Poison	Antidotes	Comments
Amfetamines	Esmolol i.v. 500 μg/kg over 1 min, then 25–200 μg/kg per min	Treatment for tachyarrhythmia
	Labetalol i.v. 0.15–0.3 mg/kg or phentolamine i.v. 0.05–0.1 mg/kg every 10 minutes	Treatment for hypertension
Benzodiazepines	Flumazenil i.v. 3–10 μg/kg, repeat 1 minute, then 3–10 μ/kg per hour	Specific receptor antagonist. Beware convulsions
β-Blockers	Glucagon i.v. 7 μg/kg, then 2–7 μg/kg per min	Stimulates non-catecholamine cAMP (preferred antidote)
	Isoprenaline i.v. 0.05–3 μg/kg per min	Beware β₂ hypotension
	Noradrenaline i.v. 0.05–1 μg/kg per min	Antagonises at receptors
Calcium channel blocker	Calcium chloride i.v. 10%, 0.2 ml/kg	Antagonises at receptors
Carbon monoxide	Oxygen 100%	Decreases carboxyhaemoglobin. May need hyperbaric oxygen
Cyanide	Dicobalt edetate i.v. 4–7.5 mg/kg	Give 50 ml 50% glucose after dose
	Hydroxocobalamin (vitamin B₁₂) i.v. 70 mg/kg	Beware anaphylaxis, hypertension
	Amyl nitrite 0.2 ml perles by inhalation until sodium nitrite 3% i.v. 0.13–0.33 ml/kg over 4 min, then sodium thiosulphate 25% i.v. 1.65 ml/kg (max 50 ml) at 3–5 minutes	Beware hypotension. Nitrites form methaemoglobin–cyanide complex. Beware excess methaemoglobin >20%. Thiosulphate forms non-toxic thiocyanate from methaemoglobin–cyanide
Digoxin	Magnesium sulphate i.v. 25–50 mg/kg (0.1–0.2 mmol/kg)	Antagonises digoxin at sarcolemma
Digoxin	Digoxin Fab i.v: acute – 10 vials per 25 tablets (0.25 mg each), 10 vials per 5 mg elixir; steady state: vials, serum digoxin(ng/ml) × BW(kg)/100	Binds digoxin
Ergotamine	Sodium nitroprusside infusion 0.5–5.0 μg/kg per min	Treats vasoconstriction. Monitor BP continuously
Ergotamine	Heparin i.v. 100 units/kg then 10–30 units/kg per hour	Monitor partial thromboplastin time
Lead	Dimercaprol (BAL) i.m. 75 mg/m² 4-hourly, six doses, then i.v. CaNa₂ edetate (EDTA) 1500 mg/m² over 5 days if blood level >3.38 μmol/l If asymptomatic and blood level 2.65–3.3 μmol/l, infuse CaNa₂EDTA 1000 mg/m² per day 5 days or oral succimer 350 mg/m² 8-hourly 5 days, then 12-hourly 14 days	Chelating agents
Heparin	Protamine 1 mg/100 units heparin	Direct neutralisation
Iron	Desferrioxamine 15 mg/kg per hour 12–24 hours if serum iron >90 μmol/l (500 μg/dl) or >63 μmol/l (350 μg/dl) and symptomatic	Give slowly, beware anaphylaxis
Methanol, ethylene glycol, glycol ethers	Ethanol i.v. loading dose 10 ml/kg 10% diluted in glucose 5%, then 0.15 ml/kg per hour to maintain blood level 0.1% (100 mg/dl)	Competes with poison for alcohol dehydrogenase
Methanol, ethylene glycol, glycol ethers	Fomepizole (4-methylpyrazole) 15 mg/kg over 30 minutes, then 10 mg/kg 12-hourly, four doses. (Not available in Australia)	Inhibits alcohol dehydrogenase
Methaemoglobinaemia	Methylene blue i.v. 1–2 mg/kg over several minutes	Reduces methaemoglobin to haemoglobin
Opiates	Naloxone i.v. 0.01–0.1 mg/kg, then 0.01 mg/kg per hour as needed	Direct receptor antagonist
Organophosphates and carbamates	Atropine i.v. 20–50 μg/kg every 15 minutes until secretions dry	Blocks muscarinic effects
Organophosphates and carbamates	Pralidoxime i.v. 25 mg/kg over 15–30 minutes then 10–20 mg/kg per hour for 18 hours or more. Not for carbamates	Reactivates cholinesterase
Paracetamol	N-acetylcysteine i.v. 150 mg/kg in dextrose 5% over 60 minutes then 10 mg/kg per hour for 20–72 hours OR oral 140 mg/kg then 17 doses of 70 mg/kg 4-hourly (total 1330 mg/kg over 68 hours)	Restores glutathione inhibiting metabolites. Give if serum paracetamol exceeds 1500 μmol/l at 2 hours, 1000 at 4 hours, 500 at 8 hours, 200 at 12 hours, 80 at 16 hours, 40 at 20 hours. Beware anaphylaxis
Phenothiazine dystonia	Benzatropine i.v or i.m. 0.01–0.03 mg/kg	Blocks dopamine reuptake
Potassium	Calcium chloride 10% i.v. 0.2 ml/kg	Antagonises cardiac effects
	Sodium bicarbonate i.v. 1 mmol/kg	Decreases serum potassium (slight effect). Beware hypocalcaemia
	Glucose i.v. 0.5 g/kg plus insulin i.v. 0.05 units/kg	Decreases serum potassium (rapid marked effect). Monitor serum glucose
	Salbutamol aerosol 0.25 mg/kg	Decreases serum potassium (rapid marked effect)
	Resonium oral or rectal 0.5–1 g/kg	Absorbs potassium (slow effect)
Sulphonyl ureas	Glucose Octreotide 1–2 μg/kg 8-hourly	Inhibits insulin release
Tricyclic antidepressants	Sodium bicarbonate i.v. 1 mmol/kg to maintain blood pH >7.45	Reduces cardiotoxicity

