Approach

A poison center should be contacted as soon as a toxic ingestion is suspected. Management of poisoned patients should proceed with the consultation of a specialist familiar with their care.

Symptomatic patients, and those with deliberate or high-risk ingestions and ingestions requiring blood level determination (e.g., acetaminophen, salicylates, warfarin) require assessment in the emergency department. Those who are symptomatic require urgent evaluation with establishment of an airway; evaluation of ventilatory effectiveness in both oxygenation and elimination of carbon dioxide; and maintenance of circulation as shown by a capillary refill of <2 seconds, an adequate BP, and end-organ perfusion. The mainstay of management is supportive care. The need for any further management (e.g., GI decontamination) should be discussed with a poison center.

Patients presenting within an hour of ingestion may benefit from GI decontamination methods to decrease absorption and enhance toxin elimination, but their use should not be routine and is best discussed with an expert experienced in the management of poisoning in children or a poison control center.

Patients may require antidotes for specific poisonings.[34][35]​ If either the antidote or a laboratory test required to guide its use are not available, the child should be transferred to a unit that has the ability to provide the antidote and perform the monitoring. There are a few ingestions that require extracorporeal drug removal to achieve complete elimination.

Prompt diagnosis and treatment lead to a good outcome in most cases.[36]​​[37][38][39]

In the US, the majority (67%) of human exposures reported to poison control centers in 2021 were managed outside of a healthcare facility (generally in the patient's own residence) with phone follow-up from the poison control center.[1]

Asymptomatic patients

All children suspected of having a toxic ingestion require observation. The minimum observation period is typically 6 hours, but children who have ingested a substance that carries a high risk of delayed toxicity require observation for 24 hours.

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.[36][37][39][40][41]

Deliberate or high-risk ingestions should be monitored in the hospital. In addition, any history of cyanide exposure should be referred to the hospital. Those with warfarin ingestion should be referred for an INR and monitoring.

Pediatric patients with all nonaccidental ingestions, or any suspicion of cough or cold/antipyretic/analgesic accidental ingestion, should be referred to the hospital to have an acetaminophen and salicylate level check, as the child may be asymptomatic on initial presentation.

Emergency management

Airway and breathing

  • Any medication that markedly reduces mental status can lead to loss of the airway and airway reflexes. Several medications depress the respiratory drive, including sedative-hypnotics, opioids, central alpha-agents such as clonidine, and antipsychotics. Some medications can increase oral and bronchial secretions (cholinergics and antipsychotics); 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, remembering that a child up to toddler age has a significantly larger head and smaller mouth and airway than adults. 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. Intubation may increase the risk of vomiting.

  • Ingestion of corrosive materials such as strong acids and bases should lower the threshold for intubation, especially if signs of stridor are present. There should also be a low threshold to intubate an unresponsive poisoned child with evidence of increased airway secretions or hypoventilation. In cases of multiple drug ingestion, depressed respiratory drive and respiratory acidosis can exacerbate the toxic effects of other medications, including salicylates, toxic alcohols and glycols, and sodium-channel agents such as tricyclic antidepressants. Metabolic acidosis causes hyperpnea and/or tachypnea, thereby increasing the tidal volume to a level sufficient to compensate for the acidosis. Intubation should be undertaken with extreme caution in these patients because any airway interventions that decrease the minute ventilation will lead to a sudden and catastrophic decrease in serum pH. If intubation is required (usually due to respiratory fatigue), care must be taken to maintain the respiratory rate and volume at the same level as was present before intubation or the onset of fatigue.

  • Most of the morbidity and mortality from toxic ingestions is due to issues of airway and breathing, so good airway management is crucial. Oxygen saturation should be monitored continuously, and capillary blood gas or arterial blood gas measurements taken regularly. Ventilation in intubated patients should be assessed using noninvasive end-tidal carbon dioxide monitoring.

Circulation

  • Hypotension: many overdoses are negative inotropes, negative chronotropes, or peripheral vasodilators resulting in hypotension. Children maintain their physiologic parameters far better than adults but then deteriorate suddenly without any reserves. Symptomatic patients require intravenous fluids to aid in dilution and elimination of the toxin. Hypotension and decreased perfusion should be treated with fluid boluses (20 mL/kg) with an isotonic fluid such as normal saline and Ringer lactate. If BP cannot be maintained using fluids alone, vasopressors should be considered. In most overdoses, the pressor of choice is an alpha agonist such as norepinephrine or mixed agent such as epinephrine. However, these pressors do not produce a response in beta-blocker or calcium-channel blocker toxicity; a lack of response should prompt consideration of these toxicities, which must be managed using the appropriate antidotes.

