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. 2011 Sep 1;11(3):125-133.
doi: 10.1053/j.nainr.2011.07.004.

Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments

Affiliations

Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments

Kimberly A Allen et al. Newborn Infant Nurs Rev. .

Abstract

Hypoxic ischemic encephalopathy (HIE) is a serious birth complication affecting full term infants: 40-60% of affected infants die by 2 years of age or have severe disabilities. The majority of the underlying pathologic events of HIE are a result of impaired cerebral blood flow and oxygen delivery to the brain with resulting primary and secondary energy failure. In the past, treatment options were limited to supportive medical therapy. Currently, several experimental treatments are being explored in neonates and animal models to ameliorate the effects of secondary energy failure. This review discusses the underlying pathophysiologic effects of a hypoxic-ischemic event and experimental treatment modalities being explored to manage infants with HIE. Further research is needed to better understand if the long-term impact of the experimental treatments and whether the combinations of experimental treatments can improve outcomes in infants with HIE.

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Figures

Figure 1
Figure 1
The Evolution of Hypoxic Ischemic Encephalopathy * formula image = increased; formula image = decreased; PaO2 = arterial oxygen; Na+ = sodium; K+ = potassium; ATP = adenosine triphosphate; Ca2+ = calcium; NMDA = N-methyl-D-aspartate; AMPA = ∝-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid; ROS = reactive oxygen species; NO = nitric oxide; DNA = deoxyribonucleic acid
Figure 2
Figure 2
Location of Brain Structures Impacted by Treatments Figure courtesy of HowStuffWorks.com

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