ODP192 Empagliflozin associated Euglycemic Diabetic Ketoacidosis and the Terrible Triad

Abstract

Abstract Background Among diabetic patients, newer drug classes such as SGLT2i have been reported to present with Euglycemic Diabetic Ketoacidosis (eDKA), wherein these patients are without signs of elevated glucose levels. However, this condition can coexist with acute pancreatitis (AP) and hypertriglyceridemia (HTG), which is also known as the terrible triad. Clinical Case We were presented with a 31-year old diabetic male maintained on empagliflozin 25mg OD and metformin 500mg OD, discontinued his medication four months ago, and recently started retaking empagliflozin one week ago. He presented with drowsiness, severe abdominal pain rated as 9/10, and vomiting. An NGT was inserted and on further workup, acidosis was present on ABG with an anion gap of 28 mEq/L. AP was noted on abdominal ultrasound with an amylase of 768 U/L. CBG was 167mg/dL, Hba1c of 7.4%, Creatinine of 1. 05mg/dL, with ketonuria on urinalysis. Hydration was started with referral to endocrinology service. Insulin drip was started, and CBGs ranged from 145-229mg/dL while on drip. Hydration was increased accordingly, considering the patient's intake and output. Further workup was done, and lipid profile revealed severe hypertriglyceridemia at 1724.78mg/dL and elevated VLDL at 342mg/dL. Statin was prescribed, and eventually, insulin drip was titrated down with resolution of acidosis. Insulin was then shifted to subcutaneous regimen. Diet was also transitioned to clear liquids and eventually into diabetic diet. The patient was sent home and was uneventful after. eDKA develops due to increased glucagon secretion and decreased insulin production, promoting glucose to fat metabolism and ultimately stimulating ketogenesis. These agents decrease the blood glucose level by increasing urinary glucose excretion leading to a reduction in insulin secretion from the pancreatic β-cells. The terrible or enigmatic triad consisting of AP, HTG, and DKA/eDKA has been well reported but has a complex process. HTG results as a product of the reduced lipoprotein lipase activity in peripheral tissues, which decreases the removal of VLDL from the plasma. In AP cases, HTG only accounts for a minority (2-7%) of cases, but the risk was increased with levels above 1000mg/dL, such as in our patient. In the study by Simons-Linares et al., having the said triad had higher odds of having SIRS, shock, sepsis, and parenteral nutrition when compared to AP patients alone. eDKA patients can present with non-specific signs and symptoms such as nausea, vomiting, and abdominal pain, which can delay the diagnosis in patients. Fortunately, it was recognized early on, and there was a quick response in managing the case. Conclusion To date, there is scarcity among reports of the terrible triad, especially with empagliflozin use. Therefore, we can stress the importance of keen assessments and history taking in detecting the triad for an early aggressive approach to prevent adverse outcomes. Presentation: No date and time listed