Abstract

Background:Intra-uterine growth-restricted (IUGR) fetuses are prone to hypoxic changes in the brain and neurodevelopmental sequelae in later life. Chronic hypoxaemia may also lead to polycythaemia in the fetal and neonatal period.Aim:To evaluate venous haematocrit and cerebral blood flow velocity (CBFV) in term IUGR neonates in the immediate postnatal period.Methods:This was a prospective observational study of 54 clinically healthy term IUGR neonates as cases and 50 term, appropriate-for-gestational-age (AGA), healthy neonates as controls. IUGR was defined as birthweight <10th per centile for gestational age. Neonates with perinatal asphyxia, sepsis and other systemic diseases were excluded. Resistance index (RI), pulsatility index (PI), peak systolic velocity (PSV) and vascular diameter were measured in the internal carotid, vertebral and middle cerebral arteries by transcranial colour Doppler ultrasound between 48 and 72 hours of life, along with the estimation of venous haematocrit. Neonates were observed for development of any complications until discharge and followed up clinically and radiologically for a minimum 6 months.Results:Significantly higher resistance (RI and PI) and lower PSV was recorded in all the cerebral arteries of the IUGR than the AGA group whereas no difference was observed in vascular diameters. Mean haematocrit was significantly higher in the IUGR than in the AGA group [55·7 (4·22) vs 45·1 (2·79) g/dl]. Haematocrit was positively correlated with RI and PI, and negatively correlated with PSV. After discharge, three infants in the IUGR group showed hypertonia and delayed developmental milestones along with hypoxic changes in MRI of the brain.Conclusions:Compared with their AGA counterparts, higher venous haematocrit and lower CBFV were observed in clinically healthy, term IUGR neonates during the early neonatal period. Delayed developmental milestones and hypoxic changes were detected by MRI in three infants. Since the study was limited by its sample size, larger studies are required to document the clinical significance of decreased CBFV and its usefulness as a marker of poor prognosis for future neurodevelopment.

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