Abstract
Hypoxic-ischemic encephalopathy (HIE) is one of the most important complications found in the newborn period. It is the result of a deprivation of oxygen and glucose to the neural tissue, which may be the result of either hypoxemia or ischemia. Experimental animal research and clinical observations in humans have noted that the pattern of injury occurs in 2 phases. The first phase is a primary energy failure related to the insult, and then a second energy failure occurs some hours later. The combined effects of cellular energy failure, acidosis, glutamate release, intracellular accumulation of calcium, lipid peroxidation, and nitric oxide neurotoxicity destroy essential components of the cell, culminating in cell death. The clinical presentation depends on the severity, timing, and duration of the insult, with symptoms typically evolving over approximately 72 hours. Hypothermia strategies are aimed at targeting this narrow window of opportunity to ameliorate the brain injury.