17 The impairment of cerebral blood flow leads to decreases in oxygen and glucose, which leads to significantly less energy (adenosine triphosphate (ATP)) and increased lactate production. Primary energy failure occurs as a result of the initial reduction of cerebral blood flow. Therefore, the purpose of this paper is to explain the key pathophysiological effects that occur after a hypoxic-ischemic event and discuss current experimental treatment modalities. Currently, several experimental treatments are available to infants with HIE and many others are being evaluated in animal models. 10 In the past, treatment options were limited to supportive medical therapy to maintain cardiopulmonary function and to manage seizure activity. fetal monitoring) aimed at preventing the hypoxic-ischemic event 9 thus much of the current neonatal research about HIE focuses on minimizing the extent of subsequent brain injury. 4– 8 The incidence of HIE has not declined even with advances in obstetric care (i.e. 4 By the age of 2 years, up to 60% of infants with HIE will die or have severe disabilities including mental retardation, epilepsy, and cerebral palsy (CP). HIE is a brain injury that prevents adequate blood flow to the infant’s brain occurring as a result of a hypoxic-ischemic event during the prenatal, intrapartum or postnatal period. Hypoxic ischemic encephalopathy (HIE) is one of the most serious birth complications affecting full term infants.
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