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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 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 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, 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 (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 and func- Poisonous mushrooms and clinical signs of mushroom poisoning vary tions. syndromes are described in Table I. according to the mushroom ingest- • Manage 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 . (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 MORE ABOUT mushrooms do not cause

Coprinus 1 - 2 days , , abdominal cramps, diarrhoea, , sweating. Self-limiting. Some may pro- Confusion, ataxia, eupho- appears intoxicated. Patient perspiration. Miosis, blurred vision, bradycardia, hypotension, bronchoconstriction. Abdominal Onset within cramps and diarrhoea may occur. 15 min - 2 h. Short-lived, subsiding within 6 - 24 h duration 4 - 5 - 30 min. Average within 10 h there is a sudden onset of nausea, vomiting, colicky failure and possibly renal become clinically apparent in the absence of alcohol toxicity , nausea, vomiting, sweating. Less common- headache, nausea, vomiting, sweating. Less ly: chest pain, hypotension, vertigo, blurred vision, confusion, respiratory problems. Poisoning may occur h of inges- if alcohol is consumed before or within 72 disulfiram effect occurstion. The within 30 min - 2 h after ingestion. latent period, 36 hours - 14 days after ingestion. latent period, 36 hours - 14 Symptoms and signs of renal failure may appear even as late as 21 days after ingestion . h (range 6 - 48 h) - 14 an average period of 10 After species. prominent, dilated pupils, confusion,

alba, A

I. hirtella, species. vertigo, Onset usually ataxia, weakness, drowsiness. . min - 2 h. be affected, others not. Onset within 15 , , and other Cholinergic syndrome: profuse salivation, lacrimation, var. var.

Psilocybe

Chlorophyllum (common ink cap) Flushing, paraesthesias, palpitations, throbbing

Agaricus semotus, (common earth ball) Subsides within 3 - 4 h. Recovery complete within species probably not tion, hepatic failure and coma. Onset usually within , , and other

Ramaria formosa

Inocybe eutheles

(yellow stainer). (yellow umbrina (false parasol or green-spored parasol). Some people may duce CNS, toxicity. musculoskeletal species — probably not found in Anorexia, nausea, vomiting, diarrhoea, headache, joint species. var. var. Gyromitra species (false morel). Known cases ofspecies (false morel). Known Nausea, vomiting, diarrhoea and abdominal cramps. species.

Agaricus placomyces xanthodermus molybdites Hebeloma Scleroderma citrinum Amanita muscaria, pantherina Clitocybe toxica, olearia Clitocybe I. obscura Psilocybe coprophila Panaeolus papillionaceus. Conocybe Stropharia aurantiaca, S. semiglobata Coprinus atramentarius Amanita phalloides, A. Phalloides phalloides Gyromitra represented in southern AfricaCortinarius 6 - 24 h after ingestion xin. It produces Mushroom poisoning syndromes -amanitin is the main to Many toxins involved, mostly unidentified Many toxins is converted to muscimolwhich structurally resembles GABA. probably alsoOther unidentified toxins involved. bind-severe hepatocellular damage by ing to nuclear RNA polymerase II.Inhibition of mRNA synthesis is themajor cause of cell death. Note: the poison is heat stable. Mortality rate of spasms and ria, disturbed vision, hyperkinetic activity, 50% Lasts for 4 - 8 h delirium. Onset within 30 - 90 min, peaking at 2 3 h. abdominal pain, profuse diarrhoea, , hypo- glycaemia, which may be associated with electrolyte a sec- by is followed and acid-base disturbances. This with a relapse on ond phase of temporary recovery, day 2 - 4. During this third stage, fulminant hepatic Coprine has a disulfiram effect (Antabuse) Series of heat-stable nephrotoxicpoisons southern Africa renal failure. Onset after a long by pain followed Psilocybin, psilocin. Related to LSD Intoxication resembles isoniazid Intoxication poisoning poisoning mainly from Europe. Poisonous inco-ordina- May develop haemolysis, , ,  Table I. Table Muscarine/histamine group Orellamine group Clinical syndromes• Clinical syndromes presenting early (within 6 hours after ingestion) Gastrointestinal group Mushrooms Symptoms and signs /ibotenic group Hallucinogenic indole group: Coprine group Monomethylhydrazine group • Clinical syndromes presenting late ( > 6 hours after ingestion) Cyclopeptide group

