Prediction of Cerebral Vasospasm in Patients Presenting with Aneurysmal Subarachnoid Hemorrhage: A Review

Harrod, Christopher G.; Bendok, Bernard R.; Batjer, H. Hunt

doi:10.1227/01.neu.0000156644.45384.92

Cited by 210 publications

(142 citation statements)

References 168 publications

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“…A comprehensive review of the literature by Harrod et al from 1996Harrod et al from to 2005 showed that the only factor that has shown to be predictive of cerebral vasospasm is the burden of blood at the time of SAH. 3 A previous study from our center corroborates this finding and stratifies the maximum clot burden into 5 categories.…”

Section: Discussionsupporting

confidence: 84%

“…3,5,10 Identifying patients at the greatest risk for cerebral vasospasm is an important prognosticator in the setting of SAH and may identify patients who will likely need hypertensive therapy, or potential endovascular treatment of vasospasm, or both. A comprehensive review of the literature by Harrod et al from 1996Harrod et al from to 2005 showed that the only factor that has shown to be predictive of cerebral vasospasm is the burden of blood at the time of SAH.…”

Section: Discussionmentioning

confidence: 99%

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The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Abla

Wilson

Williamson

et al. 2014

JNS

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Object Cerebral vasospasm following subarachnoid hemorrhage (SAH) causes significant morbidity in a delayed fashion. The authors recently published a new scale that grades the maximum thickness of SAH on axial CT and is predictive of vasospasm incidence. In this study, the authors further investigate whether different aneurysm locations result in different SAH clot burdens and whether any concurrent differences in ruptured aneurysm location and maximum SAH clot burden affect vasospasm incidence. Methods Two hundred fifty patients who were part of a prospective randomized controlled trial were reviewed. Most outcome and demographic variables were included as part of the prospective randomized controlled trial. Additional variables were also collected at a later time, including vasospasm data and maximum clot thickness. Results Aneurysms were categorized into 1 of 6 groups: intradural internal carotid artery aneurysms, vertebral artery (VA) aneurysms (including the posterior inferior cerebellar artery), basilar trunk or basilar apex aneurysms, middle cerebral artery aneurysms, pericallosal aneurysms, and anterior communicating artery aneurysms. Twenty-nine patients with nonaneurysmal SAH were excluded. Patients with pericallosal aneurysms had the least average maximum clot burden (5.3 mm), compared with 6.4 mm for the group overall, but had the highest rate of symptomatic vasospasm (56% vs 22% overall, OR 4.9, RR 2.7, p = 0.026). Symptomatic vasospasm occurrence was tallied in patients with clinical deterioration attributable to delayed cerebral ischemia. There were no significant differences in maximum clot thickness between aneurysm sites. Middle cerebral artery aneurysms resulted in the thickest mean maximum clot (7.1 mm) but rates of symptomatic and radiographic vasospasm in this group were statistically no different compared with the overall group. Vertebral artery aneurysms had the worst 1-year modified Rankin scale (mRS) scores (3.0 vs 1.9 overall, respectively; p = 0.0249). A 1-year mRS score of 0–2 (good outcome) was found in 72% of patients overall, but in only 50% of those with pericallosal and VA aneurysms, and in 56% of those with basilar artery aneurysms (p = 0.0044). Patients with stroke from vasospasm had higher mean clot thickness (9.71 vs 6.15 mm, p = 0.004). Conclusions The location of a ruptured aneurysm minimally affects the maximum thickness of the SAH clot but is predictive of symptomatic vasospasm or clinical deterioration from delayed cerebral ischemia in pericallosal aneurysms. The worst 1-year mRS outcomes in this cohort of patients were noted in those with posterior circulation aneurysms or pericallosal artery aneurysms. Patients experiencing stroke had higher mean clot burden.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Abla

