Introduction
Hypoglycemia among infants and children has traditionally been divided into transient neonatal hypoglycemia and hypoglycemia of infancy and childhood. The definition of hypoglycemia is somewhat arbitrary, depending on the age of the patient and the conditions under which the samples are obtained. For example, a plasma glucose concentration of 3.3 mmol/L (60 mg·dL^-1) can be distinctly abnormal 1 hour after a carbohydrate load for any child or adolescent, whereas healthy women who fast for 4 days can have plasma glucose values less than 2.2 mmol/L (40 mg·dL^-1) without symptoms.

Children usually have symptoms of hypoglycemia when plasma glucose concentrations decreases to approximately 2.2 mmol/L (40 mg·dL^-1).

Any child or infant who has a plasma glucose concentration less than 2.8 mmol/L (<50 mg·dL^-1) during an elective fast should be observed carefully. At concentration less than 2.2 mmol/L (<40 mg·dL^-1), the patient is considered to have hypoglycemia, and diagnostic and therapeutic intervention is initiated. The definition of hypoglycemia among newborns continues to be a source of controversy, particularly in the first hours of life.

Plasma concentration of glucose decreases over the first hours of life, a time of physiological hypoglycemia. After these first hours, plasma level of glucose less than 2.2 mmol/L (40 mg·dL^-1) is considered hypoglycemia, and appropriate treatment is initiated (feeding or intravenous glucose, depending on the patient’s maturity, clinical status, and glucose concentration).

The symptoms associated with a rapid decrease in plasma concentration of glucose reflect increased adrenergic activity (tachycardia, shaking) and cholinergic activity (sweating, weakness, and hunger). If the hypoglycemia is not relieved, manifestations of progressive symptoms of cerebral dysfunction, such as headache, irritability, mental confusion, psychotic behavior, seizures, and coma, can develop. With frequent or prolonged episodes of hypoglycemia, permanent central nervous system damage or even death can occur.

Symptoms of hypoglycemia are less obvious among neonates than they are among adults and may be overlooked. Careful, prospective monitoring of plasma concentration of glucose is indicated in the early hours of life and for longer periods in the care of infants at high risk of hypoglycemia.

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Neonatal Hypoglycemia
Hypoglycemia is caused by either decreased rates of glucose production or increased rates of use. Small-for-gestational-age infants have low glycogen, muscle, and fat stores, making them prone to hypoglycemia caused by inadequate glucose production from glycogen and by gluconeogenesis. Infants whose mothers have diabetes frequently have severe hypoglycemia after birth, presumably caused by chronic exposure to high ambient glucose concentrations during gestation with resultant β-cell hyperplasia. After birth, excessive insulin is secreted with resultant hypoglycemia. Other disorders that can cause hypoglycemia in the newborn include glucagon deficiency and disorders that increase the rates of glucose utilization such as neonatal sepsis.

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Pascal J. Vanelderen MD, Resident, Filiep M. Soetens MD, Staff Anesthesiologist, Maurits A. Soetens MD, Staff Anesthesiologist, Herman J. Janssen PhD, Professor and Andre’ M. De Wolf MDc, Professor

Department of Anesthesiology, Sint-Elisabeth Hospital, 2300 Turnhout, Belgium
Department of Physics, Limburgs Universitair Centrum, 3590 Diepenbeek, Belgium

REFERENCES

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KATZ LE , FERRY RJ JR , STANLEY CA , COLLETT-SOLBERG PF , BAKER L , COHEN P: Suppression of insulin oversecretion by subcutaneous recombinant human insulin-like growth factor I in children with congenital hyperinsulinism due to defective beta-cell sulfonylurea receptor. J Clin Endocrinol Metab 84:3117-24, 1999

SCHWITZGEBEL VM , GITELMAN SE: Neonatal hyperinsulinism. Clin Perinatol, 25:1015-1038, 1998

STANLEY CA , LIEU YK , HSU BY , et al: Hyperinsulinism and hyperammonemia in infants with regulatory mutations of the glutamate dehydrogenase gene. N Engl J Med 338:1352-1357, 1998