CHAPTER 82

Ingestions: Diagnosis and Management

Kelly D. Young, MD, MS, FAAP

Ingestions are a common problem presenting to pediatric practitioners. Three scenarios frequently encountered are accidental ingestions by preschool-age children, intentional suicide attempts by adolescents, and recreational drug use. This chapter discusses the general approach to the child who has ingested a potentially poisonous substance. Ingestions of specific substances are beyond the scope of this chapter, as is toxicity occurring by dermal, ophthalmologic, and inhalational routes. The general approach to the history, physical examination, laboratory tests and diagnostic studies, and management, especially decontamination, is useful for all ingestions, however.

Epidemiology

Most calls made to poison control centers involve pediatric patients. Poison control center data from 2016 show that pediatric patients younger than 20 years accounted for 60% of exposures and young children aged 0 to 5 years accounted for 46%. Among younger children boys were more commonly exposed, whereas girls pre-dominated in adolescence. For children aged 0 to 12 years 3.5% of exposures are intentional, whereas for adolescents aged 13 to 19 years 27% are intentional, and for adults 69% are intentional.

The most common substances ingested overall are analgesics, including acetaminophen, nonsteroidal anti-inflammatory drugs, and narcotics; household cleaning substances; and cosmetics/ personal care products. The most common fatal ingestion in children is analgesics (often narcotics that are not their own prescription). Other common pediatric fatal poisonings are stimulants and street drugs, carbon monoxide poisoning, antidepressants, and disc battery ingestions. A registry that included cases on which a medical toxicologist was consulted (presumably for serious exposures) at 31 participating centers reported on the most common agents involved for infants and toddlers age 2 years and younger: 16% cardiac drugs, 15% psychotropic drugs, 9% recreational drugs and controlled narcotics, 9% analgesics, 7% cleaning products, 5% scorpion stings, and 4% toxic alcohols.

Fatalities are uncommon overall and are more likely to occur with intentional ingestion by older children. Poison control center data from 2016 revealed 31 pediatric fatalities (age 0–12 years) and 42 adolescent fatalities (age 13–19 years). Children accounted for 2% of total toxicologic fatalities for the year, whereas adolescents accounted for 3% and adults for the remainder. Young children tend to ingest nontoxic substances or small quantities of toxic substances. Review of trends over the past few years indicates a reduction in overall calls but an increase in calls about serious exposures. Fatality rates have remained stable.

The frequency of exposures to analgesics (narcotics), cardiac drugs, and psychotropic drugs in pediatric patients is linked to an overall rise in adult prescription drug use. Cough and cold medications are an increasingly recognized source of toxicity in young children, and the US Food and Drug Administration recommends against their use in children younger than 6 years. Another new source of serious toxic exposures in children is laundry and dish-washer detergent capsules, which can have an appearance similar to candy. A rise in inadvertent pediatric marijuana exposures has been reported in states with legalized marijuana, with edible sources playing a sizeable role.

Recreational drug use is another source of serious exposures in adolescents. Narcotics, cocaine, amphetamines, and ecstasy remain popular, and newer forms of recreational drugs include energy drinks with or without alcohol, synthetic cathinones (“bath salts”), synthetic cannabinoids (“K2,” “Spice”), dextromethorphan, inhalants (especially computer cleaners), and the hallucinogenic herb salvia, which is legal in many states and also has opioid effects. Contamination of street drugs with high-potency opiates, such as carfentanil, is contributing to the rise in opioid fatalities.

Clinical Presentation

The clinical presentation following an ingestion varies considerably depending on the substance ingested. Some patients may not present with a clear history of a toxic ingestion. The physician must maintain a high index of suspicion for poisoning as the cause of symptoms such as altered behavior, depressed level of consciousness, cardiac dysrhythmia, vomiting, seizure, and autonomic changes.

