How Much of Neonatal Encephalopathy Is due to Birth Asphyxia?

Nelson, Karin B.; Leviton, Alan

doi:10.1001/archpedi.1991.02160110117034

Cited by 144 publications

(125 citation statements)

References 88 publications

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“…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.…”

Section: Perinatal Brain Injury In the Term-born Infantmentioning

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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Section: Perinatal Brain Injury In the Term-born Infantmentioning

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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“…Infants with encephalopathy were defined as term babies (≥ 37 weeks) who in the first week of life developed either seizures alone or any two of the following lasting for more than 24 hours: abnormal consciousness, abnormal tone, poor feeding of presumed central origin, and/or an inability to initiate or maintain respiration, also of presumed central origin (Nelson and Leviton 1991). Encephalopathy was graded as moderate or severe according to criteria modified from Sarnat and Sarnat (1976).…”

Section: Methodsmentioning

confidence: 99%

“…Newborn encephalopathy is a syndrome of disturbed neurological function in the first week of life associated with significant morbidity and mortality (Nelson and Leviton 1991). Most previous studies have included only those infants thought to have had intrapartum hypoxia, and most have either excluded infants with birth defects (Ziegler et al 1976, Finer et al 1981, Low et al 1985, Robertson and Finer 1985, Gaffney et al 1994, Thornberg et al 1995 or have not mentioned whether infants with birth defects had been included or excluded (Levene et al 1985, Hull andDodd 1992).…”

mentioning

confidence: 99%

Birth defects in children with newborn encephalopathy

Felix

Badawi

Kurinczuk

et al. 2000

Develop Med Child Neuro

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This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population‐based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association between birth defects and newborn encephalopathy was found with defects affecting 27.5% of children with encephalopathy and 4.3% of control children (odds ratio 8.55; 95% confidence interval 5.25 to 13.91; p<0.001). In 11.8% of infants with a birth defect the defect was not diagnosed until after the newborn period, illustrating one of the difficulties in attempting to exclude infants with birth defects from studies of newborn encephalopathy. The majority of defects (89%) were not specific anomalies of the CNS. In 36.8% of children with encephalopthy who had a birth defect, the defect was considered to be the probable cause of the encephalopathy. Infants with birth defects who had encephalopathy had a poorer prognosis than those without: they were twice as likely to die by the age of 2 years and three times more likely to have cerebral palsy. This study catalogues the spectrum of birth defects associated with newborn encephalopathy and illustrates the importance of their inclusion when investigating both the aetiology and outcome of this condition.

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“…8,9 Furthermore, implicated are antepartum insults, direct injuries or increased susceptibility to injury that occur well before the birth process, as well as congenital and metabolic birth defects. [1][2][3]10 Although the causes of neonatal encephalopathy are likely heterogeneous, a model of cerebral hypoxic-ischemic injury that begins in utero and extends into a recovery period is increasingly suggested and has been used as a model of study. 11 Hypoxic ischemic encephalopathy (HIE) is the most well-recognized and studied cause of neonatal encephalopathy.…”

Section: Introductionmentioning

confidence: 99%