Perinatal asphyxia (PA) still constitutes a common complication involving a large number of infants with or without congenital heart diseases (CHD). PA affects 0.2-0.6% of full-term neonates, 20% of which suffer mortal hypoxic-ischemic encephalopathy, and among survivors 25% exhibit permanent consequences at neuropsychological level. Each year, about one third of 1000 live births underwent to surgical intervention in early infancy and/or are at risk for ominous outcome. Advances in brain monitoring, in anesthetic and cardiothoracic surgical techniques, including selective or total body cooling, cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest, have essentially reduced mortality expanding the possibility to address functional neurologic and cardiac outcomes in long-term survivors. However, open-heart surgery constitutes a time-frame of planned ischemia-reperfusion injury, which is a price to pay in the treatment or palliation of CHD. Infants who underwent heart surgery and non-CHD infants complicated by PA share similarities in their neurodevelopmental profile and a common form of brain damage due to hypoxic–ischemic injury.
The purpose of the present review was to evaluate different mechanisms implicated in brain injury following CPB and PA and how it is possible to monitor such injury by means of available biomarkers (S100B protein, Activin A, Adrenomedullin).