Increased risk of spastic diplegia among very low birth weight children after preterm labor or prelabor rupture of membranes

Dammann, Olaf; Allred, Elizabeth N.; Veelken, N.

doi:10.1016/s0022-3476(98)70035-6

Cited by 58 publications

(36 citation statements)

References 24 publications

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“…Keeping initiators of preterm delivery separate is important for our scenario because they might carry different risk information for neonatal 24 and longterm neurocognitive outcomes. 25 …”

Section: Intrauterine Infection Inflammation and Preterm Birthmentioning

confidence: 99%

Fetal Inflammatory Response and Brain Injury in the Preterm Newborn

2009

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Preterm birth can be caused by intrauterine infection and maternal/fetal inflammatory responses. Maternal inflammation (chorioamnionitis) is often followed by a systemic fetal inflammatory response characterized by elevated levels of pro-inflammatory cytokines in the fetal circulation. The inflammation signal is likely transmitted across the blood-brain barrier, and initiates a neuroinflammatory response. Microglial activation has a central role in this process, and triggers excitotoxic, inflammatory, and oxidative damage in the developing brain. Neuroinflammation can persist over a period of time and sensitize the brain to subinjurious insults in early and chronic phases, but may offer relative tolerance in the intermediate period through activation of endogenous anti-inflammatory, protective, and repair mechanisms. Neuroinflammatory injury not only destroys what exists, but also changes what develops.

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“…Keeping initiators of preterm delivery separate is important for our scenario because they might carry different risk information for neonatal 24 and longterm neurocognitive outcomes. 25 …”

Section: Intrauterine Infection Inflammation and Preterm Birthmentioning

confidence: 99%

Fetal Inflammatory Response and Brain Injury in the Preterm Newborn

2009

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“…However, despite the presumed benefits from these therapies, PPROM infants have a higher incidence of neonatal morbidity than preterm infants born at the same GA without PPROM. 3,4 This increase in neonatal morbidity has been attributed to an increase in perinatal complications such as umbilical cord compression and cord prolapse, placental abruption and chorioamnionitis. 2,5,6 Additionally, fetal growth restriction, neonatal chronic lung disease and brain injury with adverse long-term outcomes have been reported to occur with higher incidences in PPROM pregnancies compared with preterm births due to other etiologies.…”

Section: Introductionmentioning

confidence: 99%

“…2,5,6 Additionally, fetal growth restriction, neonatal chronic lung disease and brain injury with adverse long-term outcomes have been reported to occur with higher incidences in PPROM pregnancies compared with preterm births due to other etiologies. 4,6,7 Although observed increases in maternal and neonatal morbidity with ruptured membranes >24 h in term pregnancy have led to a consensus regarding induction of labor as standard of care, 8 there is currently no consensus regarding the optimal GA for labor induction and delivery after PPROM. [9][10][11] Several studies have shown increased latency and increased rates of chorioamnionitis in late preterm PPROM women managed expectantly, but found no differences in major neonatal morbidity and mortality, regardless of whether testing for pulmonary maturity was performed.…”

Section: Introductionmentioning

confidence: 99%

Neonatal outcomes are associated with latency after preterm premature rupture of membranes

et al. 2012

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Objective: To determine factors associated with latency time to birth after preterm premature rupture of membranes (PPROM) and the impact on neonatal outcomes.Study Design: Data on singleton pregnancies with PPROM (n ¼ 1535 infants) were prospectively collected in a computerized perinatal/neonatal database at a tertiary care perinatal center. Latency was characterized as p72h versus >72 h after PPROM.Result: The percentage of women with latency to birth >72 h decreased from 67% in very preterm (gestational age (GA) 25 to 28 weeks) to 10% in late preterm women (GA 33 to 36 weeks). PPROM women with latency p72 h were more likely to have pregnancy-induced hypertension and birth weight <3%; PPROM women with latency >72 h were more likely to have received steroids and develop clinical chorioamnionitis. PPROM <32 weeks GA with latency p72 h was associated with a two-fold higher incidence of severe neonatal morbidity, while PPROM between 29 to 34 weeks GA and latency p72 h was associated with a higher incidence of moderate neonatal morbidity. Conclusion:A latency period >72 h was associated with a decreased incidence of adverse neonatal outcomes up to 32 weeks GA for severe and 34 weeks GA for moderate morbidity indices.

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“…As indicated above, the currently most frequently used Dammann/Leviton/Bartels/Dammann PROM/CAM ⇑ PVL [76] CAM ⇑ cPVL (multiple, summarized in [4]) infancy/childhood no data POOL/PROM ⇑ CP [77] CAM ⇑ CP (multiple, summarized in [4]) CAM " CP [78,79] fever ⇓ IQ [80] Fetal early neonatal IL-6/GCSF ⇑ RDS [81] cytokines ⇑ IVH [75,82,83] (funisitis, cytokinemia) late neonatal IL-6 ⇑ BPD [43] funisitis ⇑ BPD [44] fetal vasculitis " BPD [7] fetal vasculitis ⇑ EL [50,84] infancy/childhood no data funisitis ⇑ neuro/CP [48,85,86] funisitis " CP [78,79] cytokines " CP [87] ⇓ = 'Is associated with decreased risk for'; ⇑ = 'is associated with increased risk for'; " = 'is not associated with a risk change for'; BPD = bronchopulmonary dysplasia; CAM = chorioamnionitis; CP = cerebral palsy; EL = echolucency; GCSF = granulocyte colony-stimulating factor; IL = interleukin; IVH = intraventricular hemorrhage; POOL = preterm onset of labor; PROM = prelabor rupture of membranes; RDS = respiratory distress syndrome. definition is oxygen dependence at 36 weeks' post-menstrual age.…”

Section: Methodological Issuesmentioning

confidence: 99%

Lung and Brain Damage in Preterm Newborns

Dammann

Leviton²,

Bartels³

et al. 2004

Neonatology

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The relationships among bronchopulmonary dysplasia (BPD), brain white matter damage (WMD) and cerebral palsy (CP) are far from simple. Apparently, BPD and WMD are not associated, while BPD and CP are. The most likely explanation for this paradox is that ultrasound imaging does not identify all the WMD that might lead to CP (‘tip-of-the-iceberg effect’). We discuss further methodological inconsistencies, etiological peculiarities related to antenatal infection/inflammation, and intervention-related issues. In particular, we expand on the multiple-hit scenario in the etiology of BPD and offer support for the hypothesis that it is not lung disease, but factors associated with lung disease (e.g. postnatal steroid exposure) that increase the risk for developmental disability in childhood.

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Increased risk of spastic diplegia among very low birth weight children after preterm labor or prelabor rupture of membranes

Cited by 58 publications

References 24 publications

Fetal Inflammatory Response and Brain Injury in the Preterm Newborn

Fetal Inflammatory Response and Brain Injury in the Preterm Newborn

Neonatal outcomes are associated with latency after preterm premature rupture of membranes

Lung and Brain Damage in Preterm Newborns

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