MON-135 - Fulminant Starvation Ketoacidosis in Late Pregnancy Triggered by Short-Term Reduced Intake in A Non-Diabetic Woman

Introduction:

Late pregnancy is a state of accelerated starvation: placental hormones drive insulin resistance, lipolysis and ketogenesis, while continuous fetal glucose consumption lowers maternal fasting glucose and insulin, and narrows the buffering capacity via chronic respiratory alkalosis and renal bicarbonate loss. Even transient caloric deprivation can precipitate severe euglycemic ketoacidosis as an endocrine emergency.

Case Presentation:

A 24-year-old G2P1 female at 31 weeks with no history of diabetes presented with fever, myalgias and tachycardia, and admitted for presumed sepsis. Serial blood and urine cultures, respiratory viral panels, chest imaging, abdominal imaging and echocardiography were unrevealing, and antibiotics were discontinued as her fevers defervesced. During this time, she developed progressive nausea, vomiting and markedly reduced oral intake. By hospital day 5, she was afebrile, but tachycardic to 130 bpm, tachypneic and clinically volume depleted. Labs showed new hemoconcentration, severe high-anion gap metabolic acidosis with bicarbonate of 5 mmol/L (normal 22-28) and anion gap of 27 mmol/L (normal 8-12). Renal function, lactate and blood glucose were normal. B-hydroxybutyrate was markedly elevated at 73.9 mg/dL (normal < 0.6), serum osmolality 291 mOsm/kg (normal 285-295) and HgbA1c 4.8% (normal 4-5.6%). Toxicology screens were negative. She was transferred to the ICU, intubated for impending respiratory failure and managed as an endocrine metabolic emergency with isotonic crystalloid, dextrose-containing fluids to suppress lipolysis and ketogenesis, and aggressive electrolyte repletion. Within 24 hours of nutritional repletion, maternal pH normalized, bicarbonate rose to 20 mmol/L, and anion gap closed without exogenous insulin. She was extubated the next day and recovered fully.

Conclusion:

Euglycemic starvation ketoacidosis in late pregnancy reflects gestational fuel physiology, driven by placental hormone-driven insulin resistance, continuous fetal glucose extraction, and reduced bicarbonate reserve. This combination makes brief nutritional deprivation sufficient to trigger profound ketogenesis and academia. In third trimester patients with severe high anion gap metabolic acidosis, normal lactate and normoglycemia, a high index of suspicion for euglycemic starvation ketoacidosis should be maintained, especially in the setting of poor oral intake. Management should be physiology-guided, emphasizing dextrose-containing fluids to suppress lipolysis, and electrolyte derangement correction to avoid maternal decompensation.

References:

1. Frise CJ, Mackillop L, Joash K, Williamson C. Starvation ketoacidosis in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2013;167(1):1-7. doi:10.1016/j.ejogrb.2012.10.005.

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