Introduction

For most of the twentieth century the concept of perinatal brain damage centered around cerebral palsy and intrapartum asphyxia. It is only in the last 20 years that this view has been seriously challenged by clinical and epidemiological studies that have demonstrated that approximately 70–90% or more of cerebral palsy is unrelated to intrapartum events. Many term infants who subsequently develop cerebral palsy are believed to have sustained asphyxial events in mid-gestation. In some cases, prenatal injury may lead to chronically abnormal heart-rate tracings and impaired ability to adapt to labor, which may be confounded with an acute event.

Furthermore, it has become clear that the various abnormal fetal heart-rate (FHR) patterns that have been proposed to be markers for potentially injurious asphyxia are consistently only very weakly predictive for cerebral palsy. Although metabolic acidosis is more strongly associated with outcome, more than half of babies born with severe acidosis (base deficit > 16 mmol/L and pH < 7.0) do not develop encephalopathy, while conversely encephalopathy can still occur, although at low frequency, in association with relatively modest acidosis (BD 12–16 mmol/L). These data contrast with the presence of very abnormal fetal heart-rate tracings, severe metabolic acidosis, and acute cerebral lesions in the great majority of infants who do develop acute neonatal encephalopathy.

The key factor underlying all of these observations is the effectiveness of fetal adaptation to asphyxia.