Ethylene glycol poisoning with a normal anion gap caused by concurrent ethanol ingestion: importance of the osmolal gap

Abstract

Ethylene glycol poisoning classically presents as a metabolic acidosis with an increased anion gap. Metabolism of ethylene glycol to organic acids, and increased production of lactate, are responsible for the increased gap. We report the case of an alcohol user who consumed ethanol and ethylene glycol concurrently, and presented without acidosis, with a normal anion gap. Several hours later, when his serum ethanol level had declined, he developed severe acidosis with an elevated anion gap. An increased osmolal gap, not accounted for by the serum ethanol level, proved to be an important clue to the diagnosis. In this patient, ingestion of ethanol inhibited the hepatic metabolism of ethylene glycol to organic acids, obscuring the diagnosis. In intoxicated alcohol users, even in the absence of metabolic acidosis, serum osmolality measurements and calculation of the osmolal gap may facilitate the rapid diagnosis of ethylene glycol poisoning.