Cerebrospinal Fluid Lactate Dehydrogenase in Infants with Perinatal Asphyxia

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Abstract
CSF lactate dehydrogenase was determined in 19 control human infants without asphyxia (group 1), 24 infants with perinatal asphyxia (group 2), and 26 asphyxiated infants with seizures (group 3). 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 3 groups. Mean CSF lactate dehydrogenase was significantly higher in group 3 than in groups 1 and 2. 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 3, but none in groups 1 or 2. Follow-up of survivors at 10-39 mo. of age revealed neurological sequelae in 3 infants in group 1, 2 in group 2 and 5 in group 3. 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. 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.