scholarly journals Effect of early mobilization and rehabilitation on complications in aneurysmal subarachnoid hemorrhage

2017 ◽  
Vol 126 (2) ◽  
pp. 518-526 ◽  
Author(s):  
Tanja Karic ◽  
Cecilie Røe ◽  
Tonje Haug Nordenmark ◽  
Frank Becker ◽  
Wilhelm Sorteberg ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Standard Treatment ◽  
Treatment Guidelines ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Early Rehabilitation ◽  
Control Group ◽  
Chronic Hydrocephalus ◽  
Clinical Trial Registration ◽  
Aneurysm Repair

OBJECTIVE Early rehabilitation is effective in an array of acute neurological disorders but it is not established as part of treatment guidelines after aneurysmal subarachnoid hemorrhage (aSAH). This may in part be due to the fear of aggravating the development of cerebral vasospasm, which is the most feared complication of aSAH. The aim of this study was to evaluate the effect of early rehabilitation and mobilization on complications during the acute phase and within 90 days after aSAH. METHODS This was a prospective, interventional study that included patients with aSAH at the neuro-intermediate ward after aneurysm repair. The control group received standard treatment, whereas the early rehab group underwent early rehabilitation and mobilization in addition to standard treatment. Clinical and radiological characteristics of patients with aSAH, progression in mobilization, and treatment variables were registered. The frequency and severity of cerebral vasospasm, cerebral infarction acquired in conjunction with the aSAH, and acute and chronic hydrocephalus, as well as pulmonary and thromboembolic complications, were compared between the 2 groups. RESULTS Clinical and radiological characteristics of patients with aSAH were similar between the groups. The early rehab group was mobilized beginning on the first day after aneurysm repair. The significantly quicker and higher degree of mobilization in the early rehab group did not increase complications. Clinical cerebral vasospasm was not as frequent in the early rehab group and it also tended to be less severe. Each step of mobilization achieved during the first 4 days after aneurysm repair reduced the risk of severe vasospasm by 30%. Acute and chronic hydrocephalus were similar in both groups, but there was a tendency toward earlier shunt implantation among patients in the control group. Pulmonary infections, thromboembolic events, and death before discharge or within 90 days after the ictus were similar between the 2 groups. CONCLUSIONS Early rehabilitation of patients after aSAH is safe and feasible. The earlier and higher degree of mobilization does not increase neurosurgical complications. Rather, the frequency and severity of cerebral vasospasm following aSAH are alleviated and are not aggravated by early rehabilitation. Clinical trial registration no.: NCT01656317 (www.clinicaltrials.gov).

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.

THE IMPACT OF MICROSURGICAL FENESTRATION OF THE LAMINA TERMINALIS ON SHUNT-DEPENDENT HYDROCEPHALUS AND VASOSPASM AFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE

Neurosurgery ◽  
2008 ◽  
Vol 62 (1) ◽  
pp. 123-134 ◽  
Author(s):  
Ricardo J. Komotar ◽  
David K. Hahn ◽  
Grace H. Kim ◽  
Joyce Khandji ◽  
J Mocco ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Conversion Rate ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lamina Terminalis ◽  
Chronic Hydrocephalus ◽  
Microsurgical Fenestration ◽  
Postsurgical Outcomes ◽  
Rate Conversion ◽  
The Impact

Abstract OBJECTIVE Chronic hydrocephalus requiring shunt placement and cerebral vasospasm are common complications after aneurysmal subarachnoid hemorrhage. Recent publications have investigated the possibility that microsurgical fenestration of the lamina terminalis during aneurysm surgery may reduce the incidence of shunt-dependent hydrocephalus and cerebral vasospasm. We reviewed a single-surgeon series to compare postsurgical outcomes of patients who underwent fenestration of the lamina terminalis against those who did not. METHODS This study is a retrospective review of the medical records of 369 consecutive patients with aneurysmal subarachnoid hemorrhage admitted to Columbia University Medical Center between January 2000 and July 2006. All patients underwent craniotomy and clipping of at least one ruptured cerebral aneurysm by a single neurosurgeon (ESC). The incidences of shunt-dependent hydrocephalus, conversion from acute hydrocephalus on admission to chronic hydrocephalus, and clinical cerebral vasospasm were compared in patients who underwent fenestration of the lamina terminalis with those who did not. The patient cohort was thus divided into three subgroups: 1) patients whose operative records clearly indicated that they underwent fenestration of the lamina terminalis, 2) patients whose operative records clearly indicated that they did not undergo fenestration of the lamina terminalis, and 3) patients whose operative records did not indicate one way or another whether they received fenestration of the lamina terminalis. We performed two separate analyses by comparing the postsurgical outcomes in those patients who were fenestrated versus those who were definitively not fenestrated and comparing the postsurgical outcomes in those patients who were fenestrated versus those who were not plus those whose records did not document fenestration. To further control for any cohort differences, we performed a comparison between patients who were fenestrated and those who were not after matching 1:1 for presenting radiographic and clinical characteristics predictive of hydrocephalus and vasospasm. Outcomes were compared using logistic regression and multivariable analysis. RESULTS In the first model, fenestrated patients had a shunt rate, conversion rate, and rate of clinical vasospasm of 25, 50, and 23%, respectively, versus 20, 27, and 27% in nonfenestrated patients, respectively (P = 0.28, 0.21, and 0.32, respectively). In the second model, the nonfenestrated patients plus nondocumented patients had a shunt rate, conversion rate, and rate of clinical vasospasm of 16, 40, and 20%, respectively (P = 0.19, 0.33, and 0.60, respectively). In the matched cohort, fenestrated patients had a shunt rate, conversion rate, and rate of clinical vasospasm of 29, 67, and 20%, respectively, versus 20, 25, and 25% in nonfenestrated patients, respectively (P = 0.30, 0.24, and 0.20, respectively). CONCLUSION In contrast to other retrospective multisurgeon series, our retrospective single-surgeon series suggests that microsurgical fenestration of the lamina terminalis may not reduce the incidence of shunt-dependent hydrocephalus or cerebral vasospasm after aneurysmal subarachnoid hemorrhage. A prospective multicenter trial is needed to definitively address the use of this maneuver.

