Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 5139  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 »   Next article
 »   Previous article
 »   Table of Contents

 Resource Links
 »   Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
 »   Citation Manager
 »   Access Statistics
 »   Reader Comments
 »   Email Alert *
 »   Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded407    
    Comments [Add]    
    Cited by others 40    

Recommend this journal


Year : 2006  |  Volume : 54  |  Issue : 3  |  Page : 273--275

Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage

1 Department of Medicine Divisions of Pulmonary/Critical Care, New York Medical College, Valhalla, NY, USA
2 Department of Cardiology, New York Medical College, Valhalla, NY, USA
3 Department of General Internal Medicine, New York Medical College, Valhalla, NY, USA
4 Department of Neurosurgery, New York Medical College, Valhalla, NY, USA

Correspondence Address:
Dipak Chandy
Division of Pulmonary / Critical Care Medicine, Pulmonary Lab, Macy Pavilion, Westchester Medical Center, Valhalla, NY 10595
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.27151

Rights and Permissions

Background: Hyponatremia develops in approximately a third of patients with aneurysmal subarachnoid hemorrhage (SAH). Studies have been conflicting about the association between hyponatremia and cerebrovascular spasm (CVS). Aims: To investigate whether hyponatremia can signal the onset of CVS. Settings and Design: Retrospective chart review of all patients with SAH treated at a tertiary-care university hospital from January to May 2002. Materials and Methods: 106 patients were included in the study. Serum sodium levels were recorded from days 1 to 14 of hospitalization. Hyponatremia was defined as serum sodium level <135 meq/l and a fall in sodium level of >4 meq/l from the admission sodium level. The presence of CVS was determined by transcranial doppler sonography. Patients were assigned to one of four groups based on the presence or absence of CVS and hyponatremia. Statistical Analysis: Student's t-test was used for comparison of means. A logistical regression model was constructed and odds ratios (OR) were calculated. Results: 41 patients developed hyponatremia and 44 developed CVS. Among the 41 with hyponatremia, 22 (54%) had evidence of CVS, whereas among the 65 patients without hyponatremia, 22 (34%) had evidence of CVS ( P =0.023). Among those with hyponatremia, the mean sodium drop was 7.9 meq/L in those with CVS compared to 7.0 meq/L in those without CVS ( P = 0.068). More than half of those with hyponatremia and CVS (13/22) developed hyponatremia at least a day before CVS was diagnosed. Conclusion: In patients with SAH, hyponatremia is associated with a significantly greater risk of developing CVS and may precede CVS by at least one day.


Print this article     Email this article

Online since 20th March '04
Published by Wolters Kluwer - Medknow