E-024 Intra-arterial nimodipine injection for the treatment of cerebral vasospasm following aneurysm subarachnoid hemorrhageand the factors associated with delayed cerebral infarction

2017 ◽  
Author(s):  
K Park ◽  
B Kim ◽  
D Park ◽  
N Lee
Keyword(s):  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Factors Associated

Effect of Cilostazol on Cerebral Vasospasm and Outcome in Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized, Double-Blind, Placebo-Controlled Trial

2016 ◽  
Vol 42 (1-2) ◽  
pp. 97-105 ◽  
Author(s):  
Naoya Matsuda ◽  
Masato Naraoka ◽  
Hiroki Ohkuma ◽  
Norihito Shimamura ◽  
Katsuhiro Ito ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Independent Factor ◽  
Double Blind ◽  
End Points ◽  
Double Blind Placebo ◽  
Poor Outcome

Background: Several clinical studies have indicated the efficacy of cilostazol, a selective inhibitor of phosphodiesterase 3, in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). They were not double-blinded trial resulting in disunited results on assessment of end points among the studies. The randomized, double-blind, placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm. Methods: Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study: SAH on CT scan was diffuse thick, diffuse thin, or local thick, Hunt and Hess score was less than 4, administration of cilostazol or placebo could be started within 48 h of SAH. Patients were randomly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling, and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment. The primary end point was the occurrence of symptomatic vasospasm (sVS), and secondary end points were angiographic vasospasm (aVS) evaluated on digital subtraction angiography, vasospasm-related new cerebral infarction evaluated on CT scan or MRI, and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale, in which poor outcome was defined as severe disability, vegetative state, and death. All end points were evaluated with blinded assessment. Results: One hundred forty eight patients were randomly allocated to the cilostazol group (n = 74) or the control group (n = 74). The occurrence of sVS was significantly lower in the cilostazol group than in the control group (10.8 vs. 24.3%, p = 0.031), and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS (OR 0.293, 95% CI 0.099-0.568, p = 0.027). The incidence of aVS and vasospasm-related cerebral infarction were not significantly different between the groups. Poor outcome was significantly lower in the cilostazol group than in the control group (5.4 vs. 17.6%, p = 0.011), and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome (OR 0.221, 95% CI 0.054-0.903, p = 0.035). Severe adverse events due to cilostazol administration did not occur during the study period. Conclusions: Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events. A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol.

scholarly journals Factors associated with undertriage in patients classified by the need to visit a hospital by telephone triage: a retrospective cohort study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ryota Inokuchi ◽  
Xueying Jin ◽  
Masao Iwagami ◽  
Toshikazu Abe ◽  
Masatoshi Ishikawa ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cerebral Infarction ◽  
Clinic Visit ◽  
Telephone Triage ◽  
Hospital Visit ◽  
Over The Counter ◽  
Factors Associated ◽  
Patients With Diabetes ◽  
History Of ◽  
House Call

Abstract Background Prehospital telephone triage stratifies patients into five categories, “need immediate hospital visit by ambulance,” “need to visit a hospital within 1 hour,” “need to visit a hospital within 6 hours,” “need to visit a hospital within 24 hours,” and “do not need a hospital visit” in Japan. However, studies on whether present and past histories cause undertriage are limited in patients triaged as need an early hospital visit. We investigated factors associated with undertriage by comparing patient assessed to be appropriately triaged with those assessed undertriaged. Methods We included all patients classified by telephone triage as need to visit a hospital within 1 h and 6 h who used a single after-hours house call (AHHC) medical service in Tokyo, Japan, between November 1, 2019, and November 31, 2020. After home consultation, AHHC doctors classified patients as grade 1 (treatable with over-the-counter medications), 2 (requires hospital or clinic visit), or 3 (requires ambulance transportation). Patients classified as grade 2 and 3 were defined as appropriately triaged and undertriaged, respectively. Results We identified 10,742 eligible patients triaged as need to visit a hospital within 1 h and 6 h, including 10,479 (97.6%) appropriately triaged and 263 (2.4%) undertriaged patients. Multivariable logistic regression analyses revealed patients aged 16–64, 65–74, and ≥ 75 years (adjusted odds ratio [OR], 2.40 [95% confidence interval {CI} 1.71–3.36], 8.57 [95% CI 4.83–15.2], and 14.9 [95% CI 9.65–23.0], respectively; reference patients aged < 15 years); those with diabetes mellitus (2.31 [95% CI 1.25–4.26]); those with dementia (2.32 [95% CI 1.05–5.10]); and those with a history of cerebral infarction (1.98 [95% CI 1.01–3.87]) as more likely to be undertriaged. Conclusions We found that older adults and patients with diabetes mellitus, dementia, or a history of cerebral infarction were at risk of undertriage in patients triaged as need to visit a hospital within 1 h and 6 h, but further studies are needed to validate these findings.

