Cerebral perfusion, metabolism, and outcome

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Abstract
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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