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Hypoxic-ischemic encephalopathy: facts and insights

Geert Braems (UGent)
(2005) INTERNATIONAL CONGRESS SERIES. 1279. p.350-352
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Abstract
Asphyxia may cause a hypoxic-ischemic encephalopathy due to an insufficient supply of oxygenated blood to the brain, which leads to a cerebral palsy. The transition state between both is called neonatal encephalopathy. However, there are many other causes for neonatal encephalopathy, such as developmental abnormalities, metabolic abnormalities, autoimmune disorders, coagulation disorders, infections, trauma, IUGR, and chromosomal abnormalities. Therefore, the American College of Obstetricians and Gynecologists defined criteria, sufficient for an acute intrapartum event to cause a cerebral palsy. Asphyxia itself causes a redistribution of the blood flow towards the central organs, the brain and heart, but in a further stage the cerebral energy metabolism may breakdown and a cascade of events will occur: energy, i.e. ATP, fails for Na+/K+ pumps, the gradients of Na+/K+ across the cell membranes cannot any longer be maintained and cell oedema develops, furthermore, glutamate is released and exerts a neurotoxic influence, Ca2+ overflows the cells and activates lipases, proteases and nucleases, the cellular protein synthesis decreases, after the insult reperfusion of the tissue occurs, but oxygen radicals with a nefast influence are formed, interleukins are released and an inflammatory reaction takes place and proto-oncogenes are expressed. Cell death is an inevitable consequence, leading to the hypoxic-ischemic encephalopathy.

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Chicago
Braems, Geert. 2005. “Hypoxic-ischemic Encephalopathy: Facts and Insights.” In International Congress Series, 1279:350–352. Amsterdam: Elsevier.
APA
Braems, G. (2005). Hypoxic-ischemic encephalopathy: facts and insights. INTERNATIONAL CONGRESS SERIES (Vol. 1279, pp. 350–352). Presented at the 15th Congress of Gynaecology, Obstetrics and Reproductive Medicine, Amsterdam: Elsevier.
Vancouver
1.
Braems G. Hypoxic-ischemic encephalopathy: facts and insights. INTERNATIONAL CONGRESS SERIES. Amsterdam: Elsevier; 2005. p. 350–2.
MLA
Braems, Geert. “Hypoxic-ischemic Encephalopathy: Facts and Insights.” International Congress Series. Vol. 1279. Amsterdam: Elsevier, 2005. 350–352. Print.
@inproceedings{505476,
  abstract     = {Asphyxia may cause a hypoxic-ischemic encephalopathy due to an insufficient supply of oxygenated blood to the brain, which leads to a cerebral palsy. The transition state between both is called neonatal encephalopathy. However, there are many other causes for neonatal encephalopathy, such as developmental abnormalities, metabolic abnormalities, autoimmune disorders, coagulation disorders, infections, trauma, IUGR, and chromosomal abnormalities. Therefore, the American College of Obstetricians and Gynecologists defined criteria, sufficient for an acute intrapartum event to cause a cerebral palsy.
Asphyxia itself causes a redistribution of the blood flow towards the central organs, the brain and heart, but in a further stage the cerebral energy metabolism may breakdown and a cascade of events will occur: energy, i.e. ATP, fails for Na+/K+ pumps, the gradients of Na+/K+ across the cell membranes cannot any longer be maintained and cell oedema develops, furthermore, glutamate is released and exerts a neurotoxic influence, Ca2+ overflows the cells and activates lipases, proteases and nucleases, the cellular protein synthesis decreases, after the insult reperfusion of the tissue occurs, but oxygen radicals with a nefast influence are formed, interleukins are released and an inflammatory reaction takes place and proto-oncogenes are expressed. Cell death is an inevitable consequence, leading to the hypoxic-ischemic encephalopathy.},
  author       = {Braems, Geert},
  booktitle    = {INTERNATIONAL CONGRESS SERIES},
  isbn         = {0-444-51917-3},
  issn         = {0531-5131},
  language     = {eng},
  location     = {Rotterdam},
  pages        = {350--352},
  publisher    = {Elsevier},
  title        = {Hypoxic-ischemic encephalopathy: facts and insights},
  url          = {http://dx.doi.org/10.1016/j.ics.2004.12.038},
  volume       = {1279},
  year         = {2005},
}

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