Pathophysiology

The pathophysiologic profile depends on the substance. Some toxins act on a particular organ system (eg, acetaminophen on the liver, ethanol on the central nervous system), whereas others act diffusely at the cellular level (eg, cyanide). Generally, drugs are absorbed, distributed within the body, metabolized, and excreted. Drug levels obtained prior to completion of absorption and distribution may not reflect the peak level. Interventions focus on preventing absorption, sometimes on preventing metabolism into a more toxic by-product, and on enhancing excretion. Toxic effects may be delayed or prolonged when an extended-release form of a drug has been ingested, with drugs likely to form concretions (eg, iron, aspirin, theophylline), or when toxicity results from an active metabolite (eg, toxic alcohols, acetaminophen, acetonitrile, dapsone). Pharmacogenetics are increasingly recognized as having an important role in individual responses to medications and toxins. Genetic variations in enzymatic activity in drug metabolism may result in toxicity through excessively rapid metabolism of a drug to its active metabolite, or through slow metabolism of a drug to its inactive metabolite. For example, a cytochrome P-450 CYP2D6 genotype has been linked to rapid metabolism of codeine to active morphine, resulting in toxicity and even fatality. The US Food and Drug Administration has added a boxed warning on codeine and a contraindication for its use after tonsillectomy or adenoidectomy in children.

Differential Diagnosis

The differential diagnosis of toxic ingestions is broad. For the patient with a history of ingestion, the differential diagnosis is narrowed to substances available to the child. If no history of ingestion is given, the physician should include ingestion in the differential diagnosis when evaluating symptoms and signs such as altered mental status, altered behavior, metabolic derangement, cardiac dysrhythmia, hypotension and shock states, seizure, respiratory distress or apnea, cyanosis, vomiting, and diarrhea (Box 82.1). In fact, almost any symptom complex may result from a toxic ingestion.

Evaluation

A detailed history of what and how much the patient ingested is key to the evaluation. Physical examination should focus on identifying symptoms and serious complications. The patient should be monitored and reassessed frequently. Laboratory and other diagnostic studies can be tailored to the specific ingestion.

History

The most important questions address the ingestion (Box 82.2), such as, What did the patient ingest? What is the maximum possible amount that was ingested? When did the ingestion occur? What symptoms are occurring? History of previous medical conditions is also important to identify increased susceptibility to a particular toxin (eg, seizure disorder with ingestion of a substance that causes seizures); assess for factors that may have precipitated the ingestion, such as depression; and assess for medications that may interact with or exacerbate the toxic effects of the ingested substance (eg, acetaminophen ingestion in a patient taking a cytochrome P-450 inhibitor).

Parents and caregivers should be encouraged to bring in the container and any remains of the substance ingested. The physician should attempt to obtain the exact formulation because generic and brand name drugs may differ. The physician must also be aware of possible combination products. Investigative methods such as calling or sending a family member to the home to identify the product, calling the pharmacy on a prescription label, or identifying a pill by comparing its picture and imprint to those in a pharmaceuticals reference may be necessary. Internet search engines may be used to search the imprint on a pill or identify foreign medications.

Caregivers should be questioned about all available drugs or other toxic substances in the household. Sometimes caregivers must be encouraged to mention all substances in the household, even those they do not think the child could possibly have obtained. The physician must also ask about medications used by recent visitors (eg, grandparents) and the possibility of an exposure at a recently visited household or location. It is important not to overlook herbal preparations, vitamins, alternative medications, household products (including cleaning and personal care products), gardening products, chemicals used in hobbies or work, and alcohol or illicit drugs belonging to an adult. Caregivers may initially overlook these as they concentrate only on recalling “medications.” It may be helpful to interview siblings or friends of an adolescent suspected of recreational drug use. The physician must maintain a high index of suspicion for unreported co-ingestants, especially in adolescent suicide attempts.

Although often difficult, it is important to attempt to determine the quantity of drug that was available to the patient and how much is currently missing. It may be necessary to count pills or measure liquid to make the determination. For estimating liquids, the approximate volume of a swallow is 0.3 mL/kg. The physician should always assume the “worst case” (ie, the patient took all of the drug that is missing). History about the amount ingested may be inaccurate, especially when elicited from the adolescent with intentional ingestion.

