SAT110 Euglycemic Diabetes Ketoacidosis Associated With Sodium-glucose Cotransporter Inhibitors: A Case Series To Raise Awareness

Disclosure: D. Katwal: None. Y. Pokharel: None. M. Ghawji: None. Z. Liu: None. H.O. Steinberg: None. S. Dagogo-Jack: Consulting Fee; Self; AstraZeneca, Boehringer Ingelheim, Janssen Research & Development Company, Medtronic Diabetes, Merck & Co., Sanofi, Bayer, Inc. Research Investigator; Self; AstraZeneca, Novo Nordisk, Boehringer Ingelheim. Other; Self; Janacare. Introduction: Sodium-Glucose Cotransporter Inhibitors (SGLT2i) treatment is increasing partly due to its cardiovascular and renal benefits, enlarging the population at-risk for euglycemic diabetic ketoacidosis (euDKA), a potentially life-threatening adverse event associated with SGLT2i use. Unfortunately, even among healthcare providers, awareness of euDKA appears to be low, resulting in delayed treatment and increased morbidity/mortality; We describe three cases of euDKA to illustrate. Case 1: A 25-year-old morbidly obese male with recent onset of T2DM presented with nausea and vomiting for two days. A few days before his presentation, he was started on dapagliflozin 5 mg daily and metformin 500 mg BID. Symptoms began within 24 hours of starting his medications. Laboratory results were consistent with euDKA: blood glucose (BG) of 144 mg/dl (70-110 mg/dl), pH 7.05 (7.35-7.45), bicarbonate 6 mmol/L (21-31mmol/L), and anion gap (AG) 20 mmol/L (2-15mmol/L). The euDKA resolved after 48 hours on standard treatment. Case 2: A 54-year-old male with T2DM on empagliflozin 10 mg daily presented with progressive dyspnea and altered mental status for two days. He was tachypneic, tachycardic, and hypotensive. Laboratory results were consistent with euDKA with a BG of 121 mg/dl, bicarb 4 mmol/L(21-31mmol/L), pH of 6.82, and AG 30 mmol/L. In addition to standard treatment, he required pressor and antibiotics; euDKA resolved after 65 hours. Case 3: A 68-year-old male with T2DM and other comorbidities presented with nausea, coffee-ground emesis, and abdominal pain for three days. He had recently started empagliflozin 25 mg daily. He had tachycardia and a diffusely tender abdomen. Laboratory results revealed BG of 101 mg/dl, bicarb 19 mmol/L (22-32 mmol/L), and AG of 16 (5-20) progressing to a bicarb 12 mmol/L, BG of 133 mg/dl, AG>20, pH of 7.23, and beta-hydroxybutyrate 9.7 mmol (0.00-0.29 mmol). The patient was managed with standard therapy and euDKA resolved after 75 hours. Discussion: euDKA is a rare but potentially life-threatening emergency primarily seen in T1DM and rarely in T2DM. The lack of profound hyperglycemia contributes to the delay in diagnosis and treatment. Poor oral intake, pancreatitis, alcohol use, infection, and dehydration have been associated with euDKA in patients treated with SGLT2i. Increased glucagon-to-insulin ratio and excess counter-regulatory hormones have been postulated to cause euDKA. In agreement with the literature, our patients experienced euDKA between 2-360 days of initiating SGLT2i. While our patients responded to standard treatment, the duration of insulin infusion may have been longer than plain DKA. Given the increased morbidity and mortality of euDKA, it is reasonable to consider holding SGLT2i during acute illness and preemptively before elective surgery. Providing sick-day rules to patients treated with SGLT2i should also decrease the risk of euDKA. Presentation: Saturday, June 17, 2023