Filling In the Gaps: Ethylene Glycol Poisoning Presenting With Isolated Lactate and Osmolar Gaps.

Ethylene glycol (EG) is an organic compound used in antifreeze. In 2020 alone, there were 5,277 EG exposures, with only 617 reported as intentional ingestions. Therefore, encountering EG toxicity is rare; however, it is essential to identify it promptly based on a focused history, exam, and rapid identification of commonly associated EG-induced metabolic derangements. If the diagnosis is not made within 12 hours of ingestion or exposure, severe morbidity and mortality can occur. Previous reports of EG poisoning have occurred in the setting of a lactate gap (LG) and osmolar gap (OG); however, they also had commonly associated findings of EG toxicity such as high anion gap acidosis (HAGMA), acute kidney injury (AKI), hypocalcemia, calcium oxalate stones, and suggestive histories of EG ingestion. We present a case of a 57-year-old male who presented from home for slurred speech and gait imbalance. He was intubated for airway protection due to obtundation. Labs only revealed the presence of both LG and OG, non-anion gap acidosis (NAGMA), and an EG level of 112 mg/dL three days after admission. Hemodialysis (HD) was initiated solely based on these findings within eight hours of admission, and he was subsequently able to be extubated without developing an acute or chronic cardio-pulmonary or renal injury. The patient's partner reported to the care team that they found multiple empty bottles of rum and whisky, an empty anti-freeze bottle, and a Sprite bottle with a light blue substance that was nearly empty in their basement. After extubation, the patient admitted to ingesting the antifreeze with the intention of self-harm. He recovered without complication and was transferred to the inpatient psychiatric unit to manage his depression and suicidality further. The early diagnosis and treatment of EG poisoning is critical to prevent severe morbidity and mortality occurring only 12 hours after ingestion. Therefore, reliance on prompt recognition of common laboratory findings, understanding of EG toxicity-specific signs and symptoms, and awareness of other rapid diagnostic tools for EG are essential in clinching the diagnosis. This case highlights the potential atypical presentations of EG toxicity, helpful diagnostic strategies, and the importance of avoiding anchoring bias when commonly associated disease processes are absent.