In a recent article Goldberg et al1 presented data on 12 asphyxiated newborn infants with high ammonia levels concomitant with abnormal liver function tests. They pointed out that the liver dysfunction, probably secondary to the ischemic-hypoxic injury, might have contributed to ammonia elevation by decreasing urea biosynthesis. I have recently seen two asphyxiated newborn infants who had elevated ammonia levels without any liver dysfunction. Both were meconium-stained postterm neonates with Apgar scores of 1 and 4 at one and five minutes, respectively, who developed seizures, coma, and apnea on the first day of life and required mechanical ventilation for apnea and phenobarbital for seizures.