osmotic demyelination syndrome

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osmotic demyelination syndrome

(oz-mot'ik de-mi?e-li-na'shon)
Damage to the myelin sheaths that surround nerves, usually as a result of excessively rapid correction of very low serum sodium levels.

Patient care

It can be prevented by carefully monitoring serum sodium (Na+) concentrations when hyponatremic patients are rehydrated, limiting the increase in Na+ concentration to less than 10 meq/L in the first 24 hours, and 18meq/L in the first 2 days.

Synonym: myelinolysis
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MRI brain obtained at 60 hrs of admission showed mild edema of the cortex and sulci and diffuse edema of the pons and midbrain with restricted diffusion in the pons consistent with central pontine myelinolysis also known as osmotic demyelination syndrome. There was no significant change in the subdural hemorrhage (Figures 1-4).
Martin, "Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes," Neurology in Practice, vol.
Osmotic demyelination syndrome often is preventable, with considerable morbidity and mortality.
Table 1 Risk factors for developing osmotic demyelination syndrome Advanced liver disease Alcoholism Hypokalemia Malnutrition Serum sodium concentration <105 mEq/L Source: Reference 6 Table 2 Expert panel recommendations: Avoiding ODS in patients with chronic hyponatremia Goal Minimum correction of serum sodium by 4 to 8 mEq/L per day, with a lower goal of 4 to 6 mEq/L per day if risk of ODS is high Limits not to exceed For high risk of ODS: 8 mEq/L in any 24-hour period For normal risk of ODS: 10-12 mEq/L In any 24-hour period; 18 mEq/L in any 48-hour period ODS: osmotic demyelination syndrome Source: Reference 6
Best cases from the AFIP: Osmotic demyelination syndrome. Radiographics.
The drug's label includes a boxed warning that says treatment should be initiated and reinitiated in the hospital to allow serum sodium levels to be closely monitored, and points out that overly rapid correction of hyponatremia can result in osmotic demyelination syndrome (ODS), which can cause dysarthria, mutism, dysphagia, lethargy, affect changes, spastic quadriparesis, seizures, coma, and death.
Such an intervention reduces cerebral edema without risk for osmotic demyelination syndrome as may occur during the rapid correction of chronic hyponatremia, as the prerequisite compensatory adaptation of brain cells to hypo-osmolality has not yet taken place.
Hypernatremia is a potentially lethal condition, and can cause encephalopathy, rhabdomyolysis, and osmotic demyelination syndrome. [1]
Oligodendrocytes are particularly sensitive for osmotic changes therefore changes that are seen with osmotic demyelination syndrome are in distribution to oligodendroglial cells.