ABSTRACT

The brain lesion during neonatal life has been mainly related to an asphyctic event. This relationship implies an anomalous gas exchange with an oxygen decit and a carbon dioxide accumulation, subsequently producing arterial acidosis. If asphyxia persists, systemic hypotension and brain ischemia will develop. Similarly, this cascade of events could take place in utero, in which a reduced or compromised maternal perfusion could affect the fetal gas exchange and blood ow, resulting in a different degree of asphyxia. The term hypoxic-ischemic encephalopathy has been widely used in clinical practice, due to the uncertain role played either by hypoxia or ischemia or by the combination of both, as the main pathogenic determinants of the neurological damage caused by hypoxic-ischemic injury.