Poisoning

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9 Poisoning

Poisoning is one of the most common medical emergencies in young children and adolescents. Children are exposed to toxic substances more than any other age group. According to the American Association of Poison Control Centers (AAPCC), there were almost 2.5 million total human exposures in 2007, of which 65% were in children younger than 21 years old. Of these exposures, approximately 10% to 15% were intentional and include suicide attempts, and 80% to 85% of them were unintentional and occurred through exploratory behavior, environmental exposure, or neonatal exposure.

Etiology and Pathogenesis

The cause of childhood poisoning can vary dramatically from one case to another, but the most frequent causes are ingestions of readily accessible household products such as cosmetics, hair products, cleaning substances, and analgesics. The most lethal or potentially lethal poisonings, however, are most commonly related to pharmaceuticals, including antimalarials, β-blockers, calcium channel blockers, camphor, antidiarrheals, salicylates, opioids, and tricyclic antidepressants (TCAs).

The mechanism of toxicity varies from one agent to another, yet there are some classic presentations that can be seen with particular ingestions (Table 9-1). Ingestions that can be lethal in small doses are reviewed in more depth here.

Table 9-1 Clinical Manifestations of Selected Toxic Ingestions

Ingestion	Clinical Findings
Acetaminophen	Nausea, vomiting, anorexia early in course; late findings of jaundice and liver failure
Antihistamines	Initially CNS depression but stimulation in higher doses (hyperactivity, tremors, hallucinations, seizures)
Aspirin	Tachypnea, respiratory alkalosis, metabolic acidosis, tinnitus, coagulopathy, slurred speech, seizures
β-Blockers	Bradycardia, hypotension, coma or convulsions, hypoglycemia, bronchospasm
Calcium channel blockers	Bradycardia, hypotension, junctional arrhythmias, hyperglycemia, metabolic acidosis
Caustics	Coagulation necrosis (acid) or liquefaction necrosis (alkali), scarring, strictures, burning, dysphagia, glottic edema
Digoxin	Nausea, vomiting, visual disturbances, lethargy, electrolyte disturbances, hyperkalemia, prolonged AV dissociation and heart block, arrhythmias
Disc batteries	Corrosive when in contact mucosal surfaces
Ethanol	Nausea, vomiting, stupor, anorexia; late toxicity: triad of coma, hypothermia, hypoglycemia Lethal (cardiorespiratory depression) if >400-500 mg/dL (life-threatening hypoglycemia may occur at much lower levels in young children)
Ethylene glycol	CNS depression, metabolic acidosis, convulsions and coma, hypocalcemia, renal failure Laboratory findings: anion gap metabolic acidosis, osmolal gap, urine oxalate crystals
Hypoglycemic agents	Hypoglycemia, coma, seizures
Iron	Hemorrhagic necrosis of GI mucosa, hypotension, hepatotoxicity, metabolic acidosis, coma, seizure, shock
Isopropyl alcohol	Altered mental status, gastritis, hypotension Laboratory findings: elevated osmolal gap, ketonuria (no metabolic acidosis or hypoglycemia)
Lead	Abdominal pain, constipation, anorexia, listlessness, encephalopathy (peripheral neuropathy; rare in children), microcytic anemia
Methanol	CNS depression, delayed metabolic acidosis, optic disturbances Laboratory findings: anion gap metabolic acidosis, osmolal gap
Tricyclic antidepressants	Lethargy, disorientation, ataxia, urinary retention, decreased GI motility, coma, seizures Cardiovascular alterations: sinus tachycardia, widened QRS complex; may progress to hypotension, ventricular dysrhythmias, cardiovascular collapse

AV, atrioventricular; CNS, central nervous systeml; GI, gastrointestinal.

