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Ethanol overdose in children may result in hypoglycemia.
Methanol ingestion is associated with visual disturbance, metabolic acidosis, and possibly multi-organ system failure.
Ethylene glycol poisoning is associated with metabolic acidosis, renal failure, and possibly multi-organ system failure.
Isopropanol may cause CNS depression but does not usually cause metabolic acidosis.
All of the toxic alcohols can produce an osmol gap.
Fomepizole is the only FDA-approved antidote for ethylene glycol and methanol toxicity.
Hemodialysis is indicated in severe toxic alcohol ingestions not responsive to conventional medical therapy, or with evidence of end-organ damage or severe acidosis.
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According to a 2-year prospective study in Norway, of poisonings in 8 to 15 year old children, 46% involved ethanol.1 In the Slovak Republic, ethanol accounted for 34% of all intoxications in children 9–18 years old and the proportion of children admitted for ethanol intoxication increased yearly over 10 years.2 In the United States, alcohol is the drug most commonly used by youth. “Binge drinking” tendencies (five or more consecutive drinks on one occasion) have been reported in 9.5–27.4% of 8th–12th graders respectively.3 Regardless of country of origin, ethanol is a common problem among children.
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Pharmacokinetics and Pathophysiology
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Ethanol undergoes hepatic metabolism via two metabolic pathways: alcohol dehydrogenase and the microsomal ethanol oxidizing system (MEOS). Alcohol dehydrogenase is the major metabolic pathway and the rate-limiting step in converting ethanol to acetaldehyde. In general, non-tolerant individuals metabolize ethanol at 10–25 mg/dL/h and those with tolerance metabolize it up to a rate of 30 mg/dL/h. Children may ingest large amounts of ethanol in relation to their body weight, resulting in rapid development of high blood concentrations. In children younger than 5 years, the ability to metabolize ethanol is diminished because of immature hepatic dehydrogenase activity.
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Ethanol is a selective CNS depressant at low concentrations, and a general depressant at high concentrations. Initially, ethanol produces exhilaration and loss of inhibition, which progresses to lack of coordination, ataxia, slurred speech, gait disturbances, drowsiness, and, ultimately, stupor, and coma. The intoxicated child may demonstrate a flushed face, dilated pupils, excessive sweating, gastrointestinal distress, hypoventilation, hypothermia, and hypotension. Death from respiratory depression may occur at serum ethanol concentrations >500 mg/dL. Convulsions and death have been reported in children with acute ethanol intoxication owing to alcohol-induced hypoglycemia. Hypoglycemia results from inhibition of hepatic gluconeogenesis and is most common in children younger than 5 years. It does not appear to be directly related to the quantity of ethanol ingested.4
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In symptomatic children who have suspected ethanol intoxication, the most critical laboratory tests are the serum ethanol and glucose concentrations.5 Although blood ethanol concentrations roughly correlate with clinical signs, the physician must treat patients based on their clinical status, not the absolute level.5 If the ethanol level ...