TOXICOLOGY
DIAGNOSIS
■ Usually obvious from patient’s history and exam
■ Serum levels are readily available in most EDs.
■ The correlation between serum levels and patient symptoms varies widely
due to individual tolerance.TREATMENT
■ Supportive care
■ Be careful not to overlook concomitant injuries or medical illness.COMPLICATIONS
■ Chronic alcohol use is associated with a wide variety of illnesses including
hypoglycemia, alcoholic ketoacidosis, cirrhosis, pancreatitis, GI bleeding,
malnutrition, neurologic disease, trauma.MethanolMethanol is found in windshield wiper fluid, antifreeze, photocopier fluid,
and solid fuels (eg, Sterno). Patients may ingest methanol by accident, as a
suicide attempt, or as an ethanol substitute.MECHANISM/TOXICITY
■ Methanol itself has minimal toxicity: It causes mild intoxication.
■ Metabolized by alcohol dehydrogenase (ADH) to a toxic metabolite,
formic acid
■ Formic acid accumulation →anion gap metabolic acidosis, retinal
toxicity.SYMPTOMS/EXAM
■ Intoxication, headache, CNS depression
■ Visual changes: Classic description is “looking through a snow field,”
hyperemic optic discs, blindness.
■ Tachycardia, tachypnea
■ Abdominal pain, N/VDIFFERENTIAL
■ Consider other causes of acute metabolic acidosis.
■ The combination of acute onset visual changes with acidosis is highly sug-
gestive of methanol toxicity.DIAGNOSIS
■ Gold standard is direct serum measurement.
■ Suspect methanol ingestion if patient has a high osmolal gap, anion gap
metabolic acidosis, and a consistent history and exam.
■ Metabolism, and therefore toxicity, may be delayedwith coingestion of
alcohol.TREATMENT
■ Antidote = fomepizoleorethanol.
■ Blocks ADH, preventing production of formic acidOsmolal gap = measured
serum osmolality – calculated
serum osmolality
(normal = < 10 mOsm/kg).Calculated serum
osmolality =
2(Na) + (BUN/2.8) +
(glucose/18) + (ethanol/4.6).“Blind drunk,” osmolal gap,
and anion gap metabolic
acidosis = methanol toxicity.