Editorial
The feeding conundrum
Abstract
Placental insufficiency is an important contributor to the intra utero growth restriction (IUGR). Increasing severity of placental insufficiency results in fetal adaptation (diving reflex) leading to preferential blood circulation to the brain and increased comprise of the intestines and the kidneys. Antenatal Doppler abnormalities including absent or reversal of end-diastolic flow (AREDF) in the umbilical artery in IUGR fetus is a reflection of greater severity of utero placental insufficiency and more compromised intestine. Prolonged exposure to fetal hypoxia and ischemia could result in altered development of motor, secretory, mucosal functions and after birth the intestine is more susceptible to stasis, abnormal colonization, and bacterial invasion (1). Post-natal physiological flow studies report persistent mesenteric artery flow abnormalities lasting for almost a week in IUGR infants with AREDF (2,3). Pregnancy induced hypertension in association with IUGR and neonatal neutropenia could further increase the risk of early infections in these neonates. Thus these high risk preterm infants are at risk for early necrotizing enterocolitis (NEC) [odds ratio (OR) =2.13; 95% CI: 1.49–3.03] due to ischemia of mesenteric vascular bed emanating from redistribution of blood flow to vital organs in the fetus (1). IUGR and also AREDF are thus independent risk factors for NEC when adjusted for gestational age at birth.