Compiled from Eldridge DL, Van Eyk J, Kornegay C: Pediatric toxicology. Emerg Med Clin North AM 15:283-308, 2007 and Osterhoudt K, Shannon M, Burns Ewald M, Henretig F: Toxicologic emergencies. In Fleisher GR, Ludwig S (eds): Textbook of Pediatric Emergency Medicine, ed 6. Philadelphia, Lippincott Williams & Wilkins, 2010, pp 1171-1223.

Tricyclic Antidepressants

According to the 2007 AAPCC report, antidepressants were the third most common cause of fatalities secondary to poisoning. TCAs, in particular, have a potent anticholinergic effect that can present as mydriasis, urinary retention, and gastroparesis. Death most often occurs from cardiotoxicity, in particular arrhythmias and hypotension. TCAs have a dose-dependent response in that ingestions less than 5 mg/kg are often asymptomatic, but fatalities can be seen with doses of 15 mg/kg and most often with doses greater than 30 mg/kg.

Antimalarials

Although these medications are rarely used in the United States as antiparasitic agents, they are becoming more common in households because some (e.g., hydroxychloroquine) act as second-line antiinflammatory therapy for rheumatoid arthritis and lupus. The toxic effects of antimalarials result from blockage of sodium and potassium channels, which causes subsequent cardiotoxicity, arrhythmia, and hypotension. Respiratory alterations (tachypnea, dyspnea, pulmonary edema, and respiratory failure) as well as central nervous system (CNS) side effects (seizures and coma) are also observed. Chloroquine doses of 5 to 10 mg/kg are therapeutic, but ingestions of 30 to 50 mg/kg can be lethal. Given the dangers of even moderate dose exposures, patients ingesting more than 10 mg/kg should be observed for cardiac dysfunction.

Calcium Channel Blockers and Beta-Adrenergic Blockers

Calcium channel blockers are most often used to treat hypertension, angina, migraines, and glaucoma, and they work by antagonizing L-type voltage-gated calcium channels in vascular smooth muscle and cardiac tissue. By preventing calcium influx into these cells, calcium antagonists cause vasodilatation as well as depression of both myocardial conduction and contractility. In large doses, this can lead to life-threatening bradycardia, heart block, and hypotension. Beta-adrenergic blockers can have similar cardiotoxicity in overdose (Table 9-1).

Camphor

Camphor is a component found in many nasal decongestants and topical anesthetic ointments. It can be toxic by oral ingestion, inhalation, or inappropriate dermal use. If ingested, camphor can cause oropharyngeal irritation, a burning sensation, nausea, and vomiting. It can also have CNS effects of apnea, coma, agitation, anxiety, hallucinations, hyperreflexia, myoclonic jerks, and seizures. Death can occur from doses of greater than 500 mg of camphor and usually results from intractable seizures or respiratory failure.

Salicylates

Aspirin, oil of wintergreen, and Pepto-Bismol all contain various quantities of salicylates. Symptoms of salicylate poisoning include nausea, vomiting, and altered mental status. Additionally there is often a classic laboratory finding of an elevated anion gap metabolic acidosis with a respiratory alkalosis. In severe cases, usually involving doses greater than 150 mg/kg, patients may manifest with agitation, delirium, seizures, pulmonary edema, coma, cardiovascular collapse, or death.

Sulfonylureas

Oral hypoglycemic agents are dangerous because patients may present with a delayed clinical onset of hypoglycemia accompanied with behavior changes, irritability, seizures, weakness, and eventually coma. Toxicity can occur from ingestions of even one or two sulfonylurea pills, and therefore overnight (fasting) observation and glucose monitoring is recommended after ingestion of most sulfonylureas.

Opioids

Opioids are found in analgesics, cough suppressants, and antidiarrheal medications. Ingestions present with a classic triad of respiratory depression, miosis, and CNS depression; death may result from respiratory depression. Children are most commonly exposed to codeine and oxycodone, and medical attention is important for those who ingest codeine in doses greater than 5 mg/kg. Methadone, however, is a longer acting medication and can be toxic in doses as low as 5 mg. Therefore, the AAPCC recommends close observation for opioid-naïve children ingesting more than 5 mg of methadone or any dose of extended-release opioids.

