Fever in labour and neonatal encephalopathy: a prospective cohort study

Impey, Lawrence; Greenwood, Catherine; MacQuillan, Kathryn; Reynolds, Margaret; Sheil, Orla

doi:10.1111/j.1471-0528.2001.00145.x

Cited by 66 publications

(23 citation statements)

References 23 publications

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“…Perinatal brain injury often results in severe and long-lasting disabilities, like motor deficits, seizures and severe cognitive, psychological and behavioral problems, which represent an enormous burden for the child, its parents and society [1,2,3]. Importantly, the risk of developing neonatal encephalopathy is strongly increased after maternal intrapartum fever or other antenatal inflammatory conditions like chorioamnionitis [4,5,6,7]. Moreover, it is known that exposure of the fetal brain to a proinflammatory environment in utero negatively influences clinical outcome after asphyxia, including an increased risk of development of spastic cerebral palsy [8,9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Bonestroo¹,

Heijnen²,

Groenendaal

et al. 2015

Dev Neurosci

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Antenatal inflammation is associated with increased severity of hypoxic-ischemic (HI) encephalopathy and adverse outcome in human neonates and experimental rodents. We investigated the effect of lipopolysaccharide (LPS) on the timing of HI-induced cerebral tissue loss and gray matter injury, white matter injury and integrity, and the cerebral inflammatory response. On postnatal day 9, mice underwent HI by unilateral carotid artery occlusion followed by systemic hypoxia which resulted in early neuronal damage (MAP2 loss) at 3 h that did not increase up to day 15. LPS injection 14 h before HI (LPS+HI) significantly and gradually aggravated MAP2 loss from 3 h up to day 15, resulting in an acellular cystic lesion. LPS+HI increased white matter damage, reduced myelination in the corpus callosum and increased white matter fiber coherency in the cingulum. The number of oligodendrocytes throughout the lineage (Olig2-positive) was increased whereas more mature myelinating (CNPase-positive) oligodendrocytes were strongly decreased after LPS+HI. LPS+HI induced an increased and prolonged expression of cerebral cytokines/chemokines compared to HI. Additionally, LPS+HI increased macrophage/microglia activation and influx of neutrophils in the brain compared to HI. This study demonstrates the sensitizing effect of LPS on neonatal HI brain injury for an extended time-frame up to 15 days postinsult. LPS before HI induced a gradual increase in gray and white matter deficits, including reduced numbers of more mature myelinating oligodendrocytes and a decrease in white matter integrity. Moreover, LPS+HI prolonged and intensified the cerebral inflammatory response, including cellular infiltration. In conclusion, as the timing of damage and/or involved pathways are changed when HI is preceded by inflammation, experimental therapies might require modifications in the time window, dosage or combinations of therapies for efficacious neuroprotection.

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Section: Introductionmentioning

confidence: 99%

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Bonestroo¹,

Heijnen²,

Groenendaal

et al. 2015

Dev Neurosci

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“…Results of the present study suggest that antioxidant strategies may be effective in PICH prevention, especially because lobar location of PICH brings a higher risk of recurrence [23]. Thus, diet with selenium-containing food (e.g.…”

Section: Discussionmentioning

confidence: 99%

Glutathione Peroxidase 1 C593T Polymorphism Is Associated with Lobar Intracerebral Hemorrhage

Pera¹,

Słowik²,

Dziedzic³

et al. 2008

Cerebrovasc Dis

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Background: Oxidative stress plays an important role in vascular pathology and contributes to the pathophysiology of primary intracerebral hemorrhage (PICH). Glutathione peroxidase 1 (GPX1) is a key enzyme of the antioxidant system. Here, we investigated whether a functional C593T polymorphism of GPX1 gene is associated with PICH in a Polish population. Methods: Genotyping was performed in 192 PICH patients and 197 unrelated controls matched for age and sex. All were of Caucasian origin. The C593T GPX1 polymorphism was investigated using the polymerase chain reaction/restriction fragment length polymorphism method. Results: Multivariable logistic regression analysis revealed a significant association between genotypes containing the T allele and the entire PICH group (OR = 1.53; 95% CI = 1.02–2.29) and lobar PICH (OR = 2.36; 95% CI = 1.31–4.26) but not nonlobar PICH (OR = 1.19; 95% CI = 0.75–1.89). Conclusions: We found a positive association between the studied GPX1 polymorphism and lobar PICH in a Polish population.

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“…These adverse outcomes have been shown to affect primarily the respiratory [16] and neurologic systems [17,18] of the newborn, with one study showing intrapartum fever as a strong predictor of infection-related early neonatal death in term pregnancies (OR 3.16, 95% CI: 1.56, 6.40) [1]. Impey et al [17,18] demonstrated that intrapartum fever is associated with an almost 5-fold risk for neonatal encephalopathy and a 3.4-fold increase in the risk of unexplained neonatal seizures [17]. In a small retrospective study, neonates of febrile parturients had increased risk of low Apgar scores, seizures, hypotonia, and need for assisted ventilation [11].…”

Section: Discussionmentioning

confidence: 99%

Very High Intrapartum Fever in Term Pregnancies and Adverse Obstetric and Neonatal Outcomes

Dior¹,

Kogan²,

Eventov‐Friedman

et al. 2015

Neonatology

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Background: Intrapartum fever is a well-known risk factor for adverse perinatal outcomes. Maternal intrapartum fever ≥39.0°C at term is a rare event during labor, and there is scarce evidence regarding its implications. Objectives: To investigate the association between very high intrapartum maternal fever and perinatal outcomes in term pregnancies. Methods: A retrospective cohort analysis including 43,560 term, singleton live births in two medical centers between the years 2003 and 2011 was performed. We compared parturients who experienced a maximal intrapartum fever of <38.0°C with two subgroups of parturients who experienced respective maximal fevers of 38.0-38.9°C and ≥39°C. Adjusted risks for adverse perinatal outcomes were calculated by using multiple logistic regression models to control for confounders. Results: Compared with normal intrapartum temperature, intrapartum fever ≥39.0°C was associated with an extremely elevated risk for neonatal sepsis 16.08 (95% CI: 2.15, 120.3) as well as with low Apgar scores and neonatal intensive care unit admissions (p < 0.001). Additionally, very high intrapartum fever was related to significantly higher risk for operative delivery (p < 0.001). Conclusions: Extremely elevated intrapartum fever is an important indicator of severe neonatal morbidity and operative delivery.

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Fever in labour and neonatal encephalopathy: a prospective cohort study

Cited by 66 publications

References 23 publications

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Glutathione Peroxidase 1 C593T Polymorphism Is Associated with Lobar Intracerebral Hemorrhage

Very High Intrapartum Fever in Term Pregnancies and Adverse Obstetric and Neonatal Outcomes

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