Abstract WP386: Acute Catecholamine Surge in Patients with Aneurysmal Subarachnoid Hemorrhage: Characteristics and Prognostic Value

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Koichi Uramaru ◽  
Yuichiro Kikkawa ◽  
Hiroki Sato ◽  
Taro Yanagawa ◽  
Kaima Suzuki ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Subarachnoid Hemorrhage ◽  
Acute Phase ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Demographic Data ◽  
Plasma Concentrations ◽  
Clinical Grade ◽  
High Concentration ◽  
Mutual Correlation ◽  
Inflammatory Reactions

Objectives: The characteristics of serum catecholamine concentration at the hyper-acute phase of aneurysmal subarachnoid hemorrhage (SAH) and its relationship between patient outcome and delayed vasospasm were investigated. Methods: Patients with aneurysmal SAH (170) were prospectively studied between August 2008 and June 2011. Baseline demographic data and physiological parameters, including plasma concentrations of adrenaline (AD), noradrenaline (NA) and dopamine (DP) were evaluated for all patients. Results: On admission, plasma AD, NA and DP levels were significantly higher in patients with a poor clinical grade on admission (Hunt & Kosnik: IV-V), compared to those with a good clinical grade on admission (Hunt & Kosnik: I-III). AD showed a markedly high concentration immediately after the onset of SAH and then rapidly decreased. NA levels peaked within 6 hours after onset, then significantly decreased. The increase of DP with time was not significant, but showed a similar trend to that of NA. The level of each catecholamine showed significant mutual correlation. Multivariate analyses demonstrated age, poor clinical grade, plasma AD and NA levels were predictors of poor patient outcome, and.poor clinical grade, Fisher scale and plasma AD level were predictors of the development of delayed vasospasm. Conclusions: The present findings suggest that sympathetic activation in patients in the acute phase of SAH reflects the severity of SAH, and is closely related to the development of delayed vasospasm, leading to the subsequent immune response and inflammatory reactions. Strategies for suppressing catecholamine at the hyperacute phase may contribute to vasospasm prevention and improve patient outcome.

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 Baseline characteristics and outcome for aneurysmal versus non-aneurysmal subarachnoid hemorrhage: a prospective cohort study

2021 ◽  
Author(s):  
Catharina Conzen ◽  
Miriam Weiss ◽  
Walid Albanna ◽  
Katharina Seyfried ◽  
Tobias P. Schmidt ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prospective Cohort ◽  
Clinical Course ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Demographic Data ◽  
Delayed Cerebral Ischemia ◽  
Perimesencephalic Subarachnoid Hemorrhage ◽  
Glucose Levels ◽  
Shunt Dependency ◽  
Baseline Characteristics

AbstractThis study aims to investigate the characteristics of patients with mild aneurysmal and non-aneurysmal perimesencephalic and non-perimesencephalic subarachnoid hemorrhage (aSAH, pmSAH, npmSAH) with emphasis on admission biomarkers, clinical course, and outcome. A prospective cohort of 115 patients with aSAH (Hunt and Hess 1–3) and of 35 patients without aneurysms (16 pmSAH and 19 npmSAH) admitted between January 2014 and January 2020 was included. Demographic data, blood samples on admission, complications (hydrocephalus, shunt dependency, delayed cerebral ischemia DCI, DCI-related infarction, and mortality), and outcome after 6 months were analyzed. Demographic data was comparable between all groups except for age (aSAH 55 [48–65] vs. npmSAH 60 [56–68] vs. pmSAH 52 [42–60], p = 0.032) and loss of consciousness (33% vs. 0% vs. 0%, p = 0.0004). Admission biomarkers showed poorer renal function and highest glucose levels for npmSAH patients. Complication rate in npmSAH was high and comparable to that of aSAH patients (hydrocephalus, shunt dependency, DCI, DCI-related infarction, mortality), but nearly absent in patients with pmSAH. Favorable outcome after 6 months was seen in 92.9% of pmSAH, 83.3% of npmSAH, and 62.7% of aSAH (p = 0.0264). In this prospective cohort of SAH patients, npmSAH was associated with a complicated clinical course, comparable to that of patients with aSAH. In contrast, such complications were nearly absent in pmSAH patients, suggesting fundamental differences in the pathophysiology of patients with different types of non-aneurysmal hemorrhage. Our findings underline the importance for a precise terminology according the hemorrhage etiology as a basis for more vigilant management of npmSAH patients. NCT02142166, 05/20/2014, retrospectively registered.

