Chapter 105 Paediatric poisoning

EPIDEMIOLOGY

The peak incidence of poisoning in childhood is among 1–4 year olds. It usually occurs in the home when the child ingests a single prescribed or over-the-counter medication or a household product. Approximately 3500 young children are admitted to hospital each year in Australia.¹ This mode of poisoning is called ‘accidental’ – erroneously because it is usually the result of inadequate supervision or improper storage of poisons. The mortality is very low and if hospitalisation is required, it is usually brief (1–3 days). In this circumstance, care must be taken to ensure that whatever treatment is applied, it does not impose additional risk.

Occasionally, poisoning in childhood is either truly accidental as in ingestion of a decanted chemical, or is part of a syndrome of child abuse (Munchausen syndrome by proxy), or is iatrogenic as when a parent mistakes medications at home or when medical or nursing staff make errors in drug administration in hospital. Medication errors occur in approximately 5% of paediatric inpatient medication.² Self-poisoning in older children is usually with the intention to manipulate their psychosocial environment or to commit suicide, or is the result of substance abuse. All circumstances of poisoning require remedial action.

DIAGNOSIS

Commonly, the diagnosis of poisoning in paediatric practice is self-evident and supported by a history detailed by parents or guardians. Although a single poison is usually involved, the possibility of several or multiple poisons should be considered. Occasionally the diagnosis is unknown on presentation. Any child who presents with unexplained obtundation, fitting, hypoventilation, hypotension or has a metabolic derangement should have the diagnosis excluded.

A knowledge of important poisons is indispensable. A number of poisons or classes of poison are potentially fatal to a small child if taken as a single tablet or a teaspoonful. These include opiates (methadone, buprenorphine, lomotil), camphor, quinine derivatives, cyclic antidepressants, clonidine, sulphonylureas, salicylates and calcium channel blockers.³

OPTIONS FOR TREATMENT

The treatment should be determined by the poison, severity of poisoning as judged by the observed and expected effects of the poison, by the amount ingested, by the interval between ingestion and presentation and by the existence or otherwise of an antidote.

The range of treatment options is to: discharge home, observe for a short duration in the emergency department or ward, provide intensive nursing care or to treat medically. The task is to match the intensity of treatment to the severity of the poisoning, thereby avoiding under- and overtreatment.

PRINCIPLES OF MANAGEMENT

The four basic principles in management of poisoning are:

• support vital functions

• confirm the diagnosis

• remove the poison from the body

• administer an antidote. Few poisons have antidotes (Table 105.1).

Table 105.1 Antidotes to some serious poisons

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.