title: Pathophysiology of Birth Asphyxia.
abstract: The pathophysiology of asphyxia generally results from interruption of placental blood flow with resultant fetal hypoxia, hypercarbia, and acidosis. Circulatory and noncirculatory adaptive mechanisms exist that allow the fetus to cope with asphyxia and preserve vital organ function. With severe and/or prolonged insults, these compensatory mechanisms fail, resulting in hypoxic ischemic injury, leading to cell death via necrosis and apoptosis. Permanent brain injury is the most severe long-term consequence of perinatal asphyxia. The severity and location of injury is influenced by the mechanisms of injury, including degree and duration, as well as the developmental maturity of the brain.
authors.affiliation: Division of Newborn Medicine, Komansky Center for Children's Health, New York Presbyterian Hospital, Weill Cornell Medicine, 525 East 68th Street, N-506, New York, NY 10065, USA. Electronic address: Mar9198@med.cornell.edu.
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Rainaldi
authors.affiliation: Division of Newborn Medicine, Komansky Center for Children's Health, New York Presbyterian Hospital, Weill Cornell Medicine, 525 East 68th Street, N-506, New York, NY 10065, USA.
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Perlman
mesh_terms: D000138:Acidosis / Q000503:physiopathology*; D001238:Asphyxia Neonatorum / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology*; D005260:Female; D005311:Fetal Hypoxia / Q000503:physiopathology*; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology*; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007231:Infant, Newborn; D011247:Pregnancy
keywords: Birth asphyxia; Cerebral palsy; Fetal acidemia; Hypoxic–ischemic encephalopathy; Neonate; Perinatal