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Neonatal Hypoglycemia

Neonatal hypoglycemia is a common phenomenon in the newborn infant diagnosed by an abnormally low level of blood glucose (sugar), the body's chief energy source (hence the term low blood sugar). Serum glucose levels less than 40 mg/dl (2.2 mmol/L) in the first 24 hours of life and 40-50 mg/dl (2.6 mmol/L) thereafter are considered low whereas 80-90mg/dL is considered normal. Glucose is an essential nutrient for the brain. Abnormally low levels can cause an encephalopathy and have the potential to produce long-term neurological injury in infants. The level at which this potential for long-term injury is reached is controversial. There is a normal dip in blood glucose 2-4 hours postnatally so the challenge is to be able to recognize a normal dip from true metabolism errors.

INFANTS AT RISK

• Preterm
• SGA—Small for Gestational Age
• LGA—Macrosomic babies (may have hyperinsulinism)
• Infants of poorly controlled diabetic mothers
• Infant who suffers perinatal asphyxia (the oxygen supply gets cut off from the brain, either before or during birth)
• Growth restricted babies

Common symptoms of neonatal hypoglycemia include:

• Thermoregulatory problems, tremors, seizure activity, jitteriness, irritability, convulsions, and coma
• Respiratory distress, apnea (cessation of breathing) and cyanosis (blue color)
• Hypotonia (lack of muscle tone or weakness), lethargy, listlessness and poor feeding

Active intervention should only be taken after confirmation with a formal blood glucose level because Dextrostix (or other reagent strip test) under-read blood glucose in the low range. Treatment includes the following:

• Establish early regular breast feeding. (Minimum of 5 feeds in the 1st 24 hrs)
• Ingestion of glucose or sucrose with bottle or eyedropper if mother is unable to breastfeed.
• IV – 100ml/kg/fsy continuous dextrose infusion.
• Pancreatectomy—if hypoglycemia cannot be controlled with medical therapy (diazoxide)

Hyperinsulinism or mal-adaptive hypoglycemia is most often caused by an oversecretion of insulin from the pancreas triggered by stress, exercise, fasting, or disorders of the adrenal or pituitary glands, liver, or pancreas. In persons with diabetes it may result from an overdose of insulin. In infants of diabetic mothers, it is not uncommon for the infant to remain in a hyperinsulinemic state after losing the maternal glucose supply. Fetal glucose levels correspond to maternal levels as glucose crosses the placenta. Insulin production in the fetus begins early in gestation; insulin does not cross the placenta. When the newborn is deprived of maternal glucose, the pancreas continues to produce insulin at the same fetal level and newborn glucose levels are rapidly depleted. This condition is usually transient and is treated either with early initiation of carbohydrate feedings or, at times, intravenous dextrose until the infant's metabolic adaptation is able to supply adequate amounts of glucose.

In preterm infants and those born SGA adequate fetal glycogen storage has been interrupted or impaired, placing these infants at risk for hypoglycemia in the first several hours and days of life. Other perinatal events that may cause an increase in energy utilization (above those levels at which the newborn is able to supply glucose) include perinatal asphyxia, cold stress, respiratory distress, and prolonged labor. The newborn may also be at risk for hypoglycemia as a result of inborn errors of carbohydrate metabolism and amino acid metabolism. Hyperinsulinism due to nesidioblastosis (pancreas islet cell dysmaturation syndrome) in the early neonatal period also is a cause for neonatal hypoglycemia.

Persistent Severe Hypoglycemia - Mal-adaptive hypoglycemia can usually be clinically separated from pathological hypoglycemia by the amount of glucose need to maintain a normal blood sugar. Once a baby needs more than 7.5mg/kg/min of glucose a pathological cause becomes more likely. Most of these conditions are inborn errors of metabolism such as glycogen storage diseases and inborn errors of fatty acid oxidation.

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