Twelve-year single critical care center experience of nicardipine prolonged-release implants in patients with subarachnoid hemorrhage: a propensity score matching analysis

2020 ◽  
Vol 12 (8) ◽  
pp. 774-776 ◽  
Author(s):  
Yasuhiro Kuroi ◽  
Hidenori Ohbuchi ◽  
Naoyuki Arai ◽  
Yuichi Takahashi ◽  
Shinji Hagiwara ◽  
...  
Keyword(s):  
Critical Care ◽  
Subarachnoid Hemorrhage ◽  
Side Effects ◽  
Propensity Score ◽  
Cerebral Infarction ◽  
Propensity Score Matching ◽  
Cerebral Vasospasm ◽  
Care Center ◽  
Prolonged Release ◽  
Significant Difference

ObjectiveTo develop a nicardipine prolonged-release implant (NPRI) to prevent cerebral vasospasm in patients with subarachnoid hemorrhage in 1999, which may be used during craniotomy, and report the results of our recent 12-year single critical care center experience.MethodsOf 432 patients with aneurysmal subarachnoid hemorrhage treated between 2007 and 2019, 291 were enrolled. 97 Patients were aged >70 years (33%), 194 were female (67%), 138 were World Federation of Neurological Societies grades 1, 2, and 3 (47%), 218 were Fisher group 3 (75%), and 243 had an anterior circulation aneurysm (84%). Using a propensity score matching method for these five factors, the severity of cerebral vasospasm, occurrence of delayed cerebral infarction, and modified Rankin Scale (mRS) score at discharge were analyzed.ResultsOne hundred patients each with or without NPRI were selected, and the ratios of coil/clip were 0/100 and 88/12, respectively. Cerebral vasospasm and delayed cerebral infarction were both significantly less common in the NPRI group (p=0.004, OR=0.412 (95% CI 0.223 to 0.760) and p=0.005, OR=0.272 (95% CI 0.103 to 0.714, respectively); a significant difference was seen in the mRS score at discharge by Fisher’s exact test (p=0.0025). A mRS score of 6 (dead) was less common in the group with NPRI, and mRS scores of 0 and 1 were also less common. No side effects were seen.ConclusionsNPRIs significantly reduced the occurrence of cerebral vasospasm and delayed cerebral infraction without any side effects. The NPRI and non-NPRI groups showed different patterns of short-term outcomes in the single critical care center, which might have been due to selection bias and patient characteristics. Differences in outcomes may become clear in comparisons with patients treated by craniotomy.

scholarly journals Distal Balloon Angioplasty of Cerebral Vasospasm Decreases the Risk of Delayed Cerebral Infarction

2019 ◽  
Vol 40 (8) ◽  
pp. 1342-1348
Author(s):  
M.-A. Labeyrie ◽  
S. Gaugain ◽  
G. Boulouis ◽  
A. Zetchi ◽  
J. Brami ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Balloon Angioplasty

Abstract TP447: Tenascin-C: A Novel Therapeutic Target in Subarachnoid Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Masato Shiba ◽  
Masashi Fujimoto ◽  
Naoki Toma ◽  
Yoichi Miura ◽  
Fumihiro Kawakita ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Blood Brain Barrier ◽  
Cerebral Vasospasm ◽  
Neuronal Apoptosis ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Brain Barrier Disruption ◽  
Dose Dependent ◽  
Novel Therapeutic

