Hypoglycemia in infancy and childhood can result from a largevariety of hormonal and metabolic defects (Table 172-1). Hypoglycemia occurs most frequently in the early neonatal period,often as a result of transient neonatal hyperinsulinemia ininfants of diabetic mothers or as a result of inadequate energy stores to meet the disproportionately large metabolic needs of premature or small for gestational age newborns. Hypoglycemiaduring the first few days of life in an otherwise normal newbornis less frequent and warrants concern (see Chapter 6). After theinitial 2 to 3 days of life, hypoglycemia is far less common and ismore frequently the result of endocrine or metabolic disorders(although sepsis must always be ruled out).
The diagnosis of hypoglycemia should be made on the basis of a low serum glucose concentration, symptoms compatible with hypoglycemia, and resolution of the symptoms after administration of glucose.
Serum glucose concentrations less than 45 mg/dL are considered to be abnormal and necessitate treatment. Serum glucose concentrations greater than 55 mg/dL occasionally can occur in normal individuals, especially with prolonged fasting, but should be considered suspect, particularly if there are concurrent symptoms of hypoglycemia (Table 172-2).
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The symptoms and signs of hypoglycemia result from direct depression of the central nervous system owing to lack of energy substrate and the counterregulatory adrenergic response to low glucose via catecholamine secretion designed to correct hypoglycemia (see Table 172-2). Compared with older children, infants do not usually show adrenergic symptoms. The signs and symptoms of hypoglycemia in infants are relatively nonspecific and include jitteriness, feeding difficulties, pallor, hypotonia, hypothermia, episodes of apnea and bradycardia, depressed levels of consciousness, and seizures. In older children, signs and symptoms include confusion, irritability, headaches, visual changes, tremors, pallor, sweating, tachycardia, weakness, seizures, and coma.
Failure to recognize and treat severe, prolonged hypoglycemia can result in serious long-term morbidity, including mental retardation and nonhypoglycemic seizures. Younger infants and patients with more severe or prolonged hypoglycemia are at greatest risk for adverse outcomes.
Normal regulation of serum glucose concentrations requires appropriate interaction of a number of hormonal signals and metabolic pathways (Figure 172-1). In a normal individual, a decrease in serum glucose concentrations leads to a suppression of insulin secretion and increased secretion of the counterregulatory hormones (growth hormone [GH], cortisol, glucagon, and epinephrine) (see Fig. 172-1). This hormonal signal promotes the release of amino acids (particularly alanine) from muscle to fuel gluconeogenesis and the release of triglyceride from adipose tissue stores to provide free fatty acids (FFAs) for hepatic ketogenesis. FFAs and ketones serve as alternate fuels for muscle. This hormonal signal also stimulates the breakdown of hepatic glycogen and promotes gluconeogenesis. Failure of any of the components of this hormonal signal can lead to hypoglycemia.
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A lack of suppression of insulin secretion in response to low serum glucose concentrations can occur in infants but is uncommon beyond the neonatal period. This situation arises most frequently in infants of diabetic mothers who were exposed to high concentrations of maternally derived glucose in utero, resulting in fetal islet cell hyperplasia. The hyperinsulinemic state is transient, usually lasting hours to days.
Hyperinsulinism that persists beyond a few days of agecan result from distinct genetic disorders affecting glucose-regulated insulin release. These were previously referred to