Corticosteroid exposure after 34 weeks and prior to planned
caesarean birth
Our findings concur with a large RCT of pregnancies from
34+0 weeks at risk of late preterm birth8. The relative risk of any hypoglycaemia in the
corticosteroids (2 doses of 12mg of betamethasone) arm was 1.60 (95%
1.37–1.87). With a 15% incidence in the placebo arm, the definition
included much less severe hypoglycaemia than in our analysis.
Importantly, 84% of neonates were born before 37+0weeks, so the findings are less relevant than for our term cohort.
Further, in the trials assessing corticosteroids specifically prior to
planned early term caesarean birth 10-12,
hypoglycaemia has not been recorded. Our data importantly addresses this
specific group and highlights the risk of severe hypoglycaemia in these
term neonates. A particular issue is pregnancies complicated by
diabetes, on which existing literature is limited26-29. In the UK, recommendations state diabetes
should not be a ‘contraindication to antenatal corticosteroids for fetal
lung maturation’ 3. Our numbers preclude the
assessment of effects of ACS administration before 34 weeks in infants
born at term. However, we demonstrated that infants exposed to ACS at or
after 34 weeks had a higher incidence of severe hypoglycaemia compared
to those not exposed (31% vs 3.8%, aOR: 5.76, 95% CI 2.28-14.52).
Whilst respiratory benefits are likely to remain, this risk should be
considered alongside that of poorer maternal glucose control.
The relationship between SGA and ACS needs to be addressed. McKinzie et
al 22 found a higher risk of SGA among term
pregnancies who had received ACS before 34+0 weeks; we
did not (Table 1). We postulate that ACS may, and this may vary in
different units, be given more in pregnancies where SGA is suspected and
so the relationship is not causal. This is supported by our finding of
increased SGA in pregnancies exposed after 34 weeks.
The positive correlation between corticosteroid-to-birth interval and
neonatal glucose level, albeit as a univariate analysis, pictorially
demonstrates the increased risk in those who benefit least. It may also
shed light on the mechanism. Temporary maternal hyperglycaemia
frequently follows corticosteroid administration and this could cause
fetal hyperinsulinemia, but this mechanism has not been proven30. That hypoglycaemia is more common even many weeks
later suggests that longer term metabolic changes are induced.