AI Article Synopsis

  • The study aimed to investigate how adverse factors during pregnancy and childbirth contribute to neonatal encephalopathy in full-term newborns.
  • Conducted at multiple hospitals in Perth, Australia, it involved 89 cases of full-term infants with neurological issues compared to matched controls without these conditions.
  • Findings indicated an incidence of severe encephalopathy at 3.75 per 1000 live births, identifying several significant risk factors including maternal health issues and labor complications.

Article Abstract

Objective: Preliminary investigation of the contribution of adverse antepartum and intrapartum factors to neonatal encephalopathy in singleton neonates born full term.

Design: Matched case-control study based on incidence density sampling of controls.

Setting: Two major teaching hospitals (one paediatric and one obstetric) and three peripheral maternity hospitals in Perth, Western Australia (population 1.2 million).

Subjects: 89 cases, all the full term singleton neonates born during an eight month period in 1992 who fulfilled one or more of six criteria during the first week of life (seizures, abnormal conscious state, persistent hypertonia or hypotonia, and feeding or respiratory difficulties of central origin). One full term control infant without neonatal encephalopathy was matched to each case by sex, hospital of delivery, time of day and day of the week of birth, and maternal health insurance status.

Main Outcome Measures: Odds ratio estimates of relative risk of neonatal encephalopathy associated with antepartum and intrapartum factors.

Results: Estimated incidence of moderate or severe encephalopathy in first week of life was 3.75 per 1000 full term live births. Thirteen cases and no controls had evidence suggestive of important intrapartum hypoxia, and in only five of these cases was the neurological condition at birth attributed to events during the intrapartum period. Univariate conditional logistic regression analysis identified significant differences between cases and controls for maternal vaginal bleeding in pregnancy, maternal thyroxine treatment, congenital abnormalities, induction of labour, interval from membrane rupture to delivery, maternal pyrexia in labour, augmentation of labour, abnormal intrapartum cardiotocograms, and meconium in labour. Family history of convulsions also approached significance.

Conclusions: Our preliminary results suggest that intrapartum hypoxia, according to currently used criteria, was not the cause of neonatal encephalopathy in most cases in this population. Our findings suggest that many aetiologies of neonatal encephalopathy originate in the antepartum period.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2550662PMC
http://dx.doi.org/10.1136/bmj.311.7005.598DOI Listing

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