Antecedents of Neonatal Encephalopathy in the Vermont Oxford Network Encephalopathy Registry

Nelson, Karin B.; Bingham, Peter M.; Edwards, Erika M.; Horbar, Jeffrey D.; Kenny, Michael; Inder, Terrie E.; Pfister, Robert H.; Raju, Tonse N.K.; Soll, Roger F.

doi:10.1542/peds.2012-0714

Cited by 104 publications

(53 citation statements)

References 42 publications

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“…Given the vulnerability of the fetal/neonatal brain to hypoxia-ischaemia and the known association of neonatal encephalopathy with longer term cerebral palsy and mortality [26][27][28] it is important that at risk fetuses are identified antenatally and strategies put in place to minimize the risk of intrapartum compromise. The strengths of our study are its large size as well as the diverse patient population and the clinically relevant outcomes.…”

Section: Discussionmentioning

confidence: 99%

The relationship between the five minute Apgar score, mode of birth and neonatal outcomes

Thavarajah

Flatley

Kumar

2017

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective: To investigate the relationship between the five-minute Apgar score categories (low, intermediate, and normal), mode of birth and neonatal outcomes. Methods: This was a retrospective cross sectional study of term singleton deliveries at Mater Mothers' Hospital in Brisbane, Australia between January 2007 and December 2015. The five minute score was subdivided in to three categories -low (0-3), intermediate (4-6), and normal (7). These were correlated with adverse neonatal outcomes and mode of birth. The referent cohort was the normal Apgar group. Results: The study cohort consisted of 39,258 births with a recorded five minute Apgar score. Of these, 38,705 (98.6%) neonates had a normal (7) Apgar score, 439 (1.1%) had an intermediate score (4-6) and 114 (0.3%) had a low (0-3) score. Neonatal complications including respiratory distress, feeding problems, hypothermia, and seizures were all significantly associated with both low and intermediate Apgar scores. Emergency operative birth (caesarean and instrumental) conveyed a higher risk of low and intermediate scores and poorer neonatal outcomes. Conclusions: Low and intermediate five minute Apgar scores were strongly associated with mode of birth and poorer neonatal outcomes. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

The relationship between the five minute Apgar score, mode of birth and neonatal outcomes

Thavarajah

Flatley

Kumar

2017

The Journal of Maternal-Fetal & Neonatal Medicine

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“…39 In addition, previous studies in high-income settings have shown high prevalence of inflammatory indicator (24%) amongst infants with neonatal encephalopathy. 40 A recent US study, examining the association between maternal and neonatal infections and adverse outcomes after neonatal encephalopathy, reported an increase in adverse neurodevelopmental outcomes, but not death, amongst encephalopathic infants with sepsis; however, chorioamnionitis was associated with a lower risk of brain injury and adverse cognitive outcomes were less severe in infants exposed to chorioamnionitis. 41 Although it seems likely that the burden of infectious comorbidity is highest in low-income settings, a high incidence of sepsis has been seen in many of the hypothermia trials preformed in high-income settings (5-14%).…”

Section: Observations On Cytokines/chemokinesmentioning

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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“…30,31 Other studies, using a stricter definition of encephalopathy that automatically excludes most conditions with an antenatal or genetic origin, have found that intrapartum events are the main or a contributing factor in the causal pathway of HIE. 12,[32][33][34] None of the previous studies has used neonatal neuroimaging investigations to confirm the presence of acute hypoxicischemic injury of recent onset and to exclude other causes of encephalopathy.…”

Section: Figurementioning

confidence: 99%

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

et al. 2013

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WHAT'S KNOWN ON THIS SUBJECT: Etiology and timing of onset of neonatal hypoxic-ischemic encephalopathy continue to be controversial. Previous studies suggest antepartum events are the main contributing factors, but have used a broad definition of encephalopathy and included infants with genetic, congenital, and developmental abnormalities.WHAT THIS STUDY ADDS: Our study suggests that when strict criteria defining hypoxic-ischemic encephalopathy are applied with supporting neuroimaging evidence of an acute hypoxicischemic insult, intrapartum events are the final and necessary pathway leading to this condition. abstract OBJECTIVE: To determine whether antepartum factors alone, intrapartum factors alone, or both in combination, are associated with term neonatal hypoxic-ischemic encephalopathy (HIE). METHODS:A total of 405 infants $35 weeks' gestation with early encephalopathy, born between 1992 and 2007, were compared with 239 neurologically normal infants born between 1996 and 1997. All cases met criteria for perinatal asphyxia, had neuroimaging findings consistent with acute hypoxia-ischemia, and had no evidence for a non-hypoxic-ischemic cause of their encephalopathy.RESULTS: Both antepartum and intrapartum factors were associated with the development of HIE on univariate analysis. Case infants were more often delivered by emergency cesarean delivery (CD; 50% vs 11%, P , .001) and none was delivered by elective CD (vs 10% of controls). On logistic regression analysis only 1 antepartum factor (gestation $41 weeks) and 7 intrapartum factors (prolonged membrane rupture, abnormal cardiotocography, thick meconium, sentinel event, shoulder dystocia, tight nuchal cord, failed vacuum) remained independently associated with HIE (area under the curve 0.88; confidence interval 0.85-0.91; P , .001). Overall, 6.7% of cases and 43.5% of controls had only antepartum factors; 20% of cases and 5.8% of controls had only intrapartum factors; 69.5% of cases and 31% of controls had antepartum and intrapartum factors; and 3.7% of cases and 19.7% of controls had no identifiable risk factors (P , .001). CONCLUSIONS:Our results do not support the hypothesis that HIE is attributable to antepartum factors alone, but they strongly point to the intrapartum period as the necessary factor in the development of this condition. Pediatrics 2013;132:e952-e959

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Antecedents of Neonatal Encephalopathy in the Vermont Oxford Network Encephalopathy Registry

Abstract: Clinically recognized asphyxial birth events, indicators of intrauterine exposure to inflammation, fetal growth restriction, and birth defects were each observed in term infants with NE, but much of NE in this large registry remained unexplained.

Cited by 104 publications

References 42 publications

The relationship between the five minute Apgar score, mode of birth and neonatal outcomes

The relationship between the five minute Apgar score, mode of birth and neonatal outcomes

Inflammation‐induced sensitization of the brain in term infants

Antepartum and Intrapartum Factors Preceding Neonatal Hypoxic-Ischemic Encephalopathy

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