Pediatric Accidental Ingestions:
Monitoring and Treatment Options

Release Date: March 1, 2010

Expiration Date: March 31, 2012


Lela S. Fung, PharmD, BCPS
Clinical Pharmacy Specialist, Neonatology/Pediatrics,
Via Christi Regional Medical Center
Wichita, Kansas;
Adjunct Clinical Assistant Professor,
University of Kansas School of Pharmacy,
Lawrence, Kansas


Dr. Fung has no actual or potential conflicts of interest in relation to this activity.

U.S. Pharmacist does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors may express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.


acpePostgraduate Healthcare Education, LLC is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
UAN: 0430-0000-10-008-H01-P; 0430-0000-10-008-H01-T
Credits: 2.0 hours (0.20 ceu)
Type of Activity: Knowledge


This accredited activity is targeted to pharmacists and pharmacy technicians. Estimated time to complete this activity is 120 minutes.

Exam processing and other inquiries to:
CE Customer Service: (800) 825-4696 or


Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications or dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities.


To raise awareness of pediatric accidental ingestions and review accompanying monitoring and treatment options.


After completing this activity, participants should be able to:

  1. Discuss the prevalence of reported pediatric accidental ingestions of household chemicals and medications.*
  2. Identify agents that are commonly involved in accidental ingestions.*
  3. Review appropriate monitoring and treatment options for specific agents of pediatric exposures.
  4. Describe published literature and predicted outcomes according to agent(s) involved.

*Also applies to pharmacy technicians.

Accidental ingestions are unfortunate common occurrences in children. Despite efforts to increase awareness and prevention, the rates of unintentional ingestions reported by the American Association of Poison Control Centers (AAPCC) have remained stable since the early 1990s.1 When natural curiosity is combined with unprotected access to medications and household agents, young children are extremely susceptible to toxic ingestions. According to the 2007 annual report of the AAPCC, 61% of the 1 million reported human exposures in children younger than 6 years were unintentional ingestions.2 Fatalities claimed the lives of 13 children in this age group.2 Notably, the overwhelming majority of exposures are not lethal; however, preventable fatalities are tragic. Historically, the top offenders for accidental ingestions in children include household substances, OTC products, and prescription medications.

Household Substances

Cleaning Solutions: Cleaning solutions were the second most frequently ingested substances reported in children 5 years and younger.2 Alkaline materials (e.g., drain cleaners, detergents) seem to be more frequently ingested than acidic solutions (e.g., bleach, toilet bowl cleaners).3 Although many patients (44%) remain asymptomatic, the most frequent symptom following ingestion of caustic substances is vomiting (39%).3 Excessive salivation, hematemesis, and coughing are among other reported symptoms.3 Initial management should include assessment of the airway and administration of supplemental oxygen, if necessary.4 Ingested substances should be diluted with water or milk as soon as possible unless the airway is compromised.4 Attempts to neutralize the substances using weakly acidic or alkaline solutions and to stimulate emesis are not recommended.4

Significant exposures can result in esophageal burns characterized by erythema and ulceration within 24 hours of ingestion.4 In a large analysis of caustic-substances ingestions, alkaline solutions were responsible for about 87% of esophageal burns.3 Dishwasher powders were deemed most dangerous, because 55% of exposed children developed esophageal burns.3 Esophageal strictures, potentially resulting in dysphagia and increased risk of aspiration, are the most worrisome chronic complication following caustic ingestions. Strictures can develop over time and are a result of scar tissue formation.5 Corticosteroids have been studied for the prevention of esophageal strictures, but available evidence supporting their use and benefits is limited. However, their anti-inflammatory properties and potential for attenuation of granulation and fibrous tissue formation are protective mechanisms against stricture formation.5

Pesticides: Over 40,000 cases of pesticide ingestions were reported in children 5 years and younger in 2007.2 Organophosphates, commonly used as pesticides in homes, gardens, and farms, are irreversible cholinesterase inhibitors that cause high synaptic concentrations of acetylcholine, a potent neurotransmitter. The accumulation of acetylcholine leads to overstimulation and disturbances in the autonomic nervous system, neuromuscular junctions, and central nervous system (CNS).6