Wilson

Williamson

et al. 2014

JNS

View full text Add to dashboard Cite

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“…Examples of compounds in the first class would be hemoglobin (Hb)and BOXes, and examples in the second class of compounds would be endothelin or nitric oxide (Figure 2), which could be directly or indirectly induced by the BOXes. The rationale that blood itself or some metabolite of components of blood cause vasospasm is compelling since this helps explain why vasospasm tends to occur where large blood clots occur around vessels at the base of the brain (Harrod et al, 2005;Kistler et al, 1983).…”

Section: Two Classes Of Compounds That Could Cause Vasospasmmentioning

confidence: 99%

BilirubinOxidation Products (BOXes) and Their Role in Cerebral Vasospasm after Subarachnoid Hemorrhage

Clark

Sharp

2006

J Cereb Blood Flow Metab

113

110

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Many factors have been postulated to cause delayed subarachnoid hemorrhage (SAH)-induced vasospasm, including hemoglobin, nitric oxide, endothelin, and free radicals. We propose that free radicals (because of the high levels that are produced in the blood clots surrounding blood vessels after SAH) act on bilirubin, biliverdin, and possibly heme to produce BOXes (Bilirubin OXidized Products). Bilirubin oxidation products act on vascular smooth muscle cells to produce chronic vasoconstriction and vasospasm combined with a vasculopathy because of smooth muscle cell injury. This review summarizes recent evidence that BOXes play a role in SAH-induced vasospasm. The data supporting a role for BOXes includes (1) identification of molecules in cerebrospinal fluid (CSF) of patients with vasospasm after SAH that have structures consistent with BOXes; (2) BOXes are vasoactive in vitro and mimic the biochemical actions of CSF of patients with vasospasm; (3) BOXes are vasoactive in vivo, constricting rat cerebral vessels; and (4) there is a correlation between clinical occurrence of vasospasm and BOXes concentration in our preliminary study of patients with SAH. Since oxidation of bilirubin, biliverdin, and perhaps heme is proposed to produce BOXes that contribute to vasospasm, either blocking bilirubin formation, inactivating bilirubin or BOXes, or removing all of the blood clot before vasospasm are potential treatment targets.

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“…In all, 25% of patients die almost immediately after hemorrhage due to arrest of the cerebral circulation caused by acute intracranial hypertension as a consequence of the evolving hematoma (Pobereskin, 2001). Out of the remaining 75% of SAH victims, 15% die with a significant delay of several days (due to delayed cerebral ischemia or cardiopulmonary reasons); however, the remaining 60% of patients die within 48 h of the initial bleeding (Weir et al, 1978;Harrod et al, 2005) due to rebleedings (25%) or a sequence of events summarized by the term ''Early Brain Injury'' (EBI; 35%) (Pobereskin, 2001). While rebleedings can be prevented by surgical or endovascular procedures and, after years of research, new therapeutic options are emerging for the intriguing phenomenon of delayed cerebral ischemia, no treatment is available for EBI and its underlying mechanisms have only recently started to be understood (Cahill and Zhang, 2009;Pluta et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Friedrich

Müller

Feiler

et al. 2011

J Cereb Blood Flow Metab

191

196

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Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation. Pial arterioles and venules (10 to 80 lm diameter) were examined using in-vivo fluorescence microscopy, 3, 6, and 72 hours after SAH. Venular diameter or flow was not affected by SAH, while > 70% of arterioles constricted by 22% to 33% up to 3 days after hemorrhage (P < 0.05 versus sham). The smaller the investigated arterioles, the more pronounced the constriction (r 2 = 0.92, P < 0.04). Approximately 30% of constricted arterioles were occluded by microthrombi and the frequency of arteriolar microthrombosis correlated with the degree of constriction (r 2 = 0.93, P < 0.03). The current study demonstrates that SAH induces microarterial constrictions and microthrombosis in vivo. These findings may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits after SAH.

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Prediction of Cerebral Vasospasm in Patients Presenting with Aneurysmal Subarachnoid Hemorrhage: A Review

Cited by 210 publications

References 168 publications

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

BilirubinOxidation Products (BOXes) and Their Role in Cerebral Vasospasm after Subarachnoid Hemorrhage

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

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