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  Vol. 282 No. 24, December 22, 1999 TABLE OF CONTENTS
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Treatment of Hyponatremic Encephalopathy

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor: I disagree with several conclusions drawn by Drs Ayus and Arieff in their article on chronic hyponatremic encephalopathy.1

First, there was no patient randomization. This creates uncertainty as to whether the persistence of hyponatremia observed is a marker of those individual patients with poor clinical course (and outcomes) and not causal.

Second, there was little evidence to support the authors' suggestions that the presenting seizures, respiratory failure, and neurological status were caused by hyponatremia. For example, could hypoxia (independent of the observed hyponatremia) be similarly implicated as causal?

Third, the differences between group 3 and groups 1 and 2 appear to be the lack of correction of hyponatremia, not necessarily the mode of management. In other words, "fluid restriction" as an intervention (which along with intravenous sodium chloride was not specially defined) was not associated with correction of the hyponatremia. These data would suggest that the failure . . . [Full Text of this Article]



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RELATED ARTICLE

Chronic Hyponatremic Encephalopathy in Postmenopausal Women: Association of Therapies With Morbidity and Mortality
J. Carlos Ayus and Allen I. Arieff
JAMA. 1999;281(24):2299-2304.
ABSTRACT | FULL TEXT  






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