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Relationship of fetal asphyxia to neuropathology and deficits in children.
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1993
Year
NeonatologyFetal MedicineSocial SciencesOxidative StressFetal AsphyxiaBrain InjuryNeurologyTerm Fetus OccurAbnormal DevelopmentNeuropathologyHypoxia (Medicine)Maternal HealthPlacental DiseaseTerm FetusMaternal-fetal MedicineFetal NeurodevelopmentNeurophysiologyFetal Asphyxial ComplicationsPhysiologyPediatricsPregnancyNeuroscienceFetal ComplicationMedicine
Neuropathological studies suggest that the majority of the fetal asphyxial complications resulting in brain damage in either preterm or term fetus occur before the onset of labor. Anoxia because of the rapid sequence of events will usually result in death of the fetus. Hypoxia of 1-3 h duration may account for brain damage and deficits in children who survive. The threshold for brain damage is a severe acidosis with a pH < 7.0 in conjunction with systemic hypotension. The prevalence of antepartum fetal asphyxia and the frequency of deficits in such children have not been established. The prevalence of intrapartum fetal asphyxia determined biochemically is 2%. The majority of these children develop normally because of fetal cardiovascular compensatory mechanisms which protect the brain. However, beyond the threshold of asphyxia in either the preterm or term fetus, neuropathology may develop leading to deficits in some children.