Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

asymptomatic

1st line – contact poison control centre + observation or hospital referral

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ACUTE
|
asymptomatic
1st line – 

contact poison control centre + observation or hospital referral

The local poison control centre should be contacted for advice on the appropriate course of action as soon as a toxic ingestion is suspected. Management of poisoned patients should proceed with the consultation of a specialist familiar with their care.

All children suspected of having a toxic ingestion require observation. The minimum observation period is 6 hours, but children who have ingested a substance that carries a high risk of delayed toxicity require observation for 24 hours. In the US, most asymptomatic patients can remain at home with phone follow-up from the poison centre.

High-risk ingestions include acetonitrile, antimalarials (chloroquine or hydroxychloroquine), antiarrhythmics, antipsychotics, benzocaine, beta-blockers, calcium-channel blockers, camphor and other essential oils, cholinesterase inhibitors, clonidine and alpha-2 agonists, cocaine, tricyclic antidepressants, colchicine, bupropion, ethylene glycol, lindane, diphenoxylate/atropine, methanol, salicylates, opioids (especially methadone and buprenorphine), sulfonylureas, and theophylline.[40][41][43][44][45]​​ Deliberate or high-risk ingestions should be monitored in hospital. In addition, any history of cyanide exposure should be referred to hospital. Those with warfarin ingestion should be referred for an international normalised ratio and monitoring.

Paediatric patients with all non-accidental ingestions, or any suspicion of cough or cold/antipyretic/analgesic accidental ingestion, should be referred to hospital to have a paracetamol and salicylate level check, as the child may be asymptomatic on initial presentation.

Consider – activated charcoal within 1 hour of ingestion

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ACUTE
|
asymptomatic
Consider – 

activated charcoal within 1 hour of ingestion

Additional treatment recommended for SOME patients in selected patient group

Children suspected to have ingested a significant amount of the substance may be given a dose of activated charcoal.

Activated charcoal is contra-indicated in hydrocarbon and caustic ingestions.

Drugs that are absorbed by charcoal include theophylline, carbamazepine, quinine/quinidine, dapsone, thallium, and phenobarbital.

Other medications that are partially absorbed include almost all anticonvulsants and salicylates.

Drugs that are not absorbed by charcoal include heavy metals (except thallium), salts, lithium, ethanol, methanol, caustics, hydrocarbons, and ethylene glycol.

Multiple-dose activated charcoal may be considered for phenobarbital, quinine, dapsone, theophylline, or carbamazepine ingestions. The dose can be repeated every 2 to 4 hours. There is no clear evidence to support that this intervention changes clinical outcomes of poisoned patients.

Discussion with a regional poison control centre prior to the use of activated charcoal is recommended.

Primary options

activated charcoal: unknown amount of toxin: 1 g/kg orally/nasogastrically as a single dose (25-100 g/dose); known amount of toxin: 10 g of charcoal orally for every 1 g of toxin, may require multiple doses

symptomatic and/or high-risk ingestion and/or elevated drug levels

1st line – hospital admission + contact poison control centre

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
1st line – 

hospital admission + contact poison control centre

All patients who are symptomatic after 6 hours, or those who are likely to become so, require hospital admission. Oxygen saturation should be monitored continuously and capillary blood gas or arterial blood gas measurements taken regularly. Evidence of adequate perfusion should be repeatedly checked and include capillary refill as well as measures of end-organ perfusion such as urine output, mental status, and lactate production.

The regional poison control centre should be contacted for advice on the appropriate course of action as soon as a toxic ingestion is suspected. Management of poisoned patients should proceed with the consultation of a specialist familiar with their care.

High-risk ingestions include acetonitrile, antimalarials (chloroquine or hydroxychloroquine), antiarrhythmics, antipsychotics, benzocaine, beta-blockers, calcium-channel blockers, camphor and other essential oils, cholinesterase inhibitors, clonidine and alpha-2 agonists, cocaine, tricyclic antidepressants, colchicine, bupropion, ethylene glycol, lindane, diphenoxylate/atropine, methanol, salicylates, opioids (especially methadone and buprenorphine), sulfonylureas, and theophylline.[40][41][43][44][45]​​ Deliberate or high-risk ingestions should be monitored in hospital. In addition, any history of cyanide exposure should be referred to hospital. Those with warfarin ingestion should be referred for an international normalised ratio and monitoring.

Paediatric patients with all non-accidental ingestions, or any suspicion of cough or cold/antipyretic/analgesic accidental ingestion, should be referred to hospital to have paracetamol and salicylate levels checked, as the child may be asymptomatic on initial presentation.

