Mechanism OF Hypoglycemia Development in Premature Infants, Treatment Approaches
Abstract
Glucose, like oxygen, is essential for all living organisms and serves as the main energy source for the fetus and newborn during pregnancy. The placenta provides a constant supply of glucose to the fetus, whereas birth marks a sudden interruption in substrate delivery and significant metabolic adaptation. Hypoglycemia is one of the most common pathologies encountered in neonatal intensive care units, affecting a wide range of newborns. Preterm infants, small-for-gestational-age (SGA) infants, and those with intrauterine growth restriction (IUGR) are particularly vulnerable due to limited metabolic reserves and associated morbidities. Nearly 30–60% of these high-risk neonates develop hypoglycemia that requires immediate intervention. Preterm infants are especially prone to hypoglycemia and its related complications because of limited glycogen and fat stores, inability to generate new glucose via gluconeogenesis, relatively large brain size with high metabolic demands, and immature counterregulatory responses to hypoglycemia.