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Br J Obstet Gynaecol. 1999 Aug;106(8):774-82.

Antecedents of neonatal encephalopathy with fetal acidaemia at term.

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Department of Obstetrics and Research Centre for Developmental Medicine and Biology, School of Medicine, University of Auckland, New Zealand.



To identify the relative contribution of antenatal hypoxia, obstetric catastrophe during labour and fetal monitoring practice to the occurrence of neonatal encephalopathy associated with acidaemia at term.


Prospective study.


Tertiary referral hospital in Auckland, New Zealand.


Twenty-two term babies born between January 1996 and October 1997 with umbilical artery pH < or = 7.09 (median 6.88) or 5 minute Apgar score < 7 (median 5.0), and moderate to severe encephalopathy within five hours of birth.


Antenatal and intrapartum events and fetal heart rate monitoring practice were reviewed by an experienced obstetrician.


More than half the cases were associated with events beyond the control of the clinician: 5 of 22 (23%) had evidence of antenatal hypoxia and 5 of 22 (23%) experienced an obstetric catastrophe during labour. Use of continuous fetal monitoring techniques or the interpretation of fetal heart rate changes was suboptimal in 8 of 12 cases. Continuous monitoring was not performed at all in three cases. All pregnancies were of either low or medium risk; none had proteinuric hypertension and no case was breech, small for gestational age or had a gestational age > or = 42 weeks.


A significant proportion of babies with encephalopathy associated with acidaemia at term experienced either antenatal hypoxia or catastrophic events beyond the control of the clinician. Further improvements in obstetric care will require greater vigilance in low to medium risk pregnancies and improved fetal monitoring practice during both induction and labour.

[Indexed for MEDLINE]

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