[Limit of antenatal management of intrauterine growth retarded fetus].
Recent advances in perinatal medicine contributed to the survival of extremely premature infants. Nonetheless, prognosis of the fetus with intrauterine growth retardation (IUGR) especially of preterm IUGR is not satisfactory with respect to both neonatal and long term neurodevelopmental outcome. As in utero pathophysiology of the IUGR has been revealed by noninvasive fetal monitoring technique along with invasive cordocentesis to determine fetal blood gas parameters, most of the neonatal morbidity of IUGR is thought to be originated prior to birth. Excluding the IUGR due to chromosomal abnormalities, fetal anomalies and multiple gestation, severe preeclampsia contributes nearly 60 to 80% of the etiology of IUGR in our series. In IUGR with severe preeclampsia, it is noteworthy that the incidence of symmetrical IUGR is approximately 50%, suggesting disturbance in head growth is responsible for symmetrical growth. We have shown that the disturbance in head growth is particularly important not only for neurodevelopmental but also for short term neonatal mortality and morbidity. It is suggested that the reasonable timing of delivery of preterm IUGR should be before onset of fetal acidosis and/or cessation of fetal head growth for the following reasons. 1. There is a relationship between fetal acidemia at cordocentesis and subsequent neurodevelopment. 2. The incidence of neonatal morbidity including hypoglycemia, hemoconcentration and thrombocytopenia increased with the degree of disturbance in head circumference at birth. We propose that the IUGR fetus should be monitored weekly for its growth by ultrasound fetometry and noninvasive fetal monitoring methods including nonstress test, Biophysical profile scoring and Doppler velocimetry.(ABSTRACT TRUNCATED AT 250 WORDS)
Takagi
K
K
Department of Obstetrics and Gynecology, Tokyo Women's Medical College.
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology*; D005311:Fetal Hypoxia / Q000378:metabolism; D005328:Fetal Viability; D005865:Gestational Age; D006257:Head / Q000254:growth & development; D006801:Humans; D007231:Infant, Newborn; D018970:Insulin-Like Growth Factor Binding Protein 1; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D011225:Pre-Eclampsia / Q000150:complications; D011247:Pregnancy; D011379:Prognosis; D012306:Risk
D002352:Carrier Proteins; D018970:Insulin-Like Growth Factor Binding Protein 1; D007334:Insulin-Like Growth Factor I