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  • Ethanol overdose in children may result in hypoglycemia.
  • Methanol ingestion is associated with visual disturbance, metabolic acidosis, and possibly multiorgan system failure.
  • Ethylene glycol poisoning is associated with metabolic acidosis, renal failure, and possibly death.
  • Isopropanol may cause CNS depression but does not usually cause metabolic acidosis.
  • All of the toxic alcohols can produce an osmolal 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 recent 2-year prospective study in Norway, of those pediatric poisonings reported in children aging from 8 to 15 years, 46% involved ethanol.1 In addition to alcohol-containing beverages such as beer, wine, and hard liquors, children have access to more than 700 ethanol containing medicinal preparations, colognes and perfumes, as well as mouthwashes that can contain up to 75% ethanol. There has been increasing legislation in the United States regulating child-resistant packaging and product-warning labels on mouthwash products containing ethanol. Since these interventions were instituted in 1995, improved outcomes have been documented in regards to these ingestions in children.2,3

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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 pathway is the major metabolic pathway and the rate-limiting step in converting ethanol to acetaldehyde. In general, nontolerant individuals metabolize ethanol at 10 to 25 mg/dL/h and alcohol tolerant metabolize up to 30 mg/dL/h. Children may ingest large amounts of ethanol in relation to their body weight, resulting in rapid development of high blood alcohol concentrations. In children younger than 5 years, the ability to metabolize ethanol is diminished because of immature hepatic dehydrogenase activity.

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Clinical Presentation

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Ethanol is a selective CNS depressant at low concentrations, and a generalized 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 alcohol ingested.4

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Laboratory Studies

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In symptomatic, pediatric patients 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. If the ethanol level does not correlate with the clinical picture, ...

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