Neonatal Hypoglycaemia
Neonates of women exposed to ACS in the 36+0 – 36+6 weeks gestational age group had lower rates of neonatal hypoglycaemia while those exposed to ACS in the 37+0-37+6 weeks and 38+0 – 38+6 weeks gestational age groups had higher rates of neonatal hypoglycaemia requiring parenteral treatment. These differences were not statistically significant but may be clinically significant. It is biologically plausible that ACS may cause neonatal hypoglycaemia since ACS can cause maternal hyperglycemia which in turn causes fetal hyperglycemia and hyperinsulinemia leading to neonatal hypoglycemia following birth. The impact of hypoglycemia in the neonatal period should not be understated with even transient neonatal hypoglycemia associated with long term adverse outcomes including decreased proficiency in literacy and mathematic achievement tests.35 Profound and prolonged hypoglycemia has been associated with significant neurodevelopmental delay.36 Prolonged neonatal hypoglycaemia has been associated with MRI cortical changes and periventricular injury as well as long term effects on the developing nervous system which may lead to developmental delay, cerebral palsy and neuropsychiatric deficits.37 The findings of this retrospective observational study provide some reassurance that infants exposed to ACS are not at a significantly increased risk of neonatal hypoglycaemia. However, the absence of data regarding maternal glycaemic control mean that this finding should be interpreted with caution. In particular, the centre with the largest proportion of patients receiving ACS had a proactive approach to maternal glycaemic control with all women being admitted to hospital for intensive blood glucose monitoring and insulin doses were prospectively increased by approximately 25% at the time of ACS administration (prior to the development of maternal hyperglycaemia). Additional sliding scale insulin boluses were used liberally to ensure maternal hyperglycaemia was avoided during the interval between ACS administration and caesarean section. Paul et al also reported a similar proactive approach to the prevention of maternal hyperglycaemia in their small case- control study of women with gestational diabetes.17 In their study, all women who received ACS were treated with intravenous insulin and dextrose infusions although data regarding maternal glycaemic control were not reported. Despite this intensive regime, the rate of neonatal hypoglycaemia was higher in those exposed to ACS although this was not statistically significant.