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Osmotic demyelination syndrome (ODS) and overly rapid correction of hyponatremia

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


The serum sodium concentration is the primary determinant of serum tonicity (also known as "effective serum osmolality") (see "Diagnostic evaluation of adults with hyponatremia"). The fall in serum tonicity in patients with hypotonic hyponatremia promotes water movement into the brain and, if the hyponatremia is acute and severe, can lead to cerebral edema and neurologic symptoms. In response to hyponatremia, the brain makes adaptations that lower the cerebral volume toward normal and reduce the likelihood of these complications. The mechanisms responsible for this cerebral adaptation are discussed elsewhere. (See 'Brain adaptation to hyponatremia' below and "Manifestations of hyponatremia and hypernatremia in adults", section on 'Osmolytes and cerebral adaptation to hyponatremia'.)

However, brain adaptations that reduce the risk of cerebral edema make the brain vulnerable to injury if chronic hyponatremia is too rapidly corrected. The neurologic manifestations associated with overly rapid correction have been called the osmotic demyelination syndrome (ODS, formerly called central pontine myelinolysis or CPM). As will be described below, almost all patients who develop ODS present with a serum sodium concentration of 120 meq/L or less.

Issues related to ODS and the approach to the patient with unintentional overly rapid correction of hyponatremia will be reviewed here. A general overview of the treatment of hyponatremia is presented separately. (See "Overview of the treatment of hyponatremia in adults".)


A decrease in serum tonicity causes water to flow across the blood-brain barrier, increasing brain water content. The decrease in serum tonicity also causes brain cells, primarily astrocytes, to swell. Astrocytes are cells that surround brain capillaries and express water channels on their foot processes; these cells protect neurons from swelling via a cell-to-cell transfer of cellular solutes and water [1].

The brain begins to adapt to hypotonicity almost immediately after a fall in serum sodium, and the adaptation is complete within two days. If the brain were unable to adapt, even mild hyponatremia would result in life-threatening cerebral edema. However, within minutes after a fall in serum sodium, increased intracranial pressure forces interstitial sodium and water out of the brain into the cerebrospinal fluid, ameliorating the increased brain volume. In addition, astrocytes begin to lose intracellular solutes, principally potassium and organic solutes (called osmolytes), within hours of a fall in serum sodium and serum tonicity. This process permits these cells to shed excess water and to have the same tonicity as plasma without a large increase in cell water (figure 1). Cerebral adaptation to hyponatremia is discussed in more detail elsewhere. (See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Osmolytes and cerebral adaptation to hyponatremia'.)

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Literature review current through: Nov 2017. | This topic last updated: Apr 28, 2016.
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