Abstract TP454: Immunological Responses in Patients With Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Pilot Study

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Jorge A Roa ◽  
Deepon Sarkar ◽  
Mario Zanaty ◽  
David Hasan ◽  
Edgar Samaniego ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acute Phase ◽  
Immune Cells ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Intracellular Cytokine Staining ◽  
Delayed Cerebral Ischemia ◽  
Effector Proteins ◽  
Time Points ◽  
Adaptive Immune ◽  
Adaptive Immune Cells

Introduction: Cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) are frequently observed after aneurysmal subarachnoid hemorrhage (aSAH) and contribute to neurocognitive decline and worse outcomes. We hypothesize that aSAH initiates a cascade of neuroinflammatory events which contributes to the development of DCI. Methods: Patients who presented with aSAH requiring external ventricular drainage (EVD) for concomitant hydrocephalus were prospectively enrolled. Cerebrospinal fluid (CSF) samples were collected at different time-points relative to index aSAH injury: acute (days 0-1); pre-vasospasm (days 2-5); vasospasm peak (days 6-9) and post-vasospasm (days 10+). Presence and severity of CVS were assessed using CTA/CTP scans and clinical exam. VEGF and MMP9 (immune affectors) protein levels in the CSF were quantified using ELISA. Mobilization of the immune system was characterized by quantification of innate and adaptive immune cells in the CSF using flow cytometry. Production of inflammatory effector proteins was evaluated using intracellular cytokine staining. Results: Of 13 patients analyzed, 6 (46.2%) experienced CVS. Levels of VEGF and MMP9 were consistently higher in aSAH patients who developed CVS, with the highest difference occurring at the acute phase. Similarly, cellularity analysis revealed elevated counts of monocytes (CD11b + ) in the CSF during the acute phase, with progressive decline at later phases. Microglia (CD45 dim CD11b + ) cells were found to be significantly increased at the post-vasospasm phase. A higher percentage of IFN-γ production cytotoxic T helper cells were found at the acute phase, while the later time points revealed an elevated leveled of CD45RA - CD27 + cytotoxic T cells. Conclusion: Our preliminary data shows an active production of proteins with known immunological functions, mobilization of innate cells, production of inflammatory mediators by adaptive immune cells and altered differentiation status. Our overall goal is to determine if there are potential targets of immunomodulatory therapies which can be used to prevent or treat vasospasms and its related deleterious outcomes.

scholarly journals Daily systemic energy expenditure in the acute phase of aneurysmal subarachnoid hemorrhage

2019 ◽  
Vol 124 (4) ◽  
pp. 254-259 ◽  
Author(s):  
Christoffer Nyberg ◽  
Elisabeth Ronne Engström ◽  
Lars Hillered ◽  
Torbjörn Karlsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Energy Expenditure ◽  
Acute Phase ◽  
Aneurysmal Subarachnoid Hemorrhage

scholarly journals Prevalence and predictors of fatigue after aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 162 (12) ◽  
pp. 3107-3116
Author(s):  
Elin Western ◽  
Angelika Sorteberg ◽  
Cathrine Brunborg ◽  
Tonje Haug Nordenmark
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acute Phase ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Multivariable Analysis ◽  
Chronic Phase ◽  
Common Denominator ◽  
Fatigue Severity ◽  
Multivariable Regression ◽  
Subarachnoid Blood ◽  
Aneurysm Repair

Abstract Background Fatigue is a common and disabling sequel after aneurysmal subarachnoid hemorrhage (aSAH). At present, prevalence estimates of post-aSAH fatigue in the chronic phase are scarce and vary greatly. Factors from the acute phase of aSAH have hitherto barely been associated with post-aSAH fatigue in the chronic phase. Methods Prospective study assessing prevalence of fatigue using the Fatigue Severity Scale (FSS) in patients who were living independently 1 to 7 years after aSAH. We compared demographic, medical, and radiological variables from the acute phase of aSAH between patients with and without fatigue (FSS ≥ 4 versus < 4) and searched for predictors of fatigue among these variables applying univariable and multivariable regression analyses. Results Of 726 patients treated for aSAH in the period between January 2012 and December 2017, 356 patients completed the assessment. The mean FSS score was 4.7 ± 1.7, and fatigue was present in 69.7%. The frequency of patients with fatigue did not decline significantly over time. Univariable analysis identified nicotine use, loss of consciousness at ictus (LOCi), rebleed prior to aneurysm repair, reduced consciousness to Glasgow Coma Scale (GCS) < 14, large amounts of subarachnoid blood, the presence of acute hydrocephalus, and severe vasospasm as factors that were significantly associated with fatigue. In multivariable analysis, nicotine use, reduced GCS, and severe vasospasm were independent predictors that all more than doubled the risk to develop post-aSAH fatigue. Conclusions Fatigue is a frequent sequel persisting several years after aSAH. Nicotine use, reduced consciousness at admission, and severe vasospasm are independent predictors of fatigue from the acute phase of aSAH. We propose inflammatory cytokines causing dopamine imbalance to be a common denominator for post-aSAH fatigue and the presently identified predictors.

