Hypoglycaemia and neonatal brain injury

In this model infants at risk of neurological sequelae from hypoglycaemia are identified (see algorithm), and interventions to raise the BG are recommended at specified thresholds, with the caveat that acute neurological dysfunction in association with low BG at any level should prompt urgent invest...

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Published inArchives of disease in childhood. Education and practice edition Vol. 98; no. 1; pp. 2 - 6
Main Authors Boardman, James P, Wusthoff, Courtney J, Cowan, Frances M
Format Journal Article
LanguageEnglish
Published England BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health 01.02.2013
BMJ Publishing Group LTD
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ISSN1743-0585
1743-0593
1743-0593
DOI10.1136/archdischild-2012-302569

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Summary:In this model infants at risk of neurological sequelae from hypoglycaemia are identified (see algorithm), and interventions to raise the BG are recommended at specified thresholds, with the caveat that acute neurological dysfunction in association with low BG at any level should prompt urgent investigation and treatment. 2 A review of the literature supports the previous consensus that BG levels below 1.0 mmol/l that are persistent beyond 1-2 h (or are recurrent) and are associated with acute neurological dysfunction present the greatest risk for cerebral injury, and that brief episodes of hypoglycaemia in the absence of acute neurological dysfunction or an associated disorder are less likely to lead to cerebral injury and poor outcome. 3 The spectrum of cerebral injury associated with hypoglycaemia is wide and includes: white matter injury including parenchymal haemorrhage and ischaemic stroke, cortical neuronal injury, and sometimes signal change in the basal ganglia (mainly the globus pallidus) and thalami 4-15 ( figure 1 ).
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ISSN:1743-0585
1743-0593
1743-0593
DOI:10.1136/archdischild-2012-302569