Outcome In Subarachnoid Hemorrhage Patients Research Articles

The urotensin II receptor triggers an early meningeal response and a delayed macrophage-dependent vasospasm after subarachnoid hemorrhage in male mice

Subarachnoid hemorrhage (SAH) can be associated with neurological deficits and has profound consequences for mortality and morbidity. Cerebral vasospasm (CVS) and delayed cerebral ischemia affect neurological outcomes in SAH patients, but their mechanisms are not fully understood, and effective treatments are limited. Here, we report that urotensin II receptor UT plays a pivotal role in both early events and delayed mechanisms following SAH in male mice. Few days post-SAH, UT expression is triggered by blood or hemoglobin in the leptomeningeal compartment. UT contributes to perimeningeal glia limitans astrocyte reactivity, microvascular alterations and neuroinflammation independent of CNS-associated macrophages (CAMs). Later, CAM-dependent vascular inflammation and subsequent CVS develop, leading to cognitive dysfunction. In an SAH model using humanized UTh+/h+ male mice, we show that post-SAH CVS and behavioral deficits, mediated by UT through Gq/PLC/Ca2+ signaling, are prevented by UT antagonists. These results highlight the potential of targeting UT pathways to reduce early meningeal response and delayed cerebral ischemia in SAH patients.

Impact of fludrocortisone on the outcomes of subarachnoid hemorrhage patients: A retrospective analysis

BackgroundWhether the use of fludrocortisone affects outcomes of patients with aneurysmal subarachnoid hemorrhage (aSAH). MethodsWe conducted a retrospective analysis of 78 consecutive patients with a ruptured aSAH at a single academic center in the United States. The primary outcome was the score on the modified Rankin scale (mRS, range, 0 [no symptoms] to 6 [death]) at 90 days. The primary outcome was adjusted for age, hypertension, aSAH grade, and time from aSAH onset to aneurysm treatment. Secondary outcomes were neurologic and cardiopulmonary dysfunction events. ResultsAmong 78 patients at a single center, the median age was 58 years [IQR, 49 to 64.5]; 64 % were female, and 41 (53 %) received fludrocortisone. The adjusted common odds ratio, aOR, of a proportional odds regression model of fludrocortisone use with mRS was 0.33 (95 % CI, 0.14-0.80; P = 0.02), with values <1.0 favoring fludrocortisone. Organ-specific dysfunction events were not statistically different: delayed cerebral ischemia (22 % vs. 39 %, P = 0.16); cardiac dysfunction (0 % vs. 11 %; P = 0.10); and pulmonary edema (15 % vs. 8 %; P = 0.59). ConclusionsThe risk of disability or death at 90 days was lower with the use of fludrocortisone in aSAH patients.

Abstract 005: Outcomes of Heparin Induced Thrombocytopenia Type II in Aneurysmal Subarachnoid Hemorrhage Patients

Introduction Heparin‐induced thrombocytopenia (HIT) is a rare complication characterized by a decreased platelet count and hypercoagulability following heparin and light‐molecular weight heparin administration. Both anticoagulants can be used intraoperatively and postoperatively for DVT prophylaxis in patients undergoing subarachnoid hemorrhage (SAH) treatment. Patients with SAH are an understudied population in terms of assessing incidence and impact of HIT. This study aims to investigate the incidence, complications, and outcomes of SAH patients who develop HIT. Methods ICD‐9‐CM and ICD‐10‐CM codes were used to query the National Inpatient Sample for patients with SAH between 2010 and 2019. Subgroup analysis was stratified by HIT development. SAH severity was determined using the National Institute of Health Stroke Scale as a template. Patients from both groups were assessed for baseline clinical characteristics, comorbidities, interventions, complications, and outcomes. Cohorts containing ten or fewer patients must only be described qualitatively. Descriptive statistics, multivariate regressions, and propensity score‐matching were all performed using IBM SPSS 28. Results 76,387 patients were diagnosed with SAH between 2010 and 2019. 166 (.22%) had developed HIT in response to anticoagulant administration. The incidence of HIT was higher in patients who were younger (58.04 vs 61.39, p = 0.01), obese (0.4% vs 0.2%, p &lt; 0.01), on long‐term anticoagulant use (10.84% vs 5.72%, p &lt; 0.01), and had an implanted cerebrospinal fluid drainage device (p &lt; 0.01). Patients with HIT were associated with higher SAH severity (1.42 vs 1.06, p &lt; 0.01). Through both the complete cohort and propensity score‐matched cohort, patients with HIT were associated with higher rates of endovascular coiling, external ventricular drain placement (p &lt; 0.01), and ventriculoperitoneal shunt placement (p &lt; 0.01). HIT patients had significantly higher rates of deep vein thrombosis (p &lt; 0.01), pulmonary embolism (p &lt; 0.01), central venous sinus thrombosis (p = 0.01), pneumonia (p &lt; 0.01), urinary tract infection (p &lt; 0.01), acute kidney injury (p &lt; 0.01), and cerebral vasospasm (p &lt; 0.01). Patients who develop HIT had a longer length of stay (LOS) (24.04 vs 10.48, p &lt; 0.01). HIT continued to be a significant predictor of having an above average LOS (OR: 6.799, CI: 3.985 ‐ 11.6, p &lt; 0.01) when controlling for age, SAH severity, and significant comorbidities. Conclusion Our study revealed that younger SAH patients with various comorbidities are more prone to developing HIT, leading to higher rates of thrombotic events, acute kidney injury, and nosocomial infections, which can significantly prolong their hospital stay. Considering the extended postoperative recovery period for SAH, investigating the causes of HIT can facilitate earlier detection and prevention of thrombotic complications. This nationwide, multicenter, retrospective study provides valuable insights for clinicians on how to prevent and manage HIT in patients with subarachnoid hemorrhage.