Individual poisons may require specific measures. Consult toxicology texts ⁴^–⁶ for details.

The vast majority of poisoning in childhood is by ingestion. The correct choice of a gastrointestinal decontamination technique is crucial to uncomplicated recovery. The choices are induced emesis, gastric lavage, activated charcoal, whole-bowel irrigation or a combination of these techniques. The efficacy, indications, contraindications and disadvantages and complications of these techniques are discussed below. A general plan of management is presented in Figure 105.1.

Figure 105.1 General management of the poisoned child.

A crucial point in management is initial recognition that the patient is in a state of either ‘full-consciousness’ or ‘less-than-full consciousness’. Traditionally, management has been dependent on a judgement of whether the gag reflex is present or absent, but in practice this is rarely tested. Since aspiration pneumonitis is a common feature of poisoning management, particularly among (but not confined to) CNS obtunded patients, it is prudent to regard all obtunded patients as having incompetent pharyngeal reflexes.

The decision to attempt removal of a poison should always be made with due reference to two facts

• The vast majority of childhood poisonings recover with merely supportive care or no treatment at all

• Aspiration pneumonitis is more serious than most poisonings

Occasionally, removal from the circulation by charcoal haemoperfusion, plasmafiltration or haemofiltration is indicated.

INDUCED EMESIS

Induced emesis is quickly disappearing from hospital practice and should not be performed routinely in this setting.⁷ It does not improve outcome and may reduce effectiveness of the alternative treatments of activated charcoal, oral antidotes and whole-bowel irrigation.

Specific contraindications include actual or impending loss of full consciousness or ingestion of corrosives or hydrocarbons.⁷

Syrup of Ipecacuanha has superseded other more injurious substances as emetic agents. It contains alkaloids, mainly emetine and cephaeline, which induce emesis by stimulation of the chemoreceptor trigger zone of the medulla and by irritation of the gastric mucosa.

The efficacy of ipecacuanha (ipecac) is limited and decreases with time from ingestion. Although it causes vomiting in a high percentage (93–100%) of children within 25 minutes, the percentage of stomach contents ejected is small (28%) even when administered immediately after ingestion.⁸ Moreover, solids are retained in the stomach or may even be propelled into the duodenum.⁹

