Abstract: SA-PO0521
The Question of Correcting Hypocalcemia in Suspected Coingestion of Methanol and Ethylene Glycol
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Lorenzo Capps, Maria Jose, RWJBarnabas Health, Toms River, New Jersey, United States
- Rajendran, Jackson, RWJBarnabas Health, Toms River, New Jersey, United States
- Chiapaikeo-Poco, Katherine, RWJBarnabas Health, Toms River, New Jersey, United States
- Yaziji, Muataz, RWJBarnabas Health, Toms River, New Jersey, United States
Introduction
Toxic alcohol ingestions are medical emergencies that require prompt diagnosis and tailored management. Methanol and ethylene glycol are metabolized via alcohol dehydrogenase but produce distinct clinical toxicities. While methanol poisoning typically presents with visual disturbances and metabolic acidosis, ethylene glycol toxicity is more often associated with renal damage and hypocalcemia due to calcium oxalate precipitation.
Case Description
A 44-year-old male presented with abdominal pain, blurred vision, and severe anion gap metabolic acidosis following ingestion of denatured alcohol and an unidentified substance. Laboratory studies confirmed a methanol level of 137 mg/dL and a critically low corrected serum calcium of 5.6 mg/dL. Ethylene glycol was undetectable, but hypocalcemia raised concern for co-ingestion. Hemodialysis, sodium bicarbonate infusion, and ethanol loading were initiated. Despite severe hypocalcemia, calcium was withheld due to the potential risk of oxalate precipitation if ethylene glycol co-ingestion had occurred. Serum calcium normalized over 24 hours with dialysis and metabolic correction alone.
Discussion
Hypocalcemia is not typically associated with methanol poisoning. There is barely any mention of hypocalcemia and methanol poisoning in the literature. This contrasts with ethylene glycol toxicity, where hypocalcemia is a hallmark finding due to oxalate binding. 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.
Clinical Course
| Timepoint | Ethanol (mg/dl) | Methanol (mg/dl) | Ethylene Glycol (mg/dl) | Corrected Ca (mg/dl) | Osmolality (mOsm/kg) |
| Admission | <10.1 | 137 | <20 | 5.6 | 369 |
| 5 hours | 39.5 | 95 | <20 | 8.7 | 328 |
| 16 hours | <10.1 | 49 | <20 | 8.8 | 321 |
| 24 hours | <10.1 | <10 | <20 | 8.9 | 301 |