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Cerebral palsy developed as the sequel of intrapartum hypoxia, the loss of fetal heart rate variability followed by fetal brain damage is rare but important problem among paediatricians and obstetricians. As the author found that intrapartum fetal heart would be damaged by repetition of transient fetal heart rate (FHR) reductions (decelerations), then intended to numerize the deceleration with the hypoxic index (HI), namely, the HI was the sum of decelerating durations (min) divided by the lowest FHR in the decelerations, and multiplied by 100 in the intrapartum fetal heart rate monitoring, because the heart rate is fully parallel to the PaO2 if the PaO2 is lower than 50 mmHg [1], and fetal PaO2 is lower than 50mmHg [2]. As the hypoxia index was 25 and 26 in the loss of FHR baseline variability, which was the sign of severe fetal brain damage followed by cerebral palsy, whereas normal FHR variability neither followed by fetal brain damage nor cerebral palsy in cases whose hypoxia index was 20 to 24, where significant difference was found in the development of cerebral palsy among the two groups, it was decided that the lowest limit of hypoxia index to develop cerebral palsy was 25, where no cerebral palsy was expected to develop cerebral palsy, then the hypoxia index was 24 or less. Thus, a foetus who have any FHR curve changes should deliver the foetus in the stage when the hypoxia index is 24 or less to achieve an infant of no cerebral palsy [3].

Possible reduction of cerebral palsy caused by intrapartum fetal hypoxia and in preterm birth