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Pediatric Single-Dose Fatal Ingestions Clinical Presentation

  • Author: Chip Gresham, MD, FACEM; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Apr 05, 2016
 

History

Risk assessment is a specific and cognitive step taken in the assessment of all patients with possible ingestions. It involves a detailed history around the likely agent, the amount and timing of ingestion, and any current symptoms.

Some patients may present before developing significant symptoms. Other patients may present in an obtunded state and without a clear history of ingestion. Obtain collateral history from patients family, paramedics, doctor or pharmacist.

Elicit the following information:

  • What substance was ingested? If the substance was a medication, obtain the name, dosage strength, and preparation type (immediate verses sustained release).
  • What are the ingredients of the ingested substance? Learning the product name or finding the container helps determine the specific ingredients and concentrations.
  • When was the substance ingested?
  • Did anyone observe the ingestion? If so, ask to speak with the person who saw the incident, because this may help determine the amount and timing of ingestion.
  • Is the patient exhibiting any clinical features of ingestion?
  • What is the patient's medical history?
  • Is the ingestion consistent with the history provided? If the history is inconsistent, the suspicion of abuse or neglect is raised, and the incident must be reported.

Always assume a worst-case scenario. Assume all unaccounted for tablets have been taken. Do not account for spillage. Place the timing of ingestion at latest possible. If two children are involved, presume all the missing tablets were consumed by either child.

Next

Physical

Physical examination findings are variable and depend on the specific agent and amount ingested. Findings may range from normal to  obtundation or even cardiopulmonary arrest. Some examination results may offer subtle but specific clues regarding the type of ingestion. The recommended process is as follows:

  • Begin the examination by evaluating the patient's airway, breathing, and circulation (ABCs). Initiate appropriate interventions for any abnormalities.
  • Perform a complete physical examination, and record all vital signs.
  • Search for evidence of specific toxidromes (sedatives, hypnotics, sympathomimetics, serotonin toxicity, anticholinergic syndrome)
  • Perform a neurologic examination, checking for level of consciousness, pupils, tone, reflexes, ocular clonus, and lower limb clonus.
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Causes

The following medications are of most concern:

  • Calcium channel blockers (especially verapamil, nifedipine, and diltiazem)
  • Sulfonylureas
  • Opioids
  • Amphetamines
  • Sodium channel blockers (chloroquine, tricyclic antidepressants [TCAs], propranolol, dextropropoxyphene)
  • Theophylline

The drugs of abuse that are potentially fatal include all amphetamines (including methamphetamine and MDMA ) and opiates.

Non-pharmaceuticals that pose a risk of significant toxicity include the following:

  • Organophosphate and carbamate insecticides
  • Paraquat
  • Toxic alcohols
  • Hydrocarbons (solvents, eucalyptus oil, kerosene, naphthalene)
  • Camphor

The availability of non-pharmaceuticals in the community is extensive and any potential chemical ingestion requires a detailed review of the individual components. It is beyond the scope of this article to list every potential toxic ingestion. Included in the list below are case reports of fatailities associated with specific ingestions however expert assistance is required and poison centres should be contacted for detailed risk assessment.

Pharmaceuticals

Tricyclic antidepressants: A dose of 10-20 mg/kg can be fatal.[4, 5, 6, 7] Toxicity is characterised is coma, seizures, hypotension, ventricular arryhythmias. Case reports include the following:

  • Desipramine: Two 75-mg tablets may be fatal.
  • A 3-year-old boy on long-term therapy using desipramine 100-mg tablets died within 47 hours postingestion after obtaining twoor three extra tablets either from his own or a 6-year-old sibling's prescription. [8]
  • A 2-year-old boy ingested one desipramine 50-mg tablet and died a few hours postingestion. [9]
  • A 4-year-old boy died after ingesting 90 ml (450 mg) of imipramine syrup [10, 11]
  • A 6-year-old girl on long-term imipramine therapy for attention deficit disorder was found dead in her home after her mother had given the child 15-20 mg to induce sleep. [12]
  • A 9-month-old girl was given half of a 100-mg amitriptyline tablet to induce sleep. She arrived unresponsive at the emergency department (ED) 2-3 hours postingestion and died a few hours after admission. [13]
  • Amoxapine (tetracyclic compound): The minimum fatal dose is 250 mg in children; seizures are a risk. [14, 15]