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• In psychoactive mushroom poi- 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 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 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 intact. Management is symp- cific ) in a dose of 20 - the following: a hot, dry, flushed tomatic and hospitalisation is usually 50 mg/kg/day intravenously if it is skin; dry mouth, dilated pupils, uri- not necessary. available (see list of , nary retention, tachycardia, fever, p. 462). Haemodialysis may be disorientation, hallucinations, lifesaving in renal failure. For the aggressive behaviour, and delirium, removal of , haemodialysis with seizures and coma in severe or haemoperfusion has not been cases. Rhabdomyolysis is a possible shown to be of substantial bene- complication for which treatment is fit. In patients with hepatic fail- primarily symptomatic and support- ure, consult a liver specialist for ive. Patients should be closely the appropriateness of a liver observed to prevent injuries, nursed 1-6 transplant. in a dark room (photophobia), tem- References available on request. perature monitored, and adequate Beans of the plant. fluid intake should be assured. POISONOUS PLANTS Benzodiazepines may be given to calm patients and to treat seizures. The number of incidents of expo- For information on traditional medi- Urine should be monitored for the sure to oleander (Nerium oleander) cines of plant origin see p. 481. presence of myoglobin. and beans of the castor oil plant ( communis) was relatively low In an analysis of 220 consecutive Only one potentially serious compli- (11 and 5 cases, respectively) and exposures to poisonous plants cation was encountered with the only a few patients presented with processed by the Tygerberg Poison ingestion of calcium oxalate-contain- mild gastrointestinal symptoms Information Centre, most of the ing plants (42 cases). The patient (< 12%). Oleander contains cardio- symptomatic patients (100/220) developed laryngeal oedema and active and has the poten- ingested plants containing either cal- stridor. Plants containing calcium tial to cause serious . cium oxalate (42 cases) or atropine oxalate crystals include dumbcane However, the amount ingested by (11 cases), or were exposed (Dieffenbachia), elephant's ear children is usually too small to cause to plants causing dermatitis (25 (Alocasia macrorrhiza and Colocasia significant poisoning. The of cases). esculenta), arum lily (Zantedeschia the castor oil plant contain , an

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extremely toxic . All facility. Symptomatic and support- Direct chemical injury. Examples parts of the plant are poisonous, but ive care is the mainstay of therapy. of plants in this category include the its seeds are especially rich in ricin, The same general principles apply nettles (Urtica species), which pro- which remains in the fibrous residue even when a plant cannot be identi- duce contact urticaria by stinging of the seeds after the castor oil has fied. Accurate identification of the hairs; Euphorbia species, which con- been extracted from them. Ingestion plant involved can be difficult or tain irritant chemicals (diterpenoids) of the intact, unchewed does impossible. In such cases activated in the milky sap (latex); and the cal- not result in significant toxicity, charcoal is recommended, with cium oxalate-producing plants (e.g. because the hard seed coat prevents appropriate follow-up and/or obser- Dieffenbachia). Several of the local absorption of toxins. A similar tox- vation. Contact your local poison Euphorbia species can cause quite , , is found in the information centre for help. severe primary irritant dermatitis. rosary bean or love bead (Abrus pre- Species include Euphorbia ingens catorius). Symptoms and signs of (candelabra tree; naboom), ricin poisoning include gastrointes- Euphorbia mauritanica (gifmelkbos) tinal haemorrhage, haemolysis and Most childhood inges- and Euphorbia virosa. Initial symp- renal failure. Treatment of exposure toms include erythema and swelling to oleander and castor oil plant tions are non-toxic or within 2 - 8 hours, followed by vesi- beans is symptomatic and support- relatively benign and cle formation within ive. Activated charcoal is recom- 4 - 12 hours. Skin reactions usually mended within the first 2 hours of require only well- fade within 3 - 4 days. Eye contact ingestion. informed explanations may result in corneal ulceration, iri- tis, conjunctivitis, and even tempo- Four cases of Jerusalem cherry and reassurances rary blindness. ( pseudocapsicum) ingestion after the plant has were encountered. The brightly been identified. Allergic contact dermatitis. This coloured red cherries contain vary- category can be classified as follows: ing amounts of and • Immediate allergic type (hyper- atropine-like alkaloids (the solanine sensitivity type I, IgE mediated). dominates). They are only mildly Allergic reactions are often seen poisonous and the most common Plant dermatitis (phytoder- 4-9 in handlers of apples, tomatoes, toxic effects are nausea, vomiting, matitis) potatoes and celery. Symptoms headache and diarrhoea. Other The 25 plant dermatitis cases dealt and signs include erythema, plants which contain solanine with by the Tygerberg Poison oedema, urticaria, and symptoms include , unripe toma- Information Centre were caused of itching, burning or tingling at toes, as well as leaves and mainly by Euphorbia plant species, the site of contact within 1 - 2 green tubers. Treatment is sympto- the rainbow plant (Smodingium matic and supportive. argutum) and the blister bush (Peucedanum galbanum).

