Hypoxic-ischemic encephalopathy: pathophysiology and implications for therapy.
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.
Sunshine
Philip
P
Stanford University School of Medicine, Lucille Packard Children's Hospital, Palo Alto, CA, USA. cmeyers@stanford.edu
D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004234:Diuretics, Osmotic / Q000627:therapeutic use; D018691:Excitatory Amino Acid Antagonists / Q000627:therapeutic use; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006801:Humans; D007036:Hypothermia, Induced; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology* / Q000628:therapy*; D007231:Infant, Newborn; D008353:Mannitol / Q000627:therapeutic use; D013002:Somatomedins / Q000627:therapeutic use; D013997:Time Factors
D002121:Calcium Channel Blockers; D004234:Diuretics, Osmotic; D018691:Excitatory Amino Acid Antagonists; D016166:Free Radical Scavengers; D013002:Somatomedins; D008353:Mannitol