24 yrs old Samoan ,G2 P1 booked with LMC @ 12/40- BMI 41.8. Type II diabetes on Metformin and Gliclazide
Low risk MSS1, HbA1c - 50. El-LSCS 2010 for LFD 5220g.
Commenced on Insulin and metformin; attended regular ANC ; persistent macrosomia>95th centile.
At 34 weeks BMI 52, EFW 5921gms, normal dopplers ; HBA1C 47 . Planned -biweekly CTG and steroids. At 36 weeks EFW 6692g, AFI 42, normal dopplers. Weight 150kg (up from 118kg at booking)
EL/LSCS under spinal anaesthesia (37+4) – live male baby 7390g.
Apgars 9/1, 9/5, 10/10; Lactates A: 1.3, V: 1.1. Initial BSL 1.8 mmol/L , admitted to NICU for CPAP and BSL correction and monitoring.
CPAP discontinued after 16 hrs, nil further respiratory support. Initial BSL corrected with IV dextrose, no ongoing issues
EBM/AF from day two.
ECHO = Hypertrophic but structurally normal heart.
Genetics review: No dysmorphic features noted, assessed as symmetrically LGA baby, not assessed as ‘overgrowth’ syndrome.
Discussion:
Fetal overgrowth can be defined as a birth weight greater than the 90th percentile, corrected for gestational age.
The causes of macrosomia include both genetic and environmental factors. The offspring of mothers with diabetes have greater risks of adverse metabolic sequelae in childhood and later life and risks appear to be additional to genetic predisposition. Obese women are more likely to develop offspring macrosomia, with 1.7-fold risk increase compared to normal weight women but excessive gestational weight gain has been extensively proven to be an important risk factor for the development of macrosomia. Measurement of postprandial plasma FFA might be the best, clinically obtainable predictor of infant birth weight in this population, but this needs further study. The relationship between GDM and macrosomia is probably more complex than generally appreciated