Does hypoxemia prevent brain damage in birth asphyxia?
The clinical syndrome of hypoxic ischemic encephalopathy (HIE) which occurs in association with birth asphyxia, is thought to represent a reperfusion injury consequent upon the generation of cytotoxic oxygen derived free radicals. It has recently been suggested that resuscitation of asphyxiated infants with unrestricted oxygen may aggravate the brain damage by causing hyperoxia and increased free radical production. To determine whether sustained hypoxemia may be protective in birth asphyxiated infants, we investigated the relationship between HIE and persistent pulmonary hypertension of the neonate (PPHN). The latter condition is also related to intrauterine and intrapartum birth asphyxia but is associated with persistent hypoxemia in the infant. In a retrospective analysis of 39 asphyxiated neonates admitted to the neonatal intensive care unit, we found that 28 had HIE, 10 had PPHN and only 1 had both HIE and PPHN. We therefore suggest that the hypoxemia due to PPHN may limit the production of oxygen derived free radicals in asphyxiated neonates and hence protect against the development of HIE. These findings lend support to current research into air vs. oxygen resuscitation for infants with birth asphyxia.
Ballot
D E
DE
Department of Paediatrics and Child Health, Johannesburg Hospital, University of the Witwatersrand, South Africa.
Rothberg
A D
AD
Davies
V A
VA
Smith
J
J
Kirsten
G
G
D001238:Asphyxia Neonatorum / Q000150:complications* / Q000378:metabolism; D001930:Brain Injuries / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D005260:Female; D005609:Free Radicals; D006801:Humans; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism; D007231:Infant, Newborn; D008297:Male; D008954:Models, Biological; D010547:Persistent Fetal Circulation Syndrome / Q000150:complications / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species