Objective To examine the relationship between umbilical cord pH at term and serious neonatal outcomes.Design Observational cohort study. Methods Absolute risks, relative risks with 95% confidence intervals, and numbers needed to harm were calculated for different levels of arterial pH across the entire range.Main outcome measures Neonatal encephalopathy with seizures and/or death, encephalopathy within 24 hours of birth, 5-minute Apgar scores and neonatal unit admission.Results The median arterial pH was 7.22, interquartile range 7.17-7.27. The absolute risk of an adverse neurological outcome was significantly increased below 7.10 (0.36%) and was lowest between 7.26 and 7.30 (0.16%). Even below 7.00, the risk was only 2.95%. However, more than 75% of neonates with neurological outcomes examined, including seizures within 24 hours of birth, had a pH above 7.10. A small increase in risk was evident at higher pH levels.Conclusion The threshold pH for adverse neurological outcomes is 7.10 and the 'ideal' cord pH is 7.26-7.30. Above 7.00, however, neonatal acidaemia is weakly associated with adverse outcomes. Most neonates with neurological morbidity have normal cord pH values. Other variables must influence adverse outcomes and account for more of these than acidaemia. A better understanding of these is required before intrapartum fetal monitoring can improve.

National Institute for Health Research and Medical Research Council.

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Objective: To investigate risk factors for cerebral palsy in relation to gestational age. Design: Three case-control studies within a geographically defined cohort. Setting: The former Oxfordshire Health Authority. Participants: A total of 235 singleton children with cerebral palsy not of postnatal origin, born between 1984 and 1993, identified from the Oxford Register of Early Childhood Impairment; 646 controls matched for gestation in three bands: (32 weeks; 33-36 weeks; >37 weeks. Results: Markers of intrapartum hypoxia and infection were associated with an increased risk of cerebral palsy in term and preterm infants. The odds ratio (OR) for hypoxia was 12.2 (95% confidence interval 1.2 to 119) at (32 weeks and 146 (7.4 to 3651) at >37 weeks. Corresponding ORs for neonatal sepsis were 3.1 (1.8 to 5.4) and 10.6 (2.1 to 51.9). In contrast, pre-eclampsia carried an increased risk of cerebral palsy at >37 weeks (OR 5.1 (2.2 to 12.0)) but a decreased risk at (32 weeks (OR 0.4 (0.2 to 1.0)). However, all infants (32 weeks with maternal pre-eclampsia were delivered electively, and their risk of cerebral palsy was no lower than that of other electively delivered (32 week infants (OR 0.9 (0.3 to 2.7)). Nearly 60% of (32 week controls were delivered after spontaneous preterm labour, itself an abnormal event. Conclusion: Inflammatory processes, including pre-eclampsia, are important in the aetiology of cerebral palsy. The apparent reduced risk of cerebral palsy associated with pre-eclampsia in very preterm infants is driven by the characteristics of the gestation matched control group. Use of the term ''protective'' in this context should be abandoned.

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