Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 112. General Approach to the Poisoned Pediatric Patient

Timothy J.  Meehan

Timothy B.  Erickson


• The cardinal principle of the management of the poisoned patient is meticulous supportive care.

• Gastrointestinal decontamination plays a limited role in the management of poisoned patients and is indicated in only a few of them.

• Ipecac induced emesis, gastric lavage and cathartics should not be considered.

• Activated charcoal or whole bowel irrigation (WBI) are potential intervention in a limited number of patients.

• Antidotes are available for a limited number of poisonings.


Over the past several decades, fatalities associated with pediatric poisoning have fallen steadily, from 450 deaths in 1960 to just 42 in 2011.1 Interventions such as child-resistant packages, poison-education programs designed to increase household awareness of potential toxins, and improved intervention at both the poison center and hospital levels have all contributed to this decrease in pediatric mortality to just 1.5% of all poisoning deaths.1

However, pediatric exposures account for nearly two-thirds of all poisonings reported to the nation’s poison control centers, as noted by the most recent annual report from the American Association of Poison Control Centers.1Furthermore, this report also shows that 80% of all pediatric exposures occurred in patients 5 years of age or younger. Fortunately, most ingestions in this age group tend to be unintentional ingestions of small doses and thus result in minimal toxicity. However, most adolescent and adult poison exposures are purposeful involving larger doses and thus resulting in greater morbidity and mortality. These intentional exposures include suicide gestures, recreational substance use and Munchausen syndrome by proxy.2


It is often difficult to obtain an accurate history. In children who are either too young to provide specific details, or who have an altered level of consciousness from their ingestion, alternative sources of information should be considered. Essential historical points include: the specific identification of the substance, when it was ingested, the amount ingested, and what other medications or poisons are available in the home. If possible, sending a family member back to the home to collect pill bottles, including over-the-counter and herbal supplements/vitamins, can be very informative. Overall, it is prudent to assume the worst-case scenario until proven otherwise.24

The physical examination may provide valuable information regarding the ingestion or exposure. Specific focus upon vital signs and level of consciousness is paramount in assessing the degree of toxicity. Many drugs and toxic agents have specific effects on the heart rate, respiratory rate, blood pressure, and temperature; as such, vital sign monitoring is of the utmost importance (Table 112-1). The level of consciousness, pupil size, and the presence of coma or seizures may provide clues regarding the identity of the ingested poison (Tables 112-2 and 112-3). Other diagnostic clues may be obtained from examination of the skin (Table 112-4) and breath odor (Table 112-5). Several groups of poisons present with typical patterns of signs. Recognizing these toxic syndromes (toxidromes) may expedite diagnosis and management5,6 (Tables 112-1 to 112-6).

TABLE 112-1

Diagnosing Toxicity from Vital Signs


TABLE 112-2

Agents that Affect Pupil Size


TABLE 112-3

Agents that Cause Coma or Seizures


TABLE 112-4

Agents that Cause Skin Signs


TABLE 112-5

Odors that Suggest the Diagnosis


TABLE 112-6

Common Toxidromes



Laboratory studies are guided by the specific drug or poison. These include determination of organ damage; for example, a hepatic chemistry panel for acetaminophen ingestion or a renal chemistry panel for ethylene glycol ingestion and the measurement of the concentration of the poison in the blood. The latter is helpful for only a few poisons with the criterion being that there is a specific intervention for the poisoning that is guided by its concentration in the blood (Table 112-7). It may be beneficial to obtain an extra tube of blood in the event that it is later determined that additional testing might be helpful. In patients presenting with significant symptoms and signs (abnormal vital signs, coma, seizures) of unknown etiology with poisoning in the differential diagnosis more extensive laboratory studies including electrolytes, BUN, creatinine, blood sugar, hepatic chemistry panel, and a blood gas should be considered.

TABLE 112-7

Poisonings Requiring Blood Level Determination and their Specific


If a metabolic acidosis is found, calculating the anion gap can further refine the possible etiologies.

