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
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
PRINCIPLES OF MANAGEMENT
| 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 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 |
| 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 |
| 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 |
| 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 texts4–6 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.
The decision to attempt removal of a poison should always be made with due reference to two facts
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
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:
More serious, but rare complications include:
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
GASTRIC LAVAGE
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
