1685 BRAIN OXIDATIVE METABOLISM IN A SEVERELY ASPHYXIATED NEWBORN

Sequential in-vivo measurements of phosphorus-containing compounds by 31-P nuclear magnetic resonance (NMR) were obtained in a 2360 g, 36 wk gestation, meconium-stained infant born by vacuum extraction following 2 hrs of maternal fever and fetal tachycardia. Apgars were 1 at 1 min and 3 at 5 min. The infant was intubated, suctioned, ventilated, and given bicarbonate. Initial arterial blood gas was pH=7.16, PO2=43.6, PCO2=30, HCO3=10. Seizures noted at < 24 hrs were treated with phenobarbital. Cultures and cranial ultrasound were normal. EEC showed depressed, disorganized electrical activity but no epileptiform focus. The neurologic exam was remarkable for hypertonia, irritability, decreased activity, and posturing. NMR spectra obtained on 7 occasions between days 3-24 showed a sustained phosphocreatine/inorganic phosphate (PCr/Pi) < 1.0, due primarily to an abnormally high Pi, was markedly lower than PCr/Pi in normal infants (mean 1.07, range .76 - 1.49). PCr/Pi, a measure of phosphoenergetic reserve, was consistently 0.5 in the left hemisphere and increased from 0.5 to 0.9 over the 21 days of observation in the right. At day 23, the left hemisphere showed ½ the ATP of the right. These levels cause activation of glycolysis, acidosis, and further deterioration of the energy state and consequent cell disintegration. These data suggest there was an increased breakdown ol ATP and PCr to inorganic phosphate, as previously seen in areas of prenecrotic brain tissue in experimental animal models, and are much lower than those found in any surviving normal infants or animal models.