A 29-year-old woman with pre-gestational Type 1 diabetes at 31 weeks presents with vomiting, dehydration, Kussmaul breathing, and a blood glucose of 190 mg/dL. Urinary ketones are strongly positive, pH 7.18. Why can diabetic ketoacidosis develop at such a modest glucose level in pregnancy?
- A Placental insulinase destroys circulating insulin faster than in the non-pregnant state
- B Accelerated starvation from placental hormones lowers the glucose threshold at which lipolysis is triggered ✓
- C Renal glycosuria causes disproportionate loss of water over glucose, concentrating ketones
- D Fetal consumption of glucose forces the mother into a chronically catabolic state
Correct answer: B. Accelerated starvation from placental hormones lowers the glucose threshold at which lipolysis is triggered
Explanation
Human placental lactogen, progesterone and cortisol produce a state of accelerated starvation, so buffering of glucose by insulin reserve is lost earlier and lipolysis begins at blood glucose values that would be safe outside pregnancy, often 150 to 250 mg/dL. Renal glycosuria and fetal glucose consumption contribute but do not explain the low threshold. Management is fluid, intravenous insulin infusion, and potassium replacement, with continuous fetal monitoring.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.