Antecedents and Neonatal Consequences of Low Apgar Scores in Preterm Newborns

Weinberger, Barry; Anwar, Mujahid; Hegyi, Thomas; Hiatt, Mark; Koons, Anne; Paneth, Nigel

doi:10.1001/archpedi.154.3.294

Cited by 54 publications

(44 citation statements)

References 29 publications

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“…The absence of any significant differences in low Apgar scores lends support to the findings in another study that antenatal maternal history and pregnancy complications (such as pre-eclampsia and vaginal bleeding) and events in labour like the use of oxytocin, magnesium and narcotics are not clearly associated with low Apgar scores 24 .…”

Section: Discussionsupporting

confidence: 76%

Singleton preterm births in Korle bu teaching hospital, Accra, Ghana – origins and outcomes

Nkyekyer¹,

Enweronu‐Laryea²,

Boafor³

2010

Ghana Medical Journal

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SUMMARYObjective: To determine the singleton preterm birth rate, the relative proportions of the clinical categories of preterm births and to compare the outcomes in these categories. .1%]) were medically indicated (group C). The commonest indication for delivery in group C was severe pre-eclampsia/eclampsia. Although there was no significant difference in the mean gestational ages at delivery between the groups, babies in group C had significantly lower birth weights. No differences in sex ratios, stillbirth rates, or incidence of low Apgar scores were found. Babies in group C were significantly more likely to be admitted to the neonatal intensive care unit (NICU) and had a significantly higher perinatal death rate. Survivors of NICU admission among group C babies spent significantly longer periods in hospital before discharge. Conclusion:Outcomes of preterm births in Korle Bu Teaching Hospital are less favourable among indicated preterm births than among spontaneous or PPROM-related preterm births. A detailed study of the causes of neonatal morbidity and mortality is suggested to determine any differences between the three groups.

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Section: Discussionsupporting

confidence: 76%

Singleton preterm births in Korle bu teaching hospital, Accra, Ghana – origins and outcomes

Nkyekyer¹,

Enweronu‐Laryea²,

Boafor³

2010

Ghana Medical Journal

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“…It is more difficult to clinically assess encephalopathy in very premature infants than at term; however, larger premature infants from 31 to 36 weeks gestation with metabolic acidosis in cord blood do have a high rate of evolving clinical encephalopathy after birth, which in turn is associated with adverse neurological outcome (Salhab and Perlman, 2005). Consistent with this, in the wider population of premature infants, adverse neonatal and long-term outcomes are strongly associated with evidence of exposure to perinatal hypoxia as shown by metabolic acidosis, active labor, abnormal heart rate traces in labor, and subsequent low Apgar scores (Low et al, 1995;de Vries et al, 1998;Weinberger et al, 2000;Osborn et al, 2003;Bell et al, 2005).…”

Section: Timing and Etiology Of Preterm Brain Injurymentioning

confidence: 80%

Destruction and reconstruction: Hypoxia and the developing brain

Barrett

Bennet

Davidson

et al. 2007

Birth Defects Research Pt C

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Preterm infants have a high rate of neurodevelopmental handicap. Recent imaging studies have revealed that adverse outcomes are strongly associated with reduced brain growth and neural complexity in later life. Increasing data suggest that these chronic deficits primarily reflect acute neuronal and glial injury sustained during adverse in utero events, such as exposure to severe hypoxia-ischemia and inflammation. In the present review we examine recent evidence that this chronic impairment is partly due to upregulation of physiological apoptosis, related to input deprivation, and output isolation secondary to acute white and gray matter damage and axonal injury. However, progenitor cells in the subventricular zone (SVZ) are also vulnerable to injury, and loss of part of this critical population likely further compromises brain development. Based on these concepts the impact of proposed interventions such as induced hypothermia and endogenous growth factors are likely to be complex, but potentially offer focused ways of improving the outcomes of premature birth.

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“…Nevertheless, there is some evidence for a role of subtle insults, as shown, e.g., by depressed Apgar scores at birth (22). More recently, the Extremely Low Gestational Age Newborns (ELGAN) study reported that severe intrauterine growth restriction and evidence of placental vascular thrombosis consistent with longstanding, prenatal hypoxemia were associated with impaired neurodevelopmental outcome at 2 y of age (23).…”

Section: Timing and Etiology Of Preterm Brain Injurymentioning

confidence: 99%

What brakes the preterm brain? An arresting story

et al. 2013

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Children surviving premature birth have a high risk of cognitive and learning disabilities and attention deficit. In turn, adverse outcomes are associated with persistent reductions in cerebral growth on magnetic resonance imaging (MRI). It is striking that modern care has been associated with a dramatic reduction in the risk of cystic white matter damage, but modest improvements in terms of neurodevelopmental impairment. This review will explore the hypothesis that the disability is primarily associated with impaired neural connectivity rather than cell death alone. Very preterm infants exhibit reduced thalamocortical connectivity and cortical neuroplasticity compared with term-born controls. In preterm fetal sheep, moderate cerebral ischemia with no neuronal loss, but significant diffuse failure of maturation of cortical pyramidal neurons, was associated with impaired dendritic growth and synapse formation, consistent with altered connectivity. These changes were associated with delayed decline in cortical fractional anisotropy (FA) on MRI. Supporting these preclinical findings, preterm human survivors showed similar enduring impairment of microstructural development of the cerebral cortex defined by FA, consistent with delayed formation of neuronal processes. These findings offer the promise that better understanding of impairment of neural connectivity may allow us to promote normal development and growth of the cortex after preterm birth. P remature birth is one of the leading causes of morbidity and mortality. Approximately 6-13% of all births are preterm (1), and in the United States, this has been estimated to cost the community more than $26.2 billion in 2005 alone (1). Most of this cost is related not to acute care but to cerebral palsy and long-term neurodevelopmental disability in surviving very premature (≤30 wk gestation) infants. Disability is highly associated with greater prematurity (2,3), but even in "late preterm" infants at 34-36 wk gestation, the risks of injury and disability are increased sevenfold or more compared with term infants (4). Although there is evidence for modest overall improvements in survival without disability in recent cohorts (2,3), others found no apparent improvement in disability after extremely preterm (<25 wk gestation) birth (5).Historically, preterm human autopsy cases typically showed severe necrotic white matter injury (WMI) with evidence of axonal degeneration and loss of cortical neurons (6,7). This necrosis in turn was associated with cerebral palsy. The greater risk of long-term disability in boys is correlated with greater risk of WMI (8). Encouragingly, there is now evidence of a progressive reduction in the severest form of cystic WMI over time (9). In modern cohorts, severe WMI is seen in only ~1% of cases, whereas less severe (nonnecrotic), diffuse WMI is now common (9,10).It is striking that despite this apparent marked reduction in the severity of WMI, that even less severe forms of WMI injury are associated with impaired brain development and disabil...

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Antecedents and Neonatal Consequences of Low Apgar Scores in Preterm Newborns

Cited by 54 publications

References 29 publications

Singleton preterm births in Korle bu teaching hospital, Accra, Ghana – origins and outcomes

Singleton preterm births in Korle bu teaching hospital, Accra, Ghana – origins and outcomes

Destruction and reconstruction: Hypoxia and the developing brain

What brakes the preterm brain? An arresting story

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