The most common manifestations demonstrated in a study of children with acute organophosphate poisoning were neurologic and gastrointestinal (GI), with the large majority of patients presenting with multisystem involvement.6 About 70% of patients presented with neurologic symptoms that included coma, seizure, agitation, areflexia, and pinpoint pupils. Over 60% experienced GI symptoms such as salivation or foaming, abdominal pain, vomiting, diarrhea, and pancreatitis. Cardiopulmonary symptoms and complications, including tachycardia, prolonged QTc interval, pneumonia, and respiratory failure, occurred in about 52% of patients.6

Serum cholinesterase levels may be obtained but should not be used in determining acute management. Instead, the severity of clinical manifestations should guide treatment. Abnormal laboratory values may include elevated white blood cells, liver enzymes, l-lactate dehydrogenase, and blood glucose.6,7 These values may be obtained and monitored throughout the patient’s hospitalization, but again, observation of CNS manifestations should be the focus of determining progress.

Airway status and necessity for resuscitation should be evaluated immediately. Endotracheal intubation and mechanical ventilation may be necessary if there are excessive secretions or signs of decreased levels of consciousness or hemodynamic instability.7 Treatment for seizures and decontamination of the GI system by gastric lavage and activated charcoal should be initiated promptly. A summary of antidotes is listed in TABLE 1.

Table 1. Antidotes for Pediatric Toxic Ingestions
Antidote Dose Toxin(s) Comments
1-2 g/kg (up to 50 g) Many orally ingested substances; not for strong acids/bases or simple ions (i.e., iron) Most effective if given
within 1-4 h of ingestion
0.05 mg/kg IV every 5-20 min Minimum: 0.1 mg; max: 2 mg Continuous infusion:
0.02-0.08 mg/kg/h
CCBs, clonidine,
Chloride: 10-20 mg/kg (up to 1 g) IV, every 10-20 min
Continuous infusion: 20-50 mg/kg/h
Gluconate: 30-100 mg/kg (up to 1 g), every 10-20 min
Continuous infusion: 10-30 mg/kg/h
Continuous infusion: 15 mg/kg/h
Max: 6 g/day
Iron Each 100 mg of deferoxamine
chelates about 9 mg elemental iron
0.5-1 g/kg (up to 25 g) IV (repeat as
necessary); use 10% or 25% formulations; may initiate continuous infusion of D10W
In addition to insulin for
CCBs; sulfonylureas
0.025-0.1 mg/kg up to 1 mg IM, IV, SQ CCBs, sulfonylureas
High-dose continuous infusion:
0.1-1.0 U/kg/h
CCBs Use with supplemental dextrose
Ipecac syrup
No longer recommended; should not be used
0.05-0.1 mg/kg IV; may repeat in 10-15 min Diphenhydramine
0.01-0.1 mg/kg up to 2 mg IV/IO/ET every 3-5 min Clonidine
1-2 mcg/kg IV q6-8h Sulfonylureas
0.02 mg/kg/dose up to 2 mg every 10-20 min until symptoms subside or up to a max of 4 mg in 30 min Diphenhydramine
Pralidoxime 20-50 mg/kg/dose IV; may be
repeated every 30 min to 2 h

CCB: calcium channel blocker; D10W: dextrose 10% in water; ET: endotracheal tube; IM: intramuscularly; IO: intraosseously; max: maximum; SQ: subcutaneously. Source: References 4, 7, 8, 9, 13, 16, 24, 25, 26, 28, 30, 31.

Administration of anticholinergic agents is recommended for symptomatic patients.4 Atropine competitively antagonizes acetylcholine at the muscarinic synapses and relieves sweating, salivation, and lacrimation.8 Intermittent and continuous IV doses have been used.4,7-9 When administered intermittently, doses may be given every 5 to 20 minutes until decreased secretions and comfortable respirations have been observed (TABLE 1). Atropine should be continued for at least the first 24 hours.4,7 Pralidoxime (2-PAM) may be used in addition to atropine in cases of persistent muscle weakness with high atropine requirements.8 This antidote reactivates acetylcholinesterase at the nicotinic synapses, which is phosphorylated and inactivated by ingested organophosphates. Upon adequate atropinization, 2-PAM may be initiated with repeated doses every 30 minutes to 2 hours if muscle weakness persists, and additional doses at 8- to 12-hour intervals may be administered if cholinergic symptoms recur (TABLE 1).4,8,9