Neutrophil to Lymphocyte Ratio and Serum Biomarkers : A Potential Tool for Prediction of Clinically Relevant Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) is a condition characterized by bleeding in the subarachnoid space, often resulting from the rupture of a cerebral aneurysm. Delayed cerebral ischemia (DCI) caused by vasospasm is a significant cause of mortality and morbidity in SAH patients, and inflammatory markers such as systemic inflammatory response index (SIRI), systemic inflammatory index (SII), neutrophil-to-lymphocyte ratio (NLR), and derived NLR (dNLR) have shown potential in predicting clinical vasospasm and outcomes in SAH patients. This article aims to investigate the relationship between inflammatory markers and cerebral vasospasm after aneurysmatic subarachnoid hemorrhage (aSAH) and evaluate the predictive value of various indices, including systemic inflammatory response index (SIRI), systemic inflammatory index (SII), neutrophil-to-lymphocyte ratio (NLR), and derived NLR (dNLR), in predicting clinical vasospasm. A retrospective analysis was performed on a cohort of 96 patients who met the inclusion criteria out of a total of 139 patients admitted XXXXXXXXXXX hospital with a confirmed diagnosis of aneurysmal subarachnoid hemorrhage (aSAH) between January 2013 and December 2021. Diagnostic procedures, neurological examinations, and laboratory tests were performed to assess the patients' condition. The Student's t-test compared age variables, while the chi-square test compared categorical variables between the non-vasospasm (NVS) and vasospasm (VS) groups. Receiver operating characteristic (ROC) curve analyses were used to evaluate the diagnostic accuracy of laboratory parameters, calculating the area under the ROC curve (AUC), cut-off values, sensitivity, and specificity. A significance level of p < 0.05 was considered statistically significant. The study included 96 patients divided into two groups: NVS (non-vasospasm) and VS (vasospasm). Various laboratory parameters, such as NLR, SII, and dNLR, were measured daily for 15 days, and statistically significant differences were found in NLR on seven days, with specific cut-off values identified for each day. SII showed a significant difference on day 9, while dNLR had significant differences on days 2, 4, and 9. Graphs depicting the values of these markers for each day are provided. Neuroinflammatory biomarkers, when used alongside radiology and scoring scales, can aid in predicting prognosis, determining severity and treatment decisions for aneurysmal subarachnoid hemorrhage (aSAH), and further studies with larger patient groups are needed to gain more insights.

Impact of pre-hospital handling and initial time to cranial computed tomography on outcome in aneurysmal subarachnoid hemorrhage patients with out-of-hospital sudden cardiac arrest-a retrospective bi-centric study.

Aneurysmal subarachnoid hemorrhage (SAH) presents occasionally with cardiac arrest (CA). The impact of pre-hospital and emergency room (ER) treatment on outcome remains unclear. Therefore, we investigated the impact of pre-hospital treatment, focusing on lay cardiopulmonary resuscitation (CPR), and ER handling on the outcome of SAH patients with out-of-hospital CA (OHCA). In this bi-centric retrospective analysis, we reviewed SAH databases for OHCA and CPR from January 2011 to June 2021. Patients were analyzed for general clinical and epidemiological parameters. CPR data were obtained from ambulance reports and information on ER handling from the medical records. Data were correlated with patient survival at hospital discharge as a predefined outcome parameter. Of 1,120 patients with SAH, 45 (4.0%) were identified with OHCA and CPR, 38 of whom provided all required information and were included in this study. Time to resuscitation was significantly shorter with lay resuscitation (5.3 ± 5.2 min vs. 0.3 ± 1.2 min, p = 0.003). Nineteen patients were not initially scheduled for cranial computed tomography (CCT), resulting in a significantly longer time interval to first CCT (mean ± SD: 154 ± 217 min vs. 40 ± 23 min; p < 0.001). Overall survival to discharge was 31.6%. Pre-hospital lay CPR was not associated with higher survival (p = 0.632). However, we observed a shorter time to first CCT in surviving patients (p = 0.065). OHCA in SAH patients is not uncommon. Besides high-quality CPR, time to diagnosis of SAH appears to play an important role. We therefore recommend considering CCT diagnostics as part of the diagnostic algorithm in patients with OHCA.

Lower initial red blood cell count in cerebrospinal fluid predicts good functional outcome in patients with spontaneous subarachnoid haemorrhage.

Red blood cell (RBC) degradation after subarachnoid haemorrhage (SAH) negatively affects functional outcome. Although the detection of RBCs in the cerebrospinal fluid (CSF) is a widely available part of neurological routine diagnostics, the prognostic value as a biomarker remains unclear. This study was undertaken to investigate whether CSF RBC count correlates with established radiological markers of SAH volume and whether the CSF RBC count can predict functional outcome in SAH patients. A total of 121 consecutive spontaneous SAH patients were retrospectively analyzed. CSF was collected from external ventricular drain as part of routine diagnostic procedures. We used multivariable binary logistic regression to investigate associations between CSF RBC counts and functional outcome 3 months after SAH or hospital survival. Good functional outcome was defined as modified Rankin Scale ≤ 2. Patients' age was 60 ± 14 years, and the median admission Hunt & Hess grade (H&H) was 4. CSF samples were collected 2 days after intensive care unit admission. High CSF RBC counts positively correlated with radiological measurements for SAH volume, for example, modified Fisher score (p = 0