Administering betamethasone to women with gestational diabetes causes maternal hyperglycaemia, and is associated with neonatal hypoglycaemia 1. There are limited data to guide interventions to control maternal hyperglycaemia in this population, including treatment targets and endpoints.
Here we discuss results of a recently published cohort study 2 reporting safety and efficacy of a novel Pregnancy-specific Intravenous Insulin-Glucose Infusion (P-IVI) protocol, validated at John Hunter Hospital since 2017, as compared to the previous standard of care (a generic Adult IntraVenous Insulin protocol (A-IVI) not designed for pregnancy). Primary outcome was percentage of on-infusion time with capillary blood glucose (BGL) at target (3.8-7mmol/L). Secondary outcomes were percentage time with critical hyperglycaemia (BGL>10mmol/L) or hypoglycaemia (BGL <3.8mmol/L), and incidence of neonatal hypoglycaemia (BGL<2.5mmol/L in first 48 hours if betamethasone given within 2 days of birth).
We found that on-infusion time at target was 68% (95%CI 64-71%) for P-IVI compared to 55% (95%CI 50-60%) for AIVI (p=0.0002). Time with critical hyperglycaemia was lower with P-IVI compared to A-IVI (0% vs 2%, p=0.02), with lower incidence of maternal hypoglycaemia (2% vs 12%, p=0.02). Neonatal hypoglycaemia occurred in 29% of births following P-IVI, compared to 54% births following A-IVI (p=0.03). A multiple logistic regression model adjusting for potential confounders gave an odds ratio for neonatal hypoglycaemia with P-IVI of 0.27 (95%CI 0.10-0.76, p=0.01).
We conclude that an infusion protocol designed for pregnancy effectively controlled maternal hyperglycaemia following betamethasone. This is the first protocol to show a reduction in betamethasone-associated neonatal hypoglycaemia, linked with optimum maternal glycaemic control.