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Hypoglycemia in newborns
Last reviewed: 05.07.2025
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Hypoglycemia is a serum glucose level of less than 40 mg/dL (less than 2.2 mmol/L) in term infants or less than 30 mg/dL (less than 1.7 mmol/L) in preterm infants. Risk factors include prematurity and intrapartum asphyxia. The most common causes are inadequate glycogen stores and hyperinsulinemia. Symptoms of hypoglycemia include tachycardia, cyanosis, seizures, and apnea.
The diagnosis of hypoglycemia is assumed empirically and confirmed by determining the glucose level. The prognosis depends on the cause; treatment is enteral nutrition or intravenous glucose administration.
[ What causes hypoglycemia in newborns?
Hypoglycemia in neonates may be transient or persistent. Transient hypoglycemia is caused by insufficient substrate or immature enzyme function, resulting in insufficient glycogen stores. Persistent hypoglycemia is caused by hyperinsulinism, counter-insular hormone disorders, and hereditary metabolic diseases [e.g., glycogenoses, gluconeogenesis disorders, fatty acid oxidation disorders].
Insufficient glycogen stores at birth are common in very low birth weight ( VLBW) preterm infants, infants who are small for gestational age due to placental insufficiency, and infants who have experienced intrapartum asphyxia. Anaerobic glycolysis depletes glycogen stores in these infants, and hypoglycemia may develop at any time during the first few days, particularly if there is a long interval between feedings or if nutrient intake is low. Therefore, maintaining exogenous glucose is important to prevent hypoglycemia.
Transient hyperinsulinism is most common in infants of diabetic mothers. It also frequently occurs in infants small for gestational age during physiological stress. Less common causes include hyperinsulinism (inherited in both autosomal dominant and autosomal recessive patterns), severe fetal erythroblastosis, and Beckwith-Wiedemann syndrome (in which islet cell hyperplasia is associated with features of macroglossia and umbilical hernia). Hyperinsulinemia is characterized by a rapid fall in serum glucose levels in the first 1–2 hours after birth, when the continuous supply of glucose through the placenta ceases.
Hypoglycemia can also develop if intravenous glucose solution is suddenly stopped.
Symptoms of Hypoglycemia in Newborns
Many children have no symptoms of hypoglycemia. Prolonged or severe hypoglycemia causes both autonomic and neurologic signs of central origin. Autonomic signs include diaphoresis, tachycardia, weakness, and chills or tremor. Central neurologic signs of hypoglycemia include seizures, coma, episodes of cyanosis, apnea, bradycardia or respiratory distress, and hypothermia. Lethargy, poor feeding, hypotonia, and tachypnea may be present. All manifestations are nonspecific and are also observed in neonates with a history of asphyxia, sepsis, hypocalcemia, or opioid withdrawal. Therefore, at-risk patients with or without these symptoms require immediate monitoring of capillary blood glucose. Abnormally low levels are confirmed by venous glucose determination.
Treatment of hypoglycemia in newborns
Most high-risk infants are treated preventively. For example, infants of women with insulin-dependent diabetes are often given intravenous infusions of 10% glucose or oral glucose immediately after birth, as are sick, extremely premature infants, or infants with respiratory distress syndrome. At-risk infants should receive early, frequent formula feedings to provide carbohydrates.
In any neonate whose glucose level falls to less than or equal to 50 mg/dL, appropriate treatment should be initiated with enteral feedings or intravenous infusion of up to 12.5% glucose at 2 mL/kg over 10 minutes; higher concentrations may be given through a central catheter if necessary. The infusion should then be continued at a rate that delivers 4-8 mg/(kg min) glucose [i.e. 10% glucose at approximately 2.5-5 mL/(kg h)]. Serum glucose levels should be monitored to adjust the infusion rate. As the neonate's condition improves, enteral feedings may gradually replace the intravenous infusion while the glucose concentration continues to be monitored. Intravenous glucose infusion should always be tapered gradually since abrupt discontinuation may cause hypoglycemia.
If intravenous fluids are difficult to initiate in a hypoglycemic neonate, glucagon 100–300 mcg/kg intramuscularly (maximum 1 mg) usually increases glucose rapidly, an effect that lasts for 2–3 hours except in neonates with depleted glycogen stores. Hypoglycemia refractory to high-rate glucose infusion may be treated with hydrocortisone 2.5 mg/kg intramuscularly twice daily. If hypoglycemia is refractory to treatment, other causes (eg, sepsis) should be excluded, and endocrinologic testing may be indicated to detect persistent hyperinsulinism and defects in gluconeogenesis or glycogenolysis.