Figure 123

Symptoms of central pontine myelinolysis. This condition has been described all over the world, in all age groups, and can follow correction of hyponatremia of any cause. The risk for development of central pontine myelinolysis is related to the severity and chronicity of the hyponatremia. Initial symptoms include mutism and dysarthria. More than 90% of patients exhibit the classic symptoms of myelinolysis (ie, spastic quadriparesis and pseudobulbar palsy), reflecting damage to the corticospinal and corticobulbar tracts in the basis pontis. Other symptoms occur on account of extension of the lesion to other parts of the midbrain. This syndrome follows a biphasic course. Initially, a generalized encephalopathy, associated with a rapid rise in serum sodium, occurs. This is followed by the classic symptoms 2 to 3 days after correction of hyponatremia, however, this pattern does not always occur [22]. (Adapted from Laureno and Karp [22]; with permission.)

FIGURE 1-24

A, Imaging of central pontine myelinolysis. Brain imaging is the most useful diagnostic technique for central pontine myelinolysis. Magnetic resonance imaging (MRI) is more sensitive than computed tomography (CT). On CT, central pontine and extrapontine lesions appear as symmetric areas of hypodensity (not shown). On T2 images of MRI, the lesions appear as hyperintense and on T1

images, hypointense. These lesions do not enhance with gadolinium. They may not be apparent on imaging until 2 weeks into the illness. Other diagnostic tests are brainstem auditory evoked potentials, electroencephalography, and cerebrospinal fluid protein and myelin basic proteins [22]. B, Gross appearance of the pons in central pontine myelinolysis. (From Laureno and Karp [22]; with permission.)

Treatment of severe euvolemic hyponatrem-ia (<125 mmol/L). The evaluation of a hyponatremic patient involves an assessment of whether the patient is symptomatic, and if so, the duration of hyponatremia should be ascertained. The therapeutic approach to the hyponatremic patient is determined more by the presence or absence of symptoms than by the absolute level of serum sodium. Acutely hyponatremic patients are at great risk for permanent neurologic sequelae from cerebral edema if the hypona-tremia is not promptly corrected. On the other hand, chronic hyponatremia carries the risk of osmotic demyelination syndrome if corrected too rapidly. The next step involves a determination of whether the patient has any risk factors for development of neurologic complications.

The commonest setting for acute, symptomatic hyponatremia is hospitalized, postoperative patients who are receiving hypotonic fluids. In these patients, the risk of cerebral edema outweighs the risk for osmotic demyelination. In the presence of seizures, obtundation, and coma, rapid infusion of 3% sodium chloride (4 to 6 mL/kg/h) or even 50 mL of 29.2% sodium chloride has been used safely. Ongoing careful neurologic monitoring is imperative [20].

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