Abstract
Ethylene glycol is one of the most toxic alcohols; it may be accidentally or intentionally consumed as a substitute for ethanol or related to suicidal attempts. Ingestion of ethylene glycol causes a severe metabolic acidosis with increased anion and osmotic gap due to its toxic metabolites, leading to a clinical picture of central nervous system depression, cardiovascular and renal impairment. A 16-year-old boy was admitted with clinical and biological signs of ethylene glycol poisoning after simultaneous ingestion of antifreeze and ethanol. The patient had mild anion gap metabolic acidosis only at the debut, rapidly corrected with one dose of sodium bicarbonate; further evaluation did not reveal acidosis, even if the subsequent evolution included acute renal failure requiring hemodialysis. Due to the absence of a positive history and of a persistent metabolic acidosis, the diagnosis of ethylene glycol poisoning was delayed until it was confirmed by serum toxicological test. Conclusions: concomitant ingestion of ethanol may mask the symptoms of ethylene glycol poisoning; the absence of persistent metabolic acidosis does not rule out the diagnosis.
Highlights
Ethylene glycol (EG) is a toxic, colorless, odorless alcohol, found in antifreeze, brake fluid and as a stabilizer in foam agents and solvents
In the case we presented, the absence of persistent metabolic acidosis and anion gap had delayed the diagnosis until it was confirmed by toxicological test
Similar cases were described by the medical literature, caused by concurrent ingestion of EG and ethanol [10, 11], EG and methanol [12], suggesting that the lack of metabolic acidosis and anion gap does not exclude the diagnosis of EG poisoning
Summary
Ethylene glycol (EG) is a toxic, colorless, odorless alcohol, found in antifreeze, brake fluid and as a stabilizer in foam agents and solvents. Children are tempted to consume it in large quantities, leading to accidental poisoning [1]. Ethylene glycol is mostly metabolized by hepatic alcohol dehydrogenase (ADH). The main toxic metabolites are glycolic acid, contributing to a significant acidosis, and oxalic acid that binds to calcium, leading to calcium oxalate crystals formation. Deposition of crystals in various organs explains multisystem damage. The precipitation of calcium oxalate in kidney may result in tubular epithelial necrosis, associated with decreased glomerular filtration and renal failure [2]
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