| ORIGINAL ARTICLE |
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| Year : 2006 | Volume
: 54
| Issue : 3 | Page : 273--275 |
Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage
Dipak Chandy1, Roger Sy1, Wilbert S Aronow2, Wei-Nchih Lee3, George Maguire1, Raj Murali4
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
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.27151
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.
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