Which pediatric medication ingestions may require hospitalization and which probably don’t?
Originally published at www.emDocs.net and reviewed by Cynthia Santos, MD, Medical Toxicologist, Assistant Professor – Emergency Medicine and Toxicology at Rutgers University Hospital; Alex Koyfman, MD, FACEP, FAAEM; and Brit Long, MD, FACEP
Pediatric patients comprised 45.2% of the 2.6 million toxic exposure calls to U.S. poison centers in 2017. Although most of these exposures represent minor ingestions, there are at least seven different classes of substances that can lead to severe toxicity or even death with even small ingestions in children. The 2017 data from the American Association of Poison Control Centers (AAPCC) reported 25 deaths in children less than six years of age.
In children less than six-years-old, many medication-related poisonings are related to therapeutic error, such as incorrect dosing, accidental overdosing, usage of incorrect formulation or accidental administration of the wrong medication.2 The majority of these overdoses are benign, and the child can be watched at home. However, with the development of new pharmaceuticals and the expanded treatment indications for others, the availability of deadly drugs is only increasing.[1,3]
As with the assessment of any critically ill patient, the evaluation of a potentially poisoned pediatric patient begins with the ABCs (airway, breathing and circulation). The most common factor contributing to death from a drug overdose or poisoning is loss of airway protective reflexes, which leads to ventilatory failure. This is especially true in pediatric patients, as they tend to have less oxygen reserve. This is due to their horizontal ribs and flatter diaphragm, meaning they are less able to increase their tidal volume to compensate for changes in respiratory rate and oxygen demand.
It is imperative for physicians to be familiar with the presenting signs and symptoms of potentially toxic ingestions in the pediatric population in order to quickly initiate therapeutic and life-saving interventions.
Table 1: Commonly Cited ‘One Pill Can Kill’ Medications
|Class||Examples||Mechanism of Action/Toxicity||Signs & Symptoms||Treatment||Asymptomatic Observation Time|
|Sulfonylureas[5.6,7]||Glipizide, Glyburide||Inhibit ATP-dependent K+ channels on pancreatic beta cells[5,7]||Asymptomatic to overt coma,
|– Weight-based dextrose bolusa
– ACb if < 1hr[5,7]
– Octreotidec 4-5µg/kg/d q6hrs (max 50µg q 6hr)[5,6]
|24 hrs with
|Block Ca2+ entry through voltage gated L-type cellular membrane Ca2+ channels leading to arterial smooth muscle relaxation and inhibition AV/SA nodal depolarization and decreased contractility||Bradycardia, hypotension, dizziness, seizures,
GI symptoms, hyperglycemia,
|– IVF, atropine (usually ineffective), calcium chloride, vasopressors5
– High dose insulin 0.5-1 U/kg/hr +/- glucosed5
|Ingestions > 0.3mg/kg Amlodipine require 6hr observation7
6 hrs for IR, 18 hrs for ER
|Isopropanol||Metabolized to acetone||Respiratory depression, hypotension, hemorrhagic gastritis, osmol gap without anion gap acidosis||– Hemodialysis may greatly enhance serum elimination||
|Methanol||Oxidized in the liver to formaldehyde and formic acid||Abdominal pain, obtundation, visual loss/snowfield vision
Delayed onset osmolar gap and AGMAe.
– Hemodialysis for visual impairment, profound acidosis, renal failure, or levels >50mg/dL
– Methanol: Folate supplementation
– Ethylene Glycol: Thiamine and pyridoxine supplementation
|Ethylene Glycol||Oxidized to glycoaldehyde and glycolic acid, which is eventually metabolized to oxalic acid||AMS, ataxia, hallucinations, tachycardia, tachypnea, hypertension, CHFf, ARDSg, circulatory collapse, tetany, QT prolongation, nephrotoxicity, osmolar gap and AGMA|
|Central α-Agonist5||Clonidine||Central α2 receptor agonist||Opioid-like toxidrome, bradycardia, hypotension, apnea||– Naloxonei
– Treat refractory bradycardia with atropine
– Treat hypotension with IVF and dopamine
|Amitriptyline, nortriptyline, imipramine||Centrally mediated inhibition of biogenic amines, inhibition of H1 histamine and M1 muscarinic receptors, blockage of fast voltage-gated sodium channels on cardiac myocytes||Anticholinergic toxidrome, cardiovascular collapse, widened QRS with terminal R wave in aVR, seizure, coma||– AC as soon as possible
– Sodium bicarbonate IV bolus of 1-2mEq/kg for QRS ≥100ms, ventricular dysrhythmias, hypotension
Oil of wintergreen
|Stimulation of medullary respiratory center, uncoupling of oxidative phosphorylation, metabolic acidosis, increased pulmonary vascular permeability, inhibition of gluconeogenesis5,9||Lethargy, diaphoresis, coma, seizure, cardiovascular collapse, vomiting, tachypnea, diaphoresis, hypoglycemia, metabolic acidosis5,9||– AC if early after ingestion
– Aggressive rehydration with goal UOPj 2-3mg/kg/h
– Alkalinize urine with sodium bicarbonate 1-2mEq/kg bolus for goal urine pH 7.5-8.5 and goal blood pH 7.5-7.55
– Maintain glucose >100 mg/dL
– Early hemodialysis for salicylate levels >80-100 mg/dL
|Ingestions >150mg/kg ASA or more than a lick of oil of wintergreen require ED evaluation|
|Opioids5||Methadone, oxycodone, fentanyl||Interact with µ, κ, and δ opioid receptors throughout the CNS, PNS and GI tract||Dizziness, euphoria, depressed reflexes, AMS, lethargy, coma, dry mucus membranes, nausea and vomiting, bronchospasm, bradycardia, bradypnea, miosis||– Naloxone 1-2mg if respiratory depression present, may need to be repeated every 20-60 min
– Continuous infusion if repeated boluses needed starting at 2/3 dose needed to reverse respiratory depression per hour
– AC if within 1 hr of delayed-absorption of sustained release product
|Children with recurrent respiratory depression after initial naloxone treatment require admission|
|Blocks DNA and RNA synthesis||Hypotension, hypokalemia, QRS prolongation, seizures, coma, cardiac dysrhythmias, headache, nausea and vomiting||– AC for asymptomatic recent ingestions
– Sodium bicarbonate IV bolus of 1-2mEq/kg with goal pH 7.45-7.55
– Diazepam and epinephrine infusions recommended
– Consider early lipid emulsion therapyk for patients with dysrhythmia or hypotension
|Beta Blockers||Labetalol, metoprolol, propranolol||Inhibition of β1 receptors on heart à bradycardia
Blockage of GNGl à hypoglycemia
|Bradycardia, hypotension, reflex tachycardia, hypoglycemia (prominent in pediatrics)
Propranolol is highly lipid soluble (crosses BBBm) and has Na+ channel blocking effects and may lead to dysrhythmias (Torsade de Pointes)
|– Treat initial hypotension with IVF bolus. If hypotension continues, use glucagonn. If hypotension continues use vasopressors and high dose insulin therapyo, may consider lipid emulsion for refractory cases
– Atropine for bradycardia
– AC for recent, substantial ingestion
– Sodium bicarb for arrythmia
– Benzodiazepines for seizures
|Underlying cardiac or respiratory disease, maximum daily dose ingested, co-ingestion with CCB, deliberate OD = 6 hrs observation + ECG
8 hrs for extended release
- Weight based dextrose dosing includes D25 2-4mL/kg in children 1-24mo, D50 1-2mL/kg in children >24mo
- AC = Activated Charcoal
- Octreotide is a somatostatin analog that directly inhibits the release of insulin.
- With high dose insulin therapy, you must check potassium levels hourly at the initiation of therapy.
- AGMA = Anion gap metabolic acidosis
- CHF = congestive heart failure
- ARDS = Acute respiratory distress syndrome
- Fomepizole dosing: 15 mg/kg loading dose followed by 10 mg/kg q12hr for 48hrs, then 15 mg/kg q12hr until toxic dose ≤20 mg/dL
- Naloxone has been shown to reverse both cardiovascular and respiratory depression in up to 50% of case reports, but does not consistently show effect.
- UOP = urine output
- Lipid emulsion therapy dosing = 5 mL/kg of 20% lipid emulsion over 2 to 3 minutes as an IV bolus, followed by an infusion of 0.25 mL/kg/min
- GNG = gluconeogenesis
- BBB = blood brain barrier
- Glucagon dosing is 5 to 15 mg by slow IV push followed by an infusion rate of 5 to 15 mg/hour. Glucagon may cause nausea and vomiting, so caution should be used in patients without definitive airway.
- High insulin therapy = 1 unit/kilogram of insulin followed by an infusion of 0.1 to 1 units/kilogram/hour, titrated to a systolic blood pressure of greater than 90 to 100 mmHg.
- If you have a child that presents with concern for toxic ingestion, contact the poison control center.
- Identification of children with clinical toxidromes concerning for ingestion requires vigilance on the part of the clinician.
- Careful questioning of the family/caretakers is required to identify potential exposures.
- In pediatric exposures with known time of ingestion and early presentation, activated charcoal may be considered for early decontamination in asymptomatic patients who are protecting their airway.
- Due to their more horizontal ribs and flattened diaphragms, pediatric patients have less airway reserve and are more susceptible to ventilatory failure due to drug exposure.
- Remember the ingestions listed in Table 1!