THERAPEUTIC HYPOTHERMIA AS A STANDARD OF NEUROPROTECTION IN NEWBORNS WITH HYPOXIC-ISCHEMIC ENCEPHALOPATHY

Abstract

Hypoxic-ischemic encephalopathy (HIE) remains one of the leading causes of neonatal mortality and persistent neurological disability worldwide. According to epidemiological studies, the incidence of HIE in developed countries is 1.5-3 per 1000 live births, while in low-income countries this figure reaches 26 per 1000 or more [1, 2].Every year, more than 1 million newborns die due to perinatal asphyxia, which is the main cause of HIE [3]. The pathogenesis of the disease is caused by a two-phase cascade of cerebral damage: primary energy deficiency, which develops immediately at the time of hypoxia-ischemia, is replaced by a secondary phase of excitotoxicity, oxidative stress, neuroinflammation and apoptosis, which unfolds 6-15 hours after reperfusion. It is the presence of this therapeutic window that determines the pathogenetic validity and time frame of therapeutic hypothermia (TG) application [4].