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  1. Pharmacology. Ethanol (ethyl alcohol) acts as a competitive substrate for the enzyme alcohol dehydrogenase, preventing the formation of toxic metabolites from methanol or ethylene glycol. A serum ethanol concentration of 100 mg/dL, or at least a 1:4 molar ratio of ethanol to toxic alcohol/glycol, effectively saturates alcohol dehydrogenase and prevents further methanol and ethylene glycol metabolism (see also "Fomepizole [4-Methylpyrazole, 4-MP]"). Ethanol is well absorbed from the GI tract when given orally, but the onset is more rapid and predictable when it is given intravenously. The elimination of ethanol is zero order; the average rate of decline is 15 mg/dL/h. However, this is highly variable and will be influenced by prior chronic use of alcohol, recruitment of alternate metabolic pathways, and concomitant hemodialysis (eg, to remove methanol or ethylene glycol).

  2. Indications. Suspected methanol (methyl alcohol) or ethylene glycol poisoning with the following:

    1. A suggestive history of ingestion of a toxic dose but no available blood concentration measurements;

    2. Metabolic acidosis and an unexplained elevated osmol gap; or

    3. A serum methanol or ethylene glycol concentration of 20 mg/dL or higher.

    4. Note: Since the introduction of fomepizole (4-methylpyrazole), a potent inhibitor of alcohol dehydrogenase, most patients with ethylene glycol or methanol poisoning probably will be treated with this drug instead of ethanol, particularly in cases involving small children, patients taking disulfiram, patients with pancreatitis, and hospitals lacking laboratory support to perform rapid ethanol levels (for monitoring treatment). Ethanol is more difficult to dose, requires more monitoring, and has a greater risk of adverse effects. Studies suggest that despite the higher acquisition costs for fomepizole, it may be more cost-effective than ethanol.

    5. Other substances that are metabolized by alcohol dehydrogenase to toxic metabolites include propylene glycol, diethylene glycol, triethylene glycol, glycol ethers (eg, ethylene glycol ethyl ether, ethylene glycol butyl ether), and 1,4-butanediol. The criteria for ethanol therapy and evidence for improved outcomes are lacking for these substances.

  3. Contraindications. Use of interacting drugs, which may cause disulfiram-type reaction (see Item V. B below).

  4. Adverse effects

    1. Nausea, vomiting, and gastritis may occur with oral administration. Ethanol may also exacerbate pancreatitis.

    2. Inebriation, sedation, and hypoglycemia (particularly in children and malnourished adults) may occur.

    3. Intravenous use sometimes is associated with local phlebitis (especially with ethanol solutions 10%). Hyponatremia may result from large doses of sodium-free intravenous solutions.

    4. Acute flushing, palpitations, and postural hypotension may occur in patients with atypical aldehyde dehydrogenase enzyme (up to 50-80% of Japanese, Chinese, and Korean individuals).

    5. Use in pregnancy. FDA Category C (indeterminate). Ethanol crosses the placenta. Chronic overuse in pregnancy is associated with birth defects (fetal alcohol syndrome). The drug reduces uterine contractions and may slow or stop labor. However, these effects do not preclude its acute, short-term use for a seriously symptomatic patient (Introduction).

  5. Drug or laboratory interactions

    1. Ethanol potentiates the effect of CNS-depressant drugs and hypoglycemic agents.

    2. Disulfiram reaction, including flushing, palpitations, and postural hypotension, may occur in patients taking disulfiram as ...

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