Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage
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. Setti...
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creator | Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj |
description | 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. |
doi_str_mv | 10.4103/0028-3886.27151 |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_68782366</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A150779198</galeid><sourcerecordid>A150779198</sourcerecordid><originalsourceid>FETCH-LOGICAL-b479t-d9a1923cd86253b5b704599dd3925a7dfa7ecff7a4d32bd983e9e52b1af4da423</originalsourceid><addsrcrecordid>eNptkc1rGzEQxUVpaRwn597K0kNu6-hjVx_HEJqmYOilPYvZ1aytsCu5krfg_75y7SYQggRCM783POkR8onRVcOouKWU61poLVdcsZa9IwtmjK4byvl7snjuXpDLnJ_KVQjGP5ILJo2QQqsFWT8edjHAPuHkoYLgqh4Tdin-gdzPI6Qq7yBPlQ-liXM65AnGKs8dJOi3IXpXbXGKKW1hg1fkwwBjxuvzuSS_Hr7-vH-s1z--fb-_W9ddo8y-dgaY4aJ3WvJWdG2naNMa45wwvAXlBlDYD4OCxgneOaMFGmx5x2BoHDRcLMnNae4uxd8z5r2dfO5xHIvFOGcrtdJcSFnAL6_ApzinULzZ0jeCSXacVp-gDYxofRjivrxtgwETjDHg4Ev5jrVUKcOKmSVZvcGX5cof9m8Kbk-CPsWcEw52l_wE6WAZtccY7TEoewzK_ouxKD6ffc_dhO6FP-f24qHzcfQBn4k-ebD_i8GXTSXVWvwFGkmolA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>236931612</pqid></control><display><type>article</type><title>Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage</title><source>MEDLINE</source><source>Bioline International Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</creator><creatorcontrib>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</creatorcontrib><description>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.</description><identifier>ISSN: 0028-3886</identifier><identifier>EISSN: 1998-4022</identifier><identifier>DOI: 10.4103/0028-3886.27151</identifier><identifier>PMID: 16936387</identifier><language>eng</language><publisher>India: Medknow Publications on behalf of the Neurological Society of India</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Causes of ; Cerebral vasospasm, hyponatremia, subarachnoid hemorrhage ; Cerebrovascular spasm ; Complications and side effects ; Diagnosis ; Female ; Humans ; Hyponatremia ; Hyponatremia - blood ; Hyponatremia - diagnostic imaging ; Hyponatremia - epidemiology ; Hyponatremia - etiology ; Logistic Models ; Male ; Middle Aged ; Odds Ratio ; Retrospective Studies ; Sodium - blood ; Subarachnoid hemorrhage ; Subarachnoid Hemorrhage - blood ; Subarachnoid Hemorrhage - complications ; Subarachnoid Hemorrhage - diagnostic imaging ; Subarachnoid Hemorrhage - epidemiology ; Ultrasonography, Doppler, Transcranial - methods ; Vasospasm, Intracranial - blood ; Vasospasm, Intracranial - diagnostic imaging ; Vasospasm, Intracranial - epidemiology ; Vasospasm, Intracranial - etiology</subject><ispartof>Neurology India, 2006-07, Vol.54 (3), p.273-275</ispartof><rights>Copyright 2006 Neurology India.</rights><rights>COPYRIGHT 2006 Medknow Publications and Media Pvt. Ltd.</rights><rights>Copyright Medknow Publications Jul-Sep 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b479t-d9a1923cd86253b5b704599dd3925a7dfa7ecff7a4d32bd983e9e52b1af4da423</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930,79431</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16936387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</creatorcontrib><title>Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage</title><title>Neurology India</title><addtitle>Neurol India</addtitle><description>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.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Causes of</subject><subject>Cerebral vasospasm, hyponatremia, subarachnoid hemorrhage</subject><subject>Cerebrovascular spasm</subject><subject>Complications and side effects</subject><subject>Diagnosis</subject><subject>Female</subject><subject>Humans</subject><subject>Hyponatremia</subject><subject>Hyponatremia - blood</subject><subject>Hyponatremia - diagnostic imaging</subject><subject>Hyponatremia - epidemiology</subject><subject>Hyponatremia - etiology</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Retrospective Studies</subject><subject>Sodium - blood</subject><subject>Subarachnoid hemorrhage</subject><subject>Subarachnoid Hemorrhage - blood</subject><subject>Subarachnoid Hemorrhage - complications</subject><subject>Subarachnoid Hemorrhage - diagnostic imaging</subject><subject>Subarachnoid Hemorrhage - epidemiology</subject><subject>Ultrasonography, Doppler, Transcranial - methods</subject><subject>Vasospasm, Intracranial - blood</subject><subject>Vasospasm, Intracranial - diagnostic imaging</subject><subject>Vasospasm, Intracranial - epidemiology</subject><subject>Vasospasm, Intracranial - etiology</subject><issn>0028-3886</issn><issn>1998-4022</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>RBI</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1rGzEQxUVpaRwn597K0kNu6-hjVx_HEJqmYOilPYvZ1aytsCu5krfg_75y7SYQggRCM783POkR8onRVcOouKWU61poLVdcsZa9IwtmjK4byvl7snjuXpDLnJ_KVQjGP5ILJo2QQqsFWT8edjHAPuHkoYLgqh4Tdin-gdzPI6Qq7yBPlQ-liXM65AnGKs8dJOi3IXpXbXGKKW1hg1fkwwBjxuvzuSS_Hr7-vH-s1z--fb-_W9ddo8y-dgaY4aJ3WvJWdG2naNMa45wwvAXlBlDYD4OCxgneOaMFGmx5x2BoHDRcLMnNae4uxd8z5r2dfO5xHIvFOGcrtdJcSFnAL6_ApzinULzZ0jeCSXacVp-gDYxofRjivrxtgwETjDHg4Ev5jrVUKcOKmSVZvcGX5cof9m8Kbk-CPsWcEw52l_wE6WAZtccY7TEoewzK_ouxKD6ffc_dhO6FP-f24qHzcfQBn4k-ebD_i8GXTSXVWvwFGkmolA</recordid><startdate>20060701</startdate><enddate>20060701</enddate><creator>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</creator><general>Medknow Publications on behalf of the Neurological Society of India</general><general>Medknow Publications and Media Pvt. Ltd</general><general>Medknow Publications & Media Pvt. Ltd</general><scope>RBI</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20060701</creationdate><title>Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage</title><author>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b479t-d9a1923cd86253b5b704599dd3925a7dfa7ecff7a4d32bd983e9e52b1af4da423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Causes of</topic><topic>Cerebral vasospasm, hyponatremia, subarachnoid hemorrhage</topic><topic>Cerebrovascular spasm</topic><topic>Complications and side effects</topic><topic>Diagnosis</topic><topic>Female</topic><topic>Humans</topic><topic>Hyponatremia</topic><topic>Hyponatremia - blood</topic><topic>Hyponatremia - diagnostic imaging</topic><topic>Hyponatremia - epidemiology</topic><topic>Hyponatremia - etiology</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Retrospective Studies</topic><topic>Sodium - blood</topic><topic>Subarachnoid hemorrhage</topic><topic>Subarachnoid Hemorrhage - blood</topic><topic>Subarachnoid Hemorrhage - complications</topic><topic>Subarachnoid Hemorrhage - diagnostic imaging</topic><topic>Subarachnoid Hemorrhage - epidemiology</topic><topic>Ultrasonography, Doppler, Transcranial - methods</topic><topic>Vasospasm, Intracranial - blood</topic><topic>Vasospasm, Intracranial - diagnostic imaging</topic><topic>Vasospasm, Intracranial - epidemiology</topic><topic>Vasospasm, Intracranial - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</creatorcontrib><collection>Bioline International Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Neurology India</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chandy Dipak, Sy Roger, Aronow Wilbert S, Lee Wei-Nchih, Maguire George, Murali Raj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage</atitle><jtitle>Neurology India</jtitle><addtitle>Neurol India</addtitle><date>2006-07-01</date><risdate>2006</risdate><volume>54</volume><issue>3</issue><spage>273</spage><epage>275</epage><pages>273-275</pages><issn>0028-3886</issn><eissn>1998-4022</eissn><abstract>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.</abstract><cop>India</cop><pub>Medknow Publications on behalf of the Neurological Society of India</pub><pmid>16936387</pmid><doi>10.4103/0028-3886.27151</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; Bioline International Open Access; EZB-FREE-00999 freely available EZB journals |
subjects | Adolescent Adult Aged Aged, 80 and over Causes of Cerebral vasospasm, hyponatremia, subarachnoid hemorrhage Cerebrovascular spasm Complications and side effects Diagnosis Female Humans Hyponatremia Hyponatremia - blood Hyponatremia - diagnostic imaging Hyponatremia - epidemiology Hyponatremia - etiology Logistic Models Male Middle Aged Odds Ratio Retrospective Studies Sodium - blood Subarachnoid hemorrhage Subarachnoid Hemorrhage - blood Subarachnoid Hemorrhage - complications Subarachnoid Hemorrhage - diagnostic imaging Subarachnoid Hemorrhage - epidemiology Ultrasonography, Doppler, Transcranial - methods Vasospasm, Intracranial - blood Vasospasm, Intracranial - diagnostic imaging Vasospasm, Intracranial - epidemiology Vasospasm, Intracranial - etiology |
title | Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage |
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