is likely to ones and their toxins is limited. which envelopes the basal bulb be one of the Amanita species, the below ground level. patient should be admitted to hospi- tal, and hepatic and renal function Although South monitored. For the management of African mushrooms mushroom poisoning, it is recom- mended that you contact your local are well described, poison information centre for guide- information with lines. regard to the poiso- nous ones and their If the ingested mush- toxins is limited. room is likely to be one of the Amanita species, the patient From a medical point of view, it is should be admitted to more practical to divide poisonous Fig. 1. Amanita muscaria (top right), mushrooms into those that cause Amanita pantherina (middle right) and hospital, and hepatic symptoms and signs of poisoning Amanita phalloides (middle bottom), and renal function early (within 6 hours) and late (6 - all from the Tokai forest, Cape Town. 48 hours after ingestion). Although White gills are often associated with monitored. poisonous mushrooms. poisonings presenting early may be quite serious, they are usually self- limiting, clear up within hours, and Fig. 1. shows some South African Specific management in symptomatic patients have better prognoses than those mushroom species. presenting late. Symptoms and • Monitor liver and kidney func- Poisonous mushrooms and clinical signs of mushroom poisoning vary tions. syndromes are described in Table I. according to the mushroom ingest- • Manage dehydration and elec- ed, amount eaten, method of prepa- trolyte/acid-base disturbances ration and whether alcohol was con- General management where indicated. sumed. Many species of poisonous One should attempt to ascertain • For patients with a disulfiram mushrooms cause gastrointestinal how many types of mushrooms have effect, propranolol may be of symptoms only, and spontaneous been eaten, time lapse since inges- benefit. Dopamine may be indi- recovery usually occurs within a few tion and how many people were cated in the management of hours. However, cyclopeptide involved. Identification of the hypotension. (Amanita phalloides) poisoning can mushrooms should be attempted • In muscarine poisoning, atropine be fatal in 50% of cases and and all pieces of mushrooms saved may be considered, but it may accounts for 90% of all lethal mush- may be helpful in this regard. aggravate other types of mush- room poisonings. A. phalloides Where possible, a specimen of a room poisoning. CME August 2003 Vol.21 No.8 475 476 MORE ABOUT CME Table I. Mushroom poisoning syndromes August 2003 Vol.21 No.8 August 2003 Vol.21 Clinical syndromes Mushrooms Symptoms and signs • Clinical syndromes presenting early (within 6 hours after ingestion) Gastrointestinal group Agaricus placomyces, Agaricus semotus, Agaricus Nausea, vomiting, abdominal cramps, diarrhoea, Many toxins involved, mostly unidentified xanthodermus (yellow stainer). Chlorophyllum headaches, sweating. Self-limiting. Some may pro- molybdites (false parasol or green-spored parasol). duce CNS, musculoskeletal toxicity. Some people may Hebeloma species. Ramaria formosa. be affected, others not. Onset within 15 min - 2 h. Scleroderma citrinum (common earth ball) Subsides within 3 - 4 h. Recovery complete within 1 - 2 days Muscimol/ibotenic group Amanita muscaria, Amanita pantherina Patient appears intoxicated. Confusion, ataxia, eupho- Ibotenic acid is converted to muscimol ria, disturbed vision, hyperkinetic activity, spasms and which structurally resembles GABA. delirium. Onset within 30 - 90 min, peaking at 2 - 3 h. Other unidentified toxins probably also Lasts for 4 - 8 h involved. Muscarine/histamine group Clitocybe toxica, Clitocybe olearia, and other Cholinergic syndrome: profuse salivation, lacrimation, Clitocybe species. Inocybe eutheles, I. hirtella, perspiration. Miosis, blurred vision, bradycardia, I. obscura hypotension, bronchoconstriction. Abdominal cramps and diarrhoea may occur. Onset within 15 min - 2 h. Short-lived, subsiding within 6 - 24 h Hallucinogenic indole group: Psilocybe coprophila, and other Psilocybe species. Hallucinations prominent, dilated pupils, confusion, Psilocybin, psilocin. Related to LSD Panaeolus papillionaceus. Conocybe species. vertigo, ataxia, weakness, drowsiness. Onset usually Stropharia