Untangling the physiology and pathophysiology of neonatal hypoglycaemia

Hypoglycaemia remains one of the leading causes of term admission to neonatal units. Significant time is expended by clinical teams in managing infants at risk of hypoglycaemia. Challenges remain in differentiating physiological falls in glucose concentrations from a potentially preventable cause of brain injury. The current evidence for distinguishing physiological from pathological hypoglycaemia remains limited by reliance on single point values of blood glucose (BG). Srinivasan et al 1 demonstrated a postnatal nadir in glucose concentrations, rising to values typical of older children by 48 hours of age. However, these infants were predominantly bottle fed (15% breast fed) and in a hospital nursery. In contrast, the Glucose in well babies (GLOW) study2 followed a cohort of term infants, all appropriately grown, predominantly breast feeding and at home. Uniquely, they also used both continuous glucose monitoring (CGM) and point of care (POC) measurement of alternative fuels to explore the physiology of the complex metabolic adaptation postnatally. This study, therefore, provides a richer picture of physiological changes of glucose over time and in the context of the wider metabolic milieu.

The paper by Stanley et al uses data from this study to characterise healthy metabolic transition after birth, and suggests POC measurement of ketones may be a useful adjunct to identify healthy babies at most risk from hypoglycaemia.3 They characterised two phases of low glucose concentrations: the first immediately after birth associated with relative hypoketonaemia, the second lasting up to 48–72 hours associated with ketonaemia. The early phase that occurs in the first 12 hours of life was felt to result from …

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