Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9336052 | Seminars in Fetal and Neonatal Medicine | 2005 | 6 Pages |
Abstract
Transiently low blood glucose levels are common in the neonatal period and may be considered a normal feature of adaptation to extrauterine life. There is no evidence that this causes brain injury in the absence of concurrent clinical manifestations. Conversely, persistent and severe hypoglycaemia may be associated with other underlying pathologies which themselves predispose to brain injury. Attribution of brain injury therefore requires demonstration of both 'significant' hypoglycaemia and a characteristic resulting pattern of brain injury. The prevention of hypoglycaemic brain injury requires early detection in infants considered 'at risk' and appropriate intervention. No single concentration of plasma glucose can be associated universally with either the appearance of clinical signs or causation of cerebral injury. For this reason we suggest that treatment be based upon 'operational thresholds' and guided by clinical assessment, not by the plasma glucose concentration alone. For example, the infant displaying neurological signs requires more urgent elevation of blood glucose concentration than the 'asymptomatic' one, regardless of the absolute plasma glucose value.
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Authors
A.F. Williams,