Introduction: Tenascin-C (TNC) is one of pleiotropic matricellular proteins, which are non-structural and secreted extracellular matrix proteins that exert diverse functions. Recently we showed that TNC is involved in the mechanisms of cerebral vasospasm and early brain injury (EBI) after subarachnoid hemorrhage (SAH). However, the role of TNC has not been sufficiently investigated in SAH. Materials and Methods: First, TNC knockout (TNKO) mice SAH models were produced by endovascular perforation method, and examined the direct evidence that TNC is induced after SAH and causes cerebral vasospasm and EBI. Second, TNC was measured in serum from 156 aneurysmal SAH patients, and cilostazol (0-300 mg/day) was administered postoperatively, and investigated as to the dose-dependent effect of cilostazol on cerebral vasospasm, delayed cerebral ischemia and infarction. Results: In experimental SAH, TNKO prevented blood-brain barrier disruption and brain edema formation by inhibiting mitogen-activated protein kinase (MAPK)-mediated matrix metalloproteinase-9 activation. TNKO also suppressed post-SAH induction of another matricellular protein, periostin, which aggravates post-SAH EBI. TNKO also prevented neuroinflammation and neuronal apoptosis via inhibiting upregulation of Toll-like receptor 4, phosphorylation of nuclear factor-κB, and induction of proinflammatory cytokines in neurons. TNKO suppressed post-SAH cerebral vasospasm via inhibiting the activation of MAPKs. In the clinical study, cilostazol treatment suppressed plasma TNC levels from days 1-3 to days 10-12 post-SAH, and showed dose-dependent effects against delayed cerebral infarction, leading to improved outcome. Multivariate analyses revealed that 300 mg/day cilostazol treatment was an independent determinant against poor outcomes post-SAH. Conclusions: TNKO exerted protective effects against neuroinflammation, blood-brain barrier disruption, neuronal apoptosis, and cerebral vasospasm. The 300 mg/day cilostazol may improve post-SAH outcomes by reducing plasma TNC levels and delayed cerebral infarction. Further investigations may provide a novel therapeutic approach targeting TNC.

Risk factors associated with acute/subacute cerebral infarction in HIV-negative patients with cryptococcal meningitis

2016 ◽  
Vol 364 ◽  
pp. 19-23 ◽  
Author(s):  
Yan-Fang Chen ◽  
Dan-Ni Wang ◽  
Zhi-Ting Chen ◽  
Zhen-Hua Zhao ◽  
Yu Lin ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cerebral Infarction ◽  
Cryptococcal Meningitis ◽  
Factors Associated ◽  
Hiv Negative

scholarly journals Update on endovascular therapies for cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage

2006 ◽  
Vol 21 (3) ◽  
pp. 1-11 ◽  
Author(s):  
Christina M. Sayama ◽  
James K. Liu ◽  
William T. Couldwell
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Mechanism Of Action ◽  
Clinical Effect ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Calcium Channel Antagonists ◽  
Induced Hypertension

✓Cerebral vasospasm remains a major source of morbidity and death in patients with aneurysmal subarachnoid hemorrhage (SAH). When vasospasm becomes refractory to maximal medical management consisting of induced hypertension and hypervolemia and administration of calcium channel antagonists, endovascular therapies should be considered. The primary goal of endovascular treatment is to increase cerebral blood flow to prevent cerebral infarction. Two of the more frequently studied endovascular treatments are transluminal balloon angioplasty and intraarterial papaverine infusion. These two have been used either alone or in combination for the treatment of vasospasm. Other pharmacological vasodilating agents currently being investigated are intraarterial nimodipine, nicardipine, verapamil, and milrinone. Newer intraarterial agents, such as fasudil and colforsin daropate, have also been investigated. In this article the authors review the current options in terms of endovascular therapies for treatment of cerebral vasospasm. The mechanism of action, technique of administration, clinical effect and outcomes, and complications of each modality are discussed.

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