Antepartum risk factors for newborn encephalopathy: The Western Australian case-control study

TVW Telethon Institute for Child Health Research, PO Box 855, West Perth, Western Australia 6872, Australia.
BMJ Clinical Research (Impact Factor: 14.09). 01/1999; 317(7172):1549-53. DOI: 10.1136/bmj.317.7172.1549
Source: PubMed

ABSTRACT To ascertain antepartum predictors of newborn encephalopathy in term infants.
Population based, unmatched case-control study.
Metropolitan area of Western Australia, June 1993 to September 1995.
All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls.
Adjusted odds ratio estimates.
The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. The risk of newborn encephalopathy increased with increasing maternal age and decreased with increasing parity. There was an increased risk associated with having a mother who was unemployed (odds ratio 3.60), an unskilled manual worker (3.84), or a housewife (2.48). Other risk factors from before conception were not having private health insurance (3.46), a family history of seizures (2.55), a family history of neurological disease (2.73), and infertility treatment (4.43). Risk factors during pregnancy were maternal thyroid disease (9.7), severe pre-eclampsia (6.30), moderate or severe bleeding (3.57), a clinically diagnosed viral illness (2.97), not having drunk alcohol (2.91); and placenta described at delivery as abnormal (2.07). Factors related to the baby were birth weight adjusted for gestational age between the third and ninth centile (4.37) or below the third centile (38.23). The risk relation with gestational age was J shaped with 38 and 39 weeks having the lowest risk.
The causes of newborn encephalopathy are heterogeneous and many of the causal pathways start before birth.

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    • "Placental insufficiency resulting in growth restriction of the fetus is a significant predisposing ante-partum risk factor, shown to increase the probability of hypoxic-ischemic encephalopathy 40-fold [2]. Evidence indicates that up to 90% of cases of cerebral palsy and developmental disability occur prior to birth [2] [3] [4]. This, combined with the toxicity of conventional medications to the immature brain [5] [6], highlights the need for neuroprotective strategies that are safe, efficacious and preventive in nature. "
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    ABSTRACT: Chronic placental insufficiency and subsequent intrauterine growth restriction (IUGR) increase the risk of hypoxic-ischemic encephalopathy in the newborn by 40 fold. The latter, in turn, increases the risk of cerebral palsy and developmental disabilities. This study seeks to determine the effectiveness of broccoli sprouts (BrSp), a rich source of the isothiocyanate sulforaphane, as a neuroprotectant in a rat model of chronic placental insufficiency and IUGR. Placental insufficiency and IUGR was induced by bilateral uterine artery ligation (BUAL) on day E20 of gestation. Dams were fed standard chow or chow supplemented with 200mg of dried BrSp from E15 - postnatal day 14 (PD14). Controls received Sham surgery and the same dietary regime. Pups underwent neurologic reflex testing and open field testing, following which they were euthanized and their brains frozen for neuropathologic assessment. Compared to Sham, IUGR pups were delayed in attaining early reflexes and performed worse in the open field, both of which were significantly improved by maternal supplementation of BrSp (p<0.05). Neuropathology revealed diminished white matter, ventricular dilation, astrogliosis and reduction in hippocampal neurons in IUGR animals compared to Sham, whereas broccoli sprout supplementation improved outcome in all histological assessments (p<0.05). Maternal dietary supplementation with BrSp prevented the detrimental neurocognitive and neuropathologic effects of chronic intrauterine ischemia. These findings suggest a novel approach for prevention of cerebral palsy and/or developmental disabilities associated with placental insufficiency. Copyright © 2015. Published by Elsevier B.V.
    Behavioural brain research 05/2015; 291. DOI:10.1016/j.bbr.2015.05.033 · 3.03 Impact Factor
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    • "Badawi et al. (12) in Australia observed a prevalence of encephalopathy of 3.8 per 1000 term live birth neonates, while Ellis et al. (38), in Nepal found a prevalence of 6.1 per 1000. Statistically significant antepartum risk factors found were: malaria and preeclampsia/eclampsia, and prolonged rupture of membranes were the main risk factors for developing HIE. "
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    ABSTRACT: The World Health Organization (WHO) estimates that 4 million children are born with asphyxia every year, of which 1 million die and an equal number survive with severe neurologic sequelae. The purpose of this study was to identify the risk factors of birth asphyxia and the hospital outcome of affected neonates. This study was a prospective case-control study on term neonates in a tertiary hospital in Yaounde, with an Apgar score of < 7 at the 5th minute as the case group, that were matched with neonates with an Apgar score of ≥ 7 at the 5th minute as control group. Statistical analysis of relevant variables of the mother and neonates was carried out to determine the significant risk factors. The prevalence of neonatal asphyxia was 80.5 per 1000 live births. Statistically significant risk factors were the single matrimonial status, place of antenatal visits, malaria, pre-eclampsia/eclampsia, prolonged labor, arrest of labour, prolonged rupture of membranes, and non-cephalic presentation. Hospital mortality was 6.7%, that 12.2% of them had neurologic deficits and/or abnormal transfontanellar ultrasound/electroencephalogram on discharge, and 81.1% had a satisfactory outcome. The incidence of birth asphyxia in this study was 80.5% per1000 live birth with a mortality of 6.7%. Antepartum risk factors were: place of antenatal visit, malaria during pregnancy, and preeclampsia/eclampsia. Whereas prolonged labor, stationary labor, and term prolonged rupture of membranes were intrapartum risk faktors. Preventive measures during prenatal visits through informing and communicating with pregnant women should be reinforced.
    04/2013; 7(3):46-54.
    • "Both the fetus and the mother are at risk.[103104] The complications include increased perinatal deaths,[105] infantile death,[106] neonatal encephalitis.[107] Recent consensus opinions recommend the routine induction of labour at an earlier gestation age, specifically 41 weeks' gestation.[106108] "
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    ABSTRACT: The myometrium must remain relatively quiescent during pregnancy to accommodate growth and development of the feto-placental unit, and then must transform into a highly coordinated, strongly contracting organ at the time of labour for successful expulsion of the new born. The control of timing of labour is complex involving interactions between mother, fetus and the placenta. The timely onset of labour and delivery is an important determinant of perinatal outcome. Both preterm birth (delivery before 37 week of gestation) and post term pregnancy (pregnancy continuing beyond 42 weeks) are both associated with a significant increase in perinatal morbidity and mortality. There are multiple paracrine/autocrine events, fetal hormonal changes and overlapping maternal/fetal control mechanisms for the triggering of parturition in women. Our current article reviews the mechanisms for uterine distension and reduced contractions during pregnancy and the parturition cascade responsible for the timely and spontaneous onset of labour at term. It also discusses the mechanisms of preterm labour and post term pregnancy and the clinical implications thereof.
    03/2013; 17(1):50-9. DOI:10.4103/2230-8210.107841
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