Effect of Antenatal Magnesium Sulfate Exposure on Patent Ductus Arteriosus in Premature Infants

Emel Okulu; Elvis Kraja; Yasemin Ezgi Kostekci; Erdal Seker; Mehmet Seckin Ozisik; Doğacan Sarısoy; Batuhan Aslan; Maide Selin Çakır; Ferhan Demirtaş; Mehmet Gökhan Ramoğlu; Tayfun Uçar; Omer Erdeve; Begum Atasay; Acar Koc; Saadet Arsan

doi:10.1055/s-0044-1779620

Effect of Antenatal Magnesium Sulfate Exposure on Patent Ductus Arteriosus in Premature Infants

Am J Perinatol. 2024 Feb 6. doi: 10.1055/s-0044-1779620. Online ahead of print.

Authors

Affiliations

¹ Division of Neonatology, Department of Pediatrics, Ankara University Faculty of Medicine, Ankara, Turkey.
² Division of Perinatology, Department of Obstetrics and Gynecology, Ankara University Faculty of Medicine, Ankara, Turkey.
³ Department of Pediatrics, Ankara University Faculty of Medicine, Ankara, Turkey.
⁴ Department of Obstetrics and Gynecology, Ankara University Faculty of Medicine, Ankara, Turkey.
⁵ Division of Pediatric Cardiology, Department of Pediatrics, Ankara University Faculty of Medicine, Ankara, Turkey.

PMID: 38320597
DOI: 10.1055/s-0044-1779620

Abstract

Objective: Magnesium sulfate (MgSO₄) provides effective fetal neuroprotection. However, there is conflicting evidence regarding the association between antenatal MgSO₄ exposure and patent ductus arteriosus (PDA). Thus, herein, we aimed to evaluate the association between antenatal MgSO₄ exposure and PDA.

Study design: Preterm infants born between 24^0/7 and 31^6/7 weeks of gestation were included in this retrospective study. Infants who died within the first 72 hours of life and those with significant congenital anomalies were excluded from the study. Echocardiographic and clinical assessment parameters were used to define PDA and hemodynamically significant PDA (hsPDA). Treatments were planned according to the standard protocols of the unit. The following data were collected from hospital medical records: perinatal characteristics, neonatal outcomes, detailed PDA follow-up findings, and maternal characteristics including MgSO₄ exposure and doses.

Results: Of the 300 included infants, 98 (32.6%) were exposed to antenatal MgSO₄. hsPDA rates were similar in the infants exposed and not exposed to antenatal MgSO₄, when adjusted for antenatal steroid administration, gestational age, and birth weight (OR: 1.6, 95% CI: 0.849-3.118, p = 0.146). The rates of PDA ligation and open PDA at discharge were similar between the groups. A cumulative MgSO₄ dose of >20 g was associated with an increased risk of hsPDA (crude OR: 2.476, 95% CI: 0.893-6.864, p = 0.076; adjusted OR: 3.829, 95% CI: 1.068-13.728, p = 0.039). However, the cumulative dose had no effect on the rates of PDA ligation or open PDA at discharge. Rates of prematurity-related morbidities and mortality were similar between the groups.

Conclusion: Although antenatal MgSO₄ exposure may increase the incidence of hsPDA, it may not affect the rates of PDA ligation or open PDA at discharge. Further studies are required to better evaluate the dose-dependent outcomes and identify the MgSO₄ dose that not only provides neuroprotection but also has the lowest risk of adverse effects.

Key points: · Antenatal exposure of MgSO4 may cause PDA.. · Antenatal MgSO4 exposure may not increase the rates of PDA ligation or open PDA at discharge.. · Further studies are required to better evaluate the dose-dependent outcomes and optimal MgSO4 dose..