Monoamine oxidase inhibitors: Fatal ingestions have occurred with 4-mg/kg to 6-mg/kg doses.[16] . Ingestions of  one or two tablets of irreversible non-selective MAOIs maybe associated with toxicity.[17]

The antimalarial drugs chloroquine and hydroxychloroquine: Toxicity is characteristed by rapid onset of hypokalemia, coma, seizures, and cardiorespiratory arrest within 1-3 hours. ECG changes include prolonged PR, QRS, and QT intervals and ventricular dysrhythmias.[18]

With chloroquine, a single 500-mg tablet can be fatal. Case reports include the following:

  • A 24-month-old boy was found with a single tablet in his hand; his respiratory system became compromised, and he required cardiopulmonary resuscitation (CPR) shortly thereafter; lfe support was withdrawn 8 days postingestion. [19]
  • A 12-month-old boy who ingested 1 g was unresponsive 30 minutes postingestion and died within 3 days. [20]
  • Chloroquine phosphate and primaquine (Aralen): A 12-month-old child was pronounced brain dead approximately 24 hours after ingesting a single Aralen tablet and sucking the coating of 12 tablets. [21]
  • Fatal chloroquine poisoning in children has been reported with doses of 1 g and 3.5 g [22]
  • Literature review of 22 unintentional ingestions in children between 1961 and 1990 included 16 deaths (73%) and three patients left in persistent vegetative state; [23] fatalities also associated with iatrogenic exposure

Cardiovascular drugs.

Calcium channel blocker toxicity includes severe cardiovascular collapse, which may be delayed 4-16 hours after ingestion with extended-release preparations. Verapamil and nifedipine are more likely to be associated with symptomatic toxicity. Potential ingestion of an extended-release preparation mandates a prolonged observation period (minimum of 12 hours up to 24 hours).[24]

Verapamil case reports include the following:

  • One or two 240 mg tablets can be fatal
  • Literature review [24] identified five case reports of fatal verapamil ingestion; toxic doses for the sustained release preparation ranged from 12-120mg/kg.
  • A 4-year-old boy who ingested 6-10 sustained-release verapamil tablets and 2-4 cold capsules (acetaminophen, chlorpheniramine, pseudoephedrine, dextromethorphan) went into cardiac arrest approximately 5 hours postingestion and died within 24 hours of admission. [25, 26]
  • A 7-day-old boy inadvertently ingested 25 mg verapamil and died 20 hours postingestion. [27]

Nifedipine case reports include the following:

  • Literature review [24] identified 18 case reports of toxic or fatal nifedipine ingestions in toddlers; of the nine toddlers who died, three ingested only 1-2 pills, four ingested an unknown number, and two ingested more than 10 tablets.
  • A 14-month-old girl who ingested a single 10-mg nifedipine capsule died 3 hours postingestion. [28]
  • An 11-month-old boy ingested four 10-mg nifedipine capsules and died 2 days postingestion. [29]
  • A 14-month-old child ingested a single 10-mg nifedipine capsule and died 4 hours postingestion. [30]

Beta-blockers: A literature review found no documented case of death or serious toxicity related to beta-blocker ingestion in pediatric patients younger than 6 years old.[31] Reported toxicity includes hypoglycemia,[31, 32] second-degree heart block,[32] and QRS widening and ventricular arrhythmias from sodium channel blockade;  it also crosses the blood-brain barrier and may be associated with reduced Glasgow coma scale score and seizure activity.[33]

Clonidine: Ingestion of 0.1 mg/kg may cause bradycardia, hypotension, respiratory depression, and apnea. A retrospective review of American Association of Poison Control Centers National Posion Data System from January 2000 to December 2011 identified seven cardiac arrests and three deaths from clonidine.[34]

Lorcainide: Approximately 50 mg/kg can be fatal.[35]

Quinidine: Two 300-mg tablets can be fatal.

