There is an association between quality of intrapartum care and death. The findings also suggest an association between suboptimal care and cerebral palsy, but this seems to have a role in only a small proportion of all cases of cerebral palsy. The contribution of adverse antenatal factors in the origin of cerebral palsy needs further study.

95%

Neuropathological examinations were carried out at necropsy on 274 cases of intrauterine death or neonatal death at or before three days after birth. Fifty six (20.4%) subjects had evidence of prenatal ischaemic brain damage. On review of the maternal case notes to ascertain antenatal clinical associations there was an increased incidence of intrauterine growth retardation, either based on birth weight for gestational age (odds ratio (OR) 2-0; 95% confidence interval (CI) 1.1 to 3-7) or diagnosed antenatally (OR 2-7; 95% CI 13 to 5.6). Oligohydramnios was also more common (OR 2-9; 95% CI 1P2 to 7-0). The association of intrauterine growth retardation and white matter damage remained after excluding fetuses with a major congenital anomaly (OR 2*4; 95% CI 1.1 to 5.1). The findings suggest that chronic intrauterine hypoxia may be associated with damage to cerebral white matter among fetuses and infants who die. The relation between ischaemic white matter damage and cerebral palsy among survivors remains speculative.

A six stage model was applied to a geographically defined population of 210 singleton children born at term who had a diagnosis of cerebral palsy at 5 years of age. Thirty five children were identified as those most likely to have cerebral palsy ofintrapartum origin; in 26 of these there was evidence of suboptimal care.It is suggested that this simple model should be tested on populations of children with cerebral palsy and the underlying principles used when considering the likely cause of cerebral palsy in individual children. (Arch Dis Child 1995; 73: F106-F108)