EUGLYCEMIC DIABETIC KETOACIDOSIS MASQUERADING AS TOXIC ALCOHOL INGESTION

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: First reported in 1973, euglycemic diabetic ketoacidosis (euDKA) historically accounted for 0.8-1.1% of (DKA) cases [1]. Without hyperglycemia, the anion gap metabolic acidosis (AGMA) euDKA may be attributed to other causes. We present a case that was mistaken toxic alcohol poisoning. CASE PRESENTATION: A 53-year-old woman with type 2 diabetes (T2D), which she taking metformin and glyburide, presented abdominal pain nausea. She also drinking "vodka" given by stranger day prior. Labs included bicarbonate 12 mEq/L, (AG) 18, lactate 1.7 mmol/L, lipase 735 U/L, urinalysis 2+ glucose 3+ ketones. CT confirmed pancreatitis. Correctional insulin ordered but not due blood sugar 121-225 mg/dL. Repeat labs overnight revealed <5, AG >18, arterial pH 7.09. After toxicology consult, IV fomepizole transferred ICU urgent hemodialysis (HD) possible Just prior placing HD access, records obtained prescribed empagliflozin. Ultimately, panel negative beta-hydroxybutyrate elevated at 0.86 mmol/L. treated infusions crystalloid, insulin, dextrose. Her ketosis resolved 9 days, discharged on metformin. DISCUSSION: Previously seen low caloric intake, or cocaine use, liver disease, pregnancy, has recently been linked sodium cotransporter inhibitor (SGLT2I) use [2]. Since FDA approval 2013, SGLT2I steadily risen as data cardiovascular renal benefits accumulate. SGLT2Is act independent blocking proximal tubule reabsorption glucose. This can lead euglycemia despite deficiency potential an acute insult, like pancreatitis, trigger euDKA. Along lack SGLT2I-related mediated volume depletion, counterregulatory hormones, enhanced lipolysis fatty acid oxidation [3]. Notably, pancreatitis without Though initial ketonuria inebriation were, retrospect, clues presence DKA this case, report suspicious ingestion led presumptive diagnosis Indeed, untreated poisoning major disability death, prompt empiric treatment is vital if clinical suspicion exists. CONCLUSIONS: The rapid AGMA remains challenge intensive care. As continues grow, providers will increasingly encounter Importantly, does exclude DKA, must routinely considered differential unexplained severe prevent adverse outcomes from delays treatment. REFERENCE #1: Jenkins et al. Euglycaemic ketoacidosis: it exist? Acta Diabetol 1993;30:251-3. #2: Bonora Euglycemic Ketoacidosis. Review Curr Diab Rep 2020 May 19;20:25. #3: Qiu Ketosis response SGLT2 inhibitors: Basic mechanisms therapeutic perspectives. Diabetes Metab Res Rev 2017 Jul;33(5). DISCLOSURES: No relevant relationships Christos Argyropoulos, source=Web Response Matt Bouchonville, Mitchell Byrd, Melissa Fang, Umair Khan, Joao Teixeira,