An Overview about Neonatal Hypoxic Ischemic Encephalopathy

Abstract

Background:   Hypoxic ischemic brain injury describes brain injury due to exposure to hypoxia and∕ or ischemia as evidenced by biochemical [creatine kinase brain function (CK-BB)], electrophysiologic (EEG), neuroimaging (MRI and CT scan), or pathologic (postmortem examination) means. HIE is an important cause of permanent damage to CNS cells that may result in neonatal death or be manifested later as Cerebral Palsy (CP) or mental deficiency. 20 to 25 % of infants with HIE die in the neonatal period and 25-30% of survivors are left with permanent neurodevelopment abnormalities as cerebral palsy or mental retardation. Within minutes of the onset of total fetal hypoxia, bradycardia, hypotension, decreased cardiac output, and severe metabolic as well as respiratory acidosis occur. The initial circulatory response of a fetus is increased shunting through the ductus venosus, ductus arteriosus, and foramen ovale, with transient maintenance of perfusion of the brain, heart and adrenals in preference to the lung, liver, kidneys and intestine.   Following initial resuscitation and stabilization, treatment of HIE is largely supportive and should focus on adequate ventilation and perfusion, careful fluid management, avoidance of hypoglycemia and hyperglycemia and treatment of seizures. Intervention strategies aim to avoid any further brain injury in these infants