Poisoning

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9 Poisoning

Melissa Desai, Fred Henretig

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.

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