Abstract
Accumulating evidence points to an evolving process of brain injury after intrapartum hypoxia–ischemia that initiates in utero and extends into a recovery period. The processes leading to cell death include necrosis or apoptosis, and result from the combined effects of cellular energy failure, acidosis, glutamate release, intracellular Ca2+ accumulation and generation of free radicals that serve to disrupt essential components of the cell. Secondary cerebral energy failure occurs from 6 to 48 h after the primary event and involves mitochondrial dysfunction secondary to extended reactions from primary insults. Treatment strategies to prevent or ameliorate ongoing brain injury include early identification of high-risk infants, supportive therapy and neuroprotection. Currently, hypothermia offers the greatest promise as a neuroprotective strategy and has shown benefit particularly in a subset of infants who present with moderate encephalopathy and without seizures. Future directions will probably include hypothermia and additional interventions.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.