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Cerebral palsy and mental retardation in relation to indicators of perinatal asphyxia. An epidemiologic overview
Insights
Intrapartum asphyxia
Area of Science:
- Perinatal medicine
- Neonatology
- Neurology
Background:
- Intrapartum asphyxia is a known cause of perinatal loss.
- The contribution of intrapartum and neonatal asphyxia to community-wide neurologic handicap is debated.
- Epidemiologic data suggest perinatal events play a smaller role in severe mental retardation and cerebral palsy than commonly believed.
Purpose of the Study:
- To review epidemiologic information on the contribution of perinatal events to neurologic handicaps.
- To clarify the relationship between birth asphyxia and conditions like cerebral palsy and mental retardation.
- To inform clinical practice regarding resuscitation and obstetric intervention.
Main Methods:
- Review of existing epidemiologic literature.
- Analysis of data linking perinatal events to neurologic outcomes.
- Examination of the incidence of neurologic sequelae following asphyxia.
Main Results:
- Cerebral palsy is most closely linked to adverse perinatal events, but over 50% of cases lack documented birth depression.
- Perinatal events account for no more than 15% of severe mental retardation.
- Severe mental retardation without cerebral palsy is not typically linked to birth asphyxia.
- Most infants experiencing significant birth asphyxia do not develop detectable neurologic or intellectual deficits.
Conclusions:
- Resuscitative efforts in newborns should not be prematurely ceased due to fear of late sequelae.
- Obstetric interventions solely for potential later neurologic development are not scientifically justifiable.
- Antenatal and intrapartum fetal monitoring are best justified by the established links between indicators of fetal asphyxia and fetal/neonatal mortality and morbidity.
Abstract:
Although intrapartum asphyxia is established as an important cause of perinatal loss, there is little consensus as to how much of the burden of neurologic handicap in the community is attributable to intrapartum and neonatal asphyxia, as measured clinically. A review of the available epidemiologic information suggests that the role of perinatal events in the genesis of severe mental retardation and cerebral palsy is not as large as popularly thought. Of all neurologic handicaps, cerebral palsy bears the closest relationship to adverse perinatal events, but at least 50% of all cases have no documented depression at the time of birth. No more than 15% of severe mental retardation can be attributed to perinatal events. Severe mental retardation without cerebral palsy does not appear to be attributable to birth asphyxia. The majority of even quite severely asphyxiated babies suffer no detectable neurologic or intellectual sequelae. These epidemiologic observations suggest that resuscitative efforts in mature newborn infants ought not to be too quickly abandoned for fear of late sequelae. At the same time, obstetric intervention based solely on concern for later neurologic development cannot be justified. The most appropriate justification for antenatal and intrapartum monitoring of fetal condition are the established associations of indicators of fetal asphyxia with fetal and neonatal death, and with morbidity in the neonatal period.