Abstract Introduction Toxic alcohol ingestions, particularly methanol and ethylene glycol, are life-threatening emergencies. Though both are metabolized by alcohol dehydrogenase (ADH), their downstream metabolites cause distinct clinical syndromes. Methanol’s toxicity stems from formate, which primarily affects the optic nerve, while ethylene glycol's metabolite, oxalate, forms calcium oxalate crystals that precipitate renal and systemic damage. Recognizing patterns of injury is critical—especially when co-ingestion is suspected but toxicology data are inconclusive. We report a case of confirmed methanol intoxication with severe metabolic acidosis and hypocalcemia, raising concern for ethylene glycol co-ingestion and prompting a management dilemma regarding calcium replacement. Case A 44-year-old male with no significant past medical history presented to the emergency department with worsening abdominal pain and progressive blurry vision. He reported binge drinking tequila four days earlier, followed by ingestion of unknown quantities of denatured alcohol (a compound of ethanol and methanol) and an unidentified pink-colored substance to relieve ethanol withdrawal headaches. On exam, he was alert but dehydrated, with blurred vision and visual acuity limited to finger counting at ten feet. Laboratory studies revealed profound anion gap metabolic acidosis (pH 7.04, pCO2 52 mmHg, HCO3⁻ 3 mEq/L), a serum osmolality of 369 mOsm/kg, and a methanol level of 137 mg/dL. Ethylene glycol and ethanol levels were undetectable at baseline. Notably, corrected calcium was critically low at 5.6 mg/dL, with no evidence of oxalate crystalluria on urinalysis. Serum creatinine was 0.54 mg/dL. Management included initiation of a sodium bicarbonate drip, ethanol administration as an ADH inhibitor while awaiting fomepizole, and emergent hemodialysis, which led to progressive improvement in acidosis and normalization of calcium levels over 24 hours. Conclusion Hypocalcemia is not typically associated with methanol poisoning. In this case, the presence of unexplained hypocalcemia prompted a cautious approach, prioritizing systemic toxin clearance and avoidance of potentially harmful calcium administration. This case reinforces the pathophysiologic differences between methanol and ethylene glycol toxicity and supports withholding calcium unless symptoms are present. In toxic alcohol ingestion with suspected but unconfirmed ethylene glycol co-ingestion, asymptomatic hypocalcemia may be best managed conservatively. This case underscores the need for individualized, physiology-driven decision-making in toxicologic emergencies. This abstract is funded by: None
Qaiser et al. (Fri,) studied this question.