Neurological damage arising from intrapartum hypoxia/acidosis

Rei, Mariana; Ayres-de-Campos, Diogo; Bernardes, João

doi:10.1016/j.bpobgyn.2015.04.011

Cited by 18 publications

(11 citation statements)

References 39 publications

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“…Still, our study was focused on neonatal mortality, and for a general clinical assessment of the immediate needs and the prognosis of the new‐born infant, we see no need to revise the well‐established Apgar score. A low Apgar score can be caused by many other factors than asphyxia, and we welcome studies of associations between Apgar score components and reduced scores with respect to other outcomes, including neonatal asphyxia‐related morbidity and long‐term neurological outcomes . Our finding that the prognostic value of Apgar score and reduced scores with respect to neonatal mortality may be larger in very preterm infants than in moderately preterm and term infants challenges current view, and may be of clinical importance.…”

Section: Discussionmentioning

confidence: 75%

Apgar Score Components at 5 Minutes: Risks and Prediction of Neonatal Mortality

Cnattingius

Norman

Granath

et al. 2017

Paediatric Perinatal Epid

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Section: Discussionmentioning

confidence: 75%

Apgar Score Components at 5 Minutes: Risks and Prediction of Neonatal Mortality

Cnattingius

Norman

Granath

et al. 2017

Paediatric Perinatal Epid

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“…This is particularly important for developing appropriate and timely treatment options [ 4 , 5 ]. One consideration in the development of new therapies is that brain injury arising from in utero hypoxia is not uniform with some regions displaying greater vulnerability to hypoxia [ 6 ], including the hippocampus [ 7 ], cortical grey matter, and white matter [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

The Effects of In Utero Fetal Hypoxia and Creatine Treatment on Mitochondrial Function in the Late Gestation Fetal Sheep Brain

Muccini

Tran

Hale

et al. 2022

Oxidative Medicine and Cellular Longevity

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Near-term acute hypoxia in utero can result in significant fetal brain injury, with some brain regions more vulnerable than others. As mitochondrial dysfunction is an underlying feature of the injury cascade following hypoxia, this study is aimed at characterizing mitochondrial function at a region-specific level in the near-term fetal brain after a period of acute hypoxia. We hypothesized that regional differences in mitochondrial function would be evident, and that prophylactic creatine treatment would mitigate mitochondrial dysfunction following hypoxia; thereby reducing fetal brain injury. Pregnant Border-Leicester/Merino ewes with singleton fetuses were surgically instrumented at 118 days of gestation (dGa; term is ~145 dGA). A continuous infusion of either creatine ( n = 15 ; 6 mg/kg/h) or isovolumetric saline ( n = 16 ; 1.5 ml/kg/h) was administered to the fetuses from 121 dGa. After 10 days of infusion, a subset of fetuses (8 saline-, 7 creatine-treated) were subjected to 10 minutes of umbilical cord occlusion (UCO) to induce a mild global fetal hypoxia. At 72 hours after UCO, the fetal brain was collected for high-resolution mitochondrial respirometry and molecular and histological analyses. The results show that the transient UCO-induced acute hypoxia impaired mitochondrial function in the hippocampus and the periventricular white matter and increased the incidence of cell death in the hippocampus. Creatine treatment did not rectify the changes in mitochondrial respiration associated with hypoxia, but there was a negative relationship between cell death and creatine content following treatment. Irrespective of UCO, creatine increased the proportion of cytochrome c bound to the inner mitochondrial membrane, upregulated the mRNA expression of the antiapoptotic gene Bcl2, and of PCG1-α, a driver of mitogenesis, in the hippocampus. We conclude that creatine treatment prior to brief, acute hypoxia does not fundamentally modify mitochondrial respiratory function, but may improve mitochondrial structural integrity and potentially increase mitogenesis and activity of antiapoptotic pathways.

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“…[23][24][25] The reason is that poor fetal oxygenation during labor and impaired respiratory gas exchange at birth may result in permanent damage to the brain and neurological impairment in the future. 26,27 Experimental evidence suggests that hypoxia-ischemia-induced cerebral atrophy and corpus callosum injury contribute to the development of learning and memory deficits. 28 Our results suggest that children with an Apgar score of Poorolajal et al less than 8 had an OR of 3.65.…”

Section: Discussionmentioning

confidence: 99%

Autism Spectrum Disorder and Associated Risk Factors: A Matched Case-Control Study

Sadeghifar

Omidi

Shirmohammadi‐Khorram

et al. 2019

Int J Epidemiol Res

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Background and aims: Despite substantial advances in the etiology of autism spectrum disorder (ASD), the environmental risk factors have not yet been well understood. The present study investigated the association between ASD, and maternal and perinatal risk factors. Methods: This matched, case-control study was conducted in Hamadan, the west of Iran, from November 2015 to May 2016. We enrolled 41 children with ASD aged 3-17 years. We selected four controls per one case from the same hospital where patients were born. Controls were separately matched with cases for sex, age, and birth year. Results: We compared 41 ASD cases with 164 controls. After adjusting the odds ratio (95% CI), ASD was significantly associated with third-degree relatives consanguinity [3.29 (1.39, 7.75)], short birth length [4.99 (1.15, 21.60)], short head circumference [7.87 (1.48, 41.76), respiratory distress syndrome at birth 3.97 (1.91, 8.22)], respiratory assistance at birth [2.92 (1.39, 6.10)], birth hypoxia [2.85 (1.35, 5.99)], and low 1-minute Apgar score [3.65 (1.04, 12.75)]. Conclusions: Our findings suggest that ASD may be associated with multiple maternal and perinatal risk factors. Evidence based on large prospective multicenter cohort studies is required to indicate the impacts of maternal and perinatal exposures.

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Neurological damage arising from intrapartum hypoxia/acidosis

Cited by 18 publications

References 39 publications

Apgar Score Components at 5 Minutes: Risks and Prediction of Neonatal Mortality

Apgar Score Components at 5 Minutes: Risks and Prediction of Neonatal Mortality

The Effects of In Utero Fetal Hypoxia and Creatine Treatment on Mitochondrial Function in the Late Gestation Fetal Sheep Brain

Autism Spectrum Disorder and Associated Risk Factors: A Matched Case-Control Study

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