General management The following is a simplified classifi- Most childhood ingestions are non- cation of plant-induced dermatoses, toxic or relatively benign and require which is a complex subject (several only well-informed explanations and pseudoplant dermatoses are also reassurances after the plant has been recognised, where the primary irri- identified. This is because the tant/trigger is produced by arthro- amount ingested is generally small. pods (mites) and fungi inhabiting If a known poisonous plant has been the plant, but these are excluded ingested, activated charcoal is rec- from the classification): ommended if given within 2 hours Mechanical injury. These include of ingestion. If there are no symp- injuries due to thorns, barbs, etc., toms and signs of poisoning, regular with the added potential to cause follow-up is recommended. bacterial or fungal infection. Symptomatic patients, however, should be admitted to a medical Dieffenbachia.

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hours post exposure. Another a photodermatitis caused by the Food-borne poisoning pre- example in this category is ana- blister bush (Peucedanum gal- senting 1 - 6 hours post phylactoid reactions after inges- banum, family Apiaceae). After ingestion tion of nuts. accidental skin contact with the Microbial agents and their • Delayed allergic contact dermati- sap of the plant, together with toxins tis (type IV, cell-mediated, hyper- direct sunlight, dermatitis devel- sensitivity contact dermatitis). ops 24 hours or more after expo- aureus food poi- This reaction develops typically sure. The skin reaction is charac- soning is characterised by vomiting > 6 hours post exposure. Poison terised by a burning erythema (76% of cases) and diarrhoea ivy-triggered allergic contact der- with vesiculation or bullous skin (68%). Fever is less common matitis is a typical example lesions in the areas of contact. (23%). The illness is caused by a (Toxicodendron radicans). S. The lesions typically go through a preformed and out- argutum (rainbow leaf, family hyperpigmentation phase, lasting breaks are associated with foods Anacardiaceae) is the plant often for weeks to months. such as ham, poultry, potato, egg responsible for causing allergic salads and pastries. Management of phytodermatoses contact dermatitis in South includes identification and removal Bacillus cereus food poisoning is Africa. The Compositae family is of the primary cause, stabilisation of characterised by nausea and vomit- also a common cause of allergic inflammation with either antihista- ing (100%), abdominal cramps contact dermatitis. This family mines and/or corticosteroids, and (100%) and diarrhoea (33%) and is contains many garden plants, reparation of the barrier function of caused by a heat-stable toxin. such as chrysanthenums, and the skin with urea (Eulactol), lactic Outbreaks are often associated with dahlias, as well as , acid (Lacticare) or the ceramides fried rice that has been kept warm such as lettuce, artichokes, etc. (SBR lipocream). for long periods. Even a small number of orchids, as well as primrose, have been References available on request. Management includes oral rehydra- implicated. The clinical picture tion and other supportive measures.1 of allergic contact dermatitis FOOD-BORNE ranges from transient redness to (FOOD POISONING) Non-microbial toxins severe swelling, vesiculation, pru- Serious acute poisonings are often Heavy metal poisoning may be ritus and even bullous skin associated with prominent gastro- due to storage of foods in containers lesions. The dermatitis is usually intestinal symptoms and signs, a fea- lined with cadmium, copper, zinc, or limited to the site of contact, but ture often overlooked in standard antimony (enamelled cookware). may spread later. If the causative toxicology textbooks. Examples Ingestion causes nausea, is removed, the lesions may include iron, theophylline, lithium, and abdominal cramps within 5 - 15 heal within days to weeks. There arsenic, paraquat, digoxin, and mer- minutes. Symptoms usually resolve may be scaling, cracking and cury poisoning. within 2 - 3 hours after exposure to some thickening of the skin. the offending agent has been termi- With continued exposure, com- Food-borne may present nated.1 plications such as infection may with severe gastrointestinal symp- occur. toms and can result from ingestion Scrombroid poisoning — refer to of a wide variety of foods contami- the article on poisonous and ven- • Phytophotodermatitis. This is nated with pathogenic micro-organ- omous marine animals (p. 471).2,3 a light-induced plant dermatitis, isms, microbial toxins, or chemicals. which can be a phototoxic, or The ‘Chinese restaurant syn- For differential diagnostic purposes, photoallergic reaction. The furo- drome’ is an entity that develops the food-borne diseases are there- coumarins are the major pho- within 15 - 30 minutes after dining fore discussed briefly. toactive chemicals, of which the in certain Chinese restaurants.The psoralens are best known. These The diagnosis of food-borne disease symptoms usually last for two hours chemicals occur in two plant should be considered when an acute and resolve without residual effects. families, the Apiaceae (formerly illness with prominent gastrointesti- Symptoms and signs include numb- Umbelliferae) and the Rutaceae. nal symptoms (often together with ness or burning at the back of the The psoralens strongly crosslink neurological and/or cardiovascular head, radiating to both the arms and DNA and with exposure to UVA manifestations) affects two or more the back, general weakness, palpita- can result in cell damage and cell persons who have shared a meal tions, headache, flushing, sweating, death. A common local entity is during the previous 72 hours.1 nausea, abdominal cramps and

