Cerebral perfusion, metabolism, and outcome.
Factors contributing to brain damage and an adverse outcome are complex. Both severe hypoxia-ischemia and prolonged hypoxia of lesser severity may cause brain damage. Compromised cerebral perfusion leads to ischemia. Fetal brain damage may begin because of a redistribution rather than reduction of cerebral blood flow. Normal newborn cerebral blood flow is low; fetal asphyxia at birth causes delayed cerebral hyperperfusion in the neonate. The threshold of newborn cerebral blood flow that is associated with brain damage has not yet been established. Hypoxia-ischemia will disrupt cerebral metabolism. The fetus can compensate for hypoxia up to a point; however, decompensation will occur when acidosis becomes severe. Normal newborn cerebral oxygen consumption is low compared with that in the adult; however, asphyxia, causing brain damage, is associated with abnormal newborn cerebral metabolism. Supplementary glucose may have a protective effect in the newborn brain. Hypoxia-ischemia will cause brain damage in the human fetus and neonate. There is a threshold of fetal asphyxia at birth when brain damage may occur. Sustained neonatal hypotension and hypoxemia are associated with brain damage and an adverse outcome.
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Department of Obstetrics, Gynaecology, and Paediatrics, Queen's University, Kingston, Ontario, Canada.
D000818:Animals; D001238:Asphyxia Neonatorum / Q000503:physiopathology; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000503:physiopathology*; D005315:Fetal Diseases / Q000503:physiopathology; D005311:Fetal Hypoxia / Q000503:physiopathology*; D006801:Humans; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007231:Infant, Newborn