Poisoning in Children 5: Rare and Dangerous Poisons

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Poisoning uptake and reducing hepatic gluconeo- Arch Dis Child: first published as 10.1136/adc.87.5.407 on 1 November 2002. Downloaded from ...... genesis. In overdose, it can produce significant gastrointestinal disturbance. In addition to hypoglycaemia, met- Poisoning in children 5: Rare and formin can induce a profound lactic acidosis.7 Serum electrolytes, lactate, and dangerous poisons bicarbonate should be monitored. Hy- poglycaemia should be treated with M Riordan, G Rylance, K Berry intravenous dextrose infusion. Asympto- matic patients should be observed for 12 ...... hours.1 β Acarbose inhibits glucosidases in the Management of children who have ingested blockers, intestine, preventing the digestion and digoxin, oral hypoglycaemics, organophosphates, carbon absorption of complex carbohydrates. monoxide, cyanide, isopropanol, ethylene glycol, methanol, Hypoglycaemia is unlikely but diarrhoea Ecstasy, LSD, cocaine, nicotine, and isoniazid may occur, particularly if patients receive carbohydrate rich foods following ingestion. n the final paper in this series of Treatment in the first instance is with Repaglinide is a newer oral hypogly- articles on the management of poison- activated charcoal. Repeated doses caemic agent. It acts by stimulating ing, we deal with exposures to a should be considered.3 Blood pressure insulin release but has a very short dura- I 7 variety of rare, but potentially very and ECG monitoring are required. Elec- tion of action. Blood sugar should be dangerous, toxins. trolytes should be monitored frequently. checked and symptomatic children Hyperkalaemia should be corrected should receive oral glucose. Effects are β BLOCKERS using ion exchange resins, glucose and likely to be short lived. β Blockers competitively antagonise the insulin, or dialysis. Salbutamol and binding of catecholamines to β receptors. calcium infusions should be avoided ORGANOPHOSPHATES The effect of specific agents in overdose because of their potential to destabilise Organophosphates are found in insecti- depends on their receptor specificity, the myocardium. cides, sheep dip, and lice treatments. lipid solubility, partial agonist activity, Bradyarrhythmias may require treat- They produce irreversible acetylcho- and dose. ment with atropine or cardiac pacing. linesterase inhibition. Accumulation of Bradycardia and hypotension are the Tachyarrhythmias may respond to ligno- acetylcholine stimulates muscarinic re- 14 commonest signs of cardiovascular tox- caine, amiodarone, or phenytoin. There ceptors at parasympathetic postgangli- onic synapses. icity, but tachycardia and hypertension is an increased risk of inducing asystole Symptoms of organophosphate poi- can occur if a partial agonist is con- with cardioversion and this should be soning can be delayed for up to 24 hours sumed. Other signs of cardiovascular used only as a last resort. post-exposure. Symptoms, produced by toxicity include varying degrees of heart The use of digoxin antibodies should parasympathetic over stimulation, in- block, shock, and pulmonary oedema. be considered where patients are resist- clude increased secretions from salivary, Central effects can occur, particularly ant to supportive treatment or a very lacrimal, bronchial, and gastrointestinal with propanolol, and include lethargy, large amount of digoxin has been in- glands, increased peristaltic activity, http://adc.bmj.com/ hallucinations, and convulsions. Hy- gested (more than 300 µg/kg). bronchoconstriction, bradycardia and poglycaemia can also occur. Plasma digoxin concentrations can be hypotension, miosis, and loss of visual Asymptomatic children should receive determined six hours post-ingestion. acuity. Urinary and faecal incontinence activated charcoal. A period of 12 hours The upper end of the therapeutic range is occur secondary to loss of sphincter con- observation is advisable.1 Symptomatic 2 µg/l. A blood level above 15 µg/l usually trol. In severe cases, overwhelming tra- children require intensive monitoring. indicates severe toxicity. Levels between cheobronchial secretions can lead to res- Hypotension may respond to intra- these points should be interpreted with caution, as they do not correlate accu- piratory compromise. In large doses, venous fluids. In resistant cases, intra- on October 3, 2021 by guest. Protected copyright. µ rately with clinical severity. organophosphates produce muscle venous glucagon (50–150 g/kg in 5% stimulation followed by paralysis be- dextrose) is the treatment of choice. cause of a depolarising block. Hypergly- High dose glucagon stimulates myocar- ORAL HYPOGLYCAEMICS caemia and glycosuria without ketonu- dial adenylate cyclase directly, bypassing Sulphonylurea type drugs produce hy- β ria may also occur. receptors. Isoprenaline or cardiac pac- poglycaemia by depolarising pancreatic While organophosphates can be ab- ing may be required. Regular estimation β cells and increasing insulin release. sorbed via the skin, symptoms rarely of blood sugar is essential. Ingestion of a single tablet can produce result from acute exposure. Ingestion symptomatic hypoglycaemia in children. carries the highest risk of acute toxicity. DIGOXIN Activated charcoal should be adminis- Asymptomatic children should be ob- Digoxin is potentially extremely toxic in tered. Asymptomatic children should be served overnight. Symptomatic children overdose. Children with underlying car- observed overnight as effects can be require careful observation. Mild symp- diac disease are particularly at risk and delayed for up to 16 hours.5 Symptomatic toms can be treated with supportive should always receive treatment. Chil- children require intensive monitoring. therapy alone. Patients with cardiorespi- dren without a history of heart disease Hypoglycaemia should be treated with ratory compromise require intensive require treatment if they have ingested intravenous dextrose infusion. Resistant care. Atropine, often in very high dosage, more than 100 µg/kg body weight. hypoglycaemia may respond to sub- acts as an antidote—blocking mus- The toxic effects of digoxin include cutaneous injection of the somatostatin carinic receptors and preventing the nausea, vomiting, hypotension, hyperka- analogue, octreotide, which inhibits pan- excessive activity of acetylcholine. laemia, and a multitude of cardiac creatic insulin release.6 Patients not responding to treatment arrhythmias.2 Careful monitoring is es- Metformin, a biguanide, acts by in- with atropine should be treated with sential as patients can deteriorate sud- creasing glucose uptake into the pralidoxime. This drug reactivates inacti- denly. muscles, inhibiting its gastrointestinal vated acetylcholinesterase. Pralidoxime