Disopyramide: A 2-year-old child ingested 600 mg and died 12 hours postingestion.[36]

Lidocaine: Ingestion of 1 oz of 2% viscous lidocaine solution was almost fatal in a 20-month-old girl.[37]

Opioids

Opioid analgesic agents may lead to significant CNS and respiratory depression.[38] Methadone is the most toxic opioid; a single dose can lead to fatalities in children. A literature review identified 21 fatalities associated with methadone ingestion (up to 2002) and 64 cases of significant CNS/respiratory depression.[38] Case reports include the following:

  • A 2-year-old boy who ingested approximately 12 mL (10 mg/mL) of his mother's methadone died within 3 days of presentation. [12]
  • A 5-year-old girl given a single 10-mg tablet to stop coughing died 6.5 hours postingestion. [25]
  • A 12-month-old boy who drank 1.5 oz of a bottle containing 35 mg of methadone in 8 oz of formula died approximately 24 hours postingestion. [39]

Codeine may be fatal to a toddler who ingests three 60-mg tablets.[40] Limited data suggests that children who ingested >5 mg/kg of codeine require up to 6 hours of observation in the ED.[38]

Fentanyl patches have caused death in opioid-naive patients who have chewed or sucked on the patches. This has led the FDA to release a statement on the risks to children and advice for safe disposal of patches. The release comments on 12 deaths associated with inadvertent fentanyl patch exposure.[41] Case reports include the following:

  • In a retrospective review of data over 5 years at the Texas Poison Center Network, one death was recorded following the improper administration of a fentanyl patch by a care giver. [42]
  • A 1-year-old child died after ingestion of a transdermal fentayl patch. [43]

Toxicity from other opioids includes the following:

  • Five or six tablets of diphenoxylate at 2.5 mg and atropine at 0.025 mg (Lomotil) may cause coma or respiratory depression. [44]
  • Propxyphene may induce sodium channel blockade with subsequent widening of the QRS, AV blockade, and dysrhyhtmias. [38]
  • A 13-month-old child died after being found with a sublingual buprenorphine/naloxone (8 mg/2 mg) tablet in his mouth. [45]

Hypoglycemic agents

Sulfonylureas. Ingestion of 1 or 2 tablets can lead to profound hypoglycemia and fatalities if not adequately treated.[46] All children with potential sulfonylurea ingestion should be observed in hospital with blood sugar levels taken for a minimum of 8 hours and potentially longer.[47] Symptomatic hypoglycemia may occur late.

Theophylline

Symptoms of theophylline toxicity include vomiting, tremors, agitation and seizures. Metabolic changes include hyperglycemia, hypokalemia, hypophosphatemia, metabolic acidosis, and respiratory alkalosis. In addition, theophylline can cause significant arrhythmias.[48]

Ingestion of one 200-mg modifed-release tablet will lead to toxicity in a 10-kg child. Ingestion of more than one tablet may be life threatening.[49] In one case report, an 8-kg child who ingested three tablets (445 mg) of theophylline presented with delayed seizures and tachycardia of 250 beats/min.[50]

Antipsychotic drugs

Life-threatening toxicity may include the following:

  • Thioridazine: One 200-mg tablet can be fatal.
  • Chlorpromazine: A 1-year-old child went into coma and respiratory arrest after ingesting 200 mg. [51]
  • Clozapine: A 2-year-old girl who weighed 10.5 kg was found chewing a single 100-mg clozapine tablet; she was brought to the ED an hour later after becoming ataxic, and died 16 days later from cardiac arrest secondary to respiratory failure. [52]

Miscellaneous drugs

 Colchicine ingestion is potentially life-threatening. Effects are dose dependent, with doses of 0.5–0.8 mg/kg causing systemic toxicity. Doses >0.8 mg/kg lead to multi-organ failure and mortality approaches 100%. In a series of 23 cases of colchicine ingestion treated at a single pediatric intensive care unit (from November 1985 to March 2011), four patients had taken more than 0.8 mg/kg and three of them died.[53]

Iron ingestion can be life-threatening; 10 adult tablets may be fatal in a child. Children are more likely to consume more than one or two tablets of iron as the tablets are brightly colored, often sugar coated, and often considered harmless by care givers. Public education and changes in packaging has led to the reduction of significant toxicity from iron ingestion. Iron supplements were thought to be the primary cause of death in 16 pediatric patients over an 8-year period.[54]

Pseudoephedrine: A 2-year-old child was found dead after ingesting approximately seven 60-mg tablets.[36]

Topical preparations

Oil of Wintergreen (methyl salicylate): less than 5 mL (ie, 1 tsp) of oil of wintergreen is a potentially fatal dose, as it contains 7 g of salicylate. Case reports of fatal ingestions of oil of wintergreen include a 2-year-old boy who ingested 7.5 mL,[55] a 2-year-old girl who ingested 15 mL,[9] and another 2-year-old girl who ingested 10 mL.[25]

Benzocaine topical gels and liquids are contraindicated in children younger than 2 years due to a risk of methemoglobinemia. Small doses may lead to significant toxicity.

