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PubMed · 9518223

Birth asphyxia.

P Anslow
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Abstract

The term Birth asphyxia covers a number of clinical and physiological definitions. Birth asphyxia is a relatively common clinical event. In the majority of cases the outcome in terms of brain damage and future development of the child is excellent. However, a small number of children go on to develop patterns of brain damage which are then associated with disability. The article seeks to provide a basic understanding of the various mechanisms involved in producing injury.

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Asphyxia NeonatorumBrainBrain Damage, ChronicChildFetal HypoxiaHumansInfant, NewbornLeukomalacia, PeriventricularMagnetic Resonance ImagingMaleJournal Article

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BibTeXRIS

P Anslow. 1998. Birth asphyxia.. https://doi.org/10.1016/s0720-048x(97)00090-9

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PubMed1998

Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control study.

OBJECTIVE: To identify intrapartum predictors of newborn encephalopathy in term infants. DESIGN: Population based, unmatched case-control study. SETTING: Metropolitan area of Western Australia, June 1993 to September 1995. SUBJECTS: All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls. MAIN OUTCOME MEASURES: Adjusted odds ratio estimates. RESULTS: The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. Maternal pyrexia (odds ratio 3.82), a persistent occipitoposterior position (4.29), and an acute intrapartum event (4.44) were all risk factors for newborn encephalopathy. More case infants than control infants were induced (41.5% and 30.5%, respectively) and fewer case infants were delivered by caesarean section without labour (3.7% and 14.5%, respectively). Operative vaginal delivery (2.34) and emergency caesarean section (2.17) were both associated with an increased risk. There was an inverse relation between elective caesarean section (0.17) and newborn encephalopathy. After application of a set of consensus criteria for elective caesarean section only three (7%) eligible case mothers compared with 33 (65%) eligible control mothers were sectioned electively. Of all the case infants, 113 (69%) had only antepartum risk factors for newborn encephalopathy identified; 39 (24%) had antepartum and intrapartum factors; eight (5%) had only intrapartum factors; and four (2%) had no recognised antepartum or intrapartum factors. CONCLUSIONS: The causes of newborn encephalopathy are heterogeneous and many relate to the antepartum period. Elective caesarean section has an inverse association with newborn encephalopathy. Intrapartum hypoxia alone accounts for only a small proportion of newborn encephalopathy. These results question the view that most risk factors for newborn encephalopathy lie in the intrapartum period.

Asphyxia Neonatorum↗
PubMed1998

Lactate, lactate/pyruvate ratio and catecholamine interrelations in cord blood at delivery in complicated pregnancies.

The interrelationships between lactate, lactate/pyruvate (L/P) ratio and catecholamines (CA) in cord artery and vein blood were studied in 56 pregnancies who had complications in the antenatal period or during labour. This group of babies had higher CA levels and were more acidaemic than fetuses after normal pregnancies and labour. There were stronger correlations between lactate and noradrenaline (NA) (R = 0.56, P < 0.001), adrenaline (A) (R = 0.41, P = 0.002) and dopamine (DA) (R = 0.42, P = 0.001) in cord artery blood, than previously reported for normal deliveries. Correlations between L/P ratio and CAs were also significant, although weaker. Multiple regression analysis, using cord artery lactate as the dependent variable, revealed significant correlations for pH (P = 0.01) and pyruvate (P < 0.001) but not for the CAs. The subgroups with high lactate (> 75th centile) had significantly higher NA (P = 0.007) and DA (P < 0.001) in cord artery and NA (P < 0.001) and A (P < 0.001) in cord vein blood, as compared with the subgroup who had lower lactate concentrations. We conclude that fetal hypoxia induces fetal CA production as well as anaerobic metabolism with lactate production. However, the adrenergic stimulation seems not to contribute significantly to the fetal lactate production.

Asphyxia Neonatorum↗