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Table 1 Antidotes for cyanide poisoning Arch Dis Child: first published as 10.1136/adc.87.5.407 on 1 November 2002. Downloaded from

Order Antidote Dose Side effects Comments

1st line Amyl nitrite Crushable perles, vapour inhaled, Methaemoglobinaemia The mechanism of action of amyl nitrite is either directly or via a bag and Vasodilatation unclear but may relate to its action as a mask Headache vasodilator

1st line Sodium 412.5 mg/kg (1.65 ml/kg of Nausea Combines with CN to form thiocyanate; thiosulphate 25% solution), maximum 50ml, Vomiting this is non-toxic and excreted in the urine give over 10 minutes Muscle cramps Arthralgia

2nd line Sodium nitrite 0.33 ml/kg of 3% solution, Potentially fatal See amyl nitrite. For moderate to severe maximum 10 ml, over 4 minutes methaemoglobinaemia, avoid poisoning, do not use as prophylaxis excessive dose, keep metHb at about 20%

2nd line Dicobalt EDTA 4 mg/kg over 1 minute, followed In the absence of cyanide, cobalt Chelates cyanide and does not produce by 50 ml 50% dextrose toxicity can be severe metHb. For moderate to severe poisoning, Anaphylaxis do not use as prophylaxis

is most effective as an antidote when as high a concentration of inspired both natural, for example, wool and silk; given within the first 24 hours post- oxygen as circumstances permit should and synthetic, for example, polyurethane ingestion. be commenced immediately. High con- and polyacrylnitrile. Synthetic polymers centrations of oxygen hasten the disso- are used extensively in domestic furnish- CARBON MONOXIDE ciation of COHb. ings. Cyanide and carbon monoxide poi- Carbon monoxide poisoning accounts The classical sign of “cherry red” lips soning frequently coexist. Symington et for the largest group of poisoning deaths and nail beds is unusual. Signs of cardio- al found that 4% of those dying in house among children.8 vascular or neurological toxicity should fires had potentially lethal cyanide Carbon monoxide (CO) is most fre- be carefully sought. There are often asso- levels.9 quently encountered as a product of ciated injuries, such as burns or smoke Cyanide binds to ferric iron (Fe3+)in incomplete combustion. The affinity of inhalation. the cytochrome a-a3 complex, inhibiting haemoglobin for carbon monoxide is 210 Blood should be taken for acid-base its action and blocking the final step in times its affinity for oxygen. Once bound balance, electrolytes, and muscle en- oxidative phosphorylation. Aerobic me- to haemoglobin, carbon monoxide disso- zymes. Metabolic acidosis is common tabolism is halted and carbohydrate ciates very slowly. In addition, the bind- and should not be over corrected, as a metabolism is diverted to the production ing of a single CO molecule to haemo- mild metabolic acidosis will enhance of lactic acid. globin increases the strength with which oxygen dissociation in the tissues. Cyanide poisoning requires a high oxygen molecules are attached, making Wherever possible exposure should be index of suspicion; signs are very hard to confirmed by direct, end tidal measure- oxygen dissociation in the tissues harder. dissect from those of CO poisoning. Car- http://adc.bmj.com/ ment of CO in expired air. Where this is The amount of carboxyhaemoglobin dinal features are the presence of a not possible, or practicable, spectropho- (COHb) formed depends on the concen- profound, refractory acidosis and a mas- tometric measurement of COHb, from a tration in inspired air and the duration of sively increased anion gap. There may be sample of arterial or venous blood, exposure. very little difference between venous and should be undertaken. The former test is Carbon monoxide dissolved in the arterial pO2, termed arteriolisation of preferable; blood COHb levels exclude plasma acts as a direct cellular poison in venous blood, because of impaired cellu- dissolved CO and can underestimate lar respiration. Patients should be con- its own right. Reacting with other haem exposure. Measurements of CO are best sidered at high risk if they have been on October 3, 2021 by guest. Protected copyright. proteins, such as mitochondrial cyto- made as soon as possible following exposed to fumes from burning plastics, chromes, it disrupts cellular metabolism. exposure; however, the half life of CO is are profoundly unconscious, or have per- Patient with up to 20% of haemo- five hours, in patients breathing air, and sistent myocardial ischaemia in the globin affected complain of headaches measurements may still be of value after absence of elevated COHb. and nausea. At 20–40% involvement, considerable delay. patients tire and become confused. In- Patients with carbon monoxide poi- Rapid treatment is essential. Blood volvement of more than 40% haemo- soning that are pregnant, that have any levels are useful in confirming toxicity, globin results in ataxia, collapse, and neurological signs or symptoms includ- but therapeutic intervention is usually coma. Cardiac arrhythmias, cerebral ing abnormalities of balance or gait, or necessary before the level is available. oedema, and acidosis can occur. those with evidence of cardiovascular Patients should receive high concen- The increased affinity of COHb for abnormalities including abnormal ECGs, trations of inspired oxygen. Mouth to oxygen means that haemoglobin mol- or myocardial ischaemia/infarction, mouth resucitation must be avoided. ecules become saturated at very low par- should be discussed with a hyperbaric Specific antidotes should be adminis- tial pressures of oxygen. Oxygen satura- oxygen centre. Unconscious patients tered as soon as possible (see table 1). tion monitors are therefore very should undergo early cranial imaging unreliable in the presence of COHb— and may require aggressive management ISOPROPANOL saturations of 100% occurring in the to control cerebral oedema. Isopropanol is an alcohol found in some presence of significant hypoxia. Conven- nail polishes, hairsprays, antifreezes, and tional blood gas analysers can also be CYANIDE car screen washes. It is also found in misleading. Cyanide poisoning is most frequently rubbing alcohol, window cleaners, and Patients considered at risk of carbon encountered following inhalation of tape and CD cleaners. monoxide poisoning should be removed smoke containing the combustion prod- Isopropanol is absorbed rapidly from from ongoing exposure. Treatment with ucts of nitrogen containing polymers— the stomach and mucus membranes. It