Camphor: Five milliliters (ie, 1 tsp) of 20% camphor oil or more than 50 mg/kg is a potentially lethal dose.[15] A 19-month-old child who ingested 5 mL of camphorated oil died 5 days postingestion.[56] Concentrations of 0.1 to 11% when used on unbroken skin is likely to be safe. Toxicity may be more likely to occur if the oil is used on broken skin or higher concentrations are used.

Dibucaine (Proctosedyl): A 8-month-old girl who ingested approximately half of a 30-g tube (ie, 150 mg, or 15 mg/kg) died 7 hours postingestion.[52] A 17-month-old girl ingested approximately 22.5 g of ointment, developed cardiorespiratory arrest, and died approximately 4 hours postingestion.[27]

Drugs of Abuse

Nicotine. Symptoms include vomiting, tachycardia, agitation and seizures. Toxcity can progress to lethal dysrhythmias and paralysis.[57]

A lethal dose of nicotine is estimated to be 1 mg/kg. Electronic cigarette (e-cigarette) solutions come in 5-20 ml vials with concentrations that vary from 8.5-22.2 mg/ml.[58] Epidemiological studies note an increase in exposures of children to e-cigarettes with 717 exposures in children < 5 years between June 2010 and September 2013.[59] Most patients experienced only minor effects. However, there is a real risk of significant toxic ingestion of nicotine in pediatric patients.

Ingestion of a single whole cigarette can be fatal. An 11-month-old girl was found dead at home. Autopsy revealed five undigested cigarettes and one tablet of diazepam.[12]

Amphetamines produce central and peripheral sympathomimetic effects. A single methamphetamine tablet may produce life-threatening toxicity. As methamphetamine abuse grows in the community, higher numbers of methamphetamine toxicity in pediatric patients occur.[60] In one review, the most common presenting complaint was agitation; two patients developed seizures.[60]

The substance 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) can be life-threatening. Status epilepticus from MDMA was reported in a 13-month-old boy.[61] Two other case reports of seizures and significant sympathomimetic effects have been reported.[62, 63] Para-methoxyamphetamine, which may be sold as MDMA, can significantly increase blood pressure, body temperature, and pulse rate.[64] Ingestion of a single tablet is potentially fatal.

Hallucinogen toxicity includes the following:

Non-pharmaceuticals

Alcohols have been involved in fatal poisonings, at the following doses:

  • Methanol - 15 mL of 40% solution [15]
  • Ethylene glycol - 1-1.5 mL/kg [15]
  • Isopropyl alcohol - 2-4 mL/kg of 70% solution [15]
  • Ethanol -1-2 oz of cologne. Ethanol hand sanitizer. [15]

Chemical agents

Pesticide and herbicide fatalities have included the following:

  • Diquat: Ingestion of 20 mL of a 20% solution was fatal in a 2-year-old child. [65]
  • Paraquat: A dose of 25-50 mg/kg is deadly (7.5-10ml of 20%). [15] The delayed pulmonary effects of paraquat is the most significant cause of its toxicity, with initial pulmonary edema and acute lung injury followed by pulmonary fibrosis. Multi-organ failure and severe gastrointestinal corrosive injury are also associated with toxic ingestion. Most cases involving paraquat ingestion occur when drink containers are filled with left-over solutions. [66, 67]
  • Methylene iodide: A 20-month-old girl who ingested 10-15 mL developed acute hepatic failure within 2 days and died 9 days postingestion. [27]
  • Lindane (chlorinated hydrocarbon), used as a second-line pharmaceutical treatment for lice and scabies: Two teaspoons (ie, 10 mL) or 6 mg/kg can be fatal, primariliy from central nervous system toxicity. [68, 69]

Rodenticides that can cause fatal toxicity include the following:

  • Sodium monofluoroacetate (Compound 1080) and sodium fluoroacetamide (1081) were previously used as a rodenticide and are currently used in herbivore collars to kill coyotes and as poison to kill introduced mammals in Australia and New Zealand; 3-7 mg/kg is a potentially fatal dose, while 13-14 mg/kg of Compound 1080 is a potentially fatal dose. [15]
  • Strychnine: A dose of 5-8 mg/kg is deadly; an accidental taste could potentially be lethal in a toddler. [70, 15]
  • Zinc phosphide: A dose of 10 mg/kg is deadly. [15]

Other chemicals include the following:

