Endovascular Rescue Therapies for Refractory Vasospasm After Subarachnoid Hemorrhage: A Prospective Evaluation Study Using Multimodal, Continuous Event Neuromonitoring

Neurosurgery ◽  
2017 ◽  
Vol 80 (6) ◽  
pp. 942-949 ◽  
Author(s):  
Walid Albanna ◽  
Miriam Weiss ◽  
Marguerite Müller ◽  
Marc Alexander Brockmann ◽  
Annette Rieg ◽  
...  

Abstract BACKGROUND: Critical hypoperfusion and metabolic derangement are frequently encountered with refractory vasospasm. Endovascular rescue therapies (ERT) have proven beneficial in selected cases. However, angioplasty (AP) and intraarterial lysis (IAL) are measures of last resort and prospective, quantitative results regarding the efficacy (cerebral oxygenation, metabolism) are largely lacking. OBJECTIVE: To evaluate the efficacy of ERTs for medically refractory vasospasm using multimodal, continuous event neuromonitoring. METHODS: To detect cerebral compromise in a timely fashion, sedated patients with aneurysmal subarachnoid hemorrhage received continuous neuromonitoring (ptiO2 measurement, intraparenchymal microdialysis). ERT (AP and/or IAL) was considered in cases of clinically relevant vasospasm refractory to conservative treatment measures. Oxygen saturation and cerebral and systemic metabolism before and after events of ERT was recorded. RESULTS: We prospectively included 13 consecutive patients and recorded a total of 25 ERT events: AP (n = 10), IAL (n = 11), or both (AP + IAL, n = 4). Average cerebral ptiO2 was 10 ± 11 torr before and 49 ± 22 torr after ERT (P < .001), with a lactate-pyruvate ratio decreasing from 146.6 ± 119.0 to 27.9 ± 10.7 after ERT (P < .001). Comparable improvement was observed for each type of intervention (AP, IAL, or both). No significant alterations in systemic metabolism could be detected after ERT CONCLUSION: Multimodal event neuromonitoring is able to quantify treatment efficacy in subarachnoid hemorrhage-related vasospasm. In our small cohort of highly selected cases, ERT was associated with improvement in cerebral oxygenation and metabolism with reasonable outcome. Event neuromonitoring may facilitate individual and timely optimization of treatment modality according to the individual clinical course.

2007 ◽  
Vol 27 (10) ◽  
pp. 1675-1683 ◽  
Author(s):  
Martin H Maurer ◽  
Daniel Haux ◽  
Oliver W Sakowitz ◽  
Andreas W Unterberg ◽  
Wolfgang Kuschinsky

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.


2013 ◽  
Vol 33 (12) ◽  
pp. 1825-1837 ◽  
Author(s):  
Leif Østergaard ◽  
Rasmus Aamand ◽  
Sanja Karabegovic ◽  
Anna Tietze ◽  
Jakob Udby Blicher ◽  
...  

The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI may develop in the absence of angiographic vasospasms, and therapeutic reversal of angiographic vasospasms fails to improve patient outcome. The etiology of chronic neurodegenerative changes after SAH remains poorly understood. Brain oxygenation depends on both cerebral blood flow (CBF) and its microscopic distribution, the so-called capillary transit time heterogeneity (CTH). In theory, increased CTH can therefore lead to tissue hypoxia in the absence of severe CBF reductions, whereas reductions in CBF, paradoxically, improve brain oxygenation if CTH is critically elevated. We review potential sources of elevated CTH after SAH. Pericyte constrictions in relation to the initial ischemic episode and subsequent oxidative stress, nitric oxide depletion during the pericapillary clearance of oxyhemoglobin, vasogenic edema, leukocytosis, and astrocytic endfeet swelling are identified as potential sources of elevated CTH, and hence of metabolic derangement, after SAH. Irreversible changes in capillary morphology and function are predicted to contribute to long-term relative tissue hypoxia, inflammation, and neurodegeneration. We discuss diagnostic and therapeutic implications of these predictions.


