Assessment of stress index in patients with subarachnoid hemorrhage of acute phase

ObjectiveLittle is known about the prevalence of continued opioid use following aneurysmal subarachnoid hemorrhage (aSAH) despite guidelines recommending their use during the acute phase of disease. We sought to determine prevalence of opioid use following aSAH and test the hypothesis that acute pain and higher inpatient opioid dose increased outpatient opioid use.MethodsWe reviewed consecutively admitted aSAH patients from November 2015 through September 2019. We retrospectively collected pain scores and daily doses of analgesics. Pain burden was calculated as area under the pain-time curve. Univariate and multivariable regression models determined risk factors for continued opioid use at discharge and outpatient follow-up.ResultsWe identified 234 aSAH patients with outpatient follow-up. Continued opioid use was common at discharge (55% of patients) and follow-up (47% of patients, median 63 (IQR 49–96) days from admission). Pain burden, craniotomy, and racial-ethnic minority status were associated with discharge opioid prescription in multivariable analysis. At outpatient follow-up, pain burden (OR 1.88, 95% CI 1.5–2.4), depression (OR 3.1, 95% CI 1.1–8.8), and racial-ethnic minority status (OR 2.1, 95% CI 1.1–4.0) were independently associated with continued opioid use while inpatient opioid dose was not.ConclusionContinued opioid use following aSAH is prevalent and related to refractory pain during acute illness, but not inpatient opioid dose. More efficacious analgesic strategies are needed to reduce continued opioid use in patients following aSAH.Classification of evidenceThis study provides Class II evidence that continued opioid use following aSAH is associated with refractory pain during acute illness but not hospital opioid exposure.

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

Stroke ◽

10.1161/str.51.suppl_1.tp454 ◽

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.

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

Upsala Journal of Medical Sciences ◽

10.1080/03009734.2019.1659888 ◽

2019 ◽

Vol 124 (4) ◽

pp. 254-259 ◽

Cited By ~ 1

Author(s):

Christoffer Nyberg ◽

Elisabeth Ronne Engström ◽

Lars Hillered ◽

Torbjörn Karlsson

Keyword(s):

Subarachnoid Hemorrhage ◽

Energy Expenditure ◽

Acute Phase ◽

Aneurysmal Subarachnoid Hemorrhage

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Subarachnoid hemorrhage: frequency and severity of cardiac arrhythmias. A survey of 70 cases studied in the acute phase.

Stroke ◽

10.1161/01.str.18.3.558 ◽

1987 ◽

Vol 18 (3) ◽

pp. 558-564 ◽

Cited By ~ 132

Author(s):

A Andreoli ◽

G di Pasquale ◽

G Pinelli ◽

P Grazi ◽

F Tognetti ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Acute Phase ◽

Cardiac Arrhythmias

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Hypoperfusion in the Acute Phase of Subarachnoid Hemorrhage

Early Brain Injury or Cerebral Vasospasm ◽

10.1007/978-3-7091-0353-1_6 ◽

2011 ◽

pp. 35-38 ◽

Cited By ~ 6

Author(s):

Gerrit Alexander Schubert ◽

Marcel Seiz ◽

Aldemar Andrés Hegewald ◽

Jérôme Manville ◽

Claudius Thomé

Keyword(s):

Subarachnoid Hemorrhage ◽

Acute Phase

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Prevalence and predictors of fatigue after aneurysmal subarachnoid hemorrhage

Acta Neurochirurgica ◽

10.1007/s00701-020-04538-9 ◽

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.

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