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thirst. Although excessive amounts Sodium nitrite poisoning (nitrate Food-borne poisoning pre- of MSG (monosodium L-glutamate) is metabolised to nitrite). Sodium senting more than 6 hours used in food have been implicated, nitrite is used in small quantities as a post ingestion several studies did not show a causal curing agent in processed meat (200 link between the two. Other as yet - 500 ppm). Sodium nitrite has Microbial agents and their 1 unidentified substances may also been sold on the street as 'table salt', toxins play a role.4 The treatment is symp- leading to multiple cases of severe Abdominal cramps and diar- tomatic. methaemoglobinaemia and, in some rhoea within 8 - 16 hours. instances, fatalities. Less than 1 g is perfringens food poison- Paralytic shellfish poisoning — potentially lethal in children. ing is caused by an enterotoxin-pro- refer to the article on poisonous and Sodium nitrite oxidises haemoglobin duced in vivo.Vomiting and fever are venomous marine animals (p. 471). (Hb-Fe++) to methaemoglobin uncommon. An enterotoxin pro- (metHb-Fe+++), which has no oxy- ducing B. cereus causes a similar clin- gen-carrying capacity. Cyanosis ical picture. Symptoms and signs of The ‘Chinese restau- occurs when 15% of Hb has been both entities usually resolve sponta- rant syndrome’ is an converted to metHb.7 neously within 24 hours. Meat and dishes are usually implicat- entity that develops • Clinical features. If substantial ed in outbreaks. within 15 - 30 minutes amounts (> 1 g) are ingested, symptoms and signs of poisoning Fever, abdominal cramps, and after dining in certain may occur within 1 hour. These diarrhoea within 16 - 48 hours. Chinese restaurants. include: gastric irritation, nausea Pathogens responsible include sal- and vomiting, a throbbing monellae (from beef, poultry, eggs headache and dizziness. and dairy products), shigellae (egg Chocolate cyanosis of the skin, salads and lettuce), Campylobacter Miscellaneous mushroom poi- lips and nails develops when the jejuni (poultry and raw milk), Vibrio sonings.5 Various poisonous mush- metHb concentration reaches 30 parahaemolyticus (shellfish), and room species may cause severe gas- - 40%. Levels above 60% usually invasive Escherichia coli (under- trointestinal or nervous system toxic result in stupor, seizures and res- cooked ground beef and raw milk). effects within 30 minutes - 2 hours piratory failure. These food-borne diseases are post ingestion. Patients with mush- caused by tissue-invasive pathogens. room poisoning presenting within 6 • Management includes immedi- Vomiting may also be a feature in hours of ingestion usually have a ate life-support measures, such as these cases. more favourable outcome than those 100% oxygen. Activated charcoal presenting late (6 - 48 hours post is useful if administered within 1 ingestion). (See detailed discussion hour after ingestion. Methylene Clostridium perfrin- in article on mushroom poisoning blue (1 - 2 mg/kg in a 1% solu- on p. 475.) tion) should be administered if gens food poisoning the metHb concentration rises is caused by an Puffer poisoning is caused by above 20%; additional doses of the ingestion of the flesh, viscera or enterotoxin produced methylene blue may be required skin of fish containing the neurotox- and total doses of 7 mg/kg may in vivo. in . Headache, a float- be required for adequate treat- ing sensation, sweating, oral and ment although the higher doses peripheral paraesthesias occur within carry a risk of causing haemoly- Abdominal cramps and watery 10 minutes - 3 hours. Typical gas- sis. Oxygen therapy should be diarrhoea within 16 - 72 hours. trointestinal symptoms include epi- continued for at least 2 hours The major pathogens responsible gastric pain, nausea, vomiting, and after methylene blue has been include enterotoxin-producing salivation. Hypotension, bradycar- given. Exchange transfusion strains of E. coli (beef and raw milk), dia, and fixed, dilated pupils indicate should be considered in severe V. parahaemolyticus (seafood), and severe poisoning. An ascending cases. Vibrio cholerae (ingestion of contami- paralysis may lead to respiratory nated water, seafoods and other arrest within 4 - 24 hours. Puffer foods). C. jejuni, salmonellae, and fish poisoning is uncommon in shigellae may also be responsible. 6 southern Africa. Severe cholera is characterised by