Plus – airway and breathing management

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Plus – 

airway and breathing management

Treatment recommended for ALL patients in selected patient group

Any medication that markedly reduces mental status can lead to loss of the airway and airway reflexes. These include sedative-hypnotics, opioids, central alpha agents such as clonidine, and antipsychotics. Some medications can increase oral and bronchial secretions (cholinergics and antipsychotic agents); the presence of a gag reflex in these patients may not be sufficient to protect the airway.

Appropriate airway positioning to maintain patency is important. A child up to toddler age has a significantly larger head and smaller mouth. Use of airway adjuncts such as oral and nasopharyngeal airways may be necessary. Use of these adjuncts may increase the risk of vomiting.

Intubation and admission to the intensive care unit may be required in severe cases.

There should be a low threshold to intubate an unresponsive poisoned child with evidence of increased airway secretions or hypoventilation, ingestions of corrosive materials such as strong acids and bases, and multiple drug ingestions. Intubation should be undertaken with extreme caution in patients with metabolic acidosis or respiratory alkalosis because airway interventions that decrease minute ventilation lead to a sudden and catastrophic decrease in serum pH. Care must be taken to maintain the respiratory rate and volume at the same level as before intubation.

Plus – supportive care

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Plus – 

supportive care

Treatment recommended for ALL patients in selected patient group

Intravenous fluids dilute the toxin, aid in its elimination, maintain blood pressure, and assist in correction of acid-base disturbances. All patients require maintenance isotonic fluids; fluid boluses are used in hypotensive patients.

Potassium, sodium, calcium, and magnesium should be replaced intravenously as needed and monitored regularly. Patients with a long QT interval on ECG should receive magnesium supplementation to prevent torsades de pointes.

Sedation when intubated is best handled with opioid analgesia and/or benzodiazepine/propofol sedation, because these have the least effect on cardiovascular parameters and neurotransmitters. Sedation with dexmedetomidine in the poisoned patient lacks outcome data and may worsen hypotension and bradycardia.

Temperature control with external cooling and depression of muscular activity are extremely important in preventing hyperthermia, metabolic acidosis, and secondary rhabdomyolysis. Non-depolarising paralysis may be required to halt heat and acid production.

Minimal stress can overwhelm the glycogen stores and precipitate ketogenesis. This is especially true in paediatric ingestions of ethanol. Calorie and nutrient provision is therefore important.

Vasopressors may be required if blood pressure cannot be maintained using fluids alone. The pressor of choice is an alpha agonist such as noradrenaline (norepinephrine) or mixed agent such as adrenaline (epinephrine). A lack of response to these pressors should prompt consideration of beta-blocker or calcium-channel blocker toxicity and be managed using the appropriate antidote. Consult an appropriate specialist for choice of medication and dose.

Vasodilators may be required with sympathomimetic toxicity or if there is clinical evidence of end-stage organ dysfunction (cardiac, renal, or central nervous system abnormalities). Cardiovascular instability (due to either hypotension or hypertension) may require central monitoring of cardiac output and systemic vascular resistance, by either invasive or non-invasive monitoring. Consult an appropriate specialist for choice of medication and dose.

Primary options

phenylephrine injection: 0.1 to 0.5 micrograms/kg/minute intravenous infusion, titrate dose according to blood pressure

OR

noradrenaline (norepinephrine): 0.05 to 2 micrograms/kg/minute intravenous infusion, titrate dose according to blood pressure

OR

adrenaline (epinephrine): 0.1 to 1 micrograms/kg/minute intravenous infusion, titrate dose according to blood pressure

OR

phentolamine: consult specialist for guidance on dose

OR

glyceryl trinitrate: 0.25 to 5 micrograms/kg/minute intravenous infusion, titrate dose according to blood pressure

OR

sodium nitroprusside: 0.25 to 5 micrograms/kg/minute intravenous infusion, titrate dose according to blood pressure

OR

hydralazine: 0.1 to 0.2 mg/kg intravenously every 4-6 hours according to blood pressure, maximum 3.5 mg/kg/day

Consider – activated charcoal within 1 hour of ingestion

Back
ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Consider – 

activated charcoal within 1 hour of ingestion

Additional treatment recommended for SOME patients in selected patient group

Patients who are awake and alert with an intact airway may be given a dose of activated charcoal.

There is no clear evidence to support that this intervention changes clinical outcomes of poisoned patients. Activated charcoal is contra-indicated in hydrocarbon and caustic ingestions.