Obtaining an adequate exposure history, early diagnosis, and treatment are the keys to full clinical recovery. In a study conducted in adults and children, mechanical ventilation was required in 21.2% of patients, and 50% of those patients died.7 The overall mortality rate of ingestions was 27.6%. Complications reported in this study included respiratory failure, aspiration pneumonia, urinary tract infection, convulsion, and septic shock.7 The average length of stay observed in children was 2.8 days.6

OTC Products

Cough and Cold Products: Over 65,000 cases of children 5 years old and younger ingesting cough and cold preparations were reported to U.S. poison control centers in 2007.2 Due to safety concerns and lack of efficacy data in pediatric patients, the FDA has recommended that the use of OTC cough and cold products be prohibited in children younger than 6 years.10 Manufacturers of these products have also voluntarily removed preparations formulated for infants from the market. However, these initiatives do not prevent accidental ingestions of inappropriately stored products. Managing ingestion cases can be difficult since many of these products are combinations of agents that can lead to a variety of symptoms and complications.

Dextromethorphan is a cough suppressant that is sold as a single agent as well as in combination formulations. LoVecchio et al reviewed 304 cases of accidental dextromethorphan ingestions that yielded relatively benign outcomes.11 The mean age for patients included in the study was 28 months, and the average dose of dextromethorphan was 35 mg.11 (A typical dose for a patient at this age, at formerly FDA-recommended dosages, would be 2.5 to 7.5 mg.9,11) Hemodynamic instabilities were not observed in any of the patients, and about 20% presented with signs of sedation. No other neurologic symptoms were observed, and no deaths were recorded.11

Accidental ingestions of dextromethorphan in pediatric patients generally do not require treatment beyond supportive care.11 In cases of abuse or intentional overdoses, tachycardia, hypertension, agitation, disorientation, and somnolence can be seen. These clinical effects are likely due to dextromethorphan’s N-methyl-d-aspartate (NMDA) receptor antagonistic properties. Although dextromethorphan is an analogue of codeine, the drug possesses weak activity at the opioid receptors and has not demonstrated respiratorydepressing effects in cases of overdoses.11 Patients presenting after a dextromethorphan ingestion should be hemodynamically monitored and assessed for treatment and monitoring requirements in response to potential coingestants.

Diphenhydramine is an antihistamine available in many nonprescription formulations. Fatal outcomes in accidental ingestions are rare but have been described in case reports.12 Even though the AAPCC recommends seeking treatment at a medical facility for ingestions of 7.5 mg/kg or greater, a relationship between dose and symptom severity has not been demonstrated in studies.13 Serum diphenhydramine levels >0.5 mg/dL are considered lethal.12 Clinical presentation of toxic ingestions can vary and may include drowsiness, lethargy, ataxia, coma, tremors, seizures, and cardiovascular changes (i.e., hypertension, tachycardia, ventricular arrhythmias, prolonged QTc interval, left bundle branch block, cardiac arrest). Children are more susceptible to the anticholinergic effects of diphenhydramine and may be more likely to present with symptoms of CNS excitation.12

As with any ingestion, maintaining a patent airway and stable vital signs are priorities after toxic ingestions. Since diphenhydramine is absorbed relatively quickly (within 1-4 hours), proper GI decontamination should be initiated promptly. Benzodiazepines and other anticonvulsants should be utilized in patients presenting with seizures (TABLE 1).4,12 Physostigmine can be used in patients who present with hemodynamic instability, extreme agitation, and other life-threatening symptoms. Physostigmine is a cholinesterase inhibitor that crosses the blood–brain barrier and can be effective in treating anticholinergic symptoms (TABLE 1).4,12 Vital signs and symptoms should be closely monitored. The clinical value of serum diphenhydramine levels is questionable; therefore, treatment should be determined based on ingested dose and clinical presentation. The toxic effects of diphenhydramine are acute but rarely fatal. Long-term adverse effects have not been demonstrated in pediatric cases.4,12,13

Pseudoephedrine is a decongestant found in many nonprescription cough and cold medications. Pseudoephedrine is a sympathomimetic agent that is responsible for producing nervous system excitation. The stimulation of alpha- and beta-adrenergic receptors can result in effects on the central nervous, cardiovascular, and GI systems. Alpha-adrenergic receptor stimulation results in vasoconstriction and CNS excitation. Vasodilation, bronchodilation, increased cardiac inotropy, and gluconeogenesis can be seen with beta-adrenergic receptor stimulation. Children seem to be more sensitive to the sympathomimetic effects of pseudoephedrine than adults.14