  • Aniline is used in dyes and pigments, as herbicides and rubber processing. A 4.5-year-old child developed a potenitally life threatening blood methemoglobin (metHb) level of 77% at 13 hours after ingesting 5 mL of aniline. [71]
  • Hydrogen cyanide: 50 milligrams may be deadly. [70]
  • Acetonitrile is used as a solvent and has been used as false fingernail glue remover (although it has been baned in Europe since 2000). Acetonitrile is metabolised to hydrogen cyanide. There are several case reports of fatalities associated with ingestion of nail glue remover (acetonitrile). Physicians need to carefully distinguish between nail polish remover (acetone) and acetonitrile containing solutions for removal of false nails.
  • Paraldehyde: A single fatality has been reported with a 25-mL dose. [15]
  • Selenious acid (a component of gun bluing with copper sulfate and nitric acid): A single swallow may be fatal. A 22-month-old boy who ingested 15 mL of gun-bluing solution was unresponsive upon arrival at an ED 3 hours after ingestion and died after lengthy unsuccessful CPR. [72] A 30-month-old boy who ingested less than 1 oz of gun-bluing solution was unconscious when the ambulance arrived 10 minutes postingestion, and died less than 90 minutes after arrival at an ED. [25]

Hydrocarbons

  • Aliphatic hydrocarbon: An 18-month-old boy who ingested/aspirated a mouthful of saddle dressing died 20 days postingestion. [27]
  • Eucalyptus oil: Ingestion of 10mls may lead to CNS depression and seizures. [73]
  • Lighter fluid: A 14-month-old boy ingested/aspirated a mouthful of lamp oil and died. [74]
  • Motor oil: A 15-month-old boy who ingested/aspirated one swallow of motor oil died 51 days postingestion. [74]
  • Mineral oil and mineral spirits: A 2-year-old girl ingested/aspirated 15-30 mL of hair weaving remover (ie, 20% mineral oil, 30% mineral spirits) and died 2 days postingestion. [29] A 3-year-old boy who ingested/aspirated "a couple of swallows" of fabric protector containing mineral spirits died 19 days postingestion. [9]
  • Xylene: A dose of 15 mL can be deadly. [36]

Plants and natural toxins

  • Aconite found in Chinese herbal medicines. [75]
  • Amatoxin (ie, mushroom): A dose of 0.1 mg/kg is potentially fatal. [15]
  • Amygdalin is a cyanogenic glycoside (toxicity or death occurs secondary to cyanide ingestion): In separate case reports, 2 of 9 [76] and 1 of 8 [77] intoxicated children died after eating apricot seeds. Cassava and Tapioca also contain cyanogenic compounds and ingestion has been associated with fatal toxicity. [78]
  • Anticholinergic poisoning - Datura, Atropa belladonna, Henbane.
  • Cardiac Glycosides - Lily of the Valley, Foxglove, Oleander
  • Castor beans (ie, ricin): One milligram per kilogram or approximately 8 seeds can be fatal. [15]
  • Nicotinic poisoning - Poison hemlock, Wild Tobacco, Golden Chain.
  • Pennyroyal: A 12-week-old boy with a history of rhinorrhea and mild cough was administered 4 oz of tea made from 3-4 pennyroyal leaves. The child developed fulminant hepatotoxicity and died within 2.5 days postingestion. [8]
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Contributor Information and Disclosures
Author

Chip Gresham, MD, FACEM Emergency Medicine Physician and Medical Toxicologist, Department of Emergency Medicine, Clinical Director of Medication Safety, Middlemore Hospital; Senior Lecturer, Auckland University Medical School, New Zealand

Chip Gresham, MD, FACEM is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Sarah J Buller, MBChB, FACEM Consulting Physician, Department of Emergency Medicine, Auckland City Hospital, New Zealand

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Received salary from Merck for employment.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

William T Zempsky, MD Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

William T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Acknowledgements

Ann G Egland, MD Consulting Staff, Department of Operational and Emergency Medicine, Walter Reed Army Medical Center

Ann G Egland, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Association of Military Surgeons of the US, Medical Society of Virginia, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Cynthia L Morris-Kukoski, PharmD

Clinical Assistant Professor, Department of Pharmacy and Occupational Medicine, Medical College of Virginia

Cynthia L Morris-Kukoski, PharmD is a member of the following medical societies: American Academy of Clinical Toxicology

Disclosure: Nothing to disclose.

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