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Hypoxic–ischemic encephalopathy

par Taccone, Fabio ;Cariou, Alain
Référence Brain Disorders in Critical Illness: Mechanisms, Diagnosis, and Treatment, Cambridge University Press, page (373-380)
Publication Publié, 2011-01

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Résumé :

Hypoxic-ischemic encephalopathy (HIE) is a condition in which the entire brain is almost completely deprived of its oxygen supply because of inadequate blood flow or oxygenation. Brain damage that is observed following resuscitation from cardiac arrest is considered to be the most representative pattern of HIE. Although complex, the pathophysiology of HIE is well understood. Cerebral ischemia triggers a complex cascade of pathways that will result in the peroxidation of lipids with cell membrane layers, protein oxidation, and DNA fragmentation, all contributing to brain cell death. Following this initial insult, brain injury continues even after restoration of cerebral perfusion and oxygenation, in a process known as “reperfusion injury.” Particularly, the accumulation of reactive oxygen species and the early depletion of antioxidant reserves, such as glutathione, will lead to an oxidative stress that will promote damage to membrane, cytoskeletal proteins, and nucleic acids, thereby causing diffuse neuronal necrosis. Finally, even after the restoration of adequate blood supply and cellular energy stores, there can be a global hypoperfusion state that may further lead to secondary brain injury and aggravate neurological impairment after initial ischemia.