In experimental drug ingestions, approximately 50–83% of ingested experimental drug is removed if ipecac is given after 5 minutes,¹⁰ but falling to 2–44% if given at 30 or 60 minutes.¹¹^–¹⁵ In paediatric paracetamol poisoning, the 4-hour postingestion serum level was approximately 50% of controls if ipecac-induced vomiting occurred within 60 minutes of ingestion, but no benefit was derived if emesis occurred beyond 90 minutes after ingestion.¹⁶ Similarly, serum levels of paracetamol were reduced approximately 50% if ipecac was administered at home, inducing emesis at a mean of 26 minutes after ingestion, compared with ipecac administered at a medical facility at a mean of 83 minutes.¹⁷

In adults, ipecac is even less useful and has to be given immediately to have quantifiable effects.¹⁸

Induced emesis appears superior to gastric lavage but inferior to activated charcoal. In children poisoned with salicylate, emesis retrieved twice as much compared with gastric lavage.¹⁹ In adult volunteers ipecac-induced vomiting, occurring at an average of 19 minutes after ingestion, removed 54% of a tracer compared with 30% with gastric lavage performed at the equivalent times after ingestion.²⁰^–²²

The use of ipecac has potential complications:

• time-related lack of efficacy

• protracted vomiting (17%)

• diarrhoea (13%)

• lethargy (12%)²³

More serious, but rare complications include:

• gastric, oesophageal or brain haemorrhage

• pneumomediastinum

• aspiration pneumonitis may occur, even in the fully conscious

• delayed onset of vomiting which is a threat if loss of consciousness subsequently occurs

• abuse in bulimia which may cause cardiotoxicity as well as the sequelae associated with repetitive vomiting

Critics claim that induced emesis merely creates work, delays discharge from the emergency department,²⁴ increases complications²⁴ and does not benefit the patient who presents more than 1 hour after ingestion.²⁵ Importantly, ipecac did not alter the clinical outcome of patients who presented awake and alert to the emergency department.²⁶

Induced emesis has been largely abandoned by emergency departments but its use in the home is safe and is associated with fewer paediatric emergency department attendances.²⁷ Its use at home is still recommended by authoritative paediatric health organisations in the USA²⁸ and by approximately half of poison centre staff.²⁹ Although ipecac was recommended inappropriately in 20% of cases to poisons information centres, it caused little morbidity.³⁰

CONCLUSION

In hospital, it has no practical role. Even when a child presents very early after significant poisoning, oral or nasogastric charcoal is preferred. Whenever induced emesis is used the child must be fully conscious on administration and expected to be fully conscious when vomiting occurs.

GASTRIC LAVAGE

Its place in the management of the poisoned victim has also been curtailed. It is an invasive technique with questionable efficacy. Moreover, it is potentially harmful and should be reserved for the child who presents soon after life-threatening poisoning such as ingestion of iron or colchicine.

It involves passage of a large bore oro- or nasogastric tube into the stomach and the repeated instillation of fluid, usually water but some authorities advocate normal or half-normal saline. The oral route is preferred because of less potential for traumatic injury but an oropharyngeal airway may be needed to prevent tube occlusion by chomping. A smaller tube may be used if the poison is a liquid. Traditionally, the child should be placed in the left lateral position to limit stomach emptying but volume of intragastric contents rather than body position determines gastric emptying.³¹

Experimental studies with therapeutic substances in volunteers, or with liquid medicines or substances instilled into the stomachs of overdose victims, reported that gastric lavage retrieved 90% at 5 minutes,³² 45% at 10 minutes²¹ and 30% at 19 minutes²⁰ and reduced absorption or bioavailability by 20–32% at 1 hour after ingestion.^11,³³ When gastric lavage was performed 5 minutes after ingestion of tablet drugs, it failed to prevent absorption, presumedly because the tablets had not disintegrated.³⁴ In true overdose situations, gastric lavage within 4 hours of admission reduced serum paracetamol levels by 39%.³⁵

Efficacy of gastric lavage, even with large bore tubes, is poor because tablets are not removed and lavage encourages propulsion into the duodenum.⁸ In symptomatic patients, gastric lavage alone compared with gastric lavage and activated charcoal increased pneumonic aspiration and did not alter the duration of intubation or the stay in the emergency department or the intensive care unit (ICU),³⁶ and was not beneficial unless performed within 1 hour of ingestion.²⁶ A prospective randomised trial of gastric lavage in acute overdose,³⁷ although criticised on methodological grounds,^37,³⁸ suggested that it made no difference to outcome of obtunded patients when preceding activated charcoal.