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causes gastric irritation, central nervous ethanol therapy, the disadvantages of There is concern over the apparent Arch Dis Child: first published as 10.1136/adc.87.5.407 on 1 November 2002. Downloaded from system depression, and hypotension which include CNS depression and severe idiosyncratic reactions to Ecstasy. (which is often refractory). hypoglycaemia.12 Where fomepizole is These effects can occur following doses Isopropanol is converted to acetone by not available, ethanol remains an alter- that have previously been well tolerated. the action of alcohol dehydrogenase. native treatment (7.5 ml/kg 10% ethanol Reactions include coma, convulsions, Acetone is excreted through the lungs in 5% dextrose over 30 minutes, then arrhythmias, malignant hyperthermia, and kidneys. Ketoacidosis is uncommon 1.65 ml/kg/h of 5% ethanol to keep blood rhabdomyolysis, hypertension, and mul- in isopropanol poisoning. level at 1–1.5 g/l). Fomepizole should be tiorgan failure. Asymptomatic children should be en- given every 12 hours (10 mg/kg for four Asymptomatic children should receive couraged to drink and observed for two doses, then 15 mg/kg) until the plasma activated charcoal if poisoning has oc- hours. Activated charcoal does not de- ethylene glycol level falls below 200 mg/l. curred within one hour. Blood pressure, crease absorption. Gastric lavage and Patients require regular measurements temperature, and ECG monitoring are emesis are unlikely to be effective after of blood gases, renal function, and advisable. Blood levels can be performed one hour. Both are contraindicated in the plasma calcium. Patients with renal fail- to confirm exposure. In the absence of presence of central nervous system de- ure or resistant metabolic acidosis will symptoms patients can be discharged pression. require haemodialysis.13 Fomepizole is after 24 hours observation, provided that Symptomatic patients require inten- dialysed and the dosage interval should adequate parental supervision is avail- sive support. Hypotension, secondary to be decreased on dialysis. able. Children with symptoms require a peripheral vasodilatation, may require minimum of 48 hours observation. Ad- treatment with intravenous fluids and METHANOL verse effects, related to psychomotor inotropes. Haemodialysis is indicated for stimulation or hallucination, require Methanol is also found in certain anti- patients not responding to supportive only supportive treatment. These effects freezes and windscreen washes. Metha- measures or those with a blood isopropa- usually last for 4–6 hours, but can occur 10 nol is metabolised by alcohol dehydroge- nol concentration of more than 4 g/l. for up to 48 hours depending on the Successful treatment of isopropanol poi- nase to formaldehyde, which in turn is quantity of Ecstasy consumed. soning has been reported using perito- converted to formate. Toxic effects in- Patients with signs of cardiac or neal dialysis.11 This technique does not clude severe abdominal pain, retinal tox- central nervous system toxicity require require specialist equipment but may icity, acidosis, convulsions, and coma. admission to intensive care. Careful prove ineffective in patients with poor Methanol poisoning can be managed monitoring of haematological and bio- peritoneal perfusion caused by refractory in a similar manner to ethylene glycol chemical parameters is essential. Hyper- hypotension. poisoning, both ethanol and fomepizole thermia may respond to simple cooling inhibiting its metabolism. There are, measures but, should these fail, patients ETHYLENE GLYCOL however, a few important differences. should receive dantrolene 1 mg/kg intra- Ethylene glycol is found in certain types Severe symptoms of methanol poisoning venously over 10–15 minutes. If there is of antifreeze, brake fluid, and wind- tend to occur after hours rather than no response this dose may be repeated at screen wash. Ethylene glycol is metabo- minutes. In the absence of symptoms, 15 minute intervals to a cumulative lised by alcohol dehydrogenase to a vari- hypocalcaemia, acidosis, or renal dys- maximum of 10 mg/kg in 24 hours. ety of toxic metabolites, including function, treatment can be withheld Hypertension responds to labetalol. Con- glycolic and oxalic acid. Toxic effects pending the plasma methanol and for- vulsions and agitation should be treated include convulsions, coma, metabolic mate concentrations. Methanol has a

