The relationship of asphyxia in the mature fetus to long-term neurologic function.

Asphyxia may occur before or during labor in the preterm or term fetus. The development of neuropathologic lesions depends on the degree and duration of the asphyxia. Anoxia may occur, but because of the short duration of the fetal response, it usually will cause the death of the fetus. The common mechanism leading to neuropathologic lesions in the fetus is a significant degree of hypoxia present for a particular period of time. Antepartum asphyxia will cause such lesions and deficits in children. What is missing are measures to establish the prevalence of antepartum asphyxia in a large population and the epidemiologic studies to determine the association between the asphyxia so documented and the deficits in surviving children. The prevalence of intrapartum fetal asphyxia is of the order of 2%. Most of these children will have no evidence of brain damage. The key is the fetal cardiovascular compensatory response that maintains cerebral blood flow and oxygen metabolism. This compensatory phase, subject to the severity of the hypoxia, may continue for several hours. In the clinical setting during labor, this provides the "window of opportunity" when a specific blood gas and acid-base diagnosis can be made, and with appropriate intervention, brain damage can be avoided. However, if the hypoxia persists, a threshold will be reached when fetal cardiovascular decompensation will occur. The compromised cerebral oxygen metabolism will result in brain damage and deficits in the children who survive. The threshold at which brain damage may occur is when the acidosis is severe (pH, < 7.0). At this time, systemic hypotension may occur.(ABSTRACT TRUNCATED AT 250 WORDS)