Abstract: SA-PO1008
A Suspected Case of Glycolic Acid Poisoning
Session Information
- Fellows/Residents Case Reports: Fluid, Electrolytes, Acid Base
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Edmonston, Daniel, Duke University Hospital, Durham, North Carolina, United States
- Mohottige, Dinushika, Duke University Hospital, Durham, North Carolina, United States
- Morris, Jessica D, Duke University Hospital, Durham, North Carolina, United States
- Kothari, Niraj R., Duke University Hospital, Durham, North Carolina, United States
Background
The diagnosis of ethylene glycol and other toxic alcohol poisoning is often challenging. Metabolism by alcohol dehydrogenase may result in undetectable ethylene glycol levels in serum. Similarly, the elevation in osmolal gap may not be present once ethylene glycol is metabolized to its charged metabolites. One of the most toxic of these metabolites is glycolic acid. We report a case of suspected recurrent glycolic acid poisoning.
Methods
Our patient was a 38-year-old woman with a history of ethanol abuse and an 8-month span of recurrent admissions for altered mental status in the setting of severe lactic acidosis and acute kidney injury. Investigations including urine toxicology screen, ethanol levels, and volatile acid levels including ethylene glycol, methanol, and isopropyl alcohol were negative during each admission. The patient and family denied any availability of antifreeze and other toxins in the home. Metabolic evaluation for a mitochondrial disorder was negative. She was admitted for nine days for severe lactic acidosis with negative evaluation, which improved with supportive treatment of acidemia. On the day of discharge, her serum bicarbonate was 25 mmol/L. The next day, she became altered again after returning home from the drug store. Her bicarbonate was now 5 mmol/L with arterial pH of 7.13. Her osmolal gap was 5. Again, screening for toxic ingestions was negative. Given high suspicion, she was empirically started on fomepizole and continuous renal replacement therapy was initiated. She remained on pressor support with progressive acidemia, and ultimately died despite aggressive renal replacement therapy. Her autopsy was notable for extensive intravascular and perivascular oxalate crystals in the brain and kidneys. She was also noted to have a transmural acute myocardial infarction of the left ventricle.
Conclusion
Glycolic acid is found in a myriad of cosmetic products and can be toxic in lethal doses. Unfortunately, the presentation may be difficult to diagnose as the osmolal gap may be normal, lactate markedly elevated (glycolic acid can interfere with certain lab assays for lactate), and ethylene glycol level negative. Even in cases of ethylene glycol poisoning, the glycolic acid level is often a more reliable marker of toxicity. This case highlights the importance of assessment of glycolic acid level in suspected toxic alcohol poisoning.