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Antenatal and intrapartum factors associated with hypoxic-ischaemic encephalopathy

Presented at the Neonatal Society 2012 Spring Meeting.

Martinez-Biarge M1, Wusthoff C1, Diez-Sebastian J3, Rutherford MA2, Cowan FM1,2

1 Dept of Paediatrics, Imperial College and MRC Clinical Sciences Centre, Hammersmith Hospital London, UK
2 Centre for the Developing Brain, Imperial College and MRC Clinical Sciences Centre, Hammersmith Hospital London, UK
3 Dept of Statistics, La Paz University Hospital, Madrid, Spain

Background: The underlying causes of much perinatal asphyxia and hypoxic-ischaemic encephalopathy (HIE) remain unclear. Our aim was to identify antenatal and perinatal factors associated with term HIE following perinatal asphyxia in a case-control study.

Methods: From 1993-2007 all inborn and referred term infants (≥35 weeks gestation) with: 1) poor condition at birth (5-minute Apgar score <5, arterial cord blood pH <7.1 and/or need for major resuscitation); and 2) neonatal encephalopathy were included in this study. Antenatal and perinatal data were obtained and compared with those of a cohort of term-born neurologically normal infants (1). Infants were excluded if they had an identifiable metabolic disorder, severe congenital malformation or infection or genetic abnormality.

Results: 405 cases and 239 control infants were included. Of the 405 cases, the encephalopathy was mild in 61 (15%) and moderate/severe in 314 (77.5%); severity was unknown in 30 (7.5%). 393 infants (97%) had a brain MRI scan; in all cases imaging was consistent with a perinatal hypoxic-ischaemic insult (2) as interpreted by a paediatric neuroradiologist.
Infant characteristics: 56.5% HIE infants and 50.8% controls were male (P=0.16). HIE infants were of older gestational age (24.5% were ≥41 weeks gestation compared to 12% controls, P<0.001). More HIE infants had a BW <10th centile (17% vs. 10.8, P=0.042) and <3rd centile (5.8% vs. 1.7%, P=0.02).
Antepartum factors: mothers were younger in cases than in controls (29.7 ± 5.68 vs. 30.7 ± 5.11, P=0.021) and were more often primiparous (60.5% vs. 51.7%, P=0.042). Infertility treatment was more frequent in HIE cases (6% vs. 0.4%, P<0.001). No other antenatal factors were found to be statistically different between cases and controls.
Intrapartum factors: the incidence of induced labour was very similar between cases and controls. Control infants experienced artificial rupture of membranes more often (42.5% vs. 30.7%, P=0.012), but in more HIE cases there was prolonged (>24h) rupture of membranes (10% vs. 2.2%, P=0.004). Thick meconium (29% vs. 7%, p<0.001), abnormal CTG (77.5% vs. 21.5%, P<0.001), sentinel event (22% vs. 0.8%, P<0.001), shoulder dystocia (7.4% vs. 0.4%, P<0.001) and nuchal cord (11.5% vs. 6.3%, P=0.036) were significantly more prevalent in cases than in controls. HIE infants were delivered more often by emergency caesarean section (50% vs. 11.5%, P<0.001), and less frequently by instrumental vaginal delivery (17% vs. 21.5%, p=0.20) or spontaneous vaginal delivery (33% vs. 57.5%, P<0.001). No infant in the HIE group was delivered by elective caesarean section (10% in controls).
In the logistic regression analysis only one antepartum factor (GA ≥41 weeks) and 7 intrapartum factors (prolonged rupture of membranes, abnormal CTG, thick meconium, sentinel event, shoulder dystocia, cord around the neck and failed ventouse) remained significantly and independently associated with HIE. Overall, 6.7% of cases and 43.5% of controls had only antepartum factors; 20% cases and 5.8% controls had only intrapartum factors; 69.5% cases and 31% controls had antepartum and intrapartum factors and 3.7% cases and 19.7% controls had no identifiable risk factors (P<0.001).

Conclusion: In this case-control study only one antepartum, but multiple intrapartum factors were independently associated with HIE. We cannot exclude that some antepartum factors may predispose infants to experience an intrapartum event, but our results suggest that in the absence of intrapartum factors, antepartum factors in themselves are not enough to lead to HIE.

Corresponding author: f.cowan@imperial.ac.uk

References
1. Mercuri E et al. Arch Dis Child Fetal Neonatal Ed 1998;79: F185–F189.
2. Cowan et al. Lancet 2003;361:736-42.

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