Cerebral palsy and intrapartum hypoxia: current evidence and the position of Korean Society for Maternal Fetal Medicine

Cerebral palsy (CP) has long been associated with intrapartum hypoxia; however, contemporary evidence indicates that acute hypoxic-ischemic events during labor account for only a minority of cases. This narrative review summarizes the current evidence regarding the epidemiology, pathophysiology, and causation assessment of CP, focusing on the limitations of electronic fetal monitoring, umbilical cord pH, low Apgar scores, and cesarean delivery as predictors or preventive measures for CP. Prematurity, intrauterine infection and inflammation, placental pathology, perinatal arterial ischemic stroke, and genetic factors are important associated factors or contributory pathways in CP, although their population-attributable contributions remain uncertain. Recent genomic studies have identified pathogenic or likely pathogenic variants in approximately one-quarter to one-third of affected children, challenging the traditional assumption that unexplained CP is attributable to intrapartum events. Current evidence indicates that isolated fetal heart rate abnormalities, acidemia, or neonatal encephalopathy alone are insufficient to establish intrapartum hypoxia as the cause of CP. The Korean Society for Maternal Fetal Medicine emphasizes that causation assessments should rely on strict criteria, exclusion of alternative etiologies, and integrated interpretation of antenatal, intrapartum, neonatal, neuroimaging, placental, and genetic findings. A multifactorial and evidence-based approach is essential for rational clinical assessment, appropriate counseling, and avoidance of unnecessary defensive obstetric practices.