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PubMed · 2164797

[Postanoxia encephalopathies].

J P Haberer·E Hottier
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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.

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Acidosis, LacticArachidonic AcidsBarbituratesCalciumCalcium Channel BlockersCalcium ChannelsCerebrovascular CirculationCytosolHeart ArrestHumansHypoxia, BrainPrognosisEnglish AbstractJournal ArticleReview

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BibTeXRIS

J P Haberer, E Hottier. 1990. [Postanoxia encephalopathies].. https://doi.org/10.1016/s0750-7658(05)80173-x

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