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Published on: November 20, 2015
Cerebral injury in association with profound iatrogenic hyperglycemia in a neonate
Daryl Efron1, Mike South, Joseph J Volpe
1Department of Paediatrics, University of Melbourne, Royal Children's Hospital, Melbourne, Australia.
Insights
Severe hyperglycemia poses neurological risks in infants following cerebral ischemia. This first case highlights similar brain injury patterns in newborns as seen in adults, indicating shared vulnerabilities.
Area of Science:
- Neonatal Neurology
- Cerebral Ischemia Research
- Glucose Metabolism in Infants
Background:
- Established risk of hyperglycemia in adult cerebral ischemia.
- Limited data on hyperglycemia's impact on infant neurological outcomes.
- Need to assess neonatal risk factors for brain injury.
Observation:
- First case report of severe, prolonged hyperglycemia in an infant with cerebral ischemia.
- Infant sustained a major cerebral lesion.
- Magnetic resonance imaging revealed bilateral parieto-occipital cortex and subcortical white matter injury.
Findings:
- Hyperglycemia in infants with cerebral ischemia can cause significant brain lesions.
- Injury patterns in hyperglycemic infants resemble those in hypoglycemic infants.
- Suggests similar regional cerebral vulnerability to glucose metabolism alterations in newborns.
Implications:
- Extends the recognized risk of severe hyperglycemia to the neonatal population.
- Highlights potential shared vulnerability of posterior brain regions to both hypo- and hyperglycemia.
- Underscores the importance of glucose control in neonatal neurological injury.
Abstract:
The adverse effect of hyperglycemia on neurological outcome following cerebral ischemia has been established in both experimental and adult human studies. However, there is a paucity of data to assess this risk in the human infant. This case is the first to describe severe and prolonged iatrogenic hyperglycemia in association with ischemia in an infant who sustained a major cerebral lesion. The topography of the predominant cerebral injury, i.e., bilateral parieto-occipital cortex and subcortical white matter, shown by magnetic resonance imaging was similar to that documented in the hypoglycemic infant, suggesting a similarity in regional cerebral vulnerability to altered glucose metabolism. This case extends recognition of the risk of severe hyperglycemia in association with cerebral ischemia to the newborn and suggests also that the posterior cerebral predilection for injury is similar in both hypoglycemia and hyperglycemia.
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