The calculation is: [Na] - ([HCO3] + [Cl]). A “normal” gap is typically considered to be approximately 12 mEq/L; however, one should always use the reference ranges provided by their clinical laboratory.

A metabolic acidosis with an anion gap results from the presence of unmeasured serum anions, and suggests several specific toxins and disease states as noted in Table 112-8.

TABLE 112-8

Agents Causing Metabolic Acidosis/Elevated Anion Gap


When ingestion of a toxic alcohol – such as methanol, ethylene glycol, or isopropanol – is suspected, calculating the osmol gap may be beneficial. The gap is the difference between the actual serum osmolality – measured by freezing-point depression – and the calculated serum osmolarity as follows.

Calculated Osmolarity: 2*[Na] + [glucose]/18 + [BUN]/2.8 Osmol Gap: measured osmols – calculated osmols = <10 (normal). Agents that increase the osmol gap include ethanol, methanol, ethylene glycol isopropyl alcohol, mannitol, and acetone.

Toxicology “screens” of blood or urine ordered on an emergent basis rarely contribute to the management of the patient in the emergency department.7 False negatives (failure of the test to detect the poison) and false positives (a poison is present but is not causing the patients signs and symptoms) are frequent.

An abdominal x-ray is important for the assessment and management of iron poisoning.8 While other ingestants (chloral hydrate, sustained release drugs, illicit drug packets) may be detected on an abdominal radiograph it has limited specificity and sensitivity.

The use of ultrasound to identify pills still in the stomach has also been described but found to be not appropriate for the diagnosis and management of acute poisoning patients.9


The cornerstone of management of patients with a suspected overdose is supportive care, with particular attention to the airway, breathing, and circulation. Resuscitative measures are instituted prior to antidotal therapy or gastric decontamination.

In children with an altered level of consciousness or in whom a bedside blood sugar test finds hypoglycemia, the physician should administer intravenous dextrose at 0.5 to 1.0 g/kg, given as 2 to 4 mL/kg of D25 W in children or 50 mL (1 ampule) of D50 W in the adolescent. If intravenous access is difficult or unobtainable, glucagon, 1 mg, is administered intramuscularly.

Naloxone should be considered in patients with lethargy or coma particularly if they have bradypnea and mitotic pupils. Naloxone has negligible side effects, however agitation and signs of withdrawal may develop in opioid-dependent adolescents or in neonates whose mothers are opiate addicts or on methadone during pregnancy. The initial dose is 0.1 mg/kg intravenously or 2 mg for children weighing >20 kg. Often, additional doses of naloxone are required for certain opioids, such as fentanyl, codeine, methadone, and propoxyphene, which have high potency and a prolonged half-life.10 If an intravenous line cannot be established, naloxone may be administered via nebulizer or other nonvascular routes such as the endotracheal tube, intramuscularly, intranasally, or subcutaneously.11


Historically, considerable attention was given to gastrointestinal decontamination in the management of the overdose patient. The focus shifted away from this approach in the 1990s with virtual abandonment the following decade. Ipecac-induced emesis, gastric lavage, and cathartics are no longer considered in the management of these patients.1214 Activated charcoal and whole bowel irrigation (WBI) remain as considerations for a minority of overdose patients.15,16


Activated charcoal is a carbonaceous substance that has been heated and steamed under high pressure to create a large surface area/volume ratio — 1 g has a surface area of approximately 1000 m.2 It is an odorless and tasteless black powder that adsorbs various toxins. Although evidence supports decreased absorption of many medications, there are no outcome studies that show benefit in poisoned patients.15The administration of activated charcoal may be considered if the patient has ingested a potentially toxic amount of a poison which is known to be adsorbed by charcoal up to 1 hour previously.15 As it is a black, grainy liquid, many children will refuse to drink it and administration through a nasogastric tube is often necessary. Mixing it with “child friendly” drinks such as juice, soda, or chocolate milk to improve its palatability is of doubtful effectiveness and the solutes in these beverages occupy the charcoal binding sites thus decreasing the effectiveness of the charcoal.