Antidiarrheals

Antidiarrheals often contain opioids (e.g., Lomotil, a combination of diphenoxylate and atropine). The diphenoxylate inhibits gastrointestinal (GI) motility, as can the atropine. The anticholinergic effects of atropine may also cause agitation, tachycardia, dry mucous membranes, facial flushing, and hyperthermia. The expected anticholinergic effect of mydriasis may not be present; rather, miosis may be present from the opioid component. Monitoring for 24 hours after any Lomotil ingestion is recommended because of the risk of delayed or recurrent CNS and respiratory depression (as long as 12-24 hours after ingestion).

Clinical Presentation

Patients with poisonings may present with a wide array of clinical signs and symptoms. Most often, children present with nonspecific signs, including nausea and vomiting, as well as altered mental status. Depending on the exposure, patients may also have burns or rashes, alterations in their respiration, and metabolic changes that are not typically seen in a more common illness. Nevertheless, there are characteristic clinical features, representing in particular altered central and autonomic nervous system findings, which have been termed “toxidromes” (Table 9-2).

Table 9-2 Toxidromes

Evaluation and Management

As with the management of any patient, the initial focus of a patient with a possible poisoning must begin with the ABCs (airway, breathing, and circulation). The first step is to assess airway patency and reflexes, then breathing (both respiration and ventilation), and finally circulation. For patients with altered mental status, the next step is to determine their disability (e.g., neurologic status using the Glasgow Coma Score) and blood glucose. It is also imperative to place patients on cardiorespiratory monitors so their cardiac and respiratory status can be continually reassessed, as well as obtain frequent vital signs so changes can be detected as early as possible.

After initial stabilization, attention can be turned to discerning what the ingestion may have been; the most fruitful place to turn is a brief and focused history. Some patients may not present with a clear history of poisoning, but rather with an acute illness that does not quite fit with the history. The concern for ingestion should be raised in any child who presents with a suspicious clinical picture, particularly if they are toddlers or adolescents. For observed or highly suspected poisonings, gathering information on the patient with respect to who, what, where, and when the incident or illness onset occurred may lead to uncovering the cause of the poisoning. It is also important to determine a patient’s weight; what medications or chemicals are in the house; the timing of the incident; how much of the toxin was potentially ingested; and where the exposure took place, both in terms of where the patient was at the time and what body part(s) were exposed. Attention must also be paid to a patient’s coexisting medical conditions so they can be appropriately managed as well.

In addition to the history, the physical examination of a patient with a poisoning can be extremely revealing. Close attention to heart rate, respiratory pattern, pupillary response, mental status, abdominal examination, and reflexes can be clues to particular exposures. For example, patients poisoned with stimulants, including cocaine, amphetamines, caffeine, and theophylline, present with mydriasis, tremors, tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, mania, convulsions, and tachyarrhythmias (Figure 9-1). Poisoning with depressants, on the other hand, including opioids, alcohol, benzodiazepines, and muscle relaxants, can lead to lethargy, decreased responsiveness to verbal and physical stimulation, miosis (especially opioids, barbiturates, and alcohol), bradycardia, hypotension, bradypnea, hypothermia, and coma (see Figure 9-1). Other signs and symptoms characteristic of a particular substance can be characterized as a toxidrome (Table 9-2).

Figure 9-1 Stimulant and depressant effects.

The laboratory workup should begin with a bedside test for blood glucose, complete blood count, electrolytes, liver function testing, and urinalysis. Studies have shown that urine and serum toxicologic studies are less important emergently but are still often part of a patient’s initial evaluation. Additionally, if agents such as salicylates, acetaminophen, ethanol, methanol, ethylene glycol, digoxin, iron, lithium, or anticonvulsants are suspected, serum drug levels can be helpful for instituting the appropriate therapeutic management of the ingestion. Electrocardiography is essential for patients with arrhythmias or cardiotoxic drug ingestion, and chest radiography may be helpful in patients who have or are at risk of developing aspiration or pulmonary edema.

