LEADING ARTICLE 407 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 inges- tion. 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 www.archdischild.com 408 LEADING ARTICLE 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,