Role of Cerebro-placental-uterine Ratio in Prediction of Late-onset Fetal Growth Restriction: A Prospective Observational Study

Abstract

redistributing blood flow to essential organs when umbilical artery (UA) and maternal uterine arteries (UtAs) demonstrate increased resistance. 9 On comparison to UA-PI, cerebral vasodilatation is a more sensitive indicator of placental insufficiency.In case of late-onset FGR, due to long-term hypoxic conditions, vascular resistance decreases with increase in brain perfusion, known as "brain sparing effect." With the fact that FGR impacts different regions, ratios of these would help in improving the IntroductIonLate-onset fetal growth restriction (FGR) is often defined as the failure of the fetus to achieve growth potential as diagnosed after 32 weeks of gestational age. 1 FGR affects approximately 3-7% of all pregnancies which is seen sixfolds higher in underdeveloped countries than developed countries. 2 FGR prevalence in India is about 26% with late-onset FGR contributing for about 70-80%. 3 About 75% of FGR are missed for identification at early stages of gestation since the measurement of symphysiofundal height becomes challenging. 4 Late-onset FGR results in small for gestational age (SGA) babies, fetal distress, need for emergency cesarean section, neonatal acidosis, and need for NICU admission. 5 Late-onset FGR is predominantly due to uteroplacental insufficiency and associated with about 50% of stillbirths, especially after 34 weeks, contributing to 30% of all stillbirths. 6,7 Hence, in order to reduce the stillbirth rate, it is essential to identify the fetuses at risk of late-onset FGR. 8 Late-onset FGR is mainly due to uteroplacental insufficiency secondary to abnormal trophoblastic invasion, leading to altered blood flow resistance in the uterine, placental, and fetal vasculature, which can be detected using various Doppler parameters. For example, reduced middle cerebral artery (MCA) pulsatility index (PI) reflects vasodilatation of the fetal cerebral vessels.