Ethylene Glycol Poisoning: Resolution of Cranial Nerve Deficit

• Glycol intoxication may lead to delayed neurologic manifestations, which may lead to an inaccurate diagnosis.
• The traditional laboratory investigation may not indicate ethylene glycol exposure if preformed too soon after ingestion because the anion gap acidosis takes time to develop.
• Initial treatment is to maintain the airway, breathing, and circulation while minimizing the toxic load.
• Aggressive hydration with crystalloid solution (normal saline) to enhance urinary output as well as sodium bicarbonate infusion to correct metabolic acidosis are the primary aims.
• The Food and Drug Administration–approved antidote for ethylene glycol toxicity is fomepizole (Antizol) given every 12 hours intravenously.
• Clinicians should be aware that the use of corticosteroids is not an Food and Drug Administration–approved treatment for the late effect of cranial nerve deficit caused by glycol toxicity.

Ethylene glycol poisoning is a major contributor to the development of idiopathic metabolic acidosis, which may lead to renal failure. Ethylene glycol poisoning should be among suspected differentials when assessing a seemingly intoxicated patient with hypocalcemia, anion gap acidosis, and nontoxic blood alcohol levels. Glycol intoxication may lead to delayed neurologic manifestations, which may lead to an inaccurate diagnosis. No clear clinical guidelines exist to recommend treatment for this late effect. This is a case of the complete resolution of facial nerve deficit secondary to glycol poisoning after the completion of a steroid therapy course on an inpatient psychiatric unit.