Myelinolysis: A Complication of Correcting Hyponatremia

Abstract & Commentary

Source: Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57-62.

Laureno and karp have critically examined and synthesized the literature on myelinolysis, also known as central pontine myelinolysis, as a complication of the treatment of hyponatremia. Included in their review are animal studies and case series dating back 25 years. They prefer to call the disease myelinolysis because the pathologic process can affect extrapontine brain areas. The vast majority of cases of myelinolysis have occurred in association with correction of hyponatremia. The emergency physician should be aware of this complication and its manifestations.

Myelinolysis is to be distinguished from the demyelination of multiple sclerosis and related inflammatory processes. It is a symmetric process that frequently affects the midline of the basis pontis. Extrapontine involvement is also symmetrical and can affect the thalamus, cerebellum, subcortical white matter, midbrain, and medulla. Symptoms depend on the location of the pathologic process. Typically, the initial symptoms are mutism and dysarthria. Lethargy and other affective changes are common. Spastic quadriparesis and pseudobulbar palsy occur in more than 90% of patients.

The duration of hyponatremia (> 48 hours) and the rapidity of correction are directly related to the possibility of this complication. Animal data conclusively show that it is not the hyponatremia that initiates myelinolysis; it is the flux of solutes and fluid associated with the correction of hyponatremia that causes the pathologic changes approximately 24-48 hours after normalization of the serum sodium. Animal and human data show that treatment of hyponatremia with hypertonic saline has a higher association with this complication. It appears that when the rise in serum sodium is greater than 10-14 mmol/L per 24 hours, the incidence of myelinolysis is significantly increased.

In humans, the encephalopathy of hyponatremia improves with the elevation of the serum sodium. When myelinolysis ensues, this temporary improvement in neurologic function and mental status yields to the signs and symptoms described above. This biphasic presentation is not uniformly present, and the encephalopathy of hyponatremia may overlap with the encephalopathy of myelinolysis, making diagnosis more challenging. CT and MRI scans show characteristic changes, while those studies are normal in the encephalopathy of hyponatremia. Treatment is supportive. Steroids are of no benefit. Animal studies show that lowering serum sodium may be effective, but it is not yet recommended in humans.


This article highlights some points that are particularly pertinent to emergency physicians, who are occasionally called upon to initiate treatment for symptomatic hyponatremia. Hyponatremia itself can cause malaise, head aches, lethargy, confusion, seizures, coma, and death. Especially when hyponatremia develops precipitously, coma and seizures can occur. Infusion of hypertonic (typically 3%) saline is recommended. Hyponatremia that develops more slowly does not cause emergent, life-threatening complications, and it can be corrected gradually without hypertonic saline.1

With the advent of extended care/observation units and the frequency with which patients "board" in the ED when hospital beds are unavailable, emergency physicians may be called upon to not only initiate treatment for symptomatic hyponatremia, but also to monitor and adjust this treatment over a prolonged time period. It is important that we follow the recommendation that sodium be replaced slowly—a less than 10 mmol/L rise in serum sodium per 24-hour period. Profoundly low levels of serum sodium that develop gradually, which do not cause immediate life-threatening problems, should be corrected slowly without hypertonic saline. As the old adage says, treat the patient, not the lab test. When emergent use of hypertonic saline is indicated, it should be infused cautiously and discontinued once the life-threatening complications have been corrected.

In today’s health care environment, it is not inconceivable that a patient could be quickly discharged from the hospital after apparently successful correction of hyponatremia, only to "bounce back" to the ED with the typical biphasic encephalopathic presentation of myelinolysis 2-3 days later. Despite the absence of a specific treatment for this complication, it is important to identify it, provide supportive treatment, and resist the temptation to empirically treat the presenting signs and symptoms as a reoccurrence of hyponatremia.


1. Wijdicks EF, Larson TS. Absence of postoperative hyponatremia syndrome in young, healthy females. Ann Neurol 1994;35:626-628.