Antenatal and intrapartum risk factors for neonatal hypoxic ischemic encephalopathy

Peebles, Patrick J.; Duello, Theresa M.; Eickhoff, Jens; McAdams, Ryan M.

doi:10.1038/s41372-019-0531-6

Cited by 33 publications

(29 citation statements)

References 29 publications

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“…( Table 1 ) The largest number of sentinel events were abruptions (32, 41.6%), and one of these abruptions was also complicated by an eclamptic seizure. Other sentinel events were isolated eclampsia ( 3 ), shoulder dystocia ( 17 ), uterine rupture ( 12 ), cord prolapse ( 5 ), fetal-maternal hemorrhage ( 1 ), ruptured velamentous cord insertion ( 1 ), tight nuchal cord x 3 which was difficult to reduce ( 1 ), abdominal trauma status post motor vehicle accident ( 1 ), head entrapment during a breech delivery ( 1 ), and 2 home deliveries, one complicated by the baby’s head hitting the floor with rupture of the cord and the other baby delivering into the toilet with a tight nuchal cord x 3.…”

Section: Resultsmentioning

confidence: 99%

“…Hypoxic ischemic encephalopathy (HIE) is a major cause of neonatal morbidity and mortality. ( 1 ) It is a clinical syndrome that results from impaired cerebral perfusion and oxygen delivery to the fetus or newborn with resultant hypoxia, metabolic acidosis, and neurologic morbidity( 1 , 2 ) characterized by depressed consciousness, abnormal muscle tone and reflexes, seizures, and respiratory distress. ( 3 ) HIE occurs in approximately 1.5 infants per 1000 live births and globally accounts for an estimated 491,900–724,000 neonatal deaths annually.…”

Section: Introductionmentioning

confidence: 99%

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Blood biomarkers for neonatal hypoxic–ischemic encephalopathy in the presence and absence of sentinel events

et al. 2020

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OBJECTIVE To determine if neonatal serum biomarkers representing different pathways of injury differ for cases of HIE of unknown cause to gain insight into timing and mechanism of injury. STUDY DESIGN In this cohort of all neonates with HIE admitted to our NICU, newborns with sentinel events were compared to those without during the 1 st 3 days of life. Discard neonatal blood during the 1 st 3 days of life was used for analysis. RESULTS Of 277 babies with HIE treated with whole-body hypothermia, 190 (68.6%) had blood available for biomarker analysis. 71 (37.4%) were born within our system, and 119 (62.6%) were transferred in from outside hospitals. Of these babies, 77 (40.5%) had a sentinel event and 113 (59.6%) had no sentinel event. Although the degree of metabolic acidosis was similar, repeated measures analysis showed that during the initial 3 days of life neonates born with HIE in the absence of sentinel events had 41.4% decreased VEGF (p=0.027) and 62.5% increased IL-10 serum concentrations (p=0.005). CONCLUSION These changes indicate that neonatal HIE in the absence of sentinel events is not related to an unrecognized acute intrapartum event and is possibly related to chronic hypoxia of lower severity or recovery from a remote event.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blood biomarkers for neonatal hypoxic–ischemic encephalopathy in the presence and absence of sentinel events

et al. 2020

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“…Therefore, it is feasible that there is significant period of time with decreased oxygenation in utero delivery prior to recognition for urgent delivery. Furthermore, antenatal risk factors for chronic prenatal hypoxic injury, such as excessive weight gain during pregnancy, are risk factors for worse outcomes from HIE [64]. This possible detrimental effect of prenatal chronic hypoxia on acute hypoxic neonatal injury is in sharp contrast to postnatal adult stroke studies were hypoxic preconditioning is protective of acute and long-term injury [65].…”

Section: Discussion/conclusionmentioning

confidence: 99%

“…Another advantage of a prenatal model is that it would allow more direct study of the effects of different pathologies of the maternal-placental unit on the pathophysiology of HIE. Conditions that lead to chronic prenatal hypoxia, such as excessive weight gain during pregnancy, are risk factors for worse outcomes from HIE [67]. This possible detrimental effect of prenatal chronic hypoxia on acute hypoxic neonatal injury is in sharp contrast to postnatal adult stroke studies were hypoxic preconditioning is protective of acute and long-term injury [68].…”

Section: Discussion/conclusionmentioning

confidence: 99%

Deficits in seizure threshold and other behaviors in adult mice without gross neuroanatomic injury after late gestation transient prenatal hypoxia

