Abstract: PUB099
Antifreeze in the Desert: A Case Report of Accidental Ethylene Glycol Ingestion
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Tanasiuk, Jessee T., The University of Arizona College of Medicine Phoenix, Phoenix, Arizona, United States
- Rajpal, Minesh, Southwest Kidney Institute PLC, Tempe, Arizona, United States
Introduction
In the setting of rapidly increasing lactic acid without evidence of ischemia or infection in the geriatric population with dementia, alternative causes must be considered. Lactic acid levels measured with blood gas analysis can be affected by glycolic acid, a metabolite of ethylene glycol, and result falsely high [1]. Calculating osmolar gap early and maintaining a broad differential can aid in diagnosis particularly in the altered or unresponsive patient.
Case Description
71 y/o F hx vascular dementia, CKD stage 3a (b Cr 1.23) w/ AMS and lethargy found to have HAGMA. On presentation sodium was 149 mmol/L, anion gap 30, osmolar gap 65 mOsm/kg, calcium 10.5 mg/dL, lactic acid (venous) 10.4, BHB 6.7 mg/dL, salicylate <0.3 mg/dL. UA negative for UTI and UDS negative. Head CT and CXR both negative for acute findings. Initial ABG 7.14/10/129/3, lactic acid >18 mmol/L (RA). Repeat ABG after intubation and NS bolus 7.05/24/518/7, lactic acid >18. Volatile screen negative for acetone, ethanol, isopropanol, and methanol. Ethylene glycol 180 mg/dL. She was initiated on fomepizole, thiamine, and pyridoxine. She received 8 rounds of HD to clear toxic metabolites and for renal disfunction, with Cr peaking at 6.35 mg/dL, requiring HD after discharge.
Discussion
In this case the sustained lactic acid level and discrepancy between serum measurements in-lab and on ABG were due to the inability of ABG testing to differentiate between lactic acid and glycolic acid [1]. Elevation in osmolar gap should lead to consideration of toxic alcohol ingestion.