PERSISTENT INCREASES IN CEREBRAL LACTATE CONCENTRATION AFTER BIRTH ASPHYXIA

In this prospective study proton magnetic resonance spectroscopy (H-1 MRS) was used to test the hypothesis that lactate can be detected late r than 1 mo after birth in the brains of infants who display severe ne urodevelopmental impairment 1 y after transient perinatal hypoxia-isch emia. Data were obtained from three groups of infants: 1) eight infant s suffering birth asphyxia followed by perinatal encephalopathy and ab normal neurodevelopmental outcome at 1 y of age (defined as major neur ologic impairment, Griffiths quotient <85%, and low optimality score); 2) 10 infants with signs of perinatal hypoxia-ischemia but normal neu rodevelopmental outcome at 1 y; and 3) six control infants with uneven tful perinatal courses and normal neurodevelopment at 1 y. Between one and four examinations (median 1) were performed at median (range) 11 (4-68) wk after birth, and the cerebral concentration ratio of lactate to creatine plus phosphocreatine (Cr) calculated from each spectrum. Lactate was detected later than the Ist mo after birth in seven of eig ht infants with abnormal neurodevelopmental outcome [maximum detected lactate/Cr was median (range) 0.44 (0.24-0.67)]. No lactate was detect ed later than the Ist mo after birth in infants with normal neurodevel opmental outcome, nor in five of six control subjects, although a smal l amount of lactate was detected in one control infant (lactate/Cr = 0 .04). These results suggest that the pathologic postasphyxial process, indicated by persistent cerebral lactate, may not be confined to the period immediately after injury.