Association of an endogenous inhibitor of nitric oxide synthase with cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

2007 ◽  
Vol 107 (5) ◽  
pp. 945-950 ◽  
Author(s):  
Carla S. Jung ◽  
Edward H. Oldfield ◽  
Judith Harvey-White ◽  
Michael G. Espey ◽  
Michael Zimmermann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Type I ◽  
Endogenous Inhibitor ◽  
Primate Model ◽  
Delayed Cerebral Vasospasm

Object Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) may be evoked by the decreased availability of nitric oxide (NO). Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl-l-arginine (ADMA), an endogenous inhibitor of NO synthase (NOS), have been associated with the course and degree of cerebral vasospasm in a primate model of SAH. In this study, the authors sought to determine if similar changes in CSF ADMA levels are observed in patients with SAH, and whether these changes are associated with NO and NOS metabolite levels in the CSF and the presence of cerebral vasospasm. Methods Asymmetric dimethyl-l-arginine, l-arginine, l-citrulline, and nitrite levels were measured in CSF and serum samples collected during the 21-day period after a single aneurysmal SAH in 18 consecutive patients. Samples were also obtained in a control group consisting of seven patients with Chiari malformation Type I and five patients with spontaneous intracerebral hemorrhage without SAH. Vasospasm, defined as a greater than 11% reduction in the anterior circulation vessel diameter ratio compared with the ratio calculated from the initial arteriogram, was assessed on cerebral arteriography performed around Day 7. Results In 13 patients with SAH, arteriographic cerebral vasospasm developed. Cerebrospinal fluid ADMA levels in patients with SAH were higher than in those in the control group (p < 0.001). The CSF ADMA level remained unchanged in the five patients with SAH without vasospasm, but was significantly increased in patients with vasospasm after Day 3 (6.2 ± 1.7 μM) peaking during Days 7 through 9 (13.3 ± 6.7 μM; p < 0.001) and then gradually decreasing between Days 12 and 21 (8.8 ± 3.2 μM; p < 0.05). Nitrite levels in the CSF were lower in patients with vasospasm compared to patients without vasospasm (p < 0.03). Cerebrospinal fluid ADMA levels positively correlated with the degree of vasospasm (correlation coefficient [CC] = 0.88, p = 0.0001; 95% confidence interval [CI] 0.74–0.95) and negatively correlated with CSF nitrite levels (CC = −0.55; p = 0.017; 95% CI −0.81 to −0.12). Conclusions These results support the hypothesis that ADMA is involved in the progression of cerebral vasospasm. Asymmetric dimethyl-l-arginine and its metabolizing enzymes may be a future target for treatment of cerebral vasospasm after SAH.

Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial

2013 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Nobuo Senbokuya ◽  
Hiroyuki Kinouchi ◽  
Kazuya Kanemaru ◽  
Yasuhiro Ohashi ◽  
Akira Fukamachi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Symptomatic Vasospasm ◽  
Angiographic Vasospasm ◽  
Significant Difference ◽  
Length Of Hospitalization

Object Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of subsequent morbidity and mortality. Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm. Methods Patients admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH onset were enrolled at 7 neurosurgical sites in Japan. These patients were assigned to one of 2 groups: the usual therapy group (control group) or the add-on 100 mg cilostazol twice daily group (cilostazol group). The group assignments were done by a computer-generated randomization sequence. The primary study end point was the onset of symptomatic vasospasm. Secondary end points were the onset of angiographic vasospasm and new cerebral infarctions related to cerebral vasospasm, clinical outcome as assessed by the modified Rankin scale, and length of hospitalization. All end points were assessed for the intention-to-treat population. Results Between November 2009 and December 2010, 114 patients with SAH were treated by clipping within 72 hours from the onset of SAH and were screened. Five patients were excluded because no consent was given. Thus, 109 patients were randomly assigned to the cilostazol group (n = 54) or the control group (n = 55). Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021, Fisher exact test). The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055, Fisher exact test). Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm. The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304, Fisher exact test). Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period. Conclusions Oral administration of cilostazol is effective in preventing cerebral vasospasm with a low risk of severe adverse events. Clinical trial registration no. UMIN000004347, University Hospital Medical Information Network Clinical Trials Registry.