with benzodiazepines. Chlorpromazine http://adc.bmj.com/ acidosis, hypocalcaemia, and renal fail- considerably longer plasma half life than and haloperidol are best avoided as they ure. ethylene glycol (43 hours compared with may decrease seizure threshold. Vigorous Ethylene glycol is rapidly absorbed 18 hours).12 For this reason elective ﬂuid replacement is often necessary to from the stomach; symptoms can occur haemodialysis is often necessary, to rehydrate patients, promote a diuresis to within 30 minutes of ingestion, and enhance elimination and reduce the clear myoglobin, and allow for increased attempts at gastric decontamination are duration of therapy. insensible losses. However, care is neces- likely to be unproductive. Methylated spirit does not contain sary as self induced water intoxication Asymptomatic children should have sufﬁcient methanol to cause toxicity. has been described in these patients. on October 3, 2021 by guest. Protected copyright. blood taken for plasma ethylene glycol Adverse effects are related to its ethanol Fluid therapy should be guided by regu- estimation. Blood gases, serum calcium, content alone. electrolytes, and renal function should lar blood tests and invasive monitoring. also be measured. Symptoms of severe poisoning can occur rapidly and, even in ECSTASY LSD their absence, treatment is indicated if Ecstasy, 3,4-methylenedioxymetham- Lysergic acid diethylamide (LSD), a 5-HT ingestion is likely. Ethanol competes phetamine or MDMA, is an ampheta- agonist, is a potent hallucinogen. It is with ethylene glycol binding at the cata- mine derivative. In common with am- rapidly absorbed and has a short dura- lytic site of alcohol dehydrogenase. An phetamines, it produces locomotor tion of action. Symptomatic children oral loading dose of ethanol (2 ml/kg of stimulation, euphoria, excitement, and should be reassured. Gastric decontami- 40% ethanol over 30 minutes; most spir- stereotyped behaviour. In addition, nation is not indicated. Sedation with its match this criteria) will delay toxic Ecstasy has psychotomimetic effects, phenothiazines should be avoided as effects until blood results are available. altering perception and mood. The they decrease the threshold for convul- All children receiving this treatment will mechanism of action of Ecstasy is uncer- sions. In very rare instances, LSD can be require admission for overnight blood tain but appears to relate to increased associated with malignant hyperther- sugar estimation and observation. 5-hydroxytryptamine (5-HT) release mia. Symptomatic children, or those with a accompanied by a decreased 5-HT up- LSD is poorly absorbed through the plasma ethylene glycol level of more take by nerve terminals.7 skin; “LSD laced” transfer tattoos are an than 200 mg/l (3.2 mmol/l), should Ecstasy is widely available as a drug of urban myth. receive intravenous fomepizole (15 abuse. Ecstasy is not addictive as toler- mg/kg over 30 minutes). Fomepizole is a ance develops rapidly to its positive COCAINE competitive alcohol dehydrogenase an- effects, while negative effects are exacer- Cocaine is a psychomotor stimulant. It tagonist. Its use replaces intravenous bated by large doses or frequent use. acts by inhibiting the uptake of

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Correspondence to: Dr K Berry, Accident and

dopamine, noradrenaline, and 5-HT ISONIAZID Arch Dis Child: first published as 10.1136/adc.87.5.407 on 1 November 2002. Downloaded from from synapses. Cocaine is supplied as a Isoniazid is widely used in the treatment Emergency Department, Birmingham Children’s Hospital, Steelhouse Lane, Birmingham salt or, more recently, as a free base of tuberculosis. In overdose, isoniazid B4 6NH, UK; (“crack”). Crack cocaine is favoured by reacts with pyridoxine to form a com- [email protected] addicts as it can be smoked, producing pound which is rapidly excreted in the REFERENCES an effect equivalent to intravenous injec- urine. Pyridoxine is necessary for the 1 Bates N, Edwards N, Roper J, et al. tion of the salt. production of the inhibitory neurotrans- Paediatric toxicology: handbook of poisoning In acute overdose, both forms can be mitter γ-aminobutyric acid (GABA). A in children. London: Macmillan Reference Limited, 1997. equally hazardous. Effects include agita- deﬁciency of GABA results in intractable 2 Mofenson HC, Caraccio TR, Schauben J. tion, hallucinations, convulsions, hyper- seizures, resistant to most conventional Poisoning by antidysrhythmic drugs. Pediatr tension, myocardial ischaemia, and cer- anticonvulsant therapies. Clin North Am 1986;33:723–38. 