aurantiaca, S. semiglobata within 10 - 30 min. Average duration 4 - 5 h Coprine group Coprinus atramentarius (common ink cap) Flushing, paraesthesias, palpitations, throbbing Coprine has a disulfiram effect headache, nausea, vomiting, sweating. Less common- (Antabuse) ly: chest pain, hypotension, vertigo, blurred vision, confusion, respiratory problems. Poisoning may occur if alcohol is consumed before or within 72 h of inges- tion. The disulfiram effect occurs within 30 min - 2 h after ingestion. Coprinus mushrooms do not cause toxicity in the absence of alcohol • Clinical syndromes presenting late ( > 6 hours after ingestion) Cyclopeptide group Amanita phalloides, A. Phalloides var. alba, A. After an average period of 10 - 14 h (range 6 - 48 h) -amanitin is the main toxin. It produces phalloides var. umbrina there is a sudden onset of nausea, vomiting, colicky severe hepatocellular damage by bind- abdominal pain, profuse diarrhoea, tachycardia, hypo- ing to nuclear RNA polymerase II. glycaemia, which may be associated with electrolyte Inhibition of mRNA synthesis is the and acid-base disturbances. This is followed by a sec- major cause of cell death. Note: the ond phase of temporary recovery, with a relapse on poison is heat stable. Mortality rate of day 2 - 4. During this third stage, fulminant hepatic 50% failure and possibly renal failure become clinically apparent Monomethylhydrazine group Gyromitra species (false morel). Known cases of Nausea, vomiting, diarrhoea and abdominal cramps. Intoxication resembles isoniazid poisoning mainly from Europe. May develop haemolysis, seizures, fever, inco-ordina- poisoning Poisonous Gyromitra species probably not tion, hepatic failure and coma. Onset usually within represented in southern Africa 6 - 24 h after ingestion Orellamine group Cortinarius species — probably not found in Anorexia, nausea, vomiting, diarrhoea, headache, joint Series of heat-stable nephrotoxic southern Africa pain followed by renal failure. Onset after a long poisons latent period, 36 hours - 14 days after ingestion. Symptoms and signs of renal failure may appear even as late as 21 days after ingestion MORE ABOUT • In psychoactive mushroom poi- Plant ingestions1- 3 species) and delicious monster sonings (hallucinogens, etc.), (Monstera deliciosa). Chewing on The most serious toxic effects were both cholinergic and anti-cholin- parts of the abovementioned plants encountered with plants containing ergic effects can occur. No spe- may produce an immediate, intense atropine-like substances (10 out of cific treatment is necessary. The pain of the mouth, tongue and lips. 11 patients). Datura stramonium benzodiazepines may be helpful In severe cases, especially in chil- (stinkblaar) and Brugmansia species in agitated patients. dren, it may cause laryngeal oede- (moonflower) were most commonly ma. These plants may also cause • In suspected A. phalloides poison- involved. This type of poisoning contact dermatitis or keratoconjunc- ing, the use of N-acetylcysteine occurs mostly among teenagers who tivitis. Management includes clear- has been suggested (refer to may be experimenting with drugs. paracetamol poisoning regimen, ing the mouth of plant parts and p. 460). Penicillin G, in high administration of cool liquids or doses, may also be of benefit as a crushed ice. The possibility of receptor-site competitor. Fluid The most serious toxic laryngeal oedema should be kept in and electrolyte/acid-base imbal- effects were encoun- mind. ance should be treated and hypo- Ingestion of the ripe berries of the glycaemia corrected. Large tered with plants con- syringa tree (Melia azedarach) was quantities of carbohydrate appear taining atropine-like the most common plant ingestion. to protect the liver (5 - 10% dex- substances (10 out of Only 2 of 53 patients presented with trose, 4 - 5 l/24 h). Administer mild gastrointestinal symptoms vitamin K for bleeding. As soon 11 patients). (diarrhoea), which may have been as fluids can be administered due to other causes. The ripe berry orally, give fruit juices fortified by has a very hard kernel and usually glucose 120 g/l up to 4 - 5 times passes through the gastrointestinal daily. Administer silibinin (spe- The anticholinergic effects include tract
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