Purpose of review
Hypoglycemia in the newborn may be associated with both acute decompensation and long-term neuronal loss. Studies of the cause of hypoglycemic brain damage and the relationship of
hypoglycemia to disorders associated with
hyperinsulinism have aided in our understanding of this common clinical finding.
Recent findings
A recent consensus workshop concluded that there has been little progress toward a precise numerical definition of neonatal
hypoglycemia. Nonetheless, newer brain imaging modalities have provided insight into the relationship between neuronal
energy deficiency and
central nervous system damage. Laboratory studies have begun to reveal the mechanism of hypoglycemic damage. In addition, there is new information about hyperinsulinemic
hypoglycemia of genetic, environmental, and iatrogenic origin.
Summary
The quantitative definition of
hypoglycemia in the newborn remains elusive because it is a surrogate marker for
central nervous system energy deficiency. Nonetheless, the recognition that hyperinsulinemic
hypoglycemia, which produces profound
central nervous system energy deficiency, is most likely to lead to long-term
central nervous system damage, has altered management of children with
hypoglycemia. In addition, imaging studies on neonates and laboratory evaluation in animal models have provided insight into the mechanism of neuronal damage.