3 Vale JA, Krenzelok EP, Barceloux GD. ebral infarction. Cardiac arrhythmias are The effects of isoniazid toxicity appear Position statement and practice guidelines on a particular danger.14–16 within two hours of ingestion. Neuro- the use of multi-dose activated charcoal in the treatment of acute poisoning. American Asymptomatic children should receive logical symptoms predominate and sei- Academy of Clinical Toxicology; European activated charcoal if ingestion has oc- zures are likely if more than 30 mg/kg Association of Poisons Centres and Clinical curred within one hour. Blood pressure has been ingested. Lactic acidosis, hyper- Toxicologists. J Toxicol Clin Toxicol 1999;37:731–51. and ECG monitoring should be under- glycaemia, hypokalaemia, and ketonuria 4 Commerford PJ, Lloyd EA. Arrhythmias in taken. are common. patients with drug toxicity, electrolyte, and endocrine disturbances. Med Clin North Am Symptomatic children require inten- Asymptomatic children should receive 1984;68:1051–79. sive monitoring. Agitation, hallucina- activated charcoal. Symptomatic pa- 5 Quadrani DA, Spiller HA, Widder P. Five tions, and convulsions can be controlled tients should receive intravenous year retrospective evaluation of sulfonylurea ingestion in children. J Toxicol Clin Toxicol with benzodiazepines. Acidosis exacer- pyridoxine—at a dose equivalent to the 1996;34:267–70. bates cardiac toxicity and should be amount of isoniazid ingested in milli- 6 McLaughlin SA, Crandall CS, McKinney PE. Octreotide: an antidote for corrected; resistant arrhythmias may re- grams. This dose may be repeated at 10 sulfonylurea-induced hypoglycemia. Ann 17 spond to calcium antagonists. Hyper- minute intervals to control seizures.18 Emerg Med 2000;36:133–8. tension and chest pain can be treated Aggressive supportive treatment may be 7 Rang, Dale, Ritter. Pharmacology, 4th edn. 19 Edinburgh: Churchill Livingstone, 1999. with diazepam, nitrates, and calcium required. Urinary alkalinisation or 8 Department of Trade and Industry. Home antagonists. Drugs acting on noradrener- haemodialysis20 enhance isoniazid clear- and Leisure Accident Surveillance System, 1978–1997. Personal communication, 1999. gic or dopaminergic systems, for exam- ance and may be considered in patients 9 Symington IS, Anderson RA, Thomson I, et ple, β blockers or phenothiazines, should who fail to respond. al. Cyanide exposure in fires. Lancet be avoided because of the risk of unan- 1978;2:91–2. 10 Lacouture PG, Wason S, Abrams A, et al. ticipated interactions. Anticoagulation SEEKING FURTHER ADVICE Acute isopropyl alcohol intoxication. and thrombolysis should be considered if Speciﬁc, expert advice on all aspects of Diagnosis and management. Am J Med 1983;75:680–6. myocardial infarction occurs. poisoning is available to medical profes- 11 Mecikalski MB, Depner TA. Peritoneal sionals in the United Kingdom via the dialysis for isopropanol poisoning. West J NICOTINE Med 1982;137:322–4. National Poisons Information Service 12 Tenenbein M. Recent advancements in Nicotine is a toxic alkaloid found in a (NPIS). The regional centres that make pediatric toxicology. Pediatr Clin North Am range of plants, most notably tobacco. up this service have recently introduced 1999;46:1179–88, vii. 13 Watson WA. Ethylene glycol toxicity: closing Nicotine is also used as a pesticide. Nico- a single national enquiry number: in on rational, evidence-based treatment