Drugs that are absorbed by charcoal include theophylline, carbamazepine, quinine/quinidine, dapsone, thallium, and phenobarbital.

Other medications that are partially absorbed include almost all anticonvulsants and salicylates.

Drugs that are not absorbed by charcoal include heavy metals (except thallium), salts, lithium, ethanol, methanol, caustics, hydrocarbons, and ethylene glycol.

Multiple-dose activated charcoal may be considered for phenobarbital, quinine, dapsone, theophylline, or carbamazepine ingestions. The dose can be repeated every 2 to 4 hours. However, a randomised controlled trial in 2002 noted no outcome difference in the use of multiple-dose activated charcoal.[47]

Discussion with a regional poison control centre prior to the use of activated charcoal is recommended.

Primary options

activated charcoal: unknown amount of toxin: 1 g/kg orally/nasogastrically as a single dose (25-100 g/dose); known amount of toxin: 10 g of charcoal orally for every 1 g of toxin, may require multiple doses

Consider – antidotes for specific poisonings

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Consider – 

antidotes for specific poisonings

Additional treatment recommended for SOME patients in selected patient group

A poison control centre or an expert experienced in the management of poisoning in children should always be consulted for advice on specific dosing for antidotes. TOXBASE Opens in new window

Opioid toxicity: requires treatment with naloxone provided that the patient is not intubated.[52]

Paracetamol overdose: treatment of a single acute ingestion is with acetylcysteine guided by a paracetamol treatment graph. The graph used varies between countries, and physicians should consult the local paracetamol overdose protocols. In the UK, a treatment graph that covers normal and high-risk patients is used, whereas in the US, the Rumack-Matthew nomogram is widely used,​ and a similar guideline is used in Australia and New Zealand.[36][37] If the child presents >8 hours after ingestion or has had repeated supratherapeutic ingestions, the first dose of acetylcysteine should be given immediately.[53][54][55]​ Patients with repeated supratherapeutic ingestions should be treated if symptomatic (nausea/vomiting) or have elevated liver function tests regardless of paracetamol levels. If there are any concerns regarding initiating acetylcysteine or its route, dosing, or duration of therapy, consultation with an appropriate specialist is recommended.

Beta-blocker toxicity: requires treatment with glucagon first-line.[52]​ If this fails, hyperinsulin-euglycaemia therapy should be used.[52]

Calcium-channel blocker toxicity: requires treatment with calcium chloride.[52]​ If this fails, hyperinsulinaemia-euglycaemia therapy can be used.[56]

Sodium-channel blocker toxicity: requires serum alkalinisation with intravenous sodium bicarbonate, which should be started immediately if there is widening of the QRS >100 milliseconds on ECG.[57]​ Treatment should be continued for 12 hours, and then stopped. Repeat 12-hour infusions should be given until the QRS remains <100 milliseconds at normal pH. The serum potassium should be maintained at >3.8 mEq/L. Although very uncommon to have abnormal conduction without mental status changes, in the unusual instance of a child who is wide awake and alert with a QRS >100 milliseconds, the physician can consider a trial of an intravenous push of 1 to 2 mEq/kg of sodium bicarbonate. If the QRS narrows, then therapy can be continued. If not, then the widened QRS is likely to be the patient’s pre-morbid ECG.

Salicylate or phenobarbital toxicity: treatment involves urine alkalinisation with intravenous sodium bicarbonate to maintain a urine pH >7.5 until the salicylate level is <1448 to 1810 micromol/L (<20 to 25 mg/dL or 200 to 250 micrograms/mL).[58]​ The serum potassium should be maintained at >3.8 mEq/L. All children with salicylate ingestions need to be evaluated with both acid-base status and level, because the tissue end-organ effects determine toxicity and are extremely pH-dependent. Immediate administration should be started in a large ingestion (suggested by a salicylate level >1448 to 2172 micromol/L [>20-30 mg/dL or 200-300 micrograms/mL] within 1 to 2 hours of ingestion). As the hyperpnoea of salicylate toxicity, which is the first sign of symptoms, is often missed, a conservative approach would be to start urinary alkalinisation in any patient with a level >2172 to 2534 micromol/L (>30 to 35 mg/dL or 300 to 350 micrograms/mL) and who may seem 'asymptomatic', or any level >1448 micromol/L (>20 mg/dL or 200 micrograms/mL) with any acid-base disturbance (gap >14 mmol/L or 14 mEq/L). Salicylate levels should be checked 4 to 6 hours after stopping sodium bicarbonate, because a rebound rise may occur.

