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.
| Risk Due to Diminished Hepatic Glucose Production | Risk Due to Increased Glucose Utilization (Increased Metabolic Demand) | Risk Due to Excessive Transient Pancreatic Insulin Production (Hyperinsulinism) | Risk Due to Excessive and Persistent Pancreatic Insulin Production (Hyperinsulinism) | Other |
|---|---|---|---|---|
SGA infant IUGR | Perinatal stress Hypoxia | Infant of diabetic mother | Congenital hyperinsulinism | Endocrine Adrenal insufficiency (CAH) Congenital hypopituitarism Hypothyroidism |
| Prematurity | Thermal stress | LGA infant | Beckwith-Wiedemann syndrome | Delayed feeding |
| IUGR and infant of diabetic mother | Polycythemia-hyperviscosity | Severe Rh incompatibility (erythroblastosis fetalis) | Pancreatic islet cell adenoma | Iatrogenic |
| Post-term gestation | Congenital heart disease | Iatrogenic (maternal drugs)† | Adenomatosis | |
| Infants of multiple gestations | CNS abnormalities | High umbilical artery catheter | ||
| Inborn errors of metabolism | Sepsis | Exchange transfusion | ||
Glycogen storage disease Galactosemia Tyrosinemia Hereditary fructose intolerance α1-Antitrypsin deficiency |
In healthy adults, a decrease in blood glucose concentration inhibits the production of insulin and stimulates the production of glucagon. This prevents the blood glucose from dropping to less than 60 mg/dL, thus avoiding the development of typical symptoms of hypoglycemia such as diaphoresis, headache, and dizziness. In neonates there is a weaker clinical correlation between blood glucose concentrations and symptoms of hypoglycemia. Although some newborns may display nonspecific signs and symptoms of hypoglycemia (Table 129-2) others may appear completely asymptomatic despite low blood and cerebral glucose levels.
The presence of hypoglycemia is most often the result of a healthy newborn’s inability to quickly and adequately respond to the dramatic loss of maternal sources of glucose. However, hypoglycemia may also be a signal of other stresses, including sepsis, inborn errors of metabolism, hyperinsulinism, polycythemia, and congenital hypopituitarism (see Table 129-1). Symptoms of hypoglycemia are nonspecific and overlap with other systemic conditions (e.g. neonatal abstinence syndrome). In addition, hypoglycemia may be one feature of a syndrome or a multifaceted disorder (e.g. Beckwith-Wiedemann syndrome).
No specific glucose value either defines significant hypoglycemia, or predicts neurologic injury in the newborn. Consequently, there is no consensus or numerical definition for neonatal hypoglycemia. Uncertainty exists about where the appropriate lower limit of normal is for newborns, and there are limitations to a single cutoff value. In general, a conservative threshold for defining hypoglycemia is useful to avoid the systemic effects and potential neurologic sequelae of hypoglycemia. An “operational threshold” has been suggested that takes into consideration the unstable relationship between plasma glucose levels and clinical signs of hypoglycemia. The operational threshold has been defined as “that concentration of plasma or whole blood glucose at which clinicians should consider intervention.”2 The American Academy of Pediatrics (AAP) notes that the generally adopted level for an operational threshold for neonatal hypoglycemia is less than 47 mg/dL, and suggest a target glucose of >=45 mg/dL prior to feeds.3 The 2011 AAP clinical report provides a strategy that accounts for infant risk factors, symptoms, and age in hours. Screening is recommended in preterm infants, small and large-for-gestational-age infants, and infants of diabetic mothers. Normal full-term infants who are delivered without complications after a normal pregnancy do not require glucose monitoring. Regardless of risk factors, any infant with clinical signs consistent with hypoglycemia requires evaluation (see Table 129-2).
The optimal timing of screening is not known. Hypoglycemia in newborns generally appears at around 2 to 6 hours of life. As shown in Figure 129-1, the AAP recommends that infants at risk for hypoglycemia be screened within the first 1 to 2 hours after birth, with surveillance continuing before feedings for 12 to 24 hours of life.3
FIGURE 129-1.
American Academy of Pediatrics recommendations for screening and management of glucose homeostasis for small for gestational age (SGA) infants, large for gestational age (LGA) infants, infants of diabetic mothers (IDM), and late preterm infants (LPI) born 34 to 36 weeks gestation. IDM/LGA infants should be screened for first 12 hours of life; LPI/SGA infants should be screened for first 24 hours of life. (Data from American Academy of Pediatrics Committee on Fetus and Newborn. Clinical report—postnatal glucose homeostasis in late-preterm and term infants. Pediatrics. 2011;127:575-579.)
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