Abstract
Cerebral metabolism is known to be highly dependent upon glucose utilisation. In the neonate, severe hypoglycaemia is now recognized to be associated with subsequent adverse neurodevelopment and in extremis glial and neuronal cell death. However, the level at which hypoglycaemia becomes clinically important is not well understood. Clinical methods for assessing effects of hypoglycaemia are at best crude. Noninvasive assessment of neuronal function suggests that cerebral dysfunction occurs at blood glucose levels well above clinical action levels. Thus, we appear to ignore apparently asymptomatic hypoglycaemia at our and indeed the patient's peril. Furthermore, glycaemic status invariably is interpreted with scant regard to alternative catabolic substrates. In the neonate, recent evidence suggests this approach is unfounded. This presentation will review evidence that glycaemic status in neonates should no longer be considered as an entity in itself, but rather in the light of compensatory metabolic processes and treated accordingly.

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