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The level of blood glucose (BG) concentration that leads to cerebral injury in newborns and adverse neurodevelopmental outcome is unknown: low BG is observed during postnatal adaptation of healthy term infants without apparent adverse consequence, and the capacity to mobilise and use alternative cerebral fuels when BG is low varies between patient groups.1 Because of this uncertainty an ‘operational threshold’ approach to the management of neonates with hypoglycaemia has been proposed, which defines ‘the concentration of plasma or whole BG at which clinicians should intervene based on evidence currently available in the literature.’ 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 thalami4–15 (figure 1). Vulnerability of the white matter and cortex of the posterior parietal and occipital lobes has been well reported in human imaging studies,6 ,13 ,16 but the site of injury is more widespread in pathological and experimental studies of neonatal hypoglycaemia.4 ,5 ,17 In the largest series …
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