Fetal Growth Restriction and Doppler Waveform

Abstract

Background: Fetal growth restriction (FGR) is defined as the estimated fetal weight less than the 10th percentile for that gestational age on ultrasound study. There is no proven cure; management is reliant on a structured antenatal surveillance programme. Recent advances in ultrasound and Doppler have elucidated several mechanisms of growth restriction. Prediction of intrauterine hypoxia and acidemia can be done by Doppler study of fetal cardiovascular system. Objectives: To analyse the uteroplacental and fetoplacental blood flow using Doppler ultrasound in growth-restricted fetuses with reference to flow velocity and waveform indices. Materials and Methods: This prospective study employed Doppler ultrasound examination of the fetal cardiovascular system after 28 weeks of gestation in 32 singleton pregnancies with fetal growth restriction. Results: In the present study preeclampsia and maternal anaemia were found to be the most important cause of fetal growth restriction. Abnormal Doppler indices in umbilical and middles cerebral artery statistically correlated with lower birth weights, higher rate of caesarean delivery, oligohydramnios, low Apgar scores, perinatal death and higher admission to neonatal intensive care unit. Reduced end diastolic flow or complete absence of it in the umbilical artery is associated with poor perinatal outcome. Cerebroplacental Ratio (pulsatility index of middle cerebral artery/pulsatility index of umbilical artery) less than 1 is a very sensitive and specific sign of fetal compromise. Conclusion: Abnormal Doppler waveforms within the umbilical and middle cerebral arteries are indicative of redistribution of cerebral blood flow in fetal hypoxia. If there is reduced or low blood flow during diastole in umbilical arteries, the fetal perfusion becomes intermittent and fetal hypoxia develops. The blood flow redistributes to vital organs like brain and kidneys and the pulsatility index of middle cerebral artery falls in the fetus. The plausible explanation of it is, sympathetic activation in a hypoxemic fetus leading to increased cerebral perfusion. The ductus venosus flow gets reduced and reversed along with continued hypoxia.