Abstract

Hypernatremia and hyperosmolality of serum result from loss of water without sodium. Clinically, the important causes are continued insensible loss of water in the unconscious patient and urinary loss of water in the patient with classic or traumatic diabetes insipidus. Hyponatremia with hypo-osmolality of serum is produced by retention of water, by loss of sodium or both. It is always maintained by a defect in excretion of free water. In Addison's disease, loss of sodium and retention of water occur pari passu; in cardiac failure and cirrhosis, therapeutic loss of salt and water followed by ingestion of water leads to hyponatremia; in the syndrome of inappropriate secretion of antidiuretic hormone, retention of water is followed by loss of sodium: in the postoperative state, hyponatremia may result from retention of administered water alone. The defect in excretion of free water may result both from excessive proximal reabsorption of salt and water, with defective formation of free water, and from the action of antidiuretic hormone, with excessive distal reabsorption of free water. Whereas treatment of the underlying cause is clearly indicated, hypernatremia responds to administration of water and hyponatremia to withdrawal of water.

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