SUN-189 Ketogenic Diet and Superimposed Fasting State as a Precursor to Euglycemic Diabetic Ketoacidosis in Patient With Type 1 Diabetes Undergoing RIPE Therapy

Abstract A. Alcantara: None. C. Pham: None. A.L. Dominguez: None. Introduction: Euglycemic diabetic ketoacidosis (DKA) has often been reported as a complication of SGLT-2 inhibitors but uncommonly documented in other causes. Clinical Case: A 35-year-old male with type 1 DM presents for chronic cough, night sweats, and poor oral intake and was diagnosed with tuberculosis. Prior to hospitalization, he consumed a ketogenic diet as a method of glucose control and would only take correctional insulin but was on basal bolus regimen while admitted. He started RIPE therapy and subsequently developed abdominal pain, nausea, emesis, and decreased appetite. After two days of persistent vomiting, glucose level was 494 mg/dL (65-99), bicarbonate level 6 mmol/L (20-30), anion gap 36 mmol/L (10-20), and B-OH level 11.40 mmol/L (<0.28) and started on insulin drip. He was transitioned to subcutaneous insulin after gap was closed but had persistent poor appetite and vomiting. Repeat labs days later showed repeat anion gap 27 mmol/L, glucose 215 mg/dL, bicarbonate level 8 mmol/L, and B-OH level 4.64 mmol/L, confirming euglycemic DKA despite being on standing insulin and restarted on insulin drip. He subsequently transitioned again to subcutaneous insulin with aggressive anti-nausea regimen and dietary supplementation without recurrence of DKA. Conclusion: Euglycemic DKA was first documented in patients presenting with DKA and reduced carbohydrate intake. Data also suggests that people with type 1 diabetes are also more prone to developing ketosis after fasting, suggesting the mechanism behind euglycemic DKA is due to impaired hepatic glucose utilization. Other causes of euglycemic DKA such as pregnancy and alcohol use have also been reported. With the advent of SGLT2 inhibitors, euglycemic DKA due to increased glucosuria has become more prevalent. Thus, it is important to note that euglycemic DKA stems from an overall total body glucose deficiency and insulin deficiency versus only insulin deficiency as seen in classic DKA. Multiple factors contributed to the presentation of euglycemic DKA in this case, including ketogenic diet leading to poor glycogen stores, active infection leading to increased insulin demand, and initiation of RIPE therapy which is known to cause nausea and vomiting. This case illustrates that euglycemic DKA is precipitated from a low glucose utilization state and insulin deficiency. In patients presenting with euglycemic DKA without SGLT2 inhibitor use, addressing nutritional status and providing insulin therapy are two cornerstones of therapy. Sunday, June 2, 2024