CONTRAINDICATIONS

• Less-than-full consciousness patient (unless already intubated) because of the risk of aspiration pneumonitis – which is not negligible even during full consciousness ³⁶

• After ingestion of corrosives because of the risk of perforation

• After ingestion of hydrocarbons or petrochemicals because of the risk of pneumonitis

COMPLICATIONS

• Aspiration pneumonitis

• Water intoxication

• Minor trauma to oropharynx (gastro-oesophageal perforation occurs rarely)

• Intrabronchial instillation of lavage fluid

As expected, infants and children never cooperate fully for gastric lavage, thus increasing risks of complications and the degree of psychological trauma.

If lavage is indicated, i.e. for life-threatening poisoning, rapid sequence induction of anaesthesia with intubation is advised. The largest possible lubricated tube of diameter similar to an appropriate sized endotracheal tube should be used and correct placement in the stomach confirmed. Small volumes (1–2 ml/kg) of warm tap water may be used to lavage until clear. However, most water should be retrieved to avoid hyponatraemia.

ACTIVATED CHARCOAL

Charcoal is a substance which adsorbs many drugs and is regarded as a ‘universal antidote’. It is advocated as the sole treatment in most poisonings although it is overused for minor poisonings. For many poisons no data exist regarding efficacy.

Treatment of charcoal with chemicals and heat increases its surface area to approximately 950 m²/g in so-called low surface area activated charcoal and to 2000 m²/g in superactivated charcoal. The latter adsorbs paracetamol better ³⁸ and is more palatable.^39,⁴⁰ Activated charcoal is not pleasant to drink and was associated with vomiting in 20% of poisoned children.⁴¹

It is superior to induced emesis and gastric lavage in treatment of symptomatic poisoned patients.^22,^26,³⁶ Its efficacy diminishes with time after ingestion. Activated charcoal reduces absorption of ingested experimental drugs in volunteers by 85–100% when administered 5 minutes after ingestion,^10,^34,⁴² by 40–75% at 30 minutes⁹ and by 30–50% at 60 minutes.^14,⁴² At a mean time of 98 minutes (SD 44) or more than 2 hours after poisoning, it was not effective at all.^43,⁴⁴

Studies have suggested that charcoal alone is as effective as when combined with either emesis or with lavage.^37,³⁸ Furthermore, combined methods have a higher incidence of aspiration, 8.5% versus none.³⁴ Activated charcoal failed to show a benefit in asymptomatic poisoned patients.

Repeated doses of activated charcoal enhance elimination of some drugs by increasing adsorption and by achieving postabsorption elimination by interrupting enterohepatic circulation and by removing drug from the gastrointestinal mucosa (‘gastrointestinal dialysis’). Although there are multiple reports in experimental and clinical practice (Table 105.2), there is no hard evidence to show that this therapy reduces mortality or morbidity. Only in life-threatening poisoning by carbamazepine, dapsone, phenobarbital, quinine or theophylline should multiple-dose activated charcoal be considered.⁴⁵

Table 105.2 Elimination and lack of elimination of drugs by multiple dose activated charcoal ⁴⁵

Elimination increased in experimental and clinical studies	Elimination increased in volunteer studies	Elimination not increased in experimental or clinical studies
Carbamazepine	Amitriptyline	Astemizole
Dapsone	Dextropropoxyphene	Chlorpropamide
Phenobarbital	Digitoxin	Doxepin
Quinine	Digoxin	Imipramine
Theophylline	Disopyramide	Meprobamate
	Nadolol	Methotrexate
	Phenylbutazone	Phenytoin
	Phenytoin	Sodium valproate
	Piroxicam	Tobramycin
	Sotalol	Vancomycin

See text for details.

A suitable single dose is 1–2 g/kg. A multiple-dose regimen for children is 1–2 g/kg stat followed by 0.25–0.5 g/kg 4–6-hourly. An alternative is 0.25–0.5 g/kg hourly for 12–24 hours.⁴⁶

CONTRAINDICATIONS

• If ileus is present

• A less-than-fully conscious patient unless already intubated

• Substances not adsorbed – for example, strong corrosive acids and alkalis, cyanide, metals (iron, lithium, mercury, lead), alcohols, glycols, petroleum distillates (not all) and essential oils ⁴^–⁶

