SUN-523 A Case of Sudden Onset Diabetic Ketoacidosis in Pregnancy

Abstract Disclosure: N. Sherani: None. N. Kolta: None. D.G. Varghese: None. H.B. Whitlatch: None. R. Malek: None. Background: Development of fulminant diabetes during pregnancy, albeit a rare occurrence, has been documented in the literature. This can occur in any trimester and is characterized as Type 1B diabetes mellitus. Even pregnant patients who pass gestational diabetes screening exams can develop fulminant diabetes. The criteria for diagnosis of fulminant Type 1 diabetes include DKA within 7 days of symptom development, HbA1c< 8.5% with plasma glucose > 288 mg/dl and fasting c-peptide of < 0.3 ng/ml. Development of diabetic ketoacidosis during the third trimester can have catastrophic consequences and is associated with high fetal mortality. Clinical Case: 31-year-old female (G3P0110) with history of substance use disorder (managed with suboxone), hepatitis C, and morbid obesity (BMI >35) presented at 37 weeks and 6 days gestation with intrauterine fetal demise in the setting of severe diabetic ketoacidosis (DKA). She had no history of pregestational or gestational diabetes, and her HbA1c was 5.7% at her first prenatal visit. She had a normal oral 50 gm glucose challenge test (GCT) of 115 mg/dL at 30 weeks and 6 days, and trace urine glucose at the same visit. At 37 weeks gestation, she developed sudden-onset polyuria, polydipsia, and emesis with abdominal cramping. Fetal heart rate was undetectable. She was found to have elevated glucose (>800 mg/dL), beta-hydroxybutyrate 73.4 (0-3 mg/dL) with bicarbonate levels 9 (21-30 mmol/L) consistent with DKA. Her hemoglobin A1c was 10.5%. Further testing revealed triglyceride levels of 2,625 (<150mg/dL) that was attributed to uncontrolled hyperglycemia and propofol use. Triglyceride levels normalized after the propofol was discontinued. GAD-65, islet cell, and zinc transporter 8 antibodies were negative, and c-peptide was 0.6 (0.5-3.3 ng/mL) with glucose of 133mg/dL. Lipase was 200 (23-300 u/L). She was treated as per DKA protocol and had improvement in her clinical condition. She underwent a C-section with delivery of stillborn fetus. Autopsy of fetus revealed normal weight (2960gm) and no genetic abnormality. She continued to require basal/bolus insulin therapy as an outpatient. Conclusion: We describe a case of rapidly developing diabetes in a pregnant patient with otherwise normal antepartum testing (GCT and urine glucose), 28 lb weight gain in pregnancy, normal fetal growth, and an absence of diabetes-related symptoms until 37 weeks gestation. While this case does not meet all criteria for fulminant diabetes in pregnancy, it suggests that repeated diabetes screening should be considered in patients with high-risk clinical features, such as obesity and prediabetes, in order to avoid late-term maternal and fetal complications. Presentation: Sunday, July 13, 2025