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  • Title: [Perinatal asphyxia, hypoxic-ischemic encephalopathy and neurological sequelae in full-term newborns. II. Description and interrelation].
    Author: González de Dios J, Moya M.
    Journal: Rev Neurol; 1996 Aug; 24(132):969-76. PubMed ID: 8755359.
    Abstract:
    INTRODUCTION: There have been several attempts to relate either perinatal asphyxia at birth or abnormal neurological findings after asphyxia in neonatal period (hypoxic-ischemic encephalopathy), to outcome. OBJECTIVE: To investigate, in full-term infants, the relation between perinatal asphyxia, hypoxic-ischemic encephalopathy and neurologic sequelae at follow-up, and to define the main neurologic sequelae (cerebral palsy, mental retardation, neonatal death). Material and method. Prospective epidemiologic study over perinatal asphyxia in term neonates born in Universitary Hospital San Juan (Alicante, Spain) between November 1991-February 1995. Perinatal asphyxia was graded as non severe (1-minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart rate patterns and/or meconium-stained amniotic fluid, and the need for immediate neonatal resuscitation) and severe (1-minute Apgar score < or = 3 and umbilical artery pH < 7.10). Hypoxic-ischemic encephalopathy was graded as mild, moderate and severe based on classification of Levene and Sarnat & Sarnat. The abnormalities on psicomotor development are based in the neurologic 'alert signs' and in the neurologic sequelae; this sequelae was graded as mild, moderate and severe based on classification of Finer and Amiel-Tison. The relationships between these variables are studied by univariant and multivariant analysis (Cox's regression). RESULTS: The incidence of neurologic sequelae, in 115 asphyxiated full-term infants follow-up at least 12-24 months, was 16.5%; 4 cases of severe sequelae, 4 moderate and 11 mild. The overall asphyxia-related infant mortality rate was 0.87/1.000 live births. The main sequelae detected at follow-up was motor disability, and other disabilities like mental retardation, epilepsy, sensorial defects, were infrequents. The incidence of cerebral palsy was 0.87/1.000 live births, and 2.6% asphyctic term neonates. We found a statistically significant (p < 0.001) association between severity of perinatal asphyxia and/or evidence of hypoxic-ischemic-encephalopathy and the neurological development at follow-up. Of the several factors associated to risk of neurologic sequelae on univariant analysis, only two were independently associated on multivariant analysis: severe perinatal asphyxia (RR = 2.82; IC = 1.07-7.39) and postasphyctic encephalopathy (RR = 4.17; IC = 1.48-11.75). CONCLUSIONS: Most survivors of perinatal asphyxia do not have adverse sequelae. The best predictive tool for the neurological prognosis at follow-up was severe perinatal asphyxia at birth and evidence of encephalopathy in neonatal period. Our study confirm that perinatal asphyxia is infrequently the cause of cerebral palsy and mental retardation.
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