2009 ◽  
Vol 111 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Nir Lipsman ◽  
Jocelyn Tolentino ◽  
R. Loch Macdonald

Object Prognostic factors for outcome after aneurysmal subarachnoid hemorrhage (SAH) include the clinical and pathological characteristics of the patient and hemorrhage as well as some aspects of treatment. Because treatment can vary between countries and continents, the authors used a large database of patients with SAH to determine the effect of the geographic location of treatment on outcome. Methods Data obtained in 3567 patients who were entered into randomized trials of tirilazad between 1991 and 1997 were analyzed. Patients underwent treatment in 162 neurosurgical centers in 21 countries in North America, Europe, Africa, and Australia. The dependent variable was clinical outcome assessed 3 months after SAH with the Glasgow Outcome Scale, which was analyzed as a 5-point variable and dichotomized into favorable (good recovery or moderate disability) and unfavorable (severe disability, vegetative state, or death) outcomes. The effect of country or continent of treatment on outcome was assessed using univariate and multivariate logistic regression and proportional odds modeling before and after adjusting for numerous other factors significantly associated with outcome. Results The authors constructed several multivariate analysis models and demonstrated that for almost every model, country was not a significant predictor of outcome (p > 0.05). There was variation in outcome between countries, but this was mostly due to differences in other admission characteristics that influence outcome such as age, clinical grade, and subarachnoid clot thickness. Because the number of patients entered from some countries was small, countries were grouped, and the data were analyzed by continent. This grouping gave more stable estimates and created an appropriate model for both logistic and proportional odds models and again showed that continent had no significant effect on outcome. Conclusions Despite the variations in treatment that undoubtedly exist between countries and continents, the location of treatment had minimal effect on outcome. Outcome was influenced mostly by clinical characteristics on admission such as neurological grade, patient age, and amount of SAH.


1993 ◽  
Vol 79 (4) ◽  
pp. 490-493 ◽  
Author(s):  
Yves Roger Tran Dinh ◽  
Guillaume Lot ◽  
Rabah Benrabah ◽  
Oussama Baroudy ◽  
Jean Cophignon ◽  
...  

✓ A patient with cerebral vasospasm following subarachnoid hemorrhage (SAH) was investigated by serial measurement of cerebral blood flow (CBF) using the xenon-133 emission tomography method. The CBF was measured before and after acetazolamide injection. On Day 2 after SAH, there was early local hyperperfusion in the middle cerebral artery (MCA) territory, ipsilateral to the left posterior communicating artery aneurysm. The regional CBF of this arterial territory decreased slightly after acetazolamide injection, probably because of vasoplegia and the “steal” phenomenon, and thus surgery was delayed. A right hemiplegia with aphasia and disturbed consciousness occurred 4 days later (on Day 6 after SAH) due to arterial vasospasm, despite treatment with a calcium-channel blocker. The initial hyperemia of the left MCA territory was followed by ischemia. The vasodilation induced by acetazolamide administration was significantly subnormal until Day 13, at which time CBF and vasoreactivity amplitude returned to normal and the patient's clinical condition improved. Surgery on Day 14 and outcome were without complication. It is concluded that serial CBF measurements plus acetazolamide injection are useful for monitoring the development of cerebral vasospasm to determine the most appropriate time for aneurysm surgery.


2021 ◽  
pp. neurintsurg-2021-017859
Author(s):  
Rishi Gupta ◽  
Keith Woodward ◽  
David Fiorella ◽  
Henry H Woo ◽  
David Liebeskind ◽  
...  

BackgroundCerebral vasospasm (CV) after aneurysmal subarachnoid hemorrhage (aSAH) is linked to worse neurological outcomes. The NeVa VS is a novel cerebral dilation device based on predicate stent retrievers. We report the results of the Vesalio NeVa VS for the Treatment of Symptomatic Cerebral Vasospasm following aSAH (VITAL) Study.MethodsThis was a single-arm prospective multicenter trial to assess the safety and probable benefit of the NeVa VS device to treat CV. Patients were screened and treated if they had CV >50% on non-invasive imaging confirmed by cerebral angiography. The vessel diameters were measured before and after treatment by an independent core laboratory. The primary endpoint was ≥50% vessel diameter immediately after treatment with the NeVa VS device.ResultsThirty patients with a mean age of 52±11 years and mean Hunt–Hess grade of 3.1±0.9 were enrolled. A total of 74 vessels were treated with an average of 1.3 deployments per vessel (95 deployments total). The mean pre-treatment narrowing of the target vessel (n=74) was 65.6% with reduction of the narrowing to 29.4% after treatment. The primary endpoint was achieved in 64 of 74 vessels (86.5%). In three of 95 total deployments (3.2%), thrombus at the site of deployment was observed during the procedure without apparent neurological sequelae.ConclusionsThe NeVa VS device appears to be a safe treatment to regain vessel diameter in severely narrowed intracranial arteries secondary to CV associated with aSAH. This treatment offers a new tool that allows for controlled vessel expansion to treat CV.


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