Upon cardiopulmonary stabilization, gastric decontamination should be performed within 1 to 4 hours of ingestion. Gastric lavage generally should be performed between 1 and 2 hours of exposure. The recommendation for lavage in sympathomimetic ingestion cases is 1 hour.4,14 IV benzodiazepines can be administered for sedation in extreme hyperactivity and agitation or for the treatment of seizures. Beta-blockers may be required for treatment of tachycardia, dysrhythmias, and hypertension. A combined alpha- and beta-blocker, such as labetalol, may be preferred in order to prevent worsening hypertension caused by inhibiting beta2-mediated vasodilation and exposing the alpha-mediated vasoconstriction caused by the sympathomimetic.14 By promptly addressing the sympathomimetic manifestations of pseudoephedrine and other nonprescription nasal decongestants, children generally recover from acute ingestions without permanent sequelae.14

Iron: Although many nonprescription products are only associated with minor adverse events in ingestion cases, iron supplements can lead to significant clinical manifestations. Iron overdoses have been considered a leading cause of injury and death related to poisoning in young children.15 Toxicities can involve the GI, hepatic, cardiovascular, and central nervous systems.15 Recognition of the clinical stages of acute poisoning can aid in anticipating treatment and predicting outcomes. However, patients may present asymptomatically despite large doses of ingested iron or, conversely, go directly into shock without ever exhibiting GI symptoms.15 GI symptoms tend to appear first, within 3 hours of ingestion, and include vomiting, hematemesis, diarrhea, and abdominal pain. The symptoms can be a result of corrosive damages caused by large doses of iron.16 Increased iron absorption can lead to an increase in unbound concentrations that may produce excessive reactive oxygen species. These free radicals can damage proteins and cause cellular dysfunction in various organ systems.16

The GI symptoms can subside, and the patient may seem stabilized for up to 12 hours after ingestion. This may be due to unbound iron redistributing from intravascular space into the intracellular compartment.15 (Twelve to 48 hours after ingestion is the stage of mitochondrial toxicity.) The patient may experience shock, acidosis, coma, seizures, hyperglycemia, hypoglycemia, pulmonary hemorrhage, acute respiratory distress syndrome, coagulopathy, or acute tubular necrosis. Jaundice and encephalopathy related to hepatic necrosis can also occur at this stage. In severe cases, gastric scarring and gastric/pyloric strictures may develop 2 to 6 weeks after acute intoxication.15

The ingested dose of iron, serum iron levels, and total iron-binding capacity (TIBC) can help predict the level of toxicity. Since laboratory values are not immediately available and can be unreliable, symptoms should drive therapeutic decisions. Serum iron levels usually peak between 4 and 6 hours of ingestion. Doses of <20 mg/kg elemental iron and levels <350 mcg/dL with a TIBC greater than the serum iron concentration are associated with low toxicity.4,15 The presence of GI symptoms, leukocytosis, and hyperglycemia are predictive of serum levels >300 mcg/dL.4 Theoretically, free iron is absent when TIBC is greater than the serum iron level, indicating a low risk for toxicity. However, TIBC measurements are inaccurate in cases of iron overload, and studies have demonstrated toxicities even with high TIBC levels.15 Patients ingesting >60 mg/kg of elemental iron with levels >500 mcg/dL are at risk for severe toxicity.4,15

Initial management of the symptomatic patient should be resuscitation by supplemental oxygen, inotropic agents, transfusions, or fluid boluses. Once the patient is hemodynamically stable, gastric lavage should be performed. Whole bowel irrigation is an option if an abdominal x-ray confirms undissolved tablets throughout the GI tract.4,15 Activated charcoal is ineffective in binding iron and is thus not routinely recommended for iron-only toxic ingestions.15

Patients with resolving symptoms and low serum iron levels generally do not require additional treatment after gastric lavage or whole bowel irrigation.4 Those who have high serum iron levels, metabolic acidosis, or severe GI bleeding, are in shock, or are comatose should be given iron chelation therapy. Deferoxamine binds chelates to ferric ions and forms ferrioxamine for removal by the kidneys. Deferoxamine should be given as a continuous infusion and continued until the patient is clinically stable, serum iron is <100 mcg/dL, or urine is no longer rose colored. (Rosecolored urine indicates the presence of the deferoxamine-iron complex). Each 100 mg of deferoxamine can chelate approximately 9 mg of elemental iron (TABLE 1).4,15 Adverse effects of deferoxamine are associated with rapid IV infusions and include hypotension, facial flushing, rash, urticaria, tachycardia, and shock.4,17