COMPLICATIONS

Aspiration of charcoal causes severe and often fatal pneumonitis, bronchiolitis obliterans and adult respiratory distress syndrome. Intratracheal instillation of activated charcoal causes a significant increase in lung microvascular permeability and arterial blood gas derangements.⁴⁷

Constipation is common after charcoal but bowel obstruction is fortunately rare. The addition of a laxative (e.g. sorbitol or magnesium sulphate) is not recommended because although transit time through the gut is decreased, efficacy of the charcoal is reduced and life-threatening fluid and electrolyte imbalance may occur.⁴⁸

WHOLE-BOWEL IRRIGATION

Irrigation of the bowel with an iso-osmolar solution of polyethylene glycol and electrolytes is effective in reducing absorption of experimental drug by 24–67% at 1 hour after ingestion ^49,⁵⁰ and up to 73% at 4 hours after ingestion.⁵¹ However, it has not been shown conclusively to improve the outcome of poisoned patients. The technique has limited applications to sustained-release or enteric-coated drugs and remains a theoretical option for ingestions of iron, lead, zinc (substances not adsorbed by activated charcoal), packets of illicit drugs⁵² and for lithium.⁵³ Whole-bowel irrigation may be useful in delayed presentations when poisons have progressed beyond the stomach.

Irrigation solutions are adsorbed by activated charcoal and cause desorption of drug – necessitating prior administration of charcoal if a combined technique is used.⁵⁴ However, whole-bowel irrigation did not add to the benefits of activated charcoal in an experimental model of sustained-release theophylline poisoning.⁵⁵

A suitable regimen is approximately 30 ml/kg per hour for 4–8 hours until rectal effluent is clear. A regimen of 25 ml/kg per hour has been used safely for 5 days (total 44.3 litres),⁵⁶ but a total of 3 litres performed as well as 8 litres in a simulated poisoning.⁵⁷

CONTRAINDICATIONS

Risk of aspiration during:

• less-than-full consciousness

• bowel obstruction or ileus

PLAN OF MANAGEMENT

A general plan of management is suggested in Figure 105.1, but each case of poisoning mandates a specific plan of management according to circumstances. The primary determinant is the state of consciousness which relates to the risk of aspiration. Apart from that, the timing of presentation in relation to the severity of poisoning and the existence or otherwise of an effective antidote dictate if removal should be attempted, and by what means.

POISONING BY SPECIFIC SUBSTANCES

Like adults, children are poisoned regularly by therapeutic prescription or over-the-counter therapeutic drugs and substances. The poisons probably reflect their availability in the home. In a survey, the most common agents responsible for hospital admission were benzodiazepines, anticonvulsants, anti-parkinsonism drugs, paracetamol, major tranquillisers, antidepressants and cardiovascular drugs.⁵⁸ The inquisitive nature of young children, however, may lead to poisoning by substances not normally regarded as dangerous – a few of these and others which have notably different management from similar poisoning in adults are considered here, briefly.

BUTTON OR DISC BATTERIES

Ingestion may cause electrolytic injury and potentially corrosive, toxic or pressure injury. There are many types of batteries that contain a variety of substances: the most important are lithium, mercury and potassium hydroxide.

Impaction in the oesophagus is the most significant situation; this can result in oesophageal perforation and tracheo-oesophageal fistula or aorto-oesophageal fistula. An impacted battery must be removed endoscopically as soon as possible. Lithium batteries are large and impact readily and they have higher voltages than other types. Electrolysis commences as soon as the battery surfaces are immersed in oesophageal fluid. The consequence is local and surrounding tissue destruction, including the trachea.⁵⁹ Strong alkali is produced at the cathode and strong acid is produced at the anode. Mercury batteries are more likely to fragment⁶⁰ but mercury poisoning is very uncommon.

Sufficient follow-up is necessary to exclude oesophageal and tracheal damage and to ensure that a battery in the stomach or distal bowel is eliminated.

PETROLEUM DISTILLATES

Numerous by-products of petroleum distillation are utilised in industrial and domestic purposes. Ingestion of these hydrocarbons may cause CNS toxicity (comprising obtundation and convulsion), gastrointestinal irritation, occasional hepatorenal toxicity, and pneumonitis.

