SAT-524 - The Euglycemic Illusion: Euglycemic Ketoacidosis Emergency in Late Pregnancy.

Introduction

Diabetic ketoacidosis (DKA) is typically associated with severe hyperglycemia and acidosis; however, pregnancy physiology including increased insulin resistance, reduced buffering capacity, and accelerated ketosis can result in euglycemic or near-euglycemic presentations. Severe metabolic acidosis in late pregnancy is rare but carries substantial maternal–fetal risk, making early recognition essential, as profound acidemia may occur despite modest glucose elevations.

Case Description

A 31-year-old woman at 34 weeks’ gestation with diet-controlled gestational diabetes (HbA1c 5.8%) and aspirin prophylaxis for prior preeclampsia presented with 6 days of worsening dyspnea, headache, and intermittent visual symptoms. She was hypertensive on arrival and treated with magnesium sulfate and antihypertensives. Betamethasone was administered for fetal lung maturation.

Laboratory evaluation revealed profound high anion-gap metabolic acidosis with bicarbonate < 5 mmol/L and pH 7.09. Given concern for maternal deterioration, emergent cesarean delivery was performed without complication, though she remained intubated postoperatively due to persistent acidosis. Repeat arterial blood gas worsened (pH 6.82). Lactate was normal, arguing against lactic acidosis. Beta-hydroxybutyrate was markedly elevated at 8.4 mmol/L, with a normal osmolar gap. Serum glucose was initially normal (98 mg/dL) and later rose modestly to 226 mg/dL following corticosteroid administration, supporting euglycemic or near-euglycemic DKA rather than lactic acidosis or toxic ingestion.
She was treated with insulin infusion, dextrose-containing fluids to prevent hypoglycemia, and aggressive electrolyte and acid–base monitoring with multidisciplinary critical care support.

Discussion

This case highlights that life-threatening ketoacidosis can occur in late pregnancy despite excellent baseline glycemic control and no prior insulin requirement. Pregnancy physiology lowers the threshold for ketosis, and antenatal corticosteroids may precipitate rapid metabolic decompensation. Profound acidosis with elevated beta-hydroxybutyrate, normal lactate, and only modest hyperglycemia underscores the importance of early ketone testing when evaluating high anion-gap metabolic acidosis in pregnancy.

Conclusion

Euglycemic ketoacidosis can occur during late pregnancy even in patients with diet-controlled gestational diabetes and normal HbA1c. High anion-gap metabolic acidosis with normal lactate levels should prompt early beta-hydroxybutyrate testing, particularly following antenatal corticosteroid administration. Prompt recognition and protocolized therapy are critical to optimize maternal and fetal outcomes.

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