Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: The Modified Fisher Scale

Frontera, Jennifer A.; Claassen, Jan; Schmidt, J. Michael; Wartenberg, Katja E.; Temes, Richard E.; Connolly, E. Sander; Macdonald, R. Loch; Mayer, Stephan A.

doi:10.1227/01.neu.0000218821.34014.1b

Cited by 617 publications

(418 citation statements)

References 32 publications

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“…The initial neurological findings were evaluated using the Hunt and Hess grading system (H&H), and the patients were divided into two groups (mild: H&H 1-3; poor: H&H 4-5). The amount of subarachnoid hemorrhage was classified using the modified Fisher scale (MFS) (5). DCV was defined as a focal neurological deficit or deterioration of consciousness occurring 3 to 14 days after the onset of SAH, which was either confirmed of infarction on CT scan or could not be explained by other possible causes, such as a surgical procedure, re-bleeding, acute hydrocephalus, intracerebral hemorrhage, infections, seizures or electrolyte disturbances.…”

Section: █ Materials and Methodsmentioning

confidence: 99%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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ABSTRACTcytokines such as interleukin-6 (IL-6) and C-reactive protein (CRP) would increase early after SAH, inflammatory response would have been involved in the course of EBI. So far, most recent studies on inflammatory cytokines in SAH have focused on DCV while fewer studies have focused on EBI and its complications such as pneumonia, which influence the clinical course of aneurysmal SAH. Clinically, a serious initial clinical grade usually indicates a severe EBI after SAH (15), and infection is usually associated with immune dysfunction. █ INTRODUCTION D espite early surgical or endovascular treatment, aneurysmal subarachnoid hemorrhage (SAH) still has a high mortality and morbidity rate. Recently, early brain injury (EBI) was considered as an important determinant factor of outcome except delayed cerebral vasospasm (DCV) after aneurysmal SAH (6,19). The exact mechanism of EBI has still not been clearly demonstrated and the levels of inflammatory AIm: To assess the association between inflammatory response and early brain injury (EBI), and the association between inflammatory response and the following pneumonia after aneurysmal subarachnoid hemorrhage (SAH). mATERIAl and mEThODS: Eighty-nine patients with spontaneous SAH and 12 patients with unruptured aneurysm were included in this prospective study. The systemic inflammatory biomarkers such as C-reactive protein (CRP), IL-1β, IL-2,IL-6,IL-8, IL10 and T leukocyte subsets were measured within 24 hours after admission. Their clinical features and laboratory findings were clearly reviewed and univariate analysis was used to find the main predictors. RESUlTS:The levels of serum inflammatory cytokines especially IL-6 (p=0.004) and CRP (p=0.014) would significantly increase after aneurysm SAH. Higher Fisher grades on admission result in higher levels of IL-6 and IL-10 (pIL-6=0.003. pIL-10=0.002), and higher levels of IL-6, IL-10 and CRP were significantly associated with severe EBI, and increased the susceptibility to pneumonia (p<0.05). The counts of CD3+ T Cells would decrease after aneurysm rupture (p=0.001), especially in patients with a poor initial clinical grade. A reversed correlation between IL-6 level and CD3 T cells count was revealed in this study (p=0.014,r=-0.249); a lower CD4 T-Cells counts might lead to subsequent pneumonia after SAH (p=0.041). The levels of serum inflammatory cytokines were not different between aneurysmal and non-aneurysmal SAH.CONClUSION: Systemic inflammatory response would be activated after aneurysm rupture; a similar systemic inflammatory response would be noticed in non-aneurysmal SAH. The degree of inflammatory response could reflect the severity of EBI, and excessive inflammatory response could also aggravate EBI, induce immunodepression and increase the susceptibility to infections. Inflammatory cytokines such as IL-6, IL-10 and CRP are important predictors.

