title: [Postanoxia encephalopathies].
abstract: Ischaemic brain damage can follow global cerebral hypoxia, localized cerebral hypoxia and global cerebral anoxia as it occurs after circulatory arrest. The calcium-ion-mediated mechanism is one of the main routes to cerebral deterioration. Barbiturates are restricted for treatment of increased intracranial pressure and seizures. Calcium channel blockers cannot yet be recommended. Therapy remains mainly symptomatic. Hyperglycaemia should be avoided.
authors.affiliation: Département d'Anesthésie-Réanimation, CHU de Brabois, Vandoeuvre-lès-Nancy.
authors.forename: J P
authors.initials: JP
authors.lastname: Haberer
authors.forename: E
authors.initials: E
authors.lastname: Hottier
mesh_terms: D000140:Acidosis, Lactic / Q000503:physiopathology; D001095:Arachidonic Acids / Q000378:metabolism; D001463:Barbiturates / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D015220:Calcium Channels / Q000378:metabolism; D002560:Cerebrovascular Circulation; D003600:Cytosol / Q000378:metabolism; D006323:Heart Arrest / Q000150:complications*; D006801:Humans; D002534:Hypoxia, Brain / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D011379:Prognosis
chemical_list: D001095:Arachidonic Acids; D001463:Barbiturates; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002118:Calcium
vernacular_title: Encéphalopathies postanoxiques.