Pneumonitis is the most significant and it may occur during ingestion or subsequent vomiting. Although variable, these substances have low surface tensions which enable their rapid dispersement throughout contiguous mucosal surfaces which include the respiratory tree. Prime examples are petrol, kerosene, lighter fluid, lamp oil and mineral spirits. Any child who ingests a distillate must be assessed for pneumonitis and this should include clinical examination, a chest X-ray and at least a non-invasive measurement of oxygenation such as pulse oximetry. Although most children who ingest petroleum distillates do not develop pneumonitis, the onset of this complication may be within 30 minutes ⁶¹ and progress rapidly to severe lung disease. An adequate period of observation (6 hours) is necessary to exclude this complication. There is a poor correlation between the amount ingested and the severity of pulmonary toxicity.

Deliberate inhalation of volatile hydrocarbons such as petrol or aerosolised paint has the additional toxicity on myocardial tissue, including fatal tachydysrhythmia, possibly due to sensitisation to endogenous catecholamines. The deliberate inhalation of paint fumes, usually via a plastic bag, is called ‘chroming’.

ESSENTIAL OILS

The oils from certain plants contain mixtures of terpenes, alcohols, aldehydes, ketones and esters, which are used domestically for various purposes. The well-known oils are eucalyptus, turpentine, citronella, cloves, melaleuca, peppermint, wintergreen and lavender. In general, small amounts cause depression of conscious state, irritation of gastrointestinal tract, liver dysfunction and pneumonitis if inhaled. Each has different toxicity. For example, as little as 5 ml of eucalyptus oil ⁶² or 15 ml of turpentine may cause depression of conscious state.

Emesis should not be induced and gastric lavage performed only if airway protection is required.

LEAD

Children are more susceptible to lead poisoning after ingestion than are adults, possibly because of better absorption.

Acute poisoning usually occurs after ingestion of a lead salt or metallic foreign body or a lead-containing product, such as paint or traditional remedy or cosmetic. Acute poisoning by a salt may cause life-supporting cardiovascular collapse, and encephalopathy.

Chronic poisoning can occur with ingestion of lead-contaminated water, or by inhalation of leaded petrol fumes or contaminated house dust. Chronic poisoning causes multiorgan dysfunction including neuromuscular dysfunction and encephalopathy.

Treatment consists of gastric decontamination in the case of recent ingestion of lead salts. The use of chelating agents may be indicated. In the case of ingestion of a lead foreign body, serial X-rays should be taken to ensure elimination, otherwise surgical removal is indicated. In the case of multiple embedded gunshot pellets and in all cases of chronic poisoning, serum lead levels should be measured to guide chelation therapy (see Table 105.1).

PARACETAMOL

This is the most common drug ingested by children in an accidental, iatrogenic or deliberate overdose situation. Overdose has the potential for hepatic failure and, less commonly, renal failure. The onset of toxicity is delayed – up to several days. Consequently, the need for acute gastric decontamination is uncommon, but would be justifiable for acute large dose presentations. The toxicity in part is caused by the hepatic metabolite of the drug (N-acetyl-p-benzoquinoneimine) which accumulates when endogenous glutathione, which normally facilitates conversion of N-acetyl-p-benzoquinoneimine to non-toxic substances, becomes exhausted. Adequate supply of glutathione is ensured by administration of the antidote, N-acetylcysteine, a glutathione precursor which can be administered intravenously or orally (see Table 105.1).

The time of presentation after ingestion, as well as the dose, determines the management. If presentation is within 1 hour of ingestion, effective gastric removal or administration of activated charcoal may be all that is required pending a serum paracetamol level. In contrast, if presentation is several hours after ingestion, administration of the antidote, according to serum paracetamol level, takes precedence and although it may be administered orally or intravenously, the intravenous route is preferred.⁶³ Near-simultaneous administration of activated charcoal may be of some benefit but it may also cause vomiting or desorption, thus decreasing the effectiveness of the antidote. If presentation is many hours after the poisoning, activated charcoal would not be indicated, so the antidote could be administered orally if necessary according to serum paracetamol levels. In all cases, evidence of liver dysfunction mandates administration of the antidote.

