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Glucose is the preferred oxidative energy source for the central nervous system. At birth, the sudden loss of a continuous maternal glucose supply requires a neonatal response to maintain adequate serum glucose levels throughout the early feeding and fasting periods. The newborn’s plasma glucose level drops quickly after delivery and generally reaches a nadir by 2 hours of age. While otherwise healthy neonates may develop persistent hypoglycemia, up to 50% in high-risk neonates (e.g. small or late preterm infants, infants of diabetic mothers) develop persistent hypoglycemia.1 If severe, neonatal hypoglycemia may result in systemic effects and have potential neurological sequelae.


Adaptive changes in hormonal regulation at birth conspire to maintain the newborn’s plasma glucose concentration, reserve glucose for the central nervous system, and avoid hypoglycemia. Counterregulatory hormones, including glucagon, growth hormone, cortisol, and epinephrine, act together to increase blood glucose via glycogenolysis, gluconeogenesis, ketogenesis, and inhibition of peripheral glucose uptake and insulin release. These regulatory mechanisms support the transition from a continuous transplacental glucose source to an intermittent supply via feeding. The failure of one or several parts of this process can result in hypoglycemia.

Infants at higher risk for hypoglycemia are those with diminished hepatic glucose production, increased metabolic need versus substrate availability, or increased insulin production (Table 129-1). Additional metabolic challenges such as immaturity, low glycogen reserves, and thermal stress may also render the newborn more susceptible to hypoglycemia.

TABLE 129-1*Infants at Risk for Hypoglycemia*


In healthy adults, a decrease in blood glucose concentration inhibits the production of insulin and stimulates ...

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