480 CME August 2003 Vol.21 No.8 MORE ABOUT profuse watery diarrhoea, vomiting, paralysis, strongly suggests food- ever, slow or halt further progres- muscular cramps, dehydration, olig- borne botulism. In humans the dis- sion.8 uria, and cardiovascular collapse. ease is caused by one of three heat- labile , produced by the Non-microbial toxins Management of the latter two diar- anaerobic growth of Clostridium bot- Abdominal cramps and diar- rhoeal illnesses includes replacement ulinum. Growth frequently occurs rhoea within 6 - 24 hours, fol- of fluid losses. Antimicrobial agents in underprocessed, non-acid canned lowed by hepatorenal failure. are usually indicated in the treat- foods (pH > 4.6). The Mushrooms containing cyclic ment of shigellosis (a fluoro- inhibit the release of acetylcholine at oligopeptides (cyclopeptides), par- quinolone, trimethoprim-sul- peripheral nerve endings. Home- ticularly alpha-amanitin, are respon- phamethoxazole, amoxicillin), canned foods are the most common sible for this syndrome. Mushrooms cholera (tetracyclines, a fluoro- sources and vegetables, fish, , containing these oligopeptides quinolone, trimethoprim-sul- and condiments are the most com- include Amanita phalloides, A. phal- phamethoxazole), and invasive sal- mon vehicles, but beef, milk prod- loides var. alba and A. phalloides var. monellosis and typhoid (ceftriaxone, ucts, pork, and poultry have been umbrina. They occur throughout a fluoroquinolone, amoxicillin, chlo- involved. Non-canned foods, e.g. southern Africa, under broad-leafed ramphenicol, trimethoprim-sul- foil-wrapped baked potatoes and and pine trees. The illness is typical- phamethoxazole). chopped garlic in oil, have also ly triphasic. The early stage is char- caused outbreaks.8 acterised by abdominal pain, nausea and vomiting, and cholera-like diar- • Clinical features. The onset of The abrupt onset of rhoea. This is followed by an food-borne botulism is abrupt, acute gastrointestinal asymptomatic stage of 1 - 2 days’ usually within 18 - 36 hours post duration. During the third stage, symptoms, together ingestion, although the incuba- fulminant hepatic failure, and possi- tion period may vary from 4 with a descending bly acute renal failure, sets in (see hours to 8 days. Nausea, vomit- article on mushroom poisoning, weakness or paralysis, ing, abdominal cramps, and diar- p. 475). strongly suggests rhoea frequently precede neuro- food-borne botulism. logical symptoms. Neurological Of the serious non-food-borne acute symptoms and signs are charac- poisonings presenting with promi- teristically bilateral and symmet- nent gastrointestinal symptoms and rical, beginning at the cranial signs most will usually present clini- Bloody diarrhoea (haemorrhag- nerves and followed by descend- cally within 6 hours post ingestion. ic colitis) without fever within 72 ing weakness or paralysis. However, digoxin and sustained- - 120 hours.This is caused by cyto- Constipation is common after release theophylline and lithium may toxin-producing strains of E. coli neurological impairment. There often present later (6 - 12 hours (). The toxins damage are no sensory disturbances and post ingestion).5 endothelial cells in target organs fever is absent. Major complica- such as the gut and kidney. References available on request. tions include respiratory failure Haemorrhagic colitis is accompa- and pulmonary infections.8 nied by an acute onset of severe TRADITIONAL MEDICINES abdominal cramps and watery diar- • Management. AND ACUTE POISONING rhoea that typically becomes grossly and activated charcoal, if institut- bloody within 24 hours. ed early, may be helpful in cases Traditional healers (e.g. inyanga, Development of fever may indicate where consumption of contami- ngaka, sangoma) form an integral complications. Approximately 50% nated food is suspected. part of the life of most indigenous of the cases are complicated by a Respiratory impairment requires peoples of southern Africa. Health haemolytic-uraemic syndrome. management in an ICU. The professionals need to be aware that Treatment is supportive, with fluids antidote, trivalent antitoxin 60 - 80% of all South Africans con- and a bland diet. (A,B,E), should be administered sult traditional healers and use the as soon as possible. The antitoxin medicines they prescribe. They pro- Nausea, vomiting, diarrhoea, does not inactivate toxin that is vide a relatively inexpensive alterna- and paralysis within 18 - 36 already bound at the neuromus- tive form of medical care that is hours. The abrupt onset of acute cular junction; pre-existing readily accessible, even in remote gastrointestinal symptoms, together impairment cannot be reversed parts of the country. with a descending weakness or rapidly. The antitoxin may, how-

