MON-635 Case of steroid-induced DKA

Abstract Disclosure: S. Azmat: None. O. Lodhi: None. M.F. Siddiqui: None. Case of Steroid-induced DKA: Diabetic ketoacidosis (DKA) is a severe complication marked by ketonemia, acidosis, and hyperglycemia typically associated with type 1 diabetes. However steroid-induced DKA is rare with an incidence of 0-56/1000 persons. This report presents a case of a 52-year-old female with insulin-dependent type 2 diabetes mellitus who developed steroid-induced DKA. This case underscores the importance of vigilant steroid use, especially in septic shock settings, and raises awareness of the potential for steroid-induced DKA in T2DM patients. Clinical case: A 52-year-old female with past medical history of uncontrolled T2DM with an A1c of 13.6% (<5.7%) presented with diffuse abdominal pain. Her outpatient diabetes medication included Januvia 25 mg and 10 units of insulin. Upon arrival the patient was tachycardic to 110s and hypotensive BP 63/35. Labs revealed hyperglycemia and anion gap metabolic acidosis from septic shock: Glucose: 284 mg/dL(70-90 mg/dL), bicarb15 mEq/L (22-28 mEq/L), BHB 0.1 mmol/L (0.1-0.3 mmol/L), AG 10.7 mmol/L (4-11 mmol/L), Cr 3.26mg/dL (0.50-1.10 mg/dL), lactic acid 3.0 mmol/L (0.5-2.0 mmol/L), pH 7.33 (7.35-7.45), pCO2 19 mmHg(33-45 mmHg) and pO2 115mmHg (75-105 mmHg). The patient was admitted for septic shock, secondary to pyelonephritis, given pressors and stress dose steroids. She developed severe hyperglycemia with blood glucose over 500 mg/dL(70-90 mg/dL), bicar decreased from 15 to 10 mEq/L (22-28 mEq/L), AG increased from 10. 7>12.2, and BHB increased up to 1.10. Therefore, a diagnosis of steroid-induced DKA was established, the patient was treated with insulin drip per DKA protocols and dextrose fluids. DKA was resolved within two days with clinical improvement. The patient was successfully transitioned to subcutaneous basal-bolus insulin and remained euglycemic. Conclusion: The reported case details a patient with uncontrolled T2DM who developed steroid-induced DKA during treatment for septic shock. The two main mechanisms that could contribute to steroid-induced DKA include elevated peripheral insulin resistance at muscle and adipose levels through GLUT4 translocation inhibition and secondly increased glucose production through glycogenolysis and gluconeogenesis. Per the literature review, there are very few reported cases of steroid-induced DKA in T2DM patients. These cases highlight the importance of closely monitoring diabetic patients receiving steroid therapy, including those with well-managed T2DM or no prior history of diabetes. Also, physicians should be mindful of the potential for steroid-induced DKA in vulnerable patients, such as obese individuals, who are starting steroid therapy. Presentation: Monday, July 14, 2025