Treatment of a poisoning is fourfold: patient stabilization, minimizing toxin exposure and absorption, enhancing elimination (when possible), and managing the sequelae of the exposure. There are several methods of minimizing topical and inhaled toxin exposure, including irrigation of exposed eyes, removal of soiled clothing followed by washing of the skin and hair, and movement of the patient to fresh air, as appropriate. Ingested poison absorption may be mitigated by gastric decontamination, but this has raised many controversies with respect to the efficacy and safety of the various decontamination methods. The current recommendations are outlined below.

Activated Charcoal

When necessary, activated charcoal has been shown to be the most effective method of gastric decontamination if administered in a timely manner. A single dose of activated charcoal has its greatest benefit if administered within 1 hour of an ingestion, but it can be useful even several hours later in some situations (e.g., anticholinergic, salicylate, or opioid ingestion with delayed gastric emptying or intestinal motility or significant overdoses of delayed-release medications). Charcoal decontamination should be considered if the toxin is known to adsorb to charcoal, if the patient is at risk for significant toxicity, and if the patient has an intact GI tract. The complications are negligible compared with the other methods of gastric emptying, but aspiration has occurred rarely and can be fatal. Charcoal is not useful for iron, other heavy metals, lithium, alcohols, and cyanide ingestions because these compounds do not bind to charcoal.

Gastric Lavage

Lavage is not routinely used for decontamination because of variable results, lack of evidence with respect to improved outcomes, and significant adverse effects associated with its use. It should be considered when a life-threatening amount of poison has been ingested and if activated charcoal would not provide for sufficient decontamination, as might be the case with large iron or lithium ingestions. To do a lavage, a patient is placed on his or her left side, and a large orogastric tube is placed into the stomach. Fluid is aspirated back, and small aliquots of approximately 15 mL/kg (maximum, 250 mL) of water are administered and then aspirated back until the aspirate is clear. The most likely complications are aspiration, oxygen desaturation, esophageal irritation, and dysrhythmia.

Whole-Bowel Irrigation

This method of decontamination is not routinely recommended, but it is indicated for toxic ingestions of sustained-release or enteric-coated drugs, metals such as iron and lithium, and drug packets that may have a long absorption time or are not bound by charcoal. The intent of whole-bowel irrigation is to prevent absorption of ingested materials by provoking a liquid stool through administration of a large volume (≥1 L) of a polyethylene glycol electrolyte solution at a fast rate, typically via nasogastric tube. It may be effective if used within 4 hours of enteric-coated aspirin ingestion or even up to 12 to 16 hours after the ingestion of some sustained-release medications.

Dilution

The method of using water or milk to dilute a toxin is useful in situations in which local irritation or corrosion can be life threatening, but not for medication ingestions in which dilution may increase dissolution of the toxin and thereby increase absorption. It is only recommended if it can be initiated within the first few minutes after such exposures and only if there is no evidence of airway compromise.

Ipecac

The American Academy of Pediatrics issued a policy statement in 2004 recommending that ipecac no longer be used for home or health care facility decontamination because of the potential harmful side effects and the fact that positive results are so variable. The findings of various studies have ranged between a 0% to 40% decrease in drug absorption if ipecac is used within 1 hour of an ingestion, but the likelihood of administering ipecac in such a short period of time, especially outside of the home, is unlikely. Even if it can be done, the rare side effects of lethargy, diarrhea, persistent emesis, aspiration, and a delay in additional oral therapies are deemed too risky by most authorities to justify the potential positive results.