The physician should attempt to determine approximately what time the ingestion occurred. Symptoms are usually expected within a defined time range. Recommended observation periods before discharge take into account expected symptoms based on the length of time since the ingestion. Timing may also be important in determining what substance was most likely ingested. For example, ingestion of mushrooms that cause a self-limited illness usually results in gastrointestinal (GI) upset within 4 to 6 hours, whereas Amanita mushrooms that may ultimately result in hepatic failure typically present with GI upset in 6 to 12 hours.

The physician should ask about current symptoms and when they started relative to the time of the ingestion. In a patient without a definite history of ingestion, certain toxidromes (ie, recognizable combinations of symptoms suggestive of a certain class of medications or toxins) may be suggestive of a specific substance or class of substances. Whether the patient is symptomatic and what symptoms are present may guide the workup for an unknown ingestion, determine whether hospitalization is necessary, or dictate therapy.

Physical Examination

If the substance ingested is known, the physical examination should be focused on identifying expected symptoms of toxicity. A general physical examination should always be performed, however, because co-ingestion of another undisclosed substance must be considered. Particular attention should be paid to all 4 vital signs (ie, temperature, respiratory rate, heart rate, blood pressure); pupillary size and reaction; breathing (eg, Kussmaul respiration that occurs with acidosis); mental status; distinctive breath odors; presence or absence of bowel sounds; and skin color, temperature, and moisture. The patient’s weight should be measured, because toxicity is often estimated based on milligrams of drug ingested per kilogram of body weight. Because symptoms may develop or worsen if peak levels of the toxic substance have not been reached at the time of initial evaluation, continual reassessment and cardiorespiratory monitoring are imperative. If a symptomatic patient is noted to have a typical toxidrome, therapy may be initiated based on the toxidrome without confirmation of the exact substance ingested. Some common toxidromes and their treatments are listed in Table 82.1.

Laboratory Tests

Qualitative drug screening (reporting only the presence or absence of the drug) of urine or blood often is done when poisoning is part of a broader differential diagnosis for symptoms such as altered mental status or acute behavioral changes. Such drug screening is rarely helpful in the patient with acute poisoning because typically results are not rapidly reported, testing can be done for only a limited number of substances, and false-positive and -negative results may occur. Given the frequency of narcotic ingestions, it is important to note that synthetic opioids (eg, fentanyl, methadone, oxycodone, hydrocodone) are not detected by typical hospital immunoassay “tox screens.” Laboratory tests and diagnostic studies to consider for the patient with known or suspected toxic ingestion are listed in Box 82.3.

Quantitative drug levels for specific drugs can be helpful to estimate severity of expected symptoms or to rule out ingestion of that drug, however. Examples include acetaminophen, salicylate, ethanol, methanol, ethylene glycol, iron, theophylline, lithium, anticonvulsants, and levels of carboxyhemoglobin or methemoglobin by blood gas analysis. With the exception of acetaminophen and ethanol, such levels should be measured only when suggested by the history or physical examination. Many toxicology experts feel that because acetaminophen overdose produces few acute symptoms, may lead to fulminant hepatic failure, and is readily treatable with an antidote, and because acetaminophen is a frequent ingredient in combination products, acetaminophen level should be determined for all patients with a history of ingestion. In adolescents and adults, ethanol is a common co-ingestant, and ethanol levels are routinely measured. Routine salicylate levels are likely to be low yield in the absence of suspicion based on history or physical examination, although some physicians do obtain them as well.

Serum chemistries and osmolarity may offer clues about what was ingested when the substance is unknown. The anion gap is calculated as [Na] − ([Cl] + [HCO₃]) and is normally 8 to 12 mEq/L. An elevated anion gap indicates the presence of metabolic acidosis and occurs in ingestions and conditions identified by the MUDPILES mnemonic: methanol, uremia, diabetic ketoacidosis, paraldehyde and phenformin, iron and isoniazid, lactic acidosis, ethylene glycol and ethanol, and salicylates and solvents (eg, toluene). The osmolar gap is the difference between the measured serum osmolarity and the calculated osmolarity (given by the formula 2[Na] + [glucose]/18 + [BUN]/2.8). The normal osmolar gap is less than 10 mOsm. An elevated osmolar gap occurs with ingestion of alcohols such as ethanol, methanol, ethylene glycol, and isopropanol.

^a Not an exhaustive list.

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