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The dilemma of diagnosing the cause of hypernatraemia: drinking habits vs diabetes insipidus.

Fortunately, hypernatraemia is not a common problem, occurring in <1% of patients in an acute care hospital. It is serious, however, as hypernatraemia is correlated with a high mortality rate [1]. A major reason that hypernatraemia is so rare in conscious adults is the presence of powerful, highly regulated responses to a rise in plasma osmolality, namely thirst and anti-diuretic hormone (ADH) release [1]. An increase in plasma osmolality of only 2mOsm/kg above normal values stimulates thirst and ADH release, and ADH in turn causes water reabsorption by the kidney. Since osmolality is determined by the ratio of osmotically active particles to the volume of water in the body, thirst plus ADH release act to increase the volume of water in the body and correct the tendency to develop hyperosmolality/ hypernatraemia. Clearly, both thirst and ADH release are required because failure to release ADH or failure of ADH to stimulate water reabsorption by the kidney does not increase the osmolality or plasma sodium concentration as long as the subject has access to water [1]. Therefore, hypernatraemia in a conscious patient implies that there is a defect in thirst mechanisms in addition to loss of water via the kidney, gastrointestinal tract or other routes. We encountered a previously healthy young man who developed hypernatraemia (serum sodium concentration, 169mEq/l), but did not complain of thirst. Following correction of the hypernatraemia, we investigated him for disorders that could limit ADH responses as well as thirst. He was found to have a degree of partial central diabetes insipidus, but psychotic depression interfering with thirst mechanisms was the major factor accounting for hypernatraemia. With proper treatment, the hypernatraemia was reversed and has not recurred.