抽象的な

Hypoxic-ischemic encephalopathy and the modern ways of the treatment: Where we are and How long the way?

Leonid Pankratov

Perinatal asphyxia (PA) is one of the main contributors to neonatal morbidity, Long-term neurological disability and early neonatal mortality. It accounts for ~ 900 000 deaths worldwide for every year. Severe asphyxia results in hypoxic-ischemic encephalopathy (HIE) and multi-organ failure such as cardiac, hepatic and renal dysfunctions. The management of infants with HIE is supportive and includes resuscitation techniques. Effective resuscitation at birth can prevent a large proportion of neonatal deaths. Meta-analyzes show that resuscitation with room air after newborn asphyxia in term neonates gives lower mortality than resuscitation with 100% O2. The pathophysiology of PA is closely associated with the inflammation. Interleukins -1?,6,8,10 and tumor necrosis factor (TNF)-? have involved in an inflammatory response. They activate polymorphonuclear leukocytes and monocytes/macrophages and may release reactive oxygen species, toxic granules including proteolytic enzymes, myeloperoxidase and injuring cells. Moreover, oxidative stress arises from the strong cellular oxidizing potential of excess reactive oxygen species (ROS). A considerable variety of neuroprotective strategies studied in the experimental models and clinical trials. Therapeutic hypothermia (cooling) appears to be safe and effective due to reducing cellular metabolism, apoptotic cell death and suppression of the inflammatory cascade. The intervention starts up to the first 6 h after birth will improve survival rate, and reduce neuro disability. Nevertheless, some of the newborns have suffered from severe neurological sequelae as cerebral palsy (CP) and additional neuroprotective treatment at birth is necessary. The main focus of the presentation will make on the antioxidant and anti-inflammatory capabilities of noble gases and other medications after severe PA.