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Spontaneous angiogram-negative subarachnoid hemorrhage: a retrospective single center cohort study.

ABSTRACT:

Background

Spontaneous angiogram-negative subarachnoid hemorrhage (SAH) is considered a benign illness with little of the aneurysmal SAH-related complications. We describe the clinical course, SAH-related complications, and outcome of patients with angiogram-negative SAH.

Methods

We retrospectively reviewed all adult patients admitted to a neurosurgical intensive care unit during 2004-2018 due to spontaneous angiogram-negative SAH. Our primary outcome was a dichotomized Glasgow Outcome Scale (GOS) at 3 months. We assessed factors that associated with outcome using multivariable logistic regression analysis.

Results

Of the 108 patients included, 84% had a favorable outcome (GOS 4-5), and mortality was 5% within 1 year. The median age was 58 years, 51% were female, and 93% had a low-grade SAH (World Federation of Neurosurgical Societies grading I-III). The median number of angiograms performed per patient was two. Thirty percent of patients showed radiological signs of acute hydrocephalus, 28% were acutely treated with an external ventricular drain, 13% received active vasospasm treatment and 17% received a permanent shunt. In the multivariable logistic regression model, only acute hydrocephalus associated with unfavorable outcome (odds ratio = 4.05, 95% confidence interval = 1.05-15.73). Two patients had a new bleeding episode.

Conclusion

SAH-related complications such as hydrocephalus and vasospasm are common after angiogram-negative SAH. Still, most patients had a favorable outcome. Only acute hydrocephalus was associated with unfavorable outcome. The high rate of SAH-related complications highlights the need for neurosurgical care in these patients.

SUBMITTER: Achren A

PROVIDER: S-EPMC8761132 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionAneurysmal subarachnoid hemorrhage (aSAH) often necessitates prolonged sedation to manage elevated intracranial pressure (ICP) and to prevent secondary brain injury. Optimal timing and biomarkers for predicting adverse events (AEs) during interruption of sedation (IS) after prolonged sedation are not well established. To guide sedation management in aSAH, we aimed to explore the frequency, risk factors, and outcomes of IS in aSAH.MethodsIn a retrospective cohort study, a total of 148 patients with aSAH from January 2015 to April 2020 were screened. In total, 30 patients accounting for 42 IS were included in the analysis. Adverse events (AEs) during IS were used as core outcome measures and were categorized into neurological and non-neurological AEs. Baseline characteristics, clinical parameters before IS, AEs, and functional outcomes were collected using health records. Statistical analysis used generalized linear mixed-effects models with regularization to identify candidate predictors with subsequent bootstrapping to test model stability. As an exploratory analysis, multivariate linear and logistic regression was used to analyze the association between IS and intensive care unit length of stay, duration of mechanical ventilation, and functional outcomes.ResultsThe mean age was 56.9 (SD 14.8) years, and a majority of the patients presented with poor-grade SAH (16/30, 53.3%). Neurological and non-neurological AEs occurred in 60.0% (18/30) of the patients. Timing, number of IS attempts, ICP burden, craniectomy status, level of consciousness, heart rate, cerebral perfusion pressure, oxygen saturation, fraction of inspired oxygen, and temperature were selected as candidate predictors. Through bootstrapping, elapsed time since disease onset (OR 0.85, 95% confidence interval (95% CI) 0.75-0.97), ICP burden (OR 1.24, 95% CI 1.02-1.52), craniectomy (OR 0.68, 95% CI 0.48-0.69), and oxygen saturation (OR, 0.80 0.72-0.89) were revealed as relevant biomarkers for neurological AEs, while none of the pre-selected predictors was robustly associated with non-neurological AEs.ConclusionIn aSAH, complications during the definite withdrawal of sedation are frequent but can potentially be predicted using clinical parameters available at the bedside. Prospective multicenter studies are essential to validate these results and further investigate the impact of IS complications.

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Project description:Background and purposePrevious studies have described an association between pulse pressure (PP) level and mortality in stroke patients. Evidence of associations between PP level and the risk of mortality remains unknown in non-traumatic subarachnoid hemorrhage (SAH) patients. We aimed to explore the relationship between the baseline PP level and hospital mortality.MethodsThis cohort study of 693 non-traumatic SAH adults used Medical Information Mart for Intensive Care (MIMIC-IV) data from 2008-2019 admissions to Intensive Care Unit (ICU). PP level was calculated as the first value after admission to the ICU. The endpoint of the study was in-hospital mortality. Cox proportional hazards models were utilized to analyze the association between baseline PP level and hospital mortality. Restricted Cubic Splines (RCS) analysis was utilized to determine the relationship curve between hospital mortality and PP level and examine the threshold saturation effect. We further applied Kaplan-Meier survival curve analysis to examine the consistency of these correlations. The interaction test was used to identify subgroups with differences.ResultsThe mean age of the study population was 58.8 ± 14.6 years, and 304 (43.9%) of participants were female. When baseline PP level was assessed in quartiles, compared to the reference group (Q1 ≤ 56 mmHg), the adjusted hazard ratio (HR) in Q2 (57-68 mmHg), Q3(69-82 mmHg), Q4 (≥83 mmHg) were 0.55 (95% CI: 0.33-0.93, p = 0.026), 0.99 (95% CI, 0.62-1.59, p = 0.966), and 0.99 (95% CI: 0.62-1.59, p = 0.954), respectively. In the threshold analysis, for every 5 mmHg increase in PP level, there was an 18.2% decrease in hospital mortality (adjusted HR, 0.818; 95% CI, 0.738-0.907; p = 0.0001) in those with PP level less than 60 mmHg, and a 7.7% increase in hospital mortality (adjusted HR, 1.077; 95% CI, 1.018-1.139; p = 0.0096) in those with PP level was 60 mmHg or higher.ConclusionFor patients with non-traumatic SAH, the association between baseline PP and risk of hospital mortality was non-linear, with an inflection point at 60 mmHg and a minimal risk at 57 to 68 mmHg (Q2) of baseline PP level.