Early Perfusion Computed Tomography Scan for Prediction of Vasospasm and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

2019 ◽  
Vol 130 ◽  
pp. e743-e752
Author(s):  
Daniele Starnoni ◽  
Rodolfo Maduri ◽  
Steven David Hajdu ◽  
Katarzyna Pierzchala ◽  
Lorenzo Giammattei ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Computed Tomography Scan ◽  
Perfusion Computed Tomography ◽  
Tomography Scan

scholarly journals The Relationship Between Delayed Infarcts and Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2013 ◽  
Vol 72 (5) ◽  
pp. 702-708 ◽  
Author(s):  
Robert J. Brown ◽  
Abhay Kumar ◽  
Rajat Dhar ◽  
Tomoko R. Sampson ◽  
Michael N. Diringer
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Infarct Volume ◽  
Delayed Cerebral Ischemia ◽  
Computed Tomography Scan ◽  
Angiographic Vasospasm ◽  
Arterial Vasospasm ◽  
The Relationship ◽  
Tomography Scan

Abstract BACKGROUND: Delayed cerebral ischemia is common after aneurysmal subarachnoid hemorrhage (aSAH) and is a major contributor to poor outcome. Yet, although generally attributed to arterial vasospasm, neurological deterioration may also occur in the absence of vasospasm. OBJECTIVE: To determine the relationship between delayed infarction and angiographic vasospasm and compare the characteristics of infarcts related to vasospasm vs those unrelated. METHODS: A retrospective review of patients with aSAH admitted from July 2007 through June 2011. Patients were included if they were admitted within 48 hours of SAH, had a computed tomography scan both 24 to 48 hours following aneurysm treatment and ≥7 days after SAH, and had a catheter angiogram to evaluate for vasospasm. Delayed infarcts seen on late computed tomography but not postprocedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing. RESULTS: Of 276 aSAH survivors, 134 had all imaging requisite for inclusion. Fifty-four (34%) had moderate or severe vasospasm, of whom 17 (31%) had delayed infarcts, compared with only 3 (4%) of 80 patients without vasospasm (P < .001). There were a total of 29 delayed infarcts in these 20 patients; 21 were in a territory with angiographic vasospasm, but 8 (28%) were not. Infarct volume did not differ between vasospasm-related (18 ± 25 mL) and vasospasm-unrelated (11 ± 12 mL) infarcts (P = .54), but infarcts in the absence of vasospasm were more likely watershed (50% vs 10%, P = .03). CONCLUSION: Delayed infarcts following aSAH can occur in territories without angiographic vasospasm and are more likely watershed in distribution.

scholarly journals Computed tomography grading schemes used to predict cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a historical review

2006 ◽  
Vol 21 (3) ◽  
pp. 1-8 ◽  
Author(s):  
Paul Klimo ◽  
Richard H. Schmidt
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Historical Review ◽  
Science Research ◽  
Computed Tomography Scan ◽  
Major Area ◽  
Volumetric Quantification ◽  
Tomography Scan

✓The elucidation of predictive factors of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major area of both clinical and basic science research. It is becoming clear that many factors contribute to this phenomenon. The most consistent predictor of vasospasm has been the amount of SAH seen on the postictal computed tomography scan. Over the last 30 years, it has become clear that the greater the amount of blood within the basal cisterns, the greater the risk of vasospasm. To evaluate this risk, various grading schemes have been proposed, from simple to elaborate, the most widely known being the Fisher scale. Most recently, volumetric quantification and clearance models have provided the most detailed analysis. Intraventricular hemorrhage, although not supported as strongly as cisternal SAH, has also been shown to be a risk factor for vasospasm.

scholarly journals Diagnostic Threshold Values of Cerebral Perfusion Measured With Computed Tomography for Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2010 ◽  
Vol 41 (9) ◽  
pp. 1927-1932 ◽  
Author(s):  
Jan Willem Dankbaar ◽  
Nicolien Karen de Rooij ◽  
Mienke Rijsdijk ◽  
Birgitta K. Velthuis ◽  
Catharine J.M. Frijns ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Perfusion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Threshold Values ◽  
Diagnostic Threshold

Phase 1/2a Trial of ISPASM

Stroke ◽  
2021 ◽  
Author(s):  
Mario Zanaty ◽  
Lauren Allan ◽  
Edgar A. Samaniego ◽  
Anthony Piscopo ◽  
Eleanor Ryan ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Intravenous Infusion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Controlled Trial ◽  
Phase 1 ◽  
External Ventricular Drain ◽  
Delayed Cerebral Ischemia ◽  
Unique Identifier

Background and Purpose: Microthrombosis could play a role in delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Tirofiban has shown promising results in reducing delayed cerebral ischemia in retrospective studies. However, the safety of using tirofiban in aneurysmal subarachnoid hemorrhage is not rigorously established. Methods: A phase 1/2a double-blinded randomized controlled trial (2:1 randomization) to assess the safety of a 7-day intravenous infusion of tirofiban compared with placebo, in patients with aneurysmal subarachnoid hemorrhage treated with ventriculostomy placed in the operative room and coiling was conducted. The primary end point was any intracranial hemorrhage during the hospital stay. The secondary end points were: incidence of radiographic and clinical vasospasm, incidence of delayed cerebral ischemia, and incidence of cerebral ischemic changes noted on magnetic resonance imaging or computed tomography. Results: Eighteen patients received intravenous tirofiban and 12 received placebo. There was no difference in baseline characteristics except for higher male proportions in the tirofiban group. There was no difference in death, in development of new or change in existing intracranial hemorrhages, in thrombocytopenia, and need for shunts in the two arms. However, the tirofiban arm had a lower incidence of delayed cerebral ischemia compared with placebo (6% [1/18] versus 33% [4/12]; P =0.04), and less radiographic vasospasm as detected by catheter angiogram or computed tomography angiography ( P =0.01) and computed tomography perfusion ( P =0.01). Conclusions: The above preliminary results support proceeding with further testing of the safety and efficacy of 7-day intravenous infusion of tirofiban in a pragmatic (placing external ventricular drain by the bedside), multicenter setting, and using a larger population. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03691727.

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