Antenatal magnesium sulfate for both tocolysis and fetal neuroprotection in premature rupture of the membranes before 32 weeks' gestation.

Objective: We aimed to assess the impact of antenatal MgSO therapy given to women with PPROM before 32 weeks' gestation on latency, maternal outcomes, perinatal outcomes, and neurodevelopmental outcomes.

Methods: We undertook a retrospective cohort observational study of 184 singleton pregnancies complicated by PPROM at 23°-31 weeks who were hospitalized and received magnesium therapy for tocolysis (MgSO group) or did not receive tocolytic therapy (no MgSO group) between 2005 and 2013. Furthermore, patients were subdivided into two groups based on the gestational age at the onset of PPROM (23°-27 weeks' gestation and 28°-31 weeks' gestation).

Results: We included 184 women, of whom 143 received magnesium therapy and 41 did not. The latency period was significantly longer in the MgSO group compared with no MgSO group (7.9 ± 9.0 versus 4.0 ± 6.0 days, p = .0017). Antenatal magnesium therapy was significantly associated with decreased stillbirth (1.4% versus 14.6%, p = .0012) and perinatal mortality (7% versus 19.5%, p = .0375) without significant increase in the risk of neonatal morbidities and chorioamnionitis. However, neonates who were exposed to antenatal MgSO were associated with higher Mg levels (3.63 ± 1.05 mg/dl versus 2.13 ± 0.48 mg/dl, p < .0001) and phosphate levels (6.90 ± 1.36 mg/d versus 6.40 ± 1.01 mg/dl, p = .0459) than those who were not exposed. Neonates who were exposed to MgSO showed significantly reduced risks of IVH (20.4% versus 58.3%; RR, 0.35; 95%CI, 0.17-0.71) and PVL (27.8% versus 58.3%; RR, 0.48; 95%CI, 0.25-0.91) in the subgroup of 23°-27 weeks' gestation. And the incidence of developmental delay in the subgroup of 23°-27 weeks' gestation was significantly lower in the MgSO group (6.5% versus 36.4%; RR, 0.18; 95%CI, 0.05-0.69). However, there were no significant differences in the development of IVH, PVL, and developmental delay between the two groups for patients in the subgroup of 28°-31 weeks' gestation. A similar trend was observed for cerebral palsy, with 22.2% of unexposed children affected compared with only 7.0% of exposed children (RR, 0.31; 95%CI, 0.10-1.00).

Conclusions: Antenatal magnesium therapy in women with PPROM before 32 weeks' gestation could prolong latency period, allowing for corticosteroid benefit. Moreover, MgSO showed fetal neuroprotective effects for neonatal IVH and PVL, and for developmental delay in infancy while prolonging latency. However, these benefits were primarily limited to the subgroup of 23°-27 weeks' gestation and prolonged in utero exposure to MgSO was associated with bone mineralization in the neonates.