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Neonatal Hypoglycemia

by Nicholas Jospe, MD

Hypoglycemia is a serum glucose concentration < 40 mg/dL (< 2.2 mmol/L) in term neonates or < 30 mg/dL (< 1.7 mmol/L) in preterm neonates. Risk factors include prematurity, being small for gestational age, and perinatal asphyxia. The most common causes are deficient glycogen stores, delayed feeding, and hyperinsulinemia. Signs include tachycardia, cyanosis, seizures, and apnea. Diagnosis is suspected empirically and is confirmed by glucose testing. Prognosis depends on the underlying condition. Treatment is enteral feeding or IV dextrose.

Etiology

Neonatal hypoglycemia may be transient or persistent.

Causes of transient hypoglycemia are

  • Inadequate substrate

  • Immature enzyme function leading to deficient glycogen stores

Causes of persistent hypoglycemia include

  • Hyperinsulinism

  • Defective counter-regulatory hormone release

  • Inherited disorders of metabolism (eg, glycogen storage diseases, disorders of gluconeogenesis, fatty acid oxidation disorders—see Inherited Disorders of Metabolism)

Deficiency of glycogen stores at birth is common in very low-birth-weight preterm infants, infants who are small for gestational age (SGA) because of placental insufficiency, and infants who have perinatal asphyxia. Anaerobic glycolysis consumes glycogen stores in these infants, and hypoglycemia may develop at any time in the first few days, especially if there is a prolonged interval between feedings or if nutritional intake is poor. A sustained input of exogenous glucose is therefore important to prevent hypoglycemia.

Transient hyperinsulinism most often occurs in infants of diabetic mothers and is inversely related to the degree of maternal diabetic control. It also commonly occurs in physiologically stressed infants who are SGA. Less common causes include congenital hyperinsulinism (genetic conditions transmitted in both autosomal dominant and recessive fashion), severe erythroblastosis fetalis, and Beckwith-Wiedemann syndrome (in which islet cell hyperplasia accompanies features of macroglossia and umbilical hernia). Hyperinsulinemia characteristically results in a rapid fall in serum glucose in the first 1 to 2 h after birth when the continuous supply of glucose from the placenta is interrupted.

Hypoglycemia may also occur if an IV infusion of D/W is abruptly interrupted. Finally, hypoglycemia can be due to malposition of an umbilical catheter or sepsis.

Symptoms and Signs

Many infants remain asymptomatic. Prolonged or severe hypoglycemia causes both adrenergic and neuroglycopenic signs. Adrenergic signs include diaphoresis, tachycardia, lethargy or weakness, and shakiness. Neuroglycopenic signs include seizure, coma, cyanotic episodes, apnea, bradycardia or respiratory distress, and hypothermia. Listlessness, poor feeding, hypotonia, and tachypnea may occur.

Diagnosis

  • Bedside glucose check

All signs are nonspecific and also occur in neonates who have asphyxia, sepsis or hypocalcemia, or opioid withdrawal (see Opioids). Therefore, at-risk neonates with or without these signs require an immediate bedside serum glucose check from a capillary sample. Abnormally low levels are confirmed by a venous sample.

Treatment

  • IV dextrose (for prevention and treatment)

  • Enteral feeding

  • Sometimes IM glucagon

Most high-risk neonates are treated preventively. For example, infants of diabetic women who have been using insulin are often started at birth on a 10% D/W infusion IV or given oral glucose, as are those who are sick, are extremely premature, or have respiratory distress. Other at-risk neonates who are not sick should be started on early, frequent formula feedings to provide carbohydrates.

Any neonate whose glucose falls to 50 mg/dL ( 2.75 mmol/L) should begin prompt treatment with enteral feeding or with an IV infusion of up to 12.5% D/W, 2 mL/kg over 10 min; higher concentrations of dextrose can be infused if necessary through a central catheter. The infusion should then continue at a rate that provides 4 to 8 mg/kg/min of glucose (ie, 10% D/W at about 2.5 to 5 mL/kg/h). Serum glucose levels must be monitored to guide adjustments in the infusion rate. Once the neonate’s condition has improved, enteral feedings can gradually replace the IV infusion while the glucose concentration continues to be monitored. IV dextrose infusion should always be tapered, because sudden discontinuation can cause hypoglycemia.

If starting an IV infusion promptly in a hypoglycemic neonate is difficult, glucagon 100 to 300 μg/kg IM (maximum, 1 mg) usually raises the serum glucose rapidly, an effect that lasts 2 to 3 h, except in neonates with depleted glycogen stores. Hypoglycemia refractory to high rates of glucose infusion may be treated with hydrocortisone 2.5 mg/kg IM bid. If hypoglycemia is refractory to treatment, other causes (eg, sepsis) and possibly an endocrine evaluation for persistent hyperinsulinism and disorders of defective gluconeogenesis or glycogenolysis should be considered.

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