Abstract

A female infant, 5 months of age, with evidence of diffuse cerebral damage was found to have hyponatremia in the course of ordinary investigation. Measurements of total body chloride by the thiocyanate-space method at widely different concentrations of chloride in the serum yielded results within the expected normal range. The infant was unable to excrete an acute water load as rapidly as normal infants. Serum from the patient during a hyponatremic phase showed significantly greater antidiuretic activity than that of a normal child. We concluded that the hyponatremia was due to dilution of body fluids secondary to water retention on the basis of disturbed renal function. The hyponatremia was resistant to correction by administration of salt or mineralo-corticoids. A relation between fluid intake and concentration of sodium in the serum was demonstrated which suggested that on normal fluid intakes the child was unable to excrete solute-free water in a normal manner. This may represent the result of damage to the cerebral osmoreceptors as part of generalized brain damage. The data do not support the concept that the hyponatremia resulted from true salt-wasting, either cerebral or renal in mediation. If correction of such a state is desirable, the most useful therapeutic measure would appear to be limitation of the intake of fluid to slightly more than the amount needed to cover water expenditure from insensible losses, obligatory urine volume and growth requirements.

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