You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 46 No. 8, August 1989 TABLE OF CONTENTS
  Archives
  •  Online Features
  OBSERVATIONS
 This Article
 •References
 •Full text PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Sodium and Water Regulation in a Patient With Cerebral Salt Wasting

Michael Diringer, MD; Paul W. Ladenson, MD; Cecil Borel, MD; Graeme K. Hart, FFARACS; Jeffrey R. Kirsch, MD; Daniel F. Hanley, MD

Arch Neurol. 1989;46(8):928-930.


Abstract

• Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, <45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.



Author Affiliations

From the Departments of Neurology, Neuroscience Critical Care Unit (Drs Borel, Diringer, and Hanley), Anesthesiology and Critical Care Medicine (Drs Borel, Hanley, Hart, and Kirsch), and Medicine, Division of Endocrinology and Metabolism (Dr Ladenson), The Johns Hopkins Medical Institutions, Baltimore.


Footnotes

Accepted for publication Oct 19, 1988.

Reprint requests to Department of Neurology, The Johns Hopkins Medical Institutions, Meyer 8-139, 600 N Wolfe St, Baltimore, MD 21205 (Dr Diringer).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Hyponatraemic syndrome in a patient with tuberculosis always the adrenals?
Camous et al.
Nephrol Dial Transplant 2008;23:393-395.
FULL TEXT  

Personal practice: Management of hyponatraemia in patients with acute cerebral insults
Albanese et al.
Arch. Dis. Child. 2001;85:246-251.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1989 American Medical Association. All Rights Reserved.