scholarly journals Impact of smoking on course and outcome of aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 162 (12) ◽  
pp. 3117-3128
Author(s):  
H. Slettebø ◽  
T. Karic ◽  
A. Sorteberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Outcome ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Smoking Status ◽  
Clinical Grade ◽  
Poor Functional Outcome ◽  
Related Risk ◽  
Poor Outcomes ◽  
Subarachnoid Blood ◽  
Vertebrobasilar Aneurysms

Abstract Background While the smoking-related risk of experiencing an aneurysmal subarachnoid hemorrhage (aSAH) is well established, it remains unclear whether smoking has an unexpected “protective effect” in aSAH, or if smokers are more at risk for complications and poor outcomes. Methods Prospective, observational study investigating the course and outcome of aSAH in patients admitted during the years 2011 and 2012. Smoking status at admittance, demographic, medical, and radiological variables were registered along with management, complications, and outcome at 1 year in terms of mortality, modified Rankin score, and Glasgow outcome score extended. We compared current smokers with nonsmokers on group level and by paired analysis matched by aSAH severity, age, and severity of vasospasm. Results We included 237 patients, thereof 138 current smokers (58.2%). Seventy-four smoker/nonsmoker pairs were matched. Smokers presented more often in poor clinical grade, had less subarachnoid blood, and were younger than nonsmokers. Ruptured aneurysms were larger, and multiple aneurysms more common in smokers. Severe multi-vessel vasospasm was less frequent in smokers, whereas all other complications occurred at similar rates. Mortality at 30 days was lower in smokers and functional outcome was similar in smokers and nonsmokers. Poor clinical grade, age, cerebral infarction, and vertebrobasilar aneurysms were independent predictors of 1-year mortality and of poor functional outcome. Serious comorbidity was a predictor of 1-year mortality. Smoking did not predict mortality or poor functional outcome. Conclusions Notwithstanding clinically more severe aSAH, smokers developed less frequently severe vasospasm and had better outcome than expected. The risk for complications after aSAH is not increased in smokers.

Abstract TP457: Intraventricular and Intravenous Milrinone for Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Meghan Purohit ◽  
Naresh Mullaguri ◽  
Christine Ahrens ◽  
Christopher Newey ◽  
Dani Dhimant ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Demographic Data ◽  
Case Series ◽  
Standard Of Care ◽  
Mean Flow ◽  
First Case ◽  
Fisher Grade ◽  
Tertiary Center

Introduction: Cerebral vasospasm (CVS) is a complication of aneurysmal subarachnoid hemorrhage (aSAH). Intraventricular milrinone (IVtM) and intravenous milrinone (IVM) have been studied for treatment of CVS. We aimed to determine the effect of milrinone therapy on clinical and transcranial Doppler (TCD) measures of CVS. Methods: We performed a retrospective analysis of patients with aSAH treated with IVtM at a single tertiary center between 2016 and 2018. Patients were treated with IVtM if they had symptomatic CVS or TCD suggestive of critical CVS that persisted despite blood pressure augmentation or endovascular therapies. Nimodipine was given as standard of care. A subset of patients were also treated with IVM, which was dosed in a standard fashion based on Montreal Neurological Institute protocol. We collected demographic data, TCD mean flow velocity and pulsatility index, angiographic data, as well as utilization and frequency of IVtM and IVM. Results: Twenty-eight patients in our cohort had modified Fisher grade 4 (57%) or grade 3 (25%) and median Hunt-Hess score of 3 (IQR 2, 4). Twenty-one of 28 patients were treated with IVtM+IVM. Seven (25%) who received IVtM alone had no significant improvement in TCD velocities or reduction in symptomatic CVS (p=0.611). Patients received between 1 and 30 doses of IVtM. There was no significant improvement with time or with number of IVtM doses IVtM. There was also no significant improvement in TCD velocities of CVS patients nor reduction in symptomatic CVS with IVtM+IVM (p=0.69). The number of IVtM doses correlated with an increased discharge mRS (p=0.05). There were no direct complications due to IVtM or IVM. Conclusion: Neither IVtM+IVM nor IVtM alone appear to be effective treatment of CVS in aSAH. Our data represent one of the first case series reporting IVtM and IVtM+IVM utilization for the treatment of CVS.

Sign in / Sign up

Export Citation Format

Share Document