Maternal magnesium therapy, neonatal serum magnesium concentration and immediate neonatal outcomes

Narasimhulu, Deepa Maheswari; Brown, Alex; Egbert, Neha; Rojas, Mary; Haberman, Shoshana; Bhutada, Alok; Minkoff, Howard; Rastogi, Shantanu

doi:10.1038/jp.2017.132

Cited by 18 publications

(19 citation statements)

References 23 publications

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“…), including potential for increased risk of intraventricular haemorrhage and neonatal morbidity (Narasimhulu et al . ). Studies of MgSO 4 given to newborns suggest that bolus doses of between 125 and 250 mg kg −1 given repeatedly every 24 h have little effect on seizures, possibly because of the relatively limited transfer of MgSO 4 from blood to the brain (Ichiba et al .…”

Section: Discussionmentioning

confidence: 97%

Time and sex dependent effects of magnesium sulphate on post‐asphyxial seizures in preterm fetal sheep

Bennet

Galinsky

Draghi

et al. 2018

The Journal of Physiology

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Seizures are common in newborns after asphyxia at birth and are often refractory to anti-seizure agents. Magnesium sulphate (MgSO ) has anticonvulsant effects and is increasingly given to women in preterm labour for potential neuroprotection. There is limited information on its effects on perinatal seizures. We examined the hypothesis that MgSO infusion would reduce fetal seizures after asphyxia in utero. Preterm fetal sheep at 0.7 gestation (104 days, term = 147 days) were given intravenous infusions of either saline (n = 14) or MgSO (n = 12, 160 mg bolus + 48 mg h infusion over 48 h). Fetuses underwent umbilical cord occlusion (UCO) for 25 min, 24 h after the start of infusion. The start time for seizures did not differ between groups, but MgSO significantly reduced the total number of seizures (P < 0.001), peak seizure amplitude (P < 0.05) and seizure burden (P < 0.005). Within the saline-asphyxia group, male fetuses had significantly more seizures than females (P < 0.05). Within the MgSO -asphyxia group, although both sexes had fewer seizures than the saline-asphyxia group, the greatest effect of MgSO was on male fetuses, with reduced numbers of seizures (P < 0.001) and seizure burden (P < 0.005). Only 1 out of 6 MgSO males had seizures on the second day post-UCO compared to 5 out of 6 MgSO female fetuses (P = 0.08). Finally, seizures showed a circadian profile with peak seizures between 04.00 and 06.00 h on the first and second day post-UCO. Collectively, these results suggest that MgSO may have utility in treating perinatal seizures and has sexually dimorphic effects.

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Section: Discussionmentioning

confidence: 97%

Time and sex dependent effects of magnesium sulphate on post‐asphyxial seizures in preterm fetal sheep

Bennet

Galinsky

Draghi

et al. 2018

The Journal of Physiology

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“…There is still a lack of evidence, and conflicting results about the effect of antenatal MgSO 4 on both cerebral oxygenation and the incidence of severe IVH, and the reports suggest that outcomes may depend on the antenatal maternal magnesium dose/serum concentrations and neonatal serum magnesium concentrations. [21][22][23][24][25][26][27][28] Despite the uncertainty about the exact mechanism of fetal MgSO 4 neuroprotection, some factors have been asserted to have a role in lowering CP risk. MgSO 4 was shown to have multiple direct effects on the nervous tissue, such as blockade of NMDA (N-Methyl-d-aspartate) receptors and increasing angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Antenatal Neuroprotective Magnesium Sulfate Treatment on Cerebral Oxygenation in Preterm Infants

et al. 2020

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Objective Antenatal magnesium sulfate (MgSO4) treatment is associated with reduced risk of cerebral palsy in preterm infants. We aimed to investigate whether this treatment leads to any alterations on cerebral hemodynamics which could be detected by near-infrared spectroscopy (NIRS) readings in early postnatal life. Study design Infants with gestational ages (GAs) ≤ 32 weeks were divided into two groups regarding their exposure to antenatal neuroprotective MgSO4 treatment or not. NIRS monitoring was performed to all infants, and readings were recorded for 2 hours each day during the first 3 days of life. The primary aim was to compare regional cerebral oxygen saturation (rcSO2) and cerebral fractional tissue oxygen extraction (cFTOE) between the groups. Results Sixty-six infants were exposed to antenatal MgSO4, while 64 of them did not. GA and birth weight were significantly lower in the treatment group (p < 0.01). No difference was observed in rcSO2 and cFTOE levels in the first, second, and the third days of life (p > 0.05). An insignificant reduction in severe intraventricular hemorrhage rates was observed (8 vs. 15%, p = 0.24). Conclusion We could not demonstrate any effect on cerebral oxygenation of preterm infants in early postnatal life that could be attributed to antenatal neuroprotective MgSO4 treatment. Future studies are warranted to clarify the exact underlying mechanisms of neuroprotection.

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“…Provided that neonatal serum magnesium concentrations are <4.5 mEq dl −1 , MgSO 4 has powerful neuroprotective effects (Narasimhulu et al . ). Neonatal (and presumably, fetal) serum concentrations correlate closely with the total maternal dose and duration of therapy, and serum concentrations between 2.5 and 4.5 mEq dl −1 are optimal for neuroprotection, whereas concentrations >4.5 mEq dl −1 may be associated with periventricular leukomalacia (Narasimhulu et al .…”

Section: Introductionmentioning

confidence: 97%

“…Neonatal (and presumably, fetal) serum concentrations correlate closely with the total maternal dose and duration of therapy, and serum concentrations between 2.5 and 4.5 mEq dl −1 are optimal for neuroprotection, whereas concentrations >4.5 mEq dl −1 may be associated with periventricular leukomalacia (Narasimhulu et al . ). Of note, this study also identified increased risk of grade 3–4 intraventricular haemorrhage in neonates with serum concentrations <2.5 mEq dl −1 , suggesting there are some pregnancies that would benefit from maternal magnesium supplementation.…”

Section: Introductionmentioning

confidence: 97%

Antenatal prevention of cerebral palsy and childhood disability: is the impossible possible?

Ellery

Kelleher

Grigsby

et al. 2018

The Journal of Physiology

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This review covers our current knowledge of the causes of perinatal brain injury leading to cerebral palsy-like outcomes, and argues that much of this brain damage is preventable. We review the experimental evidence that there are treatments that can be safely administered to women in late pregnancy that decrease the likelihood and extent of perinatal brain damage that occurs because of acute and severe hypoxia that arises during some births, and the additional impact of chronic fetal hypoxia, infection, inflammation, growth restriction and preterm birth. We discuss the types of interventions required to ameliorate or even prevent apoptotic and necrotic cell death, and the vulnerability of all the major cell types in the brain (neurons, astrocytes, oligodendrocytes, microglia, cerebral vasculature) to hypoxia/ischaemia, and whether a pan-protective treatment given to the mother before birth is a realistic prospect.

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Maternal magnesium therapy, neonatal serum magnesium concentration and immediate neonatal outcomes

Cited by 18 publications

References 23 publications

Time and sex dependent effects of magnesium sulphate on post‐asphyxial seizures in preterm fetal sheep

Time and sex dependent effects of magnesium sulphate on post‐asphyxial seizures in preterm fetal sheep

The Effect of Antenatal Neuroprotective Magnesium Sulfate Treatment on Cerebral Oxygenation in Preterm Infants

Antenatal prevention of cerebral palsy and childhood disability: is the impossible possible?

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