THU310 A Presentation Of Diabetic Ketoacidosis In Gestational Diabetes

Abstract

Abstract Disclosure: C. Yim: None. S.L. Liu: None. T. Spaic: None. Diabetic ketoacidosis (DKA) is a diabetic emergency characterized by wide anion gap acidosis, presence of ketones (in serum and/or urine) and, frequently, uncontrolled hyperglycemia. In pregnancy, DKA more commonly occurs in women with pre-existing diabetes, usually type 1 diabetes, and is exceptionally rare in women with gestational diabetes mellitus (GDM). We report a case of a 37-year-old woman in her second pregnancy who presented to hospital with DKA at 29+3 weeks gestation shortly after diagnosis of GDM 4 days earlier. In her first pregnancy, she was diagnosed with GDM at 28 weeks, required treatment with metformin at 35 weeks, which she stopped postpartum. She conceived her second pregnancy 3 months postpartum so was not screened for diabetes postpartum. In her second pregnancy, there was no evidence of diabetes on early antenatal labwork at 7 weeks: Hemoglobin A1c (HbA1c) 5.6%, random glucose 3.6 mmol/L. Early GDM screening at 21+1 weeks with 75 gram oral glucose tolerance test (OGTT) was normal: fasting glucose 4.4 mmol/L 1-hour glucose 9.0 mmol/L, 2-hour glucose 6.5 mmol/L. She presented to hospital at 29+3 weeks gestation with a 2-day history of polyuria, polydipsia, dizziness, and decreased oral intake without nausea or vomiting. Four days prior to presentation, she was diagnosed with GDM on a 75g OGTT (fasting glucose 6.2 mmol/L, 1-hour glucose 15.1 mmol/L, 2-hour glucose 11.9mmol/L). Admission labwork showed serum glucose 34.8 mmol/L, anion gap 18, pH 7.29, bicarbonate 17 and beta-hydroxybutyrate 2.97. She was treated with IV fluids and insulin and initiated on multiple daily injections of insulin. Other than pregnancy, no clear precipitating factor was found. HbA1C was 6.4%, serum insulin and C-peptide levels were inappropriately low at 22 pmol/L and 296 pmol/L respectively. Her anti-glutamic acid decarboxylase and anti-islet cell antibodies were negative. Lipase was mildly elevated at 226U/L but improved to 144U/L with treatment. Abdominal ultrasound did not demonstrate any findings suggestive of acute pancreatitis. Her 24-hour urinary free cortisol was 366 nmol and 442 nmol, both within normal trimester-specific range. Her salivary cortisol was in the normal range (10.5nmol and 10.9nmol). Following discharge, she remained significantly insulin resistant with suboptimal glycemic control (total daily insulin requirements ∼3.5 units/kg/day, HbA1C 7.9% at 35+6 weeks). Due to increased insulin resistance in pregnancy, DKA can progress more rapidly compared to nonpregnancy. Given increased rates of perinatal morbidity and mortality associated with DKA, treatment and monitoring should be promptly initiated. A high index of suspicion is especially important given that DKA is a rare presentation in GDM. Other precipitating factors of newly decompensated diabetes should also be ruled out. Presentation: Thursday, June 15, 2023