The threshold single toxic dose of paracetamol indicating N-acetylcysteine administration is generally regarded as 150 mg/kg, although it has been suggested that a single dose less than 200 mg/kg in children less than 6 years of age may be safely managed at home.⁶⁴ However, in situations of repeated sub-150 mg/kg doses hepatotoxicity has a high mortality among children⁶⁵ and in adults.⁶⁶ Unfortunately, toxic overdosing by chronic administration is not uncommon even in paediatric institutions.⁶⁷

No sufficient data exist on which to firmly base a decision to administer N-acetylcysteine to children. Time-related serum levels of paracetamol should be measured and reference made to a guideline to administer the antidote (see Table 105.1) as derived from single toxic dose adult data.⁶⁸ The serum paracetamol level indicating antidote has been predicted as > 225 mg/l (1500 μmol/l) at 2 hours after ingestion of a single overdose of elixir in children 1–5 years of age.⁴³ If serum levels of paracetamol cannot be obtained and > 150 mg/kg has been ingested as a single dose or liver dysfunction is present after chronic poisoning, the antidote should be given.

Adverse reactions to N-acetylcysteine (approximately 8%) respond to an antihistamine ⁶⁹ and its temporary cessation.

IRON

Small quantities of elemental iron (> 20 mg/kg) are toxic to children. This dose may be reached by ingestion of few iron tablets. The initial effects are gastrointestinal, which may include gastric erosion, followed sometimes by an interval before cardiovascular failure occurs at 6–24 hours and then followed by multiorgan failure (including encephalopathy) and hepatic and renal failure up to some 48 hours after ingestion. In addition to general supportive measures, specific management should include abdominal X-ray to determine if unabsorbed tablets are present, in which case gastric lavage or whole-bowel irrigation may be useful. Activated charcoal is useless. Chelation therapy with desferrioxamine (see Table 105.1) should be guided by serum iron level and clinical status.

CAUSTIC SUBSTANCES

In a study of 743 children,⁷⁰ the incidence of oesophageal burns caused by ingestion of automatic machine dishwashing detergents was 59%, caustic soda 55% and drain cleaners 55%. All are strongly alkaline and are corrosive. Dishwasher detergents are presented as liquids, powders or tablet blocks and are commonly accessed in an open dishwasher.⁷¹ Pharyngeal and oesophageal irritation, burns or corrosion may occur. There may be simultaneous ocular and dermal toxicity. Any child presenting with a history of ingestion of a caustic substance, irrespective of clinical signs, should be considered for oesophagoscopy and follow-up since the correlation between symptoms and signs and oesophageal burns is poor⁷⁰ and significant oesophageal damage may occur in the absence of more proximal injury.⁷²

REFERENCES

1 Cripps R, Steel D. Childhood poisoning in Australia. Australian Government, Australian Institute of Health and Welfare. http://www.nisu.flinders.edu.au/pubs/reports/2006/injcat90.php

2 Kaushal R, Bates DW, Landrigan C, et al. Medication errors and adverse drug events in paediatric inpatients. JAMA. 2001;285:2114-2120.

3 Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: nine common agents that kill at low doses. Emerg Med Clin North Am. 2004;22:1019-1050.

4 Haddad LM, Shannon MW, Winchester JF. Clinical Management of Poisoning and Drug Overdose, 3rd edn. Philadelphia: WB Saunders, 1998.

5 Ellenhorn MJ, Schonwald S, Ordog G, et al. Ellenhorn’s Medical Toxicology, 2nd edn. Baltimore: Williams and Wilkins, 1997.

6 Bates N, Edwards N, Roper J, et al. Paediatric Toxicology. London: Macmillan, 1997.

7 Krenzelok EP, McGuigan M, Lheur P. Position statement: ipecac syrup. American Academy of Clinical Toxicology; European Associations of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35:699-709.

8 Corby DG, Decker WJ, Moran MJ, et al. Clinical comparisons of pharmacologic emetics in children. Pediatrics. 1968;4:361-364.

9 Saetta JP, March S, Gaunt ME, et al. Gastric emptying procedures in the self-poisoned patient: are we forcing gastric content beyond the pylorus? J Roy Soc Med. 1991;84:274-276.

10 Neuvonen PJ, Vartiainen M, Tokola O. Comparison of activated charcoal and ipecac syrup in prevention of drug absorption. Eur J Clin Pharmacol. 1983;24:557-562.

11 Tenenbein M, Cohen S, Sitar DS. Efficacy of ipecac-induced emesis, orogastric lavage, and activated charcoal for acute drug overdose. Ann Emerg Med. 1987;16:838-841.