Hypoglycaemia and the neonatal brain.
There has been much controversy and confusion regarding potential damage caused to the neonatal brain by low blood glucose levels. Previous studies of outcome after neonatal hypoglycaemia are flawed by many factors including retrospective data collection and inability to control for co-existing clinical complications. There is no doubt that hypoglycaemic brain damage does occur but the severity and duration of low blood glucose levels required to cause lasting harm varies between subjects and is related to the ability of each baby to mount a protective response such as the production of ketone bodies which are alternative cerebral fuels. Evidence from studies of humans and other animals suggests that cortical damage and long-term sequelae occur after prolonged hypoglycaemia sufficiently severe to cause neurological signs.


CONCLUSIONS
Prolonged hypoglycaemia should be avoided by close clinical observation of vulnerable infants whilst avoiding excessively invasive management in populations of neonates which may jeopardize the successful establishment of breast feeding.
Hawdon
J M
JM
Neonatal Unit, University College London Hospitals, Huntley Street, London WC1E 6AU, UK. j.hawdon@academic.uclh.thames.nhs.uk
D000818:Animals; D001927:Brain Diseases / Q000209:etiology*; D006801:Humans; D007003:Hypoglycemia / Q000150:complications* / Q000378:metabolism; D007231:Infant, Newborn; D007234:Infant, Premature; D007657:Ketone Bodies / Q000378:metabolism; D051381:Rats; D012307:Risk Factors
D007657:Ketone Bodies