Methanol or ethylene glycol toxicity: requires treatment with fomepizole. It is indicated if there is evidence of end-organ toxicity (visual disturbance, acidosis, hypotension, acute kidney injury) or signs and symptoms consistent with toxicity and a history of ingestion. Alcohol (ethyl alcohol/ethanol) may be used if fomepizole is unavailable. Haemodialysis may be required.

Cholinesterase inhibitor toxicity: requires treatment with atropine. This is indicated if there is symptomatic bradycardia. Atropine alone is sufficient in mild to moderate poisoning. Pralidoxime is required in severe poisoning.

Cyanide toxicity: hydroxocobalamin, or combination treatment with nitrites followed by thiosulfate, is indicated if there is coma, seizure, or metabolic acidosis. Treatment should not be delayed while awaiting cyanide levels.

Benzodiazepine toxicity: flumazenil may be indicated if there is respiratory depression or failure, the patient does not take benzodiazepines chronically and withdrawal is not a concern.[52]

Warfarin toxicity: fresh frozen plasma should be given in all patients with active bleeding and an international normalised ratio (INR) >5. Vitamin K (phytomenadione) can be given if INR >5-10.

Digoxin toxicity: the antidote is digoxin-specific antibody fragments (digoxin immune Fab) and should be given if there is symptomatic bradycardia, hypotension, hyperkalaemia, or any cardiac arrhythmia.[52]

Sulfonylurea toxicity: requires treatment with glucose and may require administration of octreotide.

Heavy metal toxicity: chelating agents may be required. Specific agent depends on type of metal. Treatment may be indicated in a symptomatic patient.

See local specialist protocol for guidance on doses of these agents.

Primary options

Opioid toxicity

naloxone

OR

Paracetamol toxicity

acetylcysteine

OR

Beta-blocker toxicity

glucagon

OR

Calcium-channel blocker toxicity

calcium chloride

OR

Sodium-channel blocker toxicity

sodium bicarbonate

OR

Salicylate or phenobarbital toxicity

sodium bicarbonate

OR

Methanol or ethylene glycol toxicity

fomepizole

OR

Cholinesterase inhibitor toxicity

atropine

or

pralidoxime

OR

Cyanide toxicity

hydroxocobalamin

OR

Cyanide toxicity

sodium nitrite

and

sodium thiosulfate

OR

Benzodiazepine toxicity

flumazenil

OR

Warfarin toxicity

phytomenadione

or

fresh frozen plasma

OR

Digoxin toxicity

digoxin immune Fab

OR

Sulfonylurea toxicity

glucose

and

octreotide

OR

Heavy metal toxicity

chelating agent

Secondary options

Beta-blocker toxicity

hyperinsulin-euglycemia protocol

OR

Calcium-channel blocker toxicity

hyperinsulin-euglycemia protocol

OR

Salicylate or phenobarbital toxicity

activated charcoal

OR

Methanol or ethylene glycol toxicity

ethyl alcohol

Tertiary options

Calcium-channel blocker toxicity

hyperinsulin-euglycemia protocol

OR

Methanol or ethylene glycol toxicity

dialysis

Consider – whole bowel irrigation

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Consider – 

whole bowel irrigation

Additional treatment recommended for SOME patients in selected patient group

Possible indications include ingestions of sustained-release or enteric products; multiple drug packets; and large ingestions of iron, potassium, or lithium. There is no firm outcome evidence to suggest that this technique improves clinical outcomes.[48]

The procedure involves infusion of a polyethylene glycol electrolyte solution at 20-40 mL/kg/hour (maximum rate of 1-2 L/hour) via a nasogastric tube until effluent is clear.

It is recommended that the use of whole bowel irrigation be discussed with a poison control centre.

Consider – haemodialysis or haemoperfusion

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ACUTE
|
symptomatic and/or high-risk ingestion and/or elevated drug levels
Consider – 

haemodialysis or haemoperfusion

Additional treatment recommended for SOME patients in selected patient group

Some ingestions require extracorporeal drug removal to achieve complete elimination. The options are either high flux haemodialysis, which is preferred, or haemoperfusion across a charcoal canister.

Examples of drugs amenable to haemodialysis include salicylates, lithium, methanol, ethylene glycol, and theophylline. Examples of drugs amenable to haemoperfusion include carbamazepine, valproate, and theophylline.

The decision to utilise extracorporeal treatment should take into account toxin levels, clinical evidence of severe toxicity or significant end-organ toxicity, and poor clinical response to other standard therapies.

Consideration of extracorporeal treatment should be discussed with a regional poison centre.

Primary options

haemodialysis

Secondary options

haemoperfusion

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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