  • Hypertension: sympathomimetic toxicity causes a marked elevation in BP. Benzodiazepines are the specific antidotes for this type of poisoning. However, vasodilators may also be required to lower BP if BP rises above a critical threshold (as defined by local protocols) or if there is clinical evidence of end-stage organ dysfunction (cardiac, renal, or CNS abnormalities). Vasodilators to consider include nitroglycerin, nitroprusside, phentolamine, and hydralazine.

  • 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. Cardiovascular instability may also require central monitoring of cardiac output and systemic vascular resistance, by either invasive or noninvasive monitoring. Fine adjustment of pressors and inotropes usually requires invasive monitoring.

Gastrointestinal decontamination

Activated charcoal

  • Patients who are awake and alert with an intact airway and no evidence of hydrocarbon or caustic ingestion may be given a dose of activated charcoal (if possible within 1 hour of ingestion). However, there is no clear evidence to support that this intervention changes clinical outcomes of poisoned patients.[42]

  • Activated charcoal is contraindicated in hydrocarbon and caustic ingestions, and is ineffective in lithium and some other 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 also be useful in enhancing drug elimination for phenobarbital, quinine, dapsone, theophylline, or carbamazepine. However, a randomized controlled trial in 2002 noted no outcome difference in the use of multiple-dose activated charcoal.[43]

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

Whole bowel irrigation

  • Possible indications include ingestions of sustained-release or enteric products; multiple drug packets (body packing); and large ingestions of iron, potassium, or lithium. There is no firm outcome evidence to suggest that this technique improves clinical outcomes.[44]

  • 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 regional poison control center.

Gastric lavage is rarely, if ever, required. There is poor evidence that it changes outcome, and there are significant side effects associated with it. It should only be considered by personnel who are properly trained in its use and contraindications.[45]

Ipecac syrup, cathartics, and laxatives should not be used in poisoned patients. There is no evidence to suggest that these agents improve outcomes following toxic ingestion.[46][47]

Supportive care

Electrolyte disturbances

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

Sedation

  • Sedation when intubated is important and is best handled with opioid analgesia and 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

  • External cooling and depression of muscular activity are extremely important in preventing hyperthermia, metabolic acidosis, and secondary rhabdomyolysis. Nondepolarizing paralysis may be required to halt heat and acid production.

  • Care must also be taken not to let a patient become hypothermic. This may happen with some sedatives including baclofen and carisoprodol.

Seizures

  • Should be controlled using GABA agonists such as benzodiazepines or barbiturates. Sodium-channel anticonvulsants such as phenytoin should be avoided because patients with toxic ingestions do not respond to these agents.

Nutrition

  • In patients who are hypermetabolic, even minimal stress can overwhelm the glycogen stores and precipitate ketogenesis. This is especially true in pediatric ingestions of ethanol. Calorie and nutrient provision to maintain nutritional status is therefore important.

Specific antidotes

Opioid toxicity

  • The antidote is naloxone. Treatment is indicated if there is respiratory depression or decreased mental status, provided the patient is not intubated.[48]

Acetaminophen overdose

  • The antidote is acetylcysteine. Treatment of a single acute ingestion is guided by the Rumack-Matthew nomogram.[30][31] The level of serum acetaminophen relative to the time of ingestion determines the need for subsequent treatment.

  • If the child presents >8 hours after ingestion or has had repeated supratherapeutic ingestions, the first dose of acetylcysteine should be given immediately.[49][50][51]

  • Patients with repeated supratherapeutic ingestions should be treated if symptomatic (nausea/vomiting) or have elevated liver function tests regardless of acetaminophen 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

  • Treatment is indicated if there is bradycardia and hypotension. Intravenous glucagon should be commenced.[48]

  • If there is no response to glucagon, high-dose insulin (hyperinsulinemia-euglycemia therapy) should be used instead.[48]​ This involves administration of pharmacologic doses of intravenous insulin with coadministration of dextrose to maintain blood glucose levels. Specialist advice should be sought for details of dosing.

Calcium-channel blocker toxicity

  • Treatment is indicated if there is symptomatic bradycardia and hypotension. Initial treatment is with calcium chloride.[48]

  • If the response is still inadequate, hyperinsulinemia-euglycemia therapy can be used.[52] The protocol involves administration of an intravenous insulin loading dose, followed by an infusion with dose increases every 15 to 30 minutes as required. Blood glucose is maintained using concurrent intravenous supplementation. Specialist advice should be sought for details of dosing.

Sodium-channel blocker toxicity

  • In patients in whom there is widening of the QRS >100 milliseconds on ECG, serum alkalinization with intravenous sodium bicarbonate should be started immediately.[53]​ Alkalinization cannot be achieved if the patient is hypokalemic, and appropriate potassium replacement should also be given as needed to maintain a serum potassium of >3.8 mEq/L.

  • The sodium bicarbonate infusion should be continued for 12 hours and then stopped. If widening of the QRS returns, a second 12-hour infusion should be given, and this procedure should be repeated until the QRS remains <100 milliseconds at normal pH.

