The Response of Young Infants to Ingestion of Ammonium Chloride

The results of observations of the effect of ingestion of ammonium chloride on the acid-base excretion of three premature and three full term infants are presented. Two of the three premature infants showed a definitely diminished ammonia and increased sodium excretion as compared with the full term infants. The results suggest that some premature infants may have a renal tubular disability. One of the two infants with diminished ammonia formation and the third premature infant, the two smallest in the series, became listless, refused their feedings, and developed depressed fontanelles and diminished elasticity of the skin. This could not be correlated with changes in serum CO2 content or chlorides or with the presence or absence of an adequate urinary formation of ammonia and conservation of sodium. Since the infants who became dehydrated gained weight while doing so, shifts of water and electrolytes from extracellular to vascular or intracellular compartments must have occurred. It is suggested that the tendency of young infants to disturbances of acidbase balance may be conditioned by disabilities in intracellular metabolism as well as by renal dysfunction. The implications of the limitations and variability in homeostasis for therapy are discussed.