Antepartum risk factors for newborn encephalopathy

Editor—Badawi et al’s case-control study of neonatal encephalopathy in Western Australia shows that clinical evidence of dysfunction of the central nervous system in newborn infants is associated with a wide range of disorders.¹ For most of their study population these disorders had origins before the onset of labour. We have two concerns about generalising their findings to other populations: their definition of neonatal encephalopathy, and the greater importance of intrapartum risk factors for neonatal encephalopathy in poorer populations in the developing world.

The omission of intrapartum criteria from the case definition of neonatal encephalopathy has been advocated previously and removes an important bias affecting other studies.² The investigators’ broad clinical definition of neonatal encephalopathy, however, makes comparison with prevalence studies in other settings problematic. For instance, isolated neonatal seizures are difficult to ascertain clinically.³ What proportion of the 109 infants reported to have seizures had interictal evidence of neurological dysfunction? Other investigators have chosen to exclude established causes of encephalopathy such as overt congenital infection and hypoglycaemia from prevalence studies, so it would be helpful for comparative purposes to know what proportion of the authors’ cases had evidence of these.

Finally, the inclusion of 37 infants with birth defects (23% of the cases) clearly has implications for the subsequent analysis of the likely time of the insult. In a high income setting with almost universal antenatal care and a relatively low stillbirth rate, the live birth of neurologically impaired fetuses will probably be maximised. In many low income countries mothers are stunted, do not access antenatal care, have high stillbirth rates, and receive poor obstetric care. Under these conditions intrapartum factors probably remain more important in the causation of neonatal encephalopathy.