Nimodipine pharmacokinetics after intraventricular injection of sustained-release nimodipine for subarachnoid hemorrhage

2021 ◽  
Vol 134 (1) ◽  
pp. 95-101 ◽  
Author(s):  
R. Loch Macdonald ◽  
Daniel Hänggi ◽  
Poul Strange ◽  
Hans Jakob Steiger ◽  
J Mocco ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Sustained Release ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
External Ventricular Drain ◽  
Plasma Concentrations ◽  
Intraventricular Injection ◽  
World Federation ◽  
Maximum Plasma ◽  
Clinical Trial Registration ◽  
Sustained Release Formulation

OBJECTIVEThe objective of this study was to measure the concentration of nimodipine in CSF and plasma after intraventricular injection of a sustained-release formulation of nimodipine (EG-1962) in patients with aneurysmal subarachnoid hemorrhage (SAH).METHODSPatients with SAH repaired by clip placement or coil embolization were randomized to EG-1962 or oral nimodipine. Patients were classified as grade 2–4 on the World Federation of Neurosurgical Societies grading scale for SAH and had an external ventricular drain inserted as part of their standard of care. Cohorts of 12 patients received 100–1200 mg of EG-1962 as a single intraventricular injection (9 per cohort) or they remained on oral nimodipine (3 per cohort). Plasma and CSF were collected from each patient for measurement of nimodipine concentrations and calculation of maximum plasma and CSF concentration, area under the concentration-time curve from day 0 to 14, and steady-state concentration.RESULTSFifty-four patients in North America were randomized to EG-1962 and 18 to oral nimodipine. Plasma concentrations increased with escalating doses of EG-1962, remained stable for 14 to 21 days, and were detectable at day 30. Plasma concentrations in the oral nimodipine group were more variable than for EG-1962 and were approximately equal to those occurring at the EG-1962 800-mg dose. CSF concentrations of nimodipine in the EG-1962 groups were 2–3 orders of magnitude higher than in the oral nimodipine group, in which nimodipine was only detected at low concentrations in 10% (21/213) of samples. In the EG-1962 groups, CSF nimodipine concentrations were 1000 times higher than plasma concentrations.CONCLUSIONSPlasma concentrations of nimodipine similar to those achieved with oral nimodipine and lasting for 21 days could be achieved after a single intraventricular injection of EG-1962. The CSF concentrations from EG-1962, however, were at least 2 orders of magnitude higher than those with oral nimodipine. These results supported a phase 3 study that demonstrated a favorable safety profile for EG-1962 but yielded inconclusive efficacy results due to notable differences in clinical outcome based on baseline disease severity.Clinical trial registration no.: NCT01893190 (ClinicalTrials.gov).

scholarly journals Risk factors for cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 598-604
Author(s):  
Valentina Opancina ◽  
Snezana Lukic ◽  
Slobodan Jankovic ◽  
Radisa Vojinovic ◽  
Milan Mijailovic
Keyword(s):  
Risk Factors ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Medical Center ◽  
White Blood Cells ◽  
Cerebral Aneurysms ◽  
International Normalized Ratio ◽  
Cross Sectional Study ◽  
Cross Sectional

AbstractIntroductionAneurysmal subarachnoid hemorrhage is a type of spontaneous hemorrhagic stroke, which is caused by a ruptured cerebral aneurysm. Cerebral vasospasm (CVS) is the most grievous complication of subarachnoid hemorrhage (SAH). The aim of this study was to examine the risk factors that influence the onset of CVS that develops after endovascular coil embolization of a ruptured aneurysm.Materials and methodsThe study was designed as a cross-sectional study. The patients included in the study were 18 or more years of age, admitted within a period of 24 h of symptom onset, diagnosed and treated at a university medical center in Serbia during a 5-year period.ResultsOur study showed that the maximum recorded international normalized ratio (INR) values in patients who were not receiving anticoagulant therapy and the maximum recorded white blood cells (WBCs) were strongly associated with cerebrovascular spasm, increasing its chances 4.4 and 8.4 times with an increase of each integer of the INR value and 1,000 WBCs, respectively.ConclusionsSAH after the rupture of cerebral aneurysms creates an endocranial inflammatory state whose intensity is probably directly related to the occurrence of vasospasm and its adverse consequences.

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