Hypoglycemia
Hypoglycemia (<50 mg/dL) is dangerous, because glucose is the
sole fuel source for much of the brain. Threshold levels depend on age. Signs of
hypoglycemia include irritability, seizures, bradycardia, hypotension, and respiratory
failure. Symptoms commonly occur in adults at blood glucose concentrations below
57 mg/dL or in infants with levels of 30 to 50 mg/dL. Symptoms are seen at higher
levels in diabetics than in nondiabetics and are obscured by general anesthesia.
At about 70 mg/dL, a biochemical stress response occurs, including sympathetic nervous
system stimulation and elevated levels of growth hormone or cortisol, or both. Neurologic
and electroencephalographic depression appears at 50 to 55 mg/dL in nondiabetics
and 70 to 85 mg/dL in diabetics.[101]
Selective
neuronal necrosis, not infarction, occurs in the caudate, putamen, and cortex. There
is a compensatory increase in cerebral blood flow.
During labor, maternal starvation-induced ketosis has adverse
fetal effects, including fetal ketonemia, hypoxia, and fetal lactic acidosis.[102]
Neonates are at an increased risk for hypoglycemia because of limited glycogen stores
and from large amounts of fetal insulin production in response to gestational hyperglycemic
states. Adults are also at risk for hypoglycemia from inadequate gluconeogenesis
coupled with inadequate nutritional intake or from excess insulin (e.g., from an
insulinoma, pancreatic islet cell adenoma, or carcinoma; iatrogenic overadministration).
Hypoglycemia can also follow too abrupt cessation of dextrose infusion during total
parenteral nutrition (i.e., reactive hyperinsulinemic states). Inadequate gluconeogenesis
occurs in liver failure, cortisol deficiency (primary or secondary), inadequate glucagon
response, growth hormone deficiency, and during β-adrenergic blockade. Fasting
in women is likely to produce hypoglycemia in 24 hours, whereas men tolerate about
72 hours of fasting.[63]
The incidence of hypoglycemia
in healthy infants and children is low (2 of 446) with 4 to 8 hours of fasting.[67]
Fetal hypoglycemia occurs if maternal glucose is greater than 150 mg/dL, because
glucose crosses the placenta, inducing fetal insulin secretion. Treatment consists
of an intravenous bolus of 5 g of dextrose followed by increasing the rate of dextrose
infusion by 1 to 2 mg/kg/min.
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