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Section: █ Materials and Methodsmentioning

confidence: 99%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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“…We have previously defined rebleeding, 8 symptomatic vasospasm, 9 infarction due to vasospasm, 6 and myocardial ischemia. 7 Deep venous thrombosis (DVT) was determined by Doppler ultrasonography.…”

Section: Study Outcomesmentioning

confidence: 99%

Impact of a Protocol for Acute Antifibrinolytic Therapy on Aneurysm Rebleeding After Subarachnoid Hemorrhage

Starke

Kim

Fernandez

et al. 2008

Stroke

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130

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Background and Purpose--Aminocaproic acid (EACA) is an antifibrinolytic agent used to prevent rebleeding in aneurysmal subarachnoid hemorrhage. Although studies have found that a decrease in rebleeding with long-term antifibrinolytic therapy is offset by an increase in ischemic deficits, more recent studies have indicated that early, short-term therapy may be beneficial. Methods-We instituted a protocol for acute EACA administration starting at diagnosis and continued for a maximum duration of 72 hours after subarachnoid hemorrhage onset. We compared 73 patients treated with EACA with 175 non-EACA-treated patients. We sought to identify differences in the occurrence of rebleeding, side effects, and outcome. Results-Baseline characteristics were similar in the 2 groups. There was a significant decrease in rebleeding in EACA-treated patients (2.7%) versus non-EACA patients (11.4%). There was no difference in ischemic complications between cohorts. There was a significant 8-fold increase in deep venous thrombosis in the EACA group but no increase in pulmonary embolism. There was a nonsignificant 76% reduction in mortality attributable to rebleeding, a 13.3% increase in favorable outcome in good-grade EACA-treated patients, and a 6.8% increase in poor-grade patients. Conclusions-When used acutely, short-term EACA treatment resulted in decreased rebleeding without an increase in serious side effects in our selected group of patients. Randomized placebo-controlled trials are needed to determine whether acute antifibrinolytic therapy should be accepted as the standard of care in all patients.

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“…However, further reports indicated that the presence of thick subarachnoid blood is non-essential for the development of cerebral vasospasm. For example, severe vasospasm was observed in patients with minimal hemorrhage in subarachnoid space or in patients with intraventricular hemorrhage while no subarachnoid blood was detected [4]. Vasospasm was also observed following perimesencephalic nonaneurysmal SAH in which only minimal amount of blood appeared in prepontine and interpeduncular cisterns [5].…”

Section: Discussionmentioning

confidence: 99%

Spinal Hemorrhage Leading to Cerebral Vasospasm and Infarction

2012

J Neurol Res

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Only one case of intracranial arterial vasospasm resulting cerebral infarction was previously described in the setting of spinal hemorrhage. The speculation of such symptomatic vasospasm being caused by an intracranial extension of the spinal hemorrhage has been unproven. Here we describe two patients with extensive spinal hemorrhage demonstrated on spinal magnetic resonance imaging (MRI). During their subsequent course, both patients developed cranial signs that included encephalopathy, visual deficit and aphasia. In both cases, small amount of intracranial hemorrhage was detected on head imaging, representing an extension of the spinal hemorrhage. Multiple areas of acute ischemia were seen on brain MRI in both patients. On digital subtraction angiography, diffuse vasospasm of carotid and vertebrobasilar arteries was seen which became normalized prior to discharge. Our report suggests that in treating patients with spinal hemorrhage, physicians need to be aware of possible intracranial hemorrhagic extension and subsequent cerebral vasospasm leading to ischemia. As symptoms of intracranial origin are commonly seen in patients with spinal hemorrhage, the incidence of cerebral vasospasm in this setting could be underestimated.

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Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: The Modified Fisher Scale

Abstract: The modified Fisher scale, which accounts for thick cisternal and ventricular blood, predicts symptomatic vasospasm after subarachnoid hemorrhage more accurately than original Fisher scale.

Cited by 617 publications

References 32 publications

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Impact of a Protocol for Acute Antifibrinolytic Therapy on Aneurysm Rebleeding After Subarachnoid Hemorrhage

Spinal Hemorrhage Leading to Cerebral Vasospasm and Infarction

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