Intrauterine Asphyxia: Clinical Implications for Providers of Intrapartum Care

Jenifer Fahey, CNM, MSN, MPH; Tekoa L. King, CNM, MPH


J Midwifery Womens Health. 2005;50(6):498-506. 

In This Article

The Relationship Between Intrapartum Asphyxia and Neurologic Injury in the Fetus

"Asphyxia as an initiating pathology [for cerebral palsy], usually involving the whole organism, must be distinguished from hypoxia or ischemia at the tissue level, resulting from secondary and tertiary complications of other disorders, such as infection, inflammation without infection, or vascular pathologies."[19]

Although intrauterine asphyxia is an established cause of neurologic damage, including cerebral palsy, determining the exact role of intrapartum asphyxia as a cause of permanent neurologic damage in a fetus is complicated. It is estimated that the overall incidence of neonatal encephalopathy attributable to intrapartum asphyxia alone (in the absence of antepartum abnormalities) is 1.6 per 10,000 births.[20] Prematurity and infections during pregnancy both appear to be more common causes of cerebral palsy than intrapartum events. Infants weighing <1500 g at birth constitute approximately 25% of all cases of cerebral palsy.[20] Several studies have demonstrated an association between chorioamnionitis and the development of cerebral palsy in the near-term and term fetus.[21,22] Current evidence implicates inflammatory cytokines in the pathway that connects infection to subsequent neurologic damage.[23]

Not only is causation of neurologic injury difficult to establish, but identifying the timing of the injury is also complicated.[24,25] The proportion of cerebral palsy that may be attributed to intrapartum events is small and estimated to be between 3% and 20%.[26,27] Because neonatal encephalopathy is an essential pathway to subsequent cerebral palsy, the role of preconceptional, antepartum, and intrapartum factors in the development of neonatal encephalopathy was investigated in a case-control study from western Australia. The authors examined infants born between 1993 and 1995.[24,25] Multivariate analysis of 164 cases of neonatal encephalopathy revealed that 69% of the children with neonatal encephalopathy had only antepartum risk factors, 24% had both antepartum and intrapartum risk factors, and only 5% had intrapartum risk factors only (defined as the presence of an abnormal fetal heart rate tracing or abnormal fetal heart rate on auscultation and/or fresh meconium staining, or both, with an Apgar of <3 at 1 minute and an Apgar of <7 at 5 minutes). Two percent of the children had no identifiable perinatal risk factors.[25]

Table 2 includes selected factors associated with the development of neurologic dysfunction in the neonate.[20] The low percentage of neonatal encephalopathy and cerebral palsy cases that appear to be attributable to intrapartum events partially explains why the rate of cerebral palsy in term infants in the United States has remained nearly unchanged despite obstetric interventions and increased use of fetal heart rate monitoring in labor.[28]

In the last decade, two major task forces have provided guidance on differentiating cases of neonatal encephalopathy and cerebral palsy that may be due to intrapartum events from those that are due to events predating labor. Both task forces have reviewed and evaluated the research available and solicited opinions and written contributions from leading clinicians and scientists. In 1999, the International Cerebral Palsy Task Force published its consensus statement.[29] The following year, the American College of Obstetricians and Gynecologists (ACOG) convened the Task Force on Neonatal Encephalopathy and Cerebral Palsy, and their consensus statement was published in 2003.[20] Both task forces published criteria needed to diagnose cerebral palsy as secondary to an acute intrapartum event, with slight differences, as noted in Table 3 .


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