Cathartics

Neither saccharide (sorbitol) nor saline (magnesium citrate) cathartics have been proven effective in GI decontamination. Some clinicians use cathartics for decontamination as a single dose in conjunction with activated charcoal, but repeat doses may increase diarrhea, cramping, and hypernatremic dehydration. Nevertheless, its efficacy remains equivocal.

Enhancement of toxin elimination is infrequently effective, but it may be lifesaving in select cases. Urine alkalinization is effective in increasing salicylate excretion. Additionally, hemodialysis is used for life-threatening toxicity caused by salicylates, toxic alcohols, lithium, and theophylline.

Some poisonings are amenable to specific antidotal therapy, which may counter the toxin itself or its dangerous metabolites (Table 9-3). Three treatments in particular—oxygen (for any patient with hypoxia, carbon monoxide exposure, or cyanide toxicity), glucose (for hypoglycemia caused by insulin, oral hypoglycemics, ethanol, and so on), and naloxone (for opioid-induced respiratory depression)—are important and safe enough to consider for emergent use as empiric therapy for altered mental status in suspect cases. The local poison control center is another valuable resource to help ensure adequate patient management regardless of the exposure. All poisonings or suspected poisonings should be reported to the local poison control center (800-222-1222) so they can assist with appropriate treatment and monitoring on a case-by-case basis.

Table 9-3 Antidotes and Management of Selected Toxic Exposures

Ingestion	Potential Antidote / Other management
Acetaminophen	N-acetylcysteine, activated charcoal within 4 hours
Antihistamines	Activated charcoal or WBI for extended-release formulations, anticonvulsants, physostigmine
Benzodiazepine	Flumazenil
β-adrenergic blockers	Glucagon, activated charcoal if early after ingestion, WBI for delayed-release formulations, atropine, IVF, pressors
Calcium channel blockers	Calcium, activated charcoal if early after ingestion, WBI for delayed-release formulations, atropine, IVF, pressors, insulin/glucose
Carbon monoxide	100% oxygen, hyperbaric oxygen
Caustic agents	ABCs, steroids for esophageal burns (controversial); in-hospital monitoring for mediastinitis, pneumonitis, and peritonitis
Cholinesterase inhibitors	Atropine, pralidoxime
Cyanide	ABCs, 100% oxygen, sodium nitrite/sodium thiosulfate or hydroxocobalamin
Digoxin	Digoxin immune FAb, activated charcoal, electrolyte management
Disc batteries	Removal if in esophagus; if below esophagus, watch for 3 days, and if not out, then consult regarding potential removal
Ethanol	Respiratory management, correction of hypoglycemia, temperature control, thiamine (in chronic alcoholism)
Ethylene glycol and methanol	Ethanol or 4-methylpyrazole if level >20 mg/dL, sodium bicarbonate, calcium, pyridoxine, thiamine, folate, hemodialysis
Iron	Deferoxamine, WBI, hemodynamic support for possible GI bleed, management of acidosis, hypoglycemia, and hypotension
Isoniazid	Pyridoxine
Lead	Chelation with edetate calcium disodium, 2,4-dimercaptopropanol, succimer, and anticonvulsants as needed
Methemoglobinemic agents	Methylene blue
Opioids	Naloxone
Salicylates	Correct electrolytes, fluid resuscitation, urine alkalinization, hemodialysis
Sulfonylurea	Dextrose, octreotide
TCAs	Sodium bicarbonate to reduce cardiotoxicity, pressor support prn, activated charcoal

ABCs, airway, breathing, and circulation; GI, gastrointestinal; IVF, intravenous fluids; TCA, tricyclic antidepressant; WBI, whole-bowel irrigation.

Compiled and adapted from Larsen LC, Cummings DM: Oral poisonings: guidelines for initial evaluation and treatment. Am Fam Phys 57(1):85-92, 1998 and Osterhoudt K, Shannon M, Burns Ewald M, Henretig F: Toxicologic emergencies. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, ed 5. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 951-1007.