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Most traditional medicines contain fort, nausea, vomiting and diarrhoea symptoms and signs of CNS toxicity substances of plant origin. These of varying degrees and duration. In are secondary to metabolic distur- medicines are generally not associat- severe cases, haematemesis and bances, such as acidosis, hypogly- ed with prominent or significant melaena are seen. Complications caemia, electrolyte disturbances, adverse/toxic effects. This is proba- include dehydration, disturbances in uraemia or hepatic failure. bly because the concentration of electrolyte and acid-base balance, Poisoning due to the ingestion of pharmacologically active substances haemolysis and a reduced haemo- stinkblaar seeds (Datura stramonium) in the medicines is either too low, or globin, which may compromise kid- is relatively common. The plant is no active ingredients are present at ney function. Perforation of the known as mokhura to Tswana tradi- all. Some traditional medicines, lower gastrointestinal tract should be tional healers and is used as an however, do contain potent pharma- considered in patients presenting aphrodisiac. The dry seeds are coactive chemicals which may, in with an acute abdomen. sometimes smoked with dagga. certain circumstances, cause toxic McVann et al.6 advise that in cases of Acute poisoning is caused by the side-effects or poisoning. poisoning where gastrointestinal muscarinic receptor-blocking action symptoms are prominent, cardiac of atropine and related alkaloids. Health professionals glycosides are the most likely cause The toxic effects include a hot, dry — e.g. the medicine sekanama and flushed skin, dry mouth, dilated need to be aware (Tswana), obtained from the bulb of pupils, urinary retention, tachycar- that 60 - 80% of all Urginea plant species (see table). dia, fever, disorientation, hallucina- tions, aggressive behaviour, delirium, Other organs targeted by potentially South Africans con- and seizures and coma in severe poisonous traditional medicines sult traditional heal- cases. Rhabdomyolysis is an occa- include the kidneys, liver and CNS. sional complication. ers and use the Symptoms and signs of urogenital medicines they pre- damage include dysuria, haematuria Sometimes traditional medicines scribe. and oliguria. Renal damage/failure may contain potentially poisonous is often secondary to hepatocellular substances of animal origin, e.g. can- damage. Patients with hepatic dam- tharidine, and/or of non-biological age may present with raised liver origin, such as dichromate, arsenic Most traditional medicines are mix- , an increase in prothrombin or lead. Even conventional (allo- tures of a variety of plants and are of time (or INR), metabolic acidosis pathic) medicines may be incorpo- very variable composition and con- and hypoglycaemia. Frank , rated. Hepatorenal syndrome with centration. Seasonal variation in which may occur occasionally, car- severe coagulopathy and intravascu- chemical concentration found in ries a poor prognosis. lar haemolysis has been described in some plants may also contribute poisonings due to dichromate-con- towards inconsistent concentrations taining medicines. of extracted chemicals, e.g. the bufadinaloids (cardiac glycosides) in Cantharidine, a powerful lipid-solu- slangkop (Urginea sanguinea).1-3 ble toxin/vesicant, derived from many indigenous blister beetle Table I lists some of the more com- species (family Meloidea), is the mon poisonous plants used in tradi- active ingredient in a medicine tional medicines. Target organs and known as seletsa. It is used as an main toxic effects are also listed.3-5 abortifacient and aphrodisiac. Over- enthusiastic oral use of this medicine Clinical features may cause severe necrosis of the Gastrointestinal symptoms and signs oesophageal and gastric mucosa, predominate in poisoning caused by Seeds of Datura stramonium congestion and irritation of the uri- (stinkblaar). traditional medicines. Many tradi- nary tract with dysuria, haematuria tional medicines contain potent gas- and renal failure. Liver function trointestinal irritants and purgatives, Some traditional medicines may may also be compromised. included for their ‘purifying’ actions. directly cause CNS toxic effects Ventricular dysrhythmias, coagu- Enthusiastic use of enemas may be such as confusion, delirium, halluci- lopathy and may develop in contributory. Symptoms and signs nations, respiratory failure and con- severe cases. As little as 10 mg may include upper abdominal discom- vulsions. However, in many cases be fatal.