Most patients respond well to appropriate therapy for iron intoxication.15,16 A retrospective, descriptive study discussed 21 children presenting to the emergency department after accidental iron poisoning. Thirteen of those patients ingested more than 60 mg/kg of elemental iron. Two out of three asymptomatic patients ingested 100 mg/kg or more of elemental iron. Nine patients experienced shock and/or impaired consciousness and two children had acute liver failure. The hospital course of four patients who died during the study was complicated by shock, coma, acute liver failure, blood glucose abnormalities, leukocytosis, and severe acidosis. None of the remaining children developed any long-term complications based on a follow-up period of 6 months to 3 years.16

Prescription Medications

Although oral prescription medications are required by law to be dispensed in child-resistant packaging, patients have the option to request easy-open lids. Thus, tens of thousands of prescription-medication accidental ingestions are still reported every year.2,18 Medications are often transferred to non-child-resistant containers, such as multiple-day medication organizers or plastic bags. Even a large number of those that remain in appropriate containers are accessed by determined children.1 An all-inclusive review of toxic ingestions of prescription medications cannot be completed within the scope of this article; therefore, a selection of the most common and the most toxic will be discussed.

Antihypertensives: Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are widely used for the treatment of hypertension. ACE inhibitors (e.g., captopril, enalapril) are often prescribed for pediatric patients with congenital heart defects, but ARBs have not been widely studied for use in children. Out of nine reported cases of ACE inhibitor ingestions reviewed by Balit et al, only one child exhibited clinical effects.19 A 2.5-year-old girl experienced transient hypotension (65/40 mmHg) approximately 4 hours after ingesting 28 mg of perindopril (not available in the U.S.). No treatment was given, and her blood pressure returned to normal within 20 minutes.19 Ten cases of ARB ingestions were reported, with one patient experiencing unsteadiness within an hour of ingesting 150 mg of irbesartan. Blood pressure upon presentation to the hospital was slightly low, but the child returned to baseline 3 hours postingestion.19 Based on limited studies, observation of an ACE inhibitor or ARB ingestion patient can reasonably be done at home if doses do not exceed 4 mg/kg or 100 mg of captopril, 1 mg/kg or 30 mg of enalapril, or 1 mg/kg of lisinopril.20,21

Beta-adrenergic antagonists are antihypertensives that can also be used for various health conditions including migraines, dysrhythmias, and thyrotoxicosis. In 2004, the AAPCC reported 4,077 beta-blocker ingestions in children younger than 6 years.22 Love et al observed ingestions over a 6-year time period and found 208 cases of betablocker exposures.22 Only nine of those cases exhibited signs or symptoms related to the ingestion. A correlation between ingested dose and symptoms could not be determined. These nine patients experienced altered mental status or behavioral changes. Records indicate hypotension, lethargy, ataxia, disorientation, blankly staring, and not acting like themselves. A total of 72% of patients were given activated charcoal. Symptoms spontaneously resolved and were not treated. Bradycardia and hypoglycemia were not observed in these patients. The only significant morbidity observed in this study was aspiration of charcoal.22 This study, among others, contributes to literature that reveals minimal toxicity in betablocker ingestion cases.

ACE inhibitors, ARBs, and beta-blockers have demonstrated minimal toxicity in accidental ingestions. However, not all antihypertensives can be deemed harmless. Calcium channel blockers (CCBs) rank among the top 10 causes of toxin-related deaths in children younger than 6 years.23 Toxicities of CCBs are typically exaggerations of therapeutic effects. Conduction system delays, loss of myocardial contractility, and loss of systemic vascular smooth muscle tone can be seen in toxic ingestions. Clinical presentation of toxicity can vary depending on the class of CCBs.23

Patients who have ingested diltiazem or verapamil tend to present with bradycardia, heart block, atrioventricular (AV) conduction disturbances, and myocardial dysfunction. These agents have more negative inotropic and chronotropic effects than other CCBs. Commonly reported symptoms in verapamil and diltiazem ingestions include mental status changes, vomiting, hypotension, and bradycardia. Symptoms can be seen even after ingestion of one verapamil tablet.23 Toxic doses in the sustained-release formulation of verapamil range from 12 to 120 mg/kg. The mean pediatric toxic dose for diltiazem has been determined as 5.7 mg/kg.23