Charcoal has no agonistic properties. Thus more is better and the dose is limited by the volume that the patient can retain. Consider 25 g in children younger than 6 years and 50 g in adolescents and adults. Complications to charcoal use have been reported, and include nausea/vomiting, constipation, obstruction, and aspiration; but are typically low in the pediatric population.15

There are substances that activated charcoal will not adsorb, and these include pesticides, acids, alkalis, alcohols, metals (iron, lead, lithium, borates), and solvents.15


Originally used as a preoperative bowel preparation, WBI is now used in the overdose setting to “flush” the toxin through the gastrointestinal tract and prevent further absorption.16 In theory, it may also produce a concentration gradient that allows previously absorbed toxins to diffuse back into the gastrointestinal tract.16 The solution used is nonabsorbable, isotonic polyethylene glycol electrolyte (PEG) solution that, unlike cathartic agents, does not appear to create fluid or electrolyte disturbances. The dose is 500 mL/h for small children and 1 to 2 L/h for adolescents.16 The irrigation process is continued until the rectal effluent is clear, usually within 4 to 6 hours.

While volunteer studies have demonstrated decreased bioavailability of certain drugs using WBI, there is currently no conclusive evidence that WBI improves clinical outcome of poisoned patients.16Although much of the evidence for WBI is anecdotal, this modality has been used in the pediatric population with minimal to no side effects. In patients who are hemodynamically stable and have normal bowel function and anatomy, it is reasonable to consider using WBI with specific ingestions. These include sustained release or enteric-coated drugs particularly if greater than 2 hours has elapsed since ingestion, iron, and packets of illicit drugs.16


Enhancing elimination is the process of removing a toxin from the body after absorption has occurred. Methods include multiple-dose–activated charcoal (MDAC), urinary alkalinization, and extracorporeal elimination.


MDAC is the administration of repeated doses of activated charcoal.17 Specific protocols for dose, dosing frequency, and duration are not established with recommendations typically varying from 10 to 25 g every 2 to 4 hours until the patient or the serum drug concentration has improved. Poisons for which this modality can be considered include carbamazepine, dapsone, Phenobarbital, quinine, or theophylline though no controlled studies have demonstrated clinical benefit.17 The use of MDAC as a poison treatment has been questioned.18


Urinary alkalinization by infusing sodium bicarbonate intravenously is intended to enhance the excretion of weak acids. It should be considered for salicylate or phenobarbital poisoned patients. It is difficult to alkalinize the urine of salicylate poisoned patients because they have decreased total body potassium even if normokalemic. Paradoxical aciduria (alkaline plasma pH and acidic urine pH) frequently occurs (see chapter on salicylate poisoning). Urine pH should be monitored frequently, and large doses of intravenous potassium are often required.19


Methods of extracorporeal removal, and include hemodialysis, hemoperfusion, continuous veno-venous hemofiltration (CVVH), and continuous veno-venous hemodialysis (CVVHD). They are highly technical and resource dependent interventions requiring specialists in nephrology and critical care. The emergency physician needs to be aware of which poisonings might benefit from extracorporeal elimination and to refer when indicated. These include salicylate, phenobarbital, methanol, ethylene glycol, and lithium.20


An antidote prevents the development or reverses the symptoms and signs of poisoning. Antidotes are available for a limited number of poisonings (Table 112-9). Please refer to the specific chapter for each of these poisonings for recommendations regarding the use of these antidotes.

TABLE 112-9




The disposition of a poisoned child is not always clear and depends on a multitude of factors. Not only is the actual clinical condition important to assess, but the potential toxicity of a purported ingestion as well as the social situation into which the child is to be discharged must be considered as well. Any patient showing signs of clinical instability is best observed in a critical care setting. If the patient appears stable, then an emergency department observation period of 6 to 8 hours may be adequate provided that the patient has not ingested a substance with a delayed onset of action or prolonged effect. These include modified release pharmaceuticals, sulfonylureas, clonidine, calcium channel antagonists, lithium, methadone, and monoamine oxidase inhibitors. Overdose of these substances may require up to 24 hours of observation.21 Any child who has ingested a potentially dangerous toxin requires antidotal therapy, manifests mild-to-moderate symptoms, or whose home environment is not considered safe, may also benefit from inpatient admission and observation.