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Table I. Plants used in traditional medicines reported to be associated with acute poisonings

Plant species Vernacular name(s) Toxic ingredients/target organs and features of poisoning

Asclepias fruticosa Milkweed, melkbos, tontelbos, Cardiac . GIT usinga-lwesalukazi (Zulu), modimolo (S Sotho) Boophane disticha Bushman poison bulb, gifbol, Buphanidrine and other alkaloids. iBadi (Zulu), inCwadi (Xhosa) CNS (dizziness, restlessness, hallucinations, respiratory failure) Bowiea volubilis uGibisisila (Zulu), Cardiac glycosides. GIT, cardiovascular, Mgaqaqana (Xhosa) haemolysis Chenopodium ambrosioides Setla-botsha Active ingredient not known. CNS (mucronatum) (psychosis) Callilepis laureola Ox-eye daisy, impila (Zulu) Atractyloside (-like poison). GIT, kidney, liver Corchorus tridens Ghumbughumbu Cardiac glycoside. GIT (? capsularis) Eucomis utumnalis ubuHlungu becanti (Xhosa), Haemolytic : GIT, kidney (E. undulata) uMathunga (Zulu) Gloriosa superba iHlamvu (Zulu, Xhosa) Colchicine. Mucous membrane irritation, uHlamvu (Zulu) GIT, hypotension, respiratory failure Jatropha curcas Purging nut, purgeerboontjie, Curcin and curnanoleic acid, which is Mathlapametse (Tswana) similar to ricinoleic acid (in castor oil). GIT, kidney, potent irritant , severe diarrhoea/dehydration Ledebouria spp Letswitlana Active ingredient not known. GIT, kidney, liver, CNS Rhoicissus tridentate Morokolopudi Active ingredient not known. GIT, (? cuneifolia) kidney, CNS, respiratory failure Ricinus communis Caster oil plant, kasterolieboom, Two toxic ingredients in seed (not in Mokhura (N Sotho), Umhlakuva the oil) ricinin and ricin. Ricin is extremely (Xhosa, Zulu) toxic. GIT (haemorrhage), haemolysis, kidney, liver. Ricinoleic acid is a potent GIT irritant, causes diarrhoea. Oil contains ricinoleic acid (as in castor oil) Scadoxus puniceus Red paintbrush, rooikwas, Patalensine and other alkaloids. CNS Umphompo (Zulu) (stimulation and convulsions) Scilla nervosa inGcino (Zulu), Digitalis glycosides. GIT, cardiovascular Magaqana (Xhosa) Spirostachys africana African mahogany, tamboti, Latex contains diterpenes. GIT (potent umtomboti (Xhosa, Zulu), irritant) morekuri (Sotho) Urginea sanguinea Slangkop, sekanama (Sotho, Digitalis-like glycosides. GIT, cardiovascular (? burkei) Tswana), Skanama (Zulu) system (cardiac conduction abnormalities)

CME August 2003 Vol.21 No.8 483 MORE ABOUT

Management the treatment of severe vomiting and Management strategies should diarrhoea. In patients with renal include peritoneal or haemodialysis. Management of patients with poi- failure, haemodialysis should be soning due to traditional medicines In cantharidine poisoning, IV fluids considered. should follow the same general prin- should be administered in patients ciples and guidelines as applied to with significant vomiting and/or any other poisoning. Basic life sup- diarrhoea, haematuria or gastroin- port measures should always be a Some traditional med- testinal bleeding. ECG monitoring first priority. Serum electrolytes, icines may directly is essential. In cases where renal acid-base balance, state of hydration, cause CNS toxic failure occurs, haemodialysis may be blood glucose, renal and liver func- necessary.Treatment of Datura stra- tion, full blood count and coagula- effects such as confu- monium poisoning (anticholinergic tion status should be assessed and sion, delirium, halluci- syndrome) is primarily symptomatic monitored. Fluid replacement and and supportive. Although physostig- the correction of acid-base balance nations, respiratory mine is recommended by most text- and electrolytes (especially serum failure and convul- books, its use is generally not advis- potassium) should be a priority. In sions. able. Patients should be closely cases of gastrointestinal bleeding, the watched to prevent injuries, they haematocrit and haemoglobin need should be nursed in a dark room to be monitored regularly. Because (patients are photophobic), tempera- cardiac glycosides are often the In poisoning due to Indian tradition- ture monitored and adequate fluid cause of poisoning, ECG monitoring al medicines, dichromate and other intake assured. Benzodiazepines is recommended in cases of suspect- heavy metals have been implicated. may be given to calm patients and to ed cardiac glycoside poisoning. These should also be considered in treat seizures.1-7 Urine should be screened for the patients presenting with acute renal No routine tests exist for the identi- presence of myoglobin to exclude failure, gastrointestinal haemorrhage fication of plant toxins. rhabdomyolysis. Antiemetics and and hepatic failure. antidiarrhoeals may be required for References available on request.

SINGLE SUTURE and exposure

There is a suggested link between exposure to nitrogen dioxide (NO2) as an air pollutant and respiratory dis- ease. It is also known that viral infections are a major cause of asthma exacerbations. A recent paper in Lancet

showed that high levels of NO2 in the week before the start of a respiratory viral infection, at levels within current air quality standards, were associated with an increase in the severity of a resulting asthma exacerbation.

(Chauhan AJ, et al. Lancet 2003; 361: 1939-1944.) This is an important consideration in cities such as Cape Town and Johannesburg where levels of air pollutants are far in excess of accepted international norms — Editor.

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