Case #021

Two gaps opening at once is the finding that matters. A high anion gap acidosis alone has a long differential and a raised osmolar gap alone means little, but together they say a toxic alcohol was swallowed and is partway through being metabolised: the parent alcohol is osmotically active and widens the osmolar gap early, while its acid metabolites widen the anion gap as metabolism proceeds. Appearing drunk with no smell of alcohol fits, and the empty container beside him supplies the rest. Negative ketones, a normal glucose, undetectable ethanol and salicylate, and only a modest lactate close off the other common causes of an acidosis this severe. What distinguishes ethylene glycol from methanol at the bedside is the target organ: methanol is metabolised to formic acid, which injures the optic nerve and produces the characteristic 'snowstorm' visual blurring, whereas this patient has entirely normal vision. Ethylene glycol is instead metabolised through glycolic acid to oxalic acid, which chelates calcium: producing the hypocalcemia, the prolonged QT interval, and calcium oxalate crystals that precipitate in the renal tubules and cause the acute kidney injury seen here. Treatment is directed at blocking metabolism rather than removing the parent compound: fomepizole inhibits alcohol dehydrogenase with far greater affinity than ethanol and without the sedation of an ethanol infusion, preventing formation of the toxic metabolites. Hemodialysis is added when there is severe acidosis, renal failure, or a high measured level, since it clears both the parent alcohol and the acid metabolites. Bicarbonate only buys time and does nothing about ongoing metabolite production, while thiamine and pyridoxine are given as cofactors to shunt what is already circulating away from oxalate.