RT Journal Article
SR Electronic
T1 Hypernatraemia in cerebral disorders
JF Journal of Clinical Pathology
JO J Clin Pathol
FD BMJ Publishing Group Ltd and Association of Clinical Pathologists
SP 211
OP 220
DO 10.1136/jcp.15.3.211
VO 15
IS 3
A1 Taylor, W. H.
YR 1962
UL http://jcp.bmj.com/content/15/3/211.abstract
AB Six patients are described in whom cerebral damage was associated with raised plasma sodium and chloride concentrations and with extremely low urinary outputs of sodium and chloride. The patients were not clinically dehydrated and direct determinations showed that the blood and plasma volumes, the endogenous creatinine clearance, and the urinary output of antidiuretic hormone were normal. For these and other reasons it is concluded that the metabolic picture results not from diminished circulatory volume, water deficiency, sodium deficiency, undetected diabetes insipidus or osmotic diuresis, but from the cerebral damage itself. In these and other cited cases, the cerebral damage was localized chiefly in the frontal lobes, hypothalamus or lower brain-stem, thus suggesting a descending pathway, the relationship of which to the pineal area controlling aldosterone secretion requires clarification.