also be considered for high serum methanol levels (in excess of 70 mg/dL) after alcohol dehydrogenase inhibition Ethylene Glycol The ingestion of ethylene glycol, although uncommon, causes significant morbidity and occasional mortality The toxicity of ethylene glycol, like that of methanol, is the result of drug metabolism; ethylene glycol has virtually no toxicity in its parent state However, metabolism by alcohol dehydrogenase produces several toxic intermediates, including glycolaldehyde, glycolic acid, and oxalate These metabolites result in severe metabolic acidosis and deposition of calcium oxalate crystals The clinical syndrome of ethylene glycol intoxication appears in three different stages The first stage consists predominantly of CNS manifestations and is accompanied by a profound metabolic acidosis In this early stage, mild hypertension, tachycardia, and leukocytosis are often present Nausea and vomiting commonly occur, and with larger doses, coma and convulsions may appear within a few hours Another classic finding is the presence of hypocalcemia This is believed to result from the widespread formation of calcium oxalate Hypocalcemia may be severe enough to cause tetany and cardiac conduction disturbances Urinalysis usually reveals a low specific gravity, proteinuria, microscopic hematuria, and crystalluria The second distinct state is coma and cardiopulmonary failure; it is usually the result of acidosis The third stage usually occurs after 24 to 72 hours Here, renal failure emerges, generally with a picture of acute tubular necrosis with either polyuria or anuria Urine sediment contains blood, protein, and casts Patients often require dialysis for extended periods and may be left with permanent renal insufficiency Consideration of ethylene glycol poisoning should be based either on the history or, in the absence of diabetic ketoacidosis, the presence of any of the following criteria: (i) alcohol-like intoxication without the odor of alcohol, (ii) large anion-gap metabolic acidosis, and (iii) an elevated osmolar gap in the absence of ethanol or methanol ingestion A urinalysis that demonstrates oxalate crystals, while neither highly sensitive nor specific for ethylene glycol poisoning, can help corroborate the diagnosis Serum chemistries or blood gas levels should be obtained frequently because of the rapid evolution of metabolic acidosis The availability of ethylene glycol levels varies by institution Activated charcoal negligibly adsorbs ethylene glycol As with methanol intoxication, treatment of ethylene glycol poisoning falls into three areas: supportive care, administration of pharmacologic agents, and enhancement of