Cristancho

Gadra²,

Samba³

et al. 2021

Preprint

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Intrauterine hypoxia is a common cause of brain injury in children with a wide spectrum of long-term neurodevelopmental sequela even after milder injury that does not result in significant neuroanatomical injury. Published prenatal hypoxia models generally require many days of modest hypoxia or are invasive, difficult to replicate surgery to ligate the uterine artery. Postnatal models of neonatal hypoxic brain injury are not able to study the effects of antenatal risk factors that contribute to outcomes of hypoxia to the developing brain. In addition, the most common postnatal hypoxia models induce significant cell death and large focal neuroanatomic injury through unilateral ischemia, which is not a common pattern of injury in children. Large animal models suggest that brief transient prenatal hypoxia alone is sufficient to lead to significant functional impairment to the developing brain. Thus, to further understand the mechanisms underlying hypoxic injury to the developing brain, it is vital to develop murine models that are simple to reproduce and phenocopy the lack of neuroanatomic injury but significant functional injury seen in children affected by mild intrauterine hypoxia. Here we characterized the effect of late gestation (embryonic day 17.5) transient prenatal hypoxia on long-term anatomical and neurodevelopmental outcomes. Prenatal hypoxia induced hypoxia inducible factor 1 alpha in the fetal brain. There was no difference in gestational age at birth, litter size at birth, survival, fetal brain cell death, or long-term changes in gray or white matter between offspring after normoxia and hypoxia. However, there were several long-term functional consequences from prenatal hypoxia, including sex-dichotomous changes. Both males and females have abnormalities in repetitive behaviors, hindlimb strength, and decreased seizure threshold. Males demonstrated increased anxiety. Females have deficit in social interaction. Hypoxia did not result in motor or visual learning deficits. This work demonstrates that transient late gestation prenatal hypoxia is a simple, clinically-relevant paradigm for studying putative environmental and genetic modulators of the long-term effects of transient hypoxia on the developing brain.

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“…For the purposes of this study, we de ned level of income according to the Development Assistance Committee (DAC) list of countries eligible to receive o cial development assistance [22]. Data of pre-speci ed antenatal and intrapartum risk factors associated with neonatal encephalopathy [23][24][25], physical examinations and outcomes were extracted from individual charts by the respective hospital co-investigators (NT, RA, UT, and TW), using a customized template. Resuscitation practice followed the ILCOR guideline [26,27].…”

Section: De Nitionsmentioning

confidence: 99%

Perinatal events associated with birth asphyxia and hypoxic-ischemic encephalopathy in a middle-income country: A multicenter, observational study.

Kitsommart

Thamwiriyakul

Asawakitipong

et al. 2021

Preprint

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Background: Risk factors for neonatal encephalopathy differ across high- and low-income countries. Evidence of demographic characteristics and factors associated with perinatal hypoxia of infants who are at-risk for HIE in Southeast Asia is needed. Our primary objective was to investigate the intrapartum characteristics of infants ≥32 weeks’ gestational age (GA) born with low Apgar scores. Secondary objectives were to determine perinatal hypoxic events, and the characteristics and outcomes of infants ≥35 weeks GA with hypoxic-ischemic encephalopathy (HIE). Methods: A multicenter, retrospective, study was conducted. Individual charts were reviewed of infants with 5-minute Apgar scores ≤5 who were admitted to 4 tertiary centers in Thailand over 5 years. Events associated with perinatal hypoxia and outcomes were extracted. Variables were compared using chi-square, Fisher-exact test, two-independent sample t tests, ANOVA and Mann-Whitney. Data were analyzed using SPSS Statistics version 18.0. A p-value <0.05 was considered statistically significant.Results: Among 120235 infants, 454 had 5-mintue Apgar scores ≤5 (average: 3.8 per 1000 live births). The estimated frequency of HIE in ≥32 weeks’ GA infants was 1.5 per 1000 livebirths. Ninety-seven percent of the mothers’ received antenatal care. After exclusions, 316 infants and 314 mothers comprised the final sample. Common intrapartum complications were abnormal fetal heart rate (38.5%) and meconium-stained amniotic fluid (19.1%). Infants ≥35 weeks GA had mean ± standard deviation (SD) birthweight of 3003.4 ± 590.5 g; 10% were small-for-GA. Among ≥35 weeks GA infants with HIE, 42% had metabolic acidosis, 53% experienced sentinel, hypoxic perinatal events and advanced resuscitation was instituted in 92%. The severity of encephalopathy was reported in 99% of subjects. Eighty-five infants (62.5%) met all eligibility criteria for therapeutic hypothermia (TH) and 48 (56.5% of eligible infants) received treatment. The overall mortality rate was 29.4%.Conclusion: Maternal and intrapartum characteristics of infants at-risk for perinatal asphyxia in Thailand were comparable to reports from high-income countries. To improve recruitment for TH in middle-income, South-East Asian countries, strategies to raise HIE awareness among practitioners and more simplified TH eligible criteria are warranted to encourage timely transfer to referral centers for treatment.

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Antenatal and intrapartum risk factors for neonatal hypoxic ischemic encephalopathy

Cited by 33 publications

References 29 publications

Blood biomarkers for neonatal hypoxic–ischemic encephalopathy in the presence and absence of sentinel events

Blood biomarkers for neonatal hypoxic–ischemic encephalopathy in the presence and absence of sentinel events

Deficits in seizure threshold and other behaviors in adult mice without gross neuroanatomic injury after late gestation transient prenatal hypoxia

Perinatal events associated with birth asphyxia and hypoxic-ischemic encephalopathy in a middle-income country: A multicenter, observational study.

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