J. Carlos Ayus, MD; Allen I. Arieff, MD
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Ayus J., Arieff A.; Hyponatremia and Myelinolysis. Ann Intern Med. 1997;127:163. doi: 10.7326/0003-4819-127-2-199707150-00016
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Published: Ann Intern Med. 1997;127(2):163.
TO THE EDITOR:
Drs. Laureno and Karp suggest that in humans, “rapid” correction of symptomatic hyponatremia may have detrimental sequelae, such as myelinolysis , 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 . 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 . 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  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 , the authors need look no further than Table 1 in the article by Steele and colleagues  in the same issue of Annals in which their review appears.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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