A macrosomic baby born to a mother with poorly controlled pre-gestational diabetes becomes jittery and lethargic 90 minutes after birth. Capillary glucose is 32 mg/dL. The MECHANISM of this neonatal hypoglycaemia is:
- A Maternal insulin transferred across the placenta during labour
- B Persistent fetal hyperinsulinism after abrupt withdrawal of maternal glucose supply ✓
- C Impaired hepatic glycogen synthesis caused by hyperbilirubinaemia
- D Delayed feeding leading to depleted brown fat reserves
Explanation
Chronic maternal hyperglycaemia crosses the placenta and drives fetal pancreatic beta cell hyperplasia with sustained hyperinsulinaemia. After cord clamping the maternal glucose supply stops abruptly but the fetal pancreas keeps secreting insulin, causing hypoglycaemia within the first hours. Maternal insulin does not cross the placenta because of its molecular size. These infants also face higher risks of respiratory distress syndrome, polycythaemia, hypocalcaemia and birth trauma from macrosomia.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.