  • Alkalinization is reserved for QRS >100 milliseconds. There are no data to suggest that prophylactic alkalinization prevents deterioration. The gray area is when the child is wide awake and alert with a QRS >100 milliseconds. Because it is extremely unusual to have abnormal conduction without mental status changes, if there is a question, then 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 the patient’s premorbid ECG. Specialist advice should be sought if this class of poisoning is suspected.

Salicylate or phenobarbital toxicity

  • Treatment of salicylate poisoning involves urine alkalinization, which is achieved by the administration of intravenous sodium bicarbonate.[54]​ Alkalinization cannot be achieved if the patient is hypokalemic, and appropriate potassium replacement should also be given as needed to maintain a serum potassium at >3.8 mEq/L. The aim of urinary alkalinization is a urine pH >7.5, which should be maintained until the salicylate level is <20 to 25 mg/dL with resolution of anion gap metabolic acidosis. Urine alkalinization may be considered for phenobarbital toxicity but should be discussed with a poison control center.

  • 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. A large ingestion is suggested by a salicylate level >20 to 30 mg/dL within 1 to 2 hours of ingestion, and immediate action should be taken to administer urine alkalinization. As the hyperpnea of salicylate toxicity, which is the first sign of symptoms, is often missed, a conservative approach would be to start urinary alkalinization in any patient with a level >30 to 35 mg/dL and who may seem "asymptomatic," or any level >20 mg/dL with any acid-base disturbance (gap >14 mEq/L). Specialist consultation should be sought with suspected salicylate poisoning in order to discuss whether hemodialysis is indicated.

  • Salicylate levels should be checked 4 to 6 hours after stopping the sodium bicarbonate infusion, because a rebound rise in salicylate level may occur.

  • The use of carbonic anhydrase inhibitors is not recommended as it may worsen systemic toxicity.

  • Phenobarbital elimination is enhanced by multidose activated charcoal; however, evidence regarding improved clinical outcomes with its use is less clear and should be discussed with a poison control center.

Benzodiazepine toxicity

  • Treatment with flumazenil may be indicated if there is respiratory depression or failure, but extreme caution should be taken with patients who are taking benzodiazepines chronically or are benzodiazepine tolerant.[48]​ Seizures caused by flumazenil may be unresponsive to benzodiazepines.

Methanol or ethylene glycol toxicity

  • Treatment is indicated if there is good evidence of ingestion or any evidence of end-organ toxicity (visual disturbance, acidosis, hypotension, acute kidney injury), or any symptoms consistent with reported ingestion until it can be confirmed. Ingestion of 10 mL of 100% methanol in a 10 kg child will lead to a level >40 mg/dL, so if there is a good suggestive history of ingestion, the physician may consider initiating treatment while waiting for methanol levels. The first-line treatment is fomepizole.[55] However, oral ethanol loading or an ethanol infusion can also be used if fomepizole is unavailable. Hemodialysis may be required and should be discussed with a regional poison control center or specialist experienced in the management of poisoning in children.

Cholinesterase inhibitor toxicity

  • Antidote is indicated if there is symptomatic bradycardia. Intravenous atropine alone is sufficient in mild to moderate cases. Severe cases also require intravenous pralidoxime.[56]

Cyanide toxicity

  • Treatment with hydroxocobalamin, or combination treatment with nitrites followed by thiosulfate, is indicated if there is coma, seizures, or metabolic acidosis.[57][58]

Warfarin toxicity

  • Fresh frozen plasma should be given in all patients with active bleeding and an INR >5. Vitamin K can be given if INR >5-10.

Digoxin toxicity

  • The antidote is digoxin immune Fab and should be given if there is symptomatic bradycardia, hypotension, hyperkalemia, or any cardiac arrhythmia.[48]

Sulfonylurea toxicity

  • Treatment with dextrose infusions in combination with intravenous or subcutaneous octreotide is indicated if there is recurrent hypoglycemia <40 mg/dL or if hypoglycemia is symptomatic.[59]

Heavy metal toxicity

  • Treatment with an appropriate chelating agent may be indicated in a symptomatic patient.

Hemodialysis and hemoperfusion

The options are either high flux hemodialysis, which is preferred, or hemoperfusion across a charcoal canister. The indications for extracorporeal treatment are:

  • Ingestion of agents amenable to extracorporeal treatment. Examples of drugs amenable to hemodialysis include salicylates, lithium, methanol, ethylene glycol, and theophylline. Hemoperfusion may be considered for carbamazepine, valproate, and theophylline.

  • The decision to utilize 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 center.

Peritoneal dialysis is not a useful therapy in poisonings at present. Continuous veno-venous hemofiltration is an alternative method that is being investigated.

Online treatment information

A number of online resources are available that provide information on the treatment of a wide range of known poisonings:

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