Hypoxic-ischemic encephalopathy: pathophysiology and implications for therapy.

Philip Sunshine

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PubMed · 12108076

Hypoxic-ischemic encephalopathy: pathophysiology and implications for therapy.

Philip Sunshine

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Abstract

Hypoxic-ischemic encephalopathy continues to be a major problem in perinatal medicine because of the high mortality rate and neurological and intellectual impairment in the surviving infants. In addition to the acute necrotic damage that occurs in the neurons initially, reperfusion injury and secondary neuronal damage continue for 6 to 72 hours after the initial insult. Secondary cellular energy failure, membrane breakdown, cellular influx of calcium ions, elaboration of cytokines, and oxidation of excitory amino acids all contribute to enhanced apoptosis of the neurons. Newer forms of therapy including the use of oxygen-free radical inhibitors and mild to moderate cerebral or systemic hypothermia for 72 hours following the asphyxial period are promising adjuncts as follow-up approaches to the affected newborns.

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Calcium Channel Blockers Diuretics, Osmotic Excitatory Amino Acid Antagonists Free Radical Scavengers Humans Hypothermia, Induced Hypoxia-Ischemia, Brain Infant, Newborn Mannitol Somatomedins Time Factors Journal Article Review

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Philip Sunshine. 2002. Hypoxic-ischemic encephalopathy: pathophysiology and implications for therapy.. https://pubmed.ncbi.nlm.nih.gov/12108076/

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