Abstract

In this paper data on abnormal antepartum FHR patterns are related to the state of fetal oxygenation, fetal brain abnormalities and to neurological outcome. It is concluded that in IUGR fetuses changes in heart rate (and movement) patterns are late signs of impairment. Antepartum heart rate decelerations are usually the first of the abnormalities detected and are associated with fetal hypoxaemia. A fixed or flat FHR pattern might be indicative of congenital malformations of the brain or of prenatally acquired encephalopathy. Several studies have shown that antepartum FHR abnormalities (usually late decelerations) are associated with an increased risk of subsequent handicap. This risk is related to the degree of FHR abnormality, and especially applies to infants born preterm and/or growth-retarded. Late (ante partum) FHR decelerations seem to be more important than 'asphyxia' at birth in determining (neonatal) neurological outcome. In IUGR hypoxaemia is probably associated with deprivation of other nutrients, and thus brain damage in these infants is more likely to be due to chronic malnutrition (including hypoxaemia) than to hypoxaemia alone. This reasoning is supported by morphological findings in IUGR infants. In general fetuses should be delivered before antepartum signs of hypoxaemia appear. Doppler blood--velocity waveform analyses of fetal vessels may detect fetuses at risk for antepartum decelerations, but until now there has been insufficient information about false-positive abnormal velocity waveforms to depend absolutely on these. Furthermore, delivery at an earlier age may increase the risk of other neonatal complications.

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