For any pediatric poisoning encounter, regardless of admission or discharge from the emergency department, education of the parents or primary caregivers regarding proper poison prevention should be considered. In regard to adolescents with recreational drug use or abuse, substance abuse rehabilitation programs are encouraged. Suicidal adolescents and children require a mental health evaluation after the potential for poisoning has passed.


1. Bronstein AC, Spyker DA, Cantilena LR Jr, Rumack BH, Dart RC. 2011 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th Annual Report. Clin Toxicol (Phila). 2012;50:911–1164.

2. Eldridge DL, Van Eyk J, Kornegay C. Pediatric toxicology. Emerg Med Clin North Am. 2007;25(2):283–308.

3. Erickson T. Toxicology: ingestions and smoke inhalation. In: Gausche-Hill M, Fuchs S, Yamamoto L, eds. APLS: The Pediatric Emergency Medicine Resource. AAP and ACEP. 4th ed. Boston, MA: Jones and Bartlett; 2004:234–267.

4. Henretig FM. Special considerations in the poisoned pediatric patient. Emerg Clin North Am. 1994;12:549–567.

5. Erickson T, Thompson T, Lu J. The approach to the patient with an unknown overdose. Emerg Med Clin North Am. 2007;25:249–281.

6. Meehan TJ, Bryant SM, Aks SE. Drugs of abuse: the highs and lows of altered mental states in the emergency department. Emerg Med Clin North Am. 2010;(3):663–682.

7. Tenenbein M. Do you really need that emergency drug screen? Clin Toxicol (Phila). 2009;47:286–291.

8. Savitt DL, Hawkins HH, Roberts JR. The radioopacity of ingested medications. Ann Emerg Med. 1987;16(3):331–339.

9. Taftachi F, Sanaei-Zadeh H, Zamani M, Emanhadi M. The role of ultrasound in the visualization of the ingested medications in acute poisoning – a literature review. Eur Rev Med Pharmacol Sci. 2012;16: 2175–2177.

10. Schumann H, Erickson T, Thompson TM, Zautcke JL, Denton JS. Fentanyl epidemic in Chicago and surrounding Cook County, Illinois. Clin Toxicol (Phila). 2008;46(6):501–506.

11. Baumann BM, Patterson RA, Parone DA, et al. Use and efficacy of nebulized naloxone in patients with suspected opioid intoxication. Am J Emerg Med. 2013;31(3):585–588.

12. Hojer J, Troutman WG, Hoppu K, et al. Position paper update: Ipecac syrup for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51:134–139.

13. Benson BE, Hoppu K, Troutman WG, et al. Position paper update: Gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51:140–146.

14. American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists. Position paper: Cathartics. J Toxicol Clin Toxicol. 2004;42:243–253.

15. American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists. Position paper: single-dose activated charcoal. J Toxicol Clin Toxicol. 2005;43: 61–87.

16. American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42:843–854.

17. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position statement and practice guidelines on the use of multidose activated charcoal in the treatment of acute poisoning. J Toxicol Clin Toxicol. 1999;37:731–751.

18. Tenenbein M. Multiple doses of activated charcoal: Time for reappraisal II. Ann Emerg Med. 2003;42:597–598.

19. Proudfoot AT, Krenzelok EP, Vale AT. Position paper on urinary alkalinization. J Toxicol Clin Toxicol. 2004;42:1–26.

20. Fertel BS, Nelson LS, Goldfarb DS. Extracorporeal removal techniques for the poisoned patient: A review for the intensivist. J Intensive Care Med. 2010;25:139–148.

21. Bosse GM, Matyunas NJ. Delayed toxidromes. J Emerg Med. 1999;17: 679–690.