Dihydropyridines, such as nifedipine and amlodipine, have more effects on vascular smooth muscle tone and, in contrast to the other CCBs, have little effect on cardiac conduction. In overdoses, tachycardia may be the first clinical effect produced in response to decreased systemic vascular resistance. A review of nifedipine ingestions revealed nine deaths.23 Three of these reported deaths occurred after ingestion of just one or two tablets. With standard-release formulations, symptoms occurred within 1 to 2 hours. Onset of symptoms was more variable in sustained-release formulations. Changes in mental status, bradycardia, and tachycardia were noted in ingestion cases, with hypotension being the most common adverse event. Other dihydropyridine ingestions have not been described as frequently as nifedipine. The most common symptoms of toxicity from a small number of reported amlodipine ingestions were lethargy and hypotension.23

Administration of activated charcoal should be considered within 2 hours of toxic ingestions. When given within this time frame, CCB absorption decreased by 85% to 99%.23 To treat hypotension associated with CCB intoxication, IV fluids and vasopressors may be given. IV calcium administration can provide competitive channel receptor activity. Atropine should be used for CCB-induced bradycardia. High-dose insulin with supplemental glucose improves cellular metabolism and exerts positive inotropic effects to reverse myocardial depression (TABLE 1).23,24 Adjunctive therapy with glucagon has demonstrated variable results in providing inotropic and chronotropic support, but has been used successfully in patients with hypotension refractory to fluids, atropine, calcium, and dopamine.23-25

Clonidine is a central alpha2-adrenergic agonist that is used for the treatment of hypertension and also of psychiatric conditions. With a therapeutic role in the management of attention-deficit/hyperactivity disorder, this medication has become widely available to children and thus prone to accidental ingestions. In 2003, 5,400 clonidine exposures were reported, with 32% of those being in children less than 6 years of age.24 Onset of symptoms occurred within 30 to 90 minutes in most cases, with a mean time of 1.7 hours for maximum CNS depression.25,26 Drowsiness and lethargy were noted in 72% of patients, bradycardia in 12%, hypotension in 9%, and respiratory depression requiring mechanical ventilation in 7%. Six percent of patients were comatose. The more serious effects were reported more frequently in the younger children.26

Clonidine ingestions of doses >5 mcg/kg for children 4 years and younger require direct medical evaluation. Medical attention is also recommended for children 5 to 8 years of age with ingested doses of >0.2 mg and of >0.4 mg for children older than 8 years.26 Management of clonidine ingestions begins with ensuring or establishing an adequate airway. Activated charcoal should be given within 1 hour of ingestion. Continuous cardiac monitoring and electrocardiograms should be used to rule out bradycardia, heart block, and hypotension. Since clonidine toxicity presents similarly to opioid intoxication, naloxone has been used for the treatment of severe clonidine overdose (TABLE 1). The mechanism of reversal is likely due to the close proximity within the neuron of the alpha-adrenergic receptor targeted by clonidine and the mu opioid receptors, as well as the functional overlap of the receptors.25 Bradycardia will generally respond to atropine. Hypotension can be managed with fluid resuscitation and vasopressors, if necessary.25 Death from clonidine overdose is rare, and most patients recover without permanent sequelae; but toxic effects can be seen in doses as low as 10 mcg/kg.24-26

Sulfonylureas: Sulfonylurea agents, such as chlorpropamide, glipizide, glyburide, and glimepiride, are commonly used for the management of type 2 diabetes. In 2003, over 4,000 sulfonylurea exposures were reported to poison control centers, and one-third of those ingestions involved children less than 6 years of age.24 Up to 72% of cases of unintentional sulfonylurea cases present asymptomatically.27 However, case reports have described neurologic symptoms or death resulting from just one or two tablets.28 Spiller et al prospectively evaluated 185 cases of accidental sulfonylurea ingestions.29 Thirty percent of patients presented with blood glucose (BG) concentration <60 mg/dL, and 3% of cases presented with BG levels <40 mg/dL. The mean time after ingestion to minimum BG level was 5.3 hours, and the onset of hypoglycemia was typically observed within 8 hours of ingestion.28,29

