Author(s): Hall RT, Kulkarni PB, Sheehan MB, Rhodes PG
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Abstract Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.
This article was published in Dev Med Child Neurol
and referenced in Journal of Neonatal Biology