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LETTER
Hyponatremia and Myelinolysis
J. Carlos Ayus, MD, and
Allen I. Arieff, MD
15 July 1997 | Volume 127 Issue 2 | Page 163
TO THE EDITOR:
Drs. Laureno and Karp suggest that in humans, "rapid" correction of symptomatic hyponatremia may have detrimental sequelae, such as myelinolysis [1], despite overwhelming evidence to the contrary [2, 3]. Although absolute correction of hyponatremia in laboratory animals by more than 25 mmol/L in 48 hours can lead to cerebral demyelinating lesions, the "rate" of correction of plasma sodium concentrations in both humans and laboratory animals has been shown to be irrelevant [2, 4]. Most patients who have brain damage associated with hyponatremic encephalopathy are menstruant women who have had a hypoxic episode [4]. Among 117 patients with brain damage secondary to hyponatremic encephalopathy, 96% had a hypoxic episode secondary to delayed onset of therapy and only 4% had brain damage that might have been related to overcorrection [4]. In the past, the picture might have been distorted by the increased likelihood of brain damage after an increase of plasma sodium in patients with end-stage liver disease. The authors [1] unfortunately conclude that respiratory arrest leading to hypoxic encephalopathy in hyponatremic young women "rarely occurs," even though in the study they cite, most patients with hyponatremia were not included in the computer survey. To ascertain that most patients who have brain damage associated with hyponatremia are young women who have hypoxic events [4], the authors need look no further than Table 1 in the article by Steele and colleagues [5] in the same issue of Annals in which their review appears.
In summary, brain damage from hyponatremic encephalopathy due to delayed onset of therapy is at least 24 times more likely than brain damage due to improper therapy. Most patients who have brain damage secondary to hyponatremic encephalopathy are young (menstruant) women [4], whereas those who have brain damage from a change in plasma sodium concentration usually have end-stage liver disease.
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Author and Article Information
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Baylor College of Medicine; Houston, TX 77024
University of California Medical Center; San Francisco, CA 94143
Request for Reprints: Robert H. Moser, MD, Canones Road, Box 616, Chama,NM 87520.
1. Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med. 1997; 126:57-62.
2. Sarnaik AP, Meert K, Hackbarth R, Fleischmann L. Management of hyponatremic seizures in children with hypertonic saline: a safe and effective strategy. Crit Care Med. 1991; 19:758-62.
3. Tien R, Arieff AI, Kucharczyk W, Wasik A, Kucharczyk J. Hyponatremic encephalopathy: is central pontine myelinolysis a component? Am J Med. 1992; 92:513-22.
4. Ayus JC, Arieff AI. Brain damage and postoperative hyponatremia: role of gender. Neurology. 1996; 46:323-8.
5. Steele A, Gowrishankar M, Abrahamson S, Mazer CD, Feldman RD, Halpern ML. Postoperative hyponatremia despite near-isotonic saline infusion: a phenomenon of desalination. Ann Intern Med. 1997; 126:20-5.
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