These hypoglycemic agents stimulate insulin secretion from the pancreas, inhibit gluconeogenesis, and also increase insulin sensitivity.9,29 Symptoms of sulfonylurea ingestions can present with hypoglycemia, loss of appetite, weakness, dizziness, lethargy, seizure, and coma.24,28 General principles of resuscitation and vital-sign stabilization should be applied immediately following discovery of ingestion. Activated charcoal may be useful if given within 1 hour of exposure. Blood glucose concentrations should be monitored every 1 to 2 hours until stabilized >60 mg/dL. Observation of patients for at least 24 hours is a reasonable expectation considering that discovery of hypoglycemia has been delayed for as long as 21 hours in ingestions of extended-release formulations.29,30 Patients with ingestions of ≥0.3 mg/kg of glyburide or glipizide appear to be at higher risk of hypoglycemia.29 However, these dosing parameters should not be used as guidelines for determining monitoring or treatment. Symptomatic patients with hypoglycemia should be treated with dextrose boluses. Continuous infusions of dextrose may also be considered to maintain euglycemia; however, breakthrough hypoglycemic episodes can occur. In cases where IV access is unattainable, glucagon can be given but is not always recommended because of the risk of rebound hypoglycemia.24,28,30

Octreotide has been used as adjunctive treatment of hypoglycemia from sulfonylurea ingestions. This synthetic peptide analogue of somatostatin is a potent inhibitor of insulin secretion. Doses of 1 mcg/kg up to 50 mcg given subcutaneously every 6 to 8 hours have been recommended (TABLE 1).9,24,30 Doses may be titrated up if hypoglycemia persists or worsens.30 Use of adjunctive octreotide has demonstrated decreased hypoglycemic events and decreased dextrose requirements.25,28 Diazoxide is an antihypertensive agent that also decreases beta–islet cell insulin secretion and can be used to treat hypoglycemia.25,28,30 The injectable formulation is no longer available in the U.S., and dosing of the oral formulation is not defined for the treatment of sulfonylurea-induced hypoglycemia. The unavailability of the IV formulation and the potentially harmful side effects of tachycardia, hypotension, and sodium retention make diazoxide a less-favored antidote.25,30

Treatment of Ingestions at Home

Parents were once urged to keep a single bottle of ipecac syrup in case of accidental ingestions. However, stimulation of emesis by administration of ipecac syrup for ingestions of any substance is no longer recommended by the American Academy of Pediatrics (AAP).31 Even when ipecac is administered immediately, the ingested substance is not completely expelled from the stomach. The side effects from ipecac syrup can also delay appropriate diagnosis and treatment. For example, lethargy caused by ipecac can cloud the clinical presentation, potentially making the diagnosis more difficult to obtain. Prolonged vomiting can also delay administration or decrease effectiveness of antidotes.31 The AAP stresses the importance of prevention and reminds parents to contact a poison control center (AAPCC hotline: 1-800-222-1222) in the event of an ingestion.


Generally, unintentional ingestions in pediatric patients result in mild or no symptoms. However, there are certain substances that can lead to permanent damage or even death if the ingestion and/or the symptoms resulting from ingestion are not recognized and treated in a timely manner. Even though most ingestions do not result in permanent physical harm to the patient, placing calls to poison control centers or taking a child to the hospital causes significant emotional trauma for both child and parent. Child-resistant containers are not always adequate barriers to potentially dangerous substances. Ensuring the storage of medications out of the reach of children and direct supervision of curious children are the most effective ways to prevent toxic ingestions.


