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.
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.
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.