Abstract
Diabetic ketoacidosis is one of the most common complications in children suffering from diabetes mellitus, a complication that may cause cerebral edema. After a diabetic ketoacidosis episode, some children develop cognitive impairment, which could be linked to subclinical or clinical grade cerebral edema. An analysis of scientific literature has shown that the pathophysiological mechanisms of the development of cognitive dysfunction in children with diabetic ketoacidosis-associated cerebral edema have not been fully elucidated. The key pathogenetic hypotheses under consideration include hypoxia, cerebral hypoperfusion and reperfusion, release of vasoactive substances and induction of inflammation, acute hyperglycemia and oxidative stress. Hypoxia leads to hypoxic-ischaemic injury of the brain, affecting, among others, areas responsible for memory formation. Cerebral hypoperfusion and reperfusion trigger mitochondrial dysfunction and oxidative stress, which worsens the cognitive impairment in patients with cerebral edema. Release of vasoactive substances and induction of inflammation impair the functioning of the blood-brain barrier and lead to cerebral vasospasm. Acute hypoglycemia triggers the development of brain tissue acidosis and accumulation of lactate and glutamate, aggravating the cognitive dysfunction. Oxidative stress causes neuronal damage, exacerbating the manifestations of cerebral edema. The pathophysiological mechanisms described here may cause cognitive dysfunction in the setting of cerebral edema either as individual triggers or collectively through a synergistic effect. Further research is needed to expand the knowledge of pathophysiological interconnections between cognitive dysfunction and cerebral edema in children after a diabetic ketoacidosis episode.
Published Version
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