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The relationship between subarachnoid hemorrhage volume and development of cerebral vasospasm.
Journal of Cerebrovascular and Endovascular Neurosurgery 2012 September
OBJECTIVE: The objective of this study is to verify the relationship between subarachnoid hemorrhage (SAH) volume (not Fisher grade) and development of cerebral vasospasm prospectively.
METHODS: Patients who visited our hospital with a diffuse or localized thick subarachnoid blood clot seen on computed tomography (CT), taken within 48 hours after SAH and the aneurysm was confirmed by CT Angiogram (CTA) from March 2010 to July 2011 were enrolled in this study. CTA was checked at least twice after admission. Angiographic vasospasm (AVS) on CTA was defined as irregularity or narrowing of intracranial vessels on follow up CTA compared with initial CTA. Total intracranial hemorrhage (ICH) volume (subdural, SAH, intracerebral and intraventricular) was calculated and SAH volume (all supratentorial and infratentorial cisterns) was also calculated using the MIPAV software package.
RESULTS: A total of 55 patients were included in our study. Thirty six patients did not show AVS on CTA or clinical deterioration (non vasospasm group: NVS). AVS without ischemic neurologic symptoms was observed in four patients and development of symptomatic vasospasm (SVS), defined as AVS with ischemic symptoms, was observed in 15 patients. SAH volume in SVS patients was statistically larger than that in NVS patients (p < 0.05). Total ICH volume in SVS patients was larger than that in NVS patients. However, the difference was not statistically significant.
CONCLUSION: Results of this study indicate an association of development of vasospasm with the SAH volume, not intracranial hemorrhage.
METHODS: Patients who visited our hospital with a diffuse or localized thick subarachnoid blood clot seen on computed tomography (CT), taken within 48 hours after SAH and the aneurysm was confirmed by CT Angiogram (CTA) from March 2010 to July 2011 were enrolled in this study. CTA was checked at least twice after admission. Angiographic vasospasm (AVS) on CTA was defined as irregularity or narrowing of intracranial vessels on follow up CTA compared with initial CTA. Total intracranial hemorrhage (ICH) volume (subdural, SAH, intracerebral and intraventricular) was calculated and SAH volume (all supratentorial and infratentorial cisterns) was also calculated using the MIPAV software package.
RESULTS: A total of 55 patients were included in our study. Thirty six patients did not show AVS on CTA or clinical deterioration (non vasospasm group: NVS). AVS without ischemic neurologic symptoms was observed in four patients and development of symptomatic vasospasm (SVS), defined as AVS with ischemic symptoms, was observed in 15 patients. SAH volume in SVS patients was statistically larger than that in NVS patients (p < 0.05). Total ICH volume in SVS patients was larger than that in NVS patients. However, the difference was not statistically significant.
CONCLUSION: Results of this study indicate an association of development of vasospasm with the SAH volume, not intracranial hemorrhage.
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