A pregnant woman at 26 weeks presents with vomiting, dehydration, and Kussmaul breathing. Plasma glucose is 180 mg/dL, pH 7.15, and serum ketones are strongly positive. Why does diabetic ketoacidosis develop at lower glucose concentrations in pregnancy than in the non-pregnant state?

• A Pregnancy increases renal glucose excretion, masking hyperglycaemia
• B Placental insulinase degrades administered insulin completely
• C Insulin requirements fall sharply after mid-pregnancy
• D Chronic respiratory alkalosis of pregnancy lowers bicarbonate buffering capacity while placental hormones accelerate lipolysis ✓

Explanation

Pregnancy produces a compensated respiratory alkalosis with serum bicarbonate 3 to 4 mEq/L lower than normal, so the buffer reserve available to neutralise ketoacids is reduced. Simultaneously, placental hormones promote lipolysis and accelerated starvation, so ketoacidosis can appear with glucose below 200 mg/dL, the so-called euglycemic DKA of pregnancy. Renal glycosuria explains glucosuria, not acidosis. Insulin requirements actually rise in the second and third trimesters, eliminating option C.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.