Antenatal Magnesium Sulfate and Neurologic Outcome in Preterm Infants: A Systematic Review

Doyle, Lex W.; Crowther, CA; Middleton, PF; Marret, Stéphane

doi:10.1097/01.aoa.0000370508.70490.34

Cited by 54 publications

(60 citation statements)

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“…To date, systematic review of the use of antenatal MgSO 4 has found that for trials reporting neurodevelopmental outcomes, there is a significant reduction in cerebral palsy and substantial gross motor impairment which are probably measuring the same injury. 26 Reported data to date do not allow confident conclusions regarding the mechanism by which MgSO 4 prevents cerebral palsy. MgSO 4 has been associated with a variety of maternal and neonatal cardiovascular effects, some of which have the potential for harm including maternal hypotension and tachycardia, 6 and the reports of reduced neonatal cerebral blood flow and perfusion pressure, 9 and this study that found an increase in use of volume expansion in infants exposed to MgSO 4 .…”

Section: Discussionmentioning

confidence: 99%

Randomized controlled trial of magnesium sulfate in women at risk of preterm delivery—neonatal cardiovascular effects

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Randomized controlled trial of magnesium sulfate in women at risk of preterm delivery—neonatal cardiovascular effects

et al. 2011

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“…Several studies have reported effects of antenatal MgSO 4 on the neurodevelopmental outcomes of newborns exposed to antenatal MgSO 4 [9,10,37] . However, there are few reports of its effects on the gastrointestinal system, despite the finding that mesenteric arteries have greater sensitivity than the cerebral arteries to MgSO 4 -induced vasodilation [22] .…”

Section: Discussionmentioning

confidence: 99%

Effects of Maternal Magnesium Sulfate Administration on Intestinal Blood Flow Velocity in Preterm Neonates

et al. 2011

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Background: Antenatal MgSO₄ administration is used extensively as a tocolytic agent and to treat preeclampsia. Various effects on the fetus and newborn have been reported, and MgSO₄ has well-documented vasoactive effects. Objective: To determine if antenatal MgSO₄ administration affects intestinal blood flow velocity in newborn preterm infants. Methods: Peak, mean and end-diastolic velocities in the superior mesenteric artery were measured on day 1 of life. Maternal medical records were reviewed to identify infants whose mothers had been administered MgSO₄ for preterm labor or preeclampsia within 24 h of delivery. Result: Fifty-six infants were studied: 27 were exposed and 29 were not exposed to antenatal MgSO₄. Mean birth weight (1,371 ± 349 and 1,401 ± 469 g, respectively), gestational age (29.7 ± 2.0 and 30.0 ± 2.9 weeks, respectively) and infant hemodynamic and clinical variables (other than clinical indication for antenatal MgSO₄ administration) were similar between groups. There were no significant differences between the exposed and unexposed groups in intestinal blood flow velocities. For the exposed group, however, there was a significant negative correlation between mean velocity and the number of hours from birth to the time superior mesenteric artery blood flow velocity measurements were made (p = 0.002); there was no correlation for the unexposed group (p = 0.852). Conclusion: Group mean values indicate that antenatal exposure to MgSO₄ does not significantly affect intestinal blood flow velocity in newborn preterm infants. However, the significant negative relationship between mean blood flow velocity and time from birth to blood flow velocity measurement in exposed infants suggests that there may be measurable effects of MgSO₄ exposure within the hours immediately after birth. Trials that prospectively evaluate the development of intestinal blood flow velocities are needed to further clarify potential effects of antenatal MgSO₄ on the gastrointestinal tract of preterm infants.

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“…106,107 There is now evidence from a meta-analysis of randomized controlled trials of infants born preterm that antenatal administration of magnesium is associated with a reduced risk of CP in early childhood. 108 In term-born infants with neonatal encephalopathy, a key mechanism of tissue protection by hypothermia is the inhibition of the pro-inflammatory cascade induced by hypoxia-ischaemia. 109 However, the pro-inflammatory response may not be entirely harmful; some reactions are helpful for tissue repair, and hypothermia is likely to inhibit both beneficial and detrimental inflammatory responses.…”

Section: Clinical and Translational Observationsmentioning

confidence: 99%

Inflammation‐induced sensitization of the brain in term infants

Fleiss

Tann

Degos

et al. 2015

Develop Med Child Neuro

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COXPerinatal insults are a leading cause of infant mortality and amongst survivors are frequently associated with neurocognitive impairment, cerebral palsy (CP), and seizure disorders. The events leading to perinatal brain injury are multifactorial. This review describes how one subinjurious factor affecting the brain sensitizes it to a second injurious factor, causing an exacerbated injurious cascade. We will review the clinical and experimental evidence, including observations of high rates of maternal and fetal infections in term-born infants with neonatal encephalopathy and cerebral palsy. In addition, we will discuss preclinical evidence for the sensitizing effects of inflammation on injuries, such as hypoxia-ischaemia, our current understanding of the mechanisms underpinning the sensitization process, and the possibility for neuroprotection. PERINATAL BRAIN INJURY IN THE TERM-BORN INFANTIntrapartum neonatal deaths are the third leading cause of global childhood mortality. 1 In addition, each year perinatal insults are estimated to be responsible for more than one million new cases of neonatal encephalopathy, and nearly half a million infants with impairments such as cerebral palsy (CP).2 Infants exposed to a perinatal insult typically present with encephalopathy, a descriptive term for a clinical constellation of neurological dysfunctions in the term-born that includes difficulty with initiating and maintaining respiration; depression of tone and reflexes; subnormal levels of consciousness; and seizures.3 Whilst often assumed to result solely from acute intrapartum hypoxic-ischaemia, the precise contribution of hypoxia is likely to vary according to the definition of encephalopathy used, the range of competing risks, and the care setting. 3,4 Presumed hypoxia-ischaemia is diagnosed based on reduced Apgar scores and acidosis, 5 and the combination of progressive hypoxia, hypercarbia, and acidosis is often referred to as asphyxia. 6 Encephalopathy resulting from hypoxia-ischaemia can be clearly diagnosed only in a small number of cases in which a sentinel event, such as placental abruption, uterine rupture, cord prolapse, or shoulder dystocia, is clearly present. Clinical studies have identified a number of other important antepartum and intrapartum risk factors for neonatal encephalopathy. [7][8][9][10] In low-income settings, where access to skilled birth attendants and emergency obstetric intervention is often limited, the probability of intrapartum hypoxic events contributing to neonatal encephalopathy is increased.2,9,11 However, in general, neonatal encephalopathy is likely to be a multifactorial condition with complex aetiology, encompassing several causal events, with strong evidence that fetal exposure to infection contributes. 12 CONCEPT OF INFLAMMATION-INDUCED SENSITIZATIONAn increasingly common model for the complex and multifactorial process of perinatal brain injury involves sensitization, 13-15 whereby factors not severe enough by themselves to induce significant brain damage make the developi...

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Antenatal Magnesium Sulfate and Neurologic Outcome in Preterm Infants: A Systematic Review

Cited by 54 publications

References 0 publications

Randomized controlled trial of magnesium sulfate in women at risk of preterm delivery—neonatal cardiovascular effects

Randomized controlled trial of magnesium sulfate in women at risk of preterm delivery—neonatal cardiovascular effects

Effects of Maternal Magnesium Sulfate Administration on Intestinal Blood Flow Velocity in Preterm Neonates

Inflammation‐induced sensitization of the brain in term infants

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