tine stimulates nicotinic acetylcholine 0870 600 6266. [editorial; comment]. Ann Emerg Med http://adc.bmj.com/ receptors throughout the central and 2000;36:139–41. A wide range of easily accessible and 14 Wang RY. pH-dependent cocaine-induced autonomic nervous systems. In severe highly practical advice is available cardiotoxicity. Am J Emerg Med poisoning confusion and convulsions are through the NPIS website.21 This free 1999;17:364–9. 15 Billman GE. Cocaine: a review of its toxic accompanied by arrhythmias and para- service is restricted to medical profes- actions on cardiac function. Crit Rev Toxicol sympathetic over stimulation (see orga- sionals. On line registration is available 1995;25:113–32. nophosphate poisoning). at http://www.spib.axl.co.uk/toxbase/. 16 Kloner RA, Hale S, Alker K, et al. The effects of acute and chronic cocaine use on the heart. Children most frequently encounter Arch Dis Child 2002;87:407–410 Circulation 1992;85:407–19. nicotine in the form of cigarette or ciga- 17 Nahas G, Trouve R, Demus JR, et al.A on October 3, 2021 by guest. Protected copyright. calcium-channel blocker as antidote to the rette butt ingestion. Vomiting is the cardiac effects of cocaine intoxication [letter]. commonest symptom following cigarette ...... N Engl J Med 1985;313:519–20. ingestion and tends to limit toxicity. 18 Romero JA, Kuczler FJ. Isoniazid overdose: Authors’ affiliations recognition and management. Am Fam Asymptomatic children who have in- M F Riordan, Department of Pediatrics, Yale Physician 1998;57:749–52. gested less than one cigarette or two University Medical School, USA 19 Yarbrough BE. Current management of the cigarette butts should be observed for G W Rylance, Department of General poisoned patient. South Med J 1988;81: 892–901. Paediatrics, Royal Victoria Infirmary, Newcastle two hours. No speciﬁc treatment is 20 Orlowski JP, Paganini EP, Pippenger CE. required. Children who have consumed upon Tyne, UK Treatment of a potentially lethal dose isoniazid K Berry, Accident and Emergency Department, ingestion. Ann Emerg Med 1988;17:73–6. more than this amount, should receive Birmingham Children’s Hospital, Birmingham, 21 Good AM, Bateman DN. TOXBASE on the activated charcoal. UK Internet. J Accid Emerg Med 1999;16:399.