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NeoReviews Vol.9 No.11 2008 e513
© 2008 American Academy of Pediatrics
* Perinatal Center, The Queen Silvia Children`s Hospital, Göteborg, Sweden
Perinatal asphyxia remains an often devastating event that results in death or impaired survival despite extensive resuscitative efforts at birth. The hypoxic-ischemic brain injury after severe birth asphyxia is largely dependent on a neurotoxic cascade that is initiated during reoxygenation and reperfusion. This results in secondary energy failure and neuronal death within hours to days after resuscitation. The mechanisms leading to secondary brain injury include release of excitatory amino acids, free radical formation, induction of apoptosis, and inflammatory activation. The interval between the primary insult and the development of permanent injury opens a time window for therapeutic interventions to improve brain outcome. Early identification of high-risk infants who may benefit from such neuroprotective treatment is, thus, important and is based on strict criteria for birth asphyxia combined with clinical and electroencephalographic signs of significant encephalopathy. Moderate hypothermia is the most studied intervention, and reduced impairment in survivors has been reported. Promising pharmacologic agents are being investigated, but further research is needed to determine their role in improving outcome.
Abbreviations: aEEG: amplitude integrated electroencephalography NMDA: N-methyl-D-aspartate NO: nitric oxide TNF: tumor necrosis factor
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