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.