  1. McFee RB, Caraccio TR. “Hang up your pocketbook”—an easy intervention for the granny syndrome: grandparents as a risk factor in unintentional pediatric exposures to pharmaceuticals. J Am Osteopath Assoc. 2006;106:405-411.
  2. Bronstein AC, Spyker DA, Cantilena LR Jr, et al. 2007 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 25th annual report. Clin Toxicol. 2008;46:927-1057.
  3. Casasnovas AB, Martinez EE, Cives RV, et al. A retrospective analy sis of ingestion of caustic substances by children. Ten-year statistics in Galicia. Eur J Pediatr. 1997;156:410-414.
  4. Barkin RM, Rosen P. Emergency Pediatrics: A Guide to Ambulatory Care. 6th ed. Philadelphia, PA: CV Mosby Company; 2003.
  5. Fulton JA, Hoffman RS. Steroids in second-degree caustic burns of the esophagus: a systematic pooled analysis of fifty years of human data: 1956-2006. Clin Toxicol. 2007;45:402-408.
  6. Levy-Khademi F, Tenenbaum AN, Wexler ID, Amitai Y. Unintentional organophosphate intoxication in children. Pediatr Emerg Care. 2007;23:716-718.
  7. Sungur M, Guven M. Intensive care management of organophosphate insecticide poisoning. Crit Care. 2001;5:211-215.
  8. White ML, Liebelt EL. Updates on antidotes for pediatric poisoning. Pediatr Emerg Care. 2006;22:740-749.
  9. Taketomo CK, Hodding JH, Kraus DM, eds. Pediatric Dosage Handbook. 15th ed. Hudson, OH: Lexi-Comp; 2008.
  10. Dart RC, Paul IM, Bond GR, et al. Pediatric fatalities associated with over the counter (nonprescription) cough and cold medications. Ann Emerg Med. 2009;53:411-417.
  11. LoVecchio F, Pizon A, Riley B, et al. Accidental dextromethorphan ingestions in children less than 5 years old. J Med Toxicol. 2008;4:251-253.
  12. Goetz CM, Lopez G, Dean BS, Krenzelok EP. Accidental child hood death from diphenhydramine overdosage. Am J Emerg Med. 1990;8:321-322.
  13. Stojanovski SD, Baker SD, Casavant MJ, et al. Implications of diphenhydramine single-dose unintended ingestions in young children. Pediatr Emerg Care. 2007;23:465-468.
  14. Sauder KL, Brady WJ, Hennes H. Visual hallucinations in a toddler: accidental ingestion of a sympathomimetic over-the-counter nasal decongestant. Am J Emerg Med. 1997;15:521-526.
  15. Singhi S, Baranwal AK, Jayashree M. Acute iron poisoning: clinical picture, intensive care needs and outcome. Indian Pediatr. 2003;40:1177-1182.
  16. Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr. 2003;40:534-540.
  17. Morris CC. Pediatric iron poisonings in the United States. South Med J. 2000;93:352-358.
  18. Jacobson BJ, Rock AR, Cohn MS, Litovitz T. Accidental ingestions of oral prescription drugs: a multicenter survey. Am J Public Health. 1989;79:853-856.
  19. Balit CR, Gilmore SP, Isbister GK. Unintentional paediatric ingestions of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists. J Paediatr Child Health. 2007;43:686-688.
  20. Hogue-Murray K, Horowitz R, Dart R. Outcome of ACE inhib itor ingestion in children under the age of six years. J Toxicol Clin Toxicol. 1995;33:509-510.
  21. Spiller HA, Udicious TM, Muir S. Angiotensin converting enzyme inhibitor ingestion in children. J Toxicol Clin Toxicol. 1989;27:345-353.
  22. Love JN, Howell JM, Klein-Schwartz W, Litovitz TL. Lack of toxicity from pediatric beta-blocker exposures. Hum Exp Toxicol.2006;25:341-346.
  23. Ranniger C, Roche C. Are one or two dangerous? Calcium channel blocker exposure in toddlers. J Emerg Med. 2007;33:145-154.
  24. Henry K, Harris CR. Deadly ingestions. Pediatr Clin N Am. 2006;53:293-315.
  25. Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: nine common agents that kill at low doses. Emerg Med Clin N Am. 2004;22:1019-1050.
  26. Spiller HA, Klein-Schwartz W, Colvin JM, et al. Toxic clonidine ingestion in children. J Pediatr. 2005;146:263-266.
  27. Quadrani DA, Spiller HA, Widder P. Five year retrospective evalu ation of sulfonylurea ingestion in children. J Toxicol Clin Toxicol. 1996;34:267-271.
  28. Little GL, Boniface KS. Are one or two dangerous? Sulfonylurea exposure in toddlers. J Emerg Med. 2005;28:305-310.
  29. Spiller HA, Villalobos D, Krenzelok EP, et al. Prospective multi center study of sulfonylurea ingestion in children. J Pediatr.1997;131:141-146.
  30. Calello DP, Kelly A, Osterhoudt KC. Case files of the Medical Toxicology Fellowship Training Program at Children’s Hospital of Phil adelphia: a pediatric exploratory sulfonylurea ingestion. J Med Toxicol. 2006;2:19-24.
  31. American Academy of Pediatrics Committee on Injury, Violence, and Poison Prevention. Policy statement: poison treatment in the home. Pediatrics. 2003;112:1182-1185.

Back to Top

  Take Test  |  View Questions