Hyponatremia as predictor of symptomatic vasospasm in aneurysmal subarachnoid hemorrhage

Abstract OBJECTIVE The development of delayed ischemia caused by cerebral vasospasm remains a common cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage. Preliminary studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may decrease the risk of vasospasm, but additional study is required. METHODS Beginning in May 2006, our treatment protocol for patients presenting with subarachnoid hemorrhage was altered to routinely include the use of 80 mg of simvastatin per day for 14 days. Before this time, only patients with other indications for statins were treated. The charts of 203 consecutive patients over a period of 27 months were retrospectively reviewed, and 150 patients were included in the analysis, of whom 71 patients received statins. These patients were compared with 79 untreated patients to determine whether or not the use of statins was associated with a reduction in the occurrence of vasospasm, delayed infarction, or poor outcome (death, vegetative state, or severe disability). RESULTS Patients who were treated with statins and those who were not had similar baseline characteristics, although more patients in the former group were managed with endovascular coil embolization. There were no statistically significant differences in the proportion of patients developing at least moderate radiographic vasospasm (41% with statins versus 42% without, P = 0.91), symptomatic vasospasm (32% with statins versus 25% without, P = 0.34), delayed infarction (23% with statins versus 28% without, P = 0.46), or poor outcome (39% with statins versus 35% without, P = 0.61). After adjustment for differences in baseline characteristics, including the method of aneurysm treatment, statins were still not significantly protective. CONCLUSION The addition of statins to standard care was not associated with any reduction in the development of vasospasm or improvement in outcomes after aneurysmal subarachnoid hemorrhage. If there is a benefit to statin use, it may be smaller than suggested by previous studies. However, further randomized controlled trials are awaited.

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Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.2002.97.6.1302 ◽

2002 ◽

Vol 97 (6) ◽

pp. 1302-1305 ◽

Cited By ~ 34

Author(s):

Takao Kamezaki ◽

Kiyoyuki Yanaka ◽

Sohji Nagase ◽

Keishi Fujita ◽

Noriyuki Kato ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Lipid Peroxides ◽

Medical Complication ◽

Content Type ◽

Poor Outcome ◽

Symptomatic Vasospasm ◽

Delayed Cerebral Vasospasm ◽

Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

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Intra-Arterial Nimodipine Infusion for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage

Interventional Neuroradiology ◽

10.1177/159101991101700205 ◽

2011 ◽

Vol 17 (2) ◽

pp. 169-178 ◽

Cited By ~ 23

Author(s):

W-S. Cho ◽

H-S. Kang ◽

J.E. Kim ◽

O-K. Kwon ◽

C.W. Oh ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Clinical Outcome ◽

Clinical Response ◽

Clinical Improvement ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Related Complication ◽

Improvement Rate ◽

Deterioration Rate ◽

Symptomatic Vasospasm ◽

Favorable Clinical Outcome

This study evaluated the efficacy of intra-arterial nimodipine infusion for symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). Clinical data collected from 42 consecutive patients with symptomatic vasospasm after aSAH were retrospectively reviewed. Forty-two patients underwent 101 sessions of intra-arterial nimodipine infusion. Angiographic response, immediate clinical response, and clinical outcome were evaluated at discharge and six months later. Angiographic improvement was achieved in 82.2% of patients. The immediate clinical improvement rate was 68.3%, while the deterioration rate was 5.0%. A favorable clinical outcome was achieved in 76.2% at discharge and 84.6% six months. Vasospasm-related infarction occurred in 21.4%. There was no drug-related complication. The nimodipine group showed satisfactory outcomes. Nimodipine can be recommended as an effective and safe intra-arterial agent for the treatment of symptomatic vasospasm after aSAH.

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Prevention of Symptomatic Vasospasm After Aneurysmal Subarachnoid Hemorrhage by Intraoperative Cisternal Fibrinolysis Using Tissue-Type Plasminogen Activator Combined With Continuous Cisternal Drainage

Neurologia medico-chirurgica ◽

10.2176/nmc.44.569 ◽

2004 ◽

Vol 44 (11) ◽

pp. 569-577 ◽

Cited By ~ 22

Author(s):

Hiroyuki KINOUCHI ◽

Kuniaki OGASAWARA ◽

Hiroaki SHIMIZU ◽

Kazuo MIZOI ◽

Takashi YOSHIMOTO

Keyword(s):

Subarachnoid Hemorrhage ◽

Plasminogen Activator ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Tissue Type ◽

Tissue Type Plasminogen Activator ◽

Symptomatic Vasospasm ◽

Type Plasminogen Activator ◽

Cisternal Drainage

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Identification of Early Markers for Symptomatic Vasospasm in Human Cerebral Microdialysate after Subarachnoid Hemorrhage: Preliminary Results of a Proteome-Wide Screening

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/sj.jcbfm.9600466 ◽

2007 ◽

Vol 27 (10) ◽

pp. 1675-1683 ◽

Cited By ~ 28

Author(s):

Martin H Maurer ◽

Daniel Haux ◽

Oliver W Sakowitz ◽

Andreas W Unterberg ◽

Wolfgang Kuschinsky

Keyword(s):

Subarachnoid Hemorrhage ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Expression Profiles ◽

Major Complication ◽

High Risk Group ◽

Individual Risk ◽

Two Dimensional Gel Electrophoresis ◽

Symptomatic Vasospasm ◽

Early Markers ◽

The Individual

A major complication of aneurysmal subarachnoid hemorrhage (SAH) is symptomatic vasospasm, a complex syndrome consisting of neurological deterioration and exclusion of other sources of ischemia. Approximately 30% of SAH patients are affected. Although symptomatic vasospasm is associated with high mortality and poor clinical outcome, it is not possible to identify the individual risk on a molecular level for patients before symptoms have developed. In this study, we hypothesize that protein changes occur in the cerebral microdialysate of patients who later develop symptomatic vasospasm which are not found in matched-pairs control subjects. We searched for changes in protein concentrations in microdialysate sampled from the fronto-temporal brain tissue of five vasospastic and five nonvasospastic SAH patients using proteomics technology based on two-dimensional gel electrophoresis and mass spectrometry. Microdialysate samples were taken at least 1.5 days before the onset of symptomatic vasospasm. Comparing protein expression profiles, we found that the protein concentrations of several isoforms of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were 1.79-fold ± 1.29 ( N = 5, P < 0.05) higher in the group which later developed symptomatic vasospasm, whereas heat—shock cognate 71 kDa protein (HSP7C) isoforms were decreased to 0.50-fold ± 0.19 ( N = 5, P < 0.05; all expression data means ± s.d.). The changes in protein concentrations were detected 3.8 ± 1.7 days ( N = 5, P < 0.05) before symptomatic vasospasm developed. We conclude that GAPDH and HSP7C may be used as early markers indicating the later development of symptomatic vasospasm after SAH, enabling selective early therapeutic intervention in this high-risk group of patients.

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Effect of Transluminal Angioplasty on Cerebral Blood Flow in the Management of Symptomatic Vasospasm Following Aneurysmal Subarachnoid Hemorrhage

Journal of Neuro-Ophthalmology ◽

10.1097/00041327-199712000-00058 ◽

1997 ◽

Vol 17 (4) ◽

pp. 290

Author(s):

A D Firlik ◽

A M Kaufmann ◽

C A Jungreis ◽

H. Yonas

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Subarachnoid Hemorrhage ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Transluminal Angioplasty ◽

Symptomatic Vasospasm

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The Postoperative C-reactive Protein Level can be a Useful Prognostic Factor for Poor Outcome and Symptomatic Vasospasm in Patients With Aneurysmal Subarachnoid Hemorrhage

Journal of Neurosurgical Anesthesiology ◽

10.1097/ana.0b013e31826047a2 ◽

2012 ◽

Vol 24 (4) ◽

pp. 317-324 ◽

Cited By ~ 27

Author(s):

Young-Tae Jeon ◽

Ju-Hyun Lee ◽

Hannnah Lee ◽

Hye-Kyoung Lee ◽

Jung-Won Hwang ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Prognostic Factor ◽

Protein Level ◽

Aneurysmal Subarachnoid Hemorrhage ◽

C Reactive Protein ◽

Reactive Protein ◽

Poor Outcome ◽

Symptomatic Vasospasm

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167 High Throughput Metabolite Profiling Identifies Plasma Anandamide as a Biomarker of Functional Outcome After Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽

10.1093/neuros/nyx417.167 ◽

2017 ◽

Vol 64 (CN_suppl_1) ◽

pp. 242-243

Author(s):

Christopher J Stapleton ◽

Hannah Irvine ◽

Zoe Wolcott ◽

Aman B Patel ◽

Jonathan Rosand ◽

...

Keyword(s):

Logistic Regression ◽

Subarachnoid Hemorrhage ◽

Functional Outcome ◽

High Throughput ◽

Metabolite Profiling ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Plasma Samples ◽

Symptomatic Vasospasm ◽

Good Functional Outcome ◽

Fisher Grade

Abstract INTRODUCTION The quantification of metabolites in plasma samples in patients with aneurysmal subarachnoid hemorrhage (aSAH) can highlight important alterations in critical metabolic pathways. As metabolites reflect changes associated with disease conditions, metabolite profiling (metabolomics) can identify candidate biomarkers for disease and potentially uncover pathways for intervention. METHODS We performed high throughput metabolite profiling across a broad spectrum of chemical classes (173 metabolites) on plasma samples taken from 119 patients with aSAH. Samples were drawn at 3 time points following ictus: 2–4, 7–10, and 12–14 days. Univariate and logistic regression analyses were performed to examine the relation of each metabolite with multiple outcome variables, including short- and long-term functional outcome (modified Rankin Scale, mRS). RESULTS >A good functional outcome (mRS 0–2) was found in 63.1% and 66.7% of patients at 30 and 90 days, respectively, following aSAH. Plasma concentrations of the endogenous cannabinoid anandamide during days 2–4 after aneurysmal SAH were decreased by 48.1% (P < 0.0001) and 57.6% (P <0.0001) in patients with mRS 0–2 at 30 and 90 days, respectively. A similar statistical result was noted with plasma anandamide concentrations averaged across all time periods. Logistic regression further demonstrated that anandamide remained an independent predictor of functional outcome (30 days: P = 0.04; 90 days: P = 0.03), even after adjusting for other factors that influence outcome, including age, World Federation of Neurological Surgeons grade (WFNS), Fisher grade, and symptomatic vasospasm. CONCLUSION Decreased plasma anandamide following aSAH predicts a good functional outcome at 30 and 90 days. While a role for anandamide in aneurysmal SAH has not been previously reported, elevated anandamide levels have been implicated in neuronal apoptosis and cerebral edema in the acutely injured brain. These data highlight the increasing capability of metabolomics techniques in profiling large-sized cohorts to illuminate novel markers of disease and potential metabolic regulators.

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