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Manifestations of hyponatremia and hypernatremia in adults

Richard H Sterns, MD
Section Editor
Michael Emmett, MD
Deputy Editor
John P Forman, MD, MSc


Symptoms of hyponatremia or hypernatremia are primarily neurologic. They are related to the severity and, in particular, the rapidity of the change in the serum sodium concentration [1-3]. Patients with hyponatremia and hypernatremia may also have complaints related to concurrent volume depletion and possible underlying neurologic diseases that predispose to the electrolyte abnormality. These include a wide variety of neurologic disorders that can lead sequentially to either the inappropriate secretion of antidiuretic hormone, water retention, and hyponatremia, or to the lack of expression of thirst, which is normally the major protective mechanism against the development of hypernatremia.

The cerebral adaptation and clinical manifestations of hyponatremia and hypernatremia will be reviewed here. The etiology and treatment of hyponatremia and hypernatremia are presented elsewhere. (See "Causes of hyponatremia in adults" and "Overview of the treatment of hyponatremia in adults" and "Etiology and evaluation of hypernatremia in adults" and "Treatment of hypernatremia".)


The symptoms directly attributable to hyponatremia primarily occur with acute and marked reductions in the serum sodium concentration and reflect neurologic dysfunction induced by cerebral edema [1,2,4,5], and possibly adaptive responses of brain cells to osmotic swelling [1]. In this setting, the associated fall in serum osmolality creates an osmolal gradient that favors water movement into the cells, leading to brain edema.

The development of cerebral edema in hyponatremic patients is dependent upon the transfer of water from plasma and cerebrospinal fluid into the brain. Insight into this process is provided by studies in mice without the genes for aquaporin-4, a water channel expressed at the interface between the brain and blood and between the brain and cerebrospinal fluid [6]. Compared with wild-type mice, knockout mice exhibit considerably less brain edema, morbidity, and mortality after the induction of acute hyponatremia, suggesting that aquaporin-4 mediates a substantial portion of osmotic water transport into the brain.

Hyponatremia-induced cerebral edema occurs primarily with rapid reductions in the serum sodium concentration, usually less than 24 hours [5], as most often occurs in postoperative patients given large quantities of hypotonic fluid and in patients with self-induced water intoxication due to primary polydipsia or exercise-associated hyponatremia. Hypoxic brain injury also may contribute to the neurologic deficit if respiratory arrest has occurred [7]. (See "Exercise-associated hyponatremia".)

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Literature review current through: Oct 2017. | This topic last updated: Jan 05, 2016.
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