Pathophysiology of Birth Asphyxia

Matthew A Rainaldi; Jeffrey M Perlman

doi:10.1016/j.clp.2016.04.002

Pathophysiology of Birth Asphyxia

Clin Perinatol. 2016 Sep;43(3):409-22. doi: 10.1016/j.clp.2016.04.002. Epub 2016 Jun 17.

Authors

Matthew A Rainaldi¹, Jeffrey M Perlman²

Affiliations

¹ 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.
² 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.

PMID: 27524444
DOI: 10.1016/j.clp.2016.04.002

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.

Keywords: Birth asphyxia; Cerebral palsy; Fetal acidemia; Hypoxic–ischemic encephalopathy; Neonate; Perinatal.

Publication types

Review

MeSH terms

Acidosis / physiopathology*
Asphyxia Neonatorum / physiopathology*
Brain / physiopathology*
Female
Fetal Hypoxia / physiopathology*
Humans
Hypercapnia / physiopathology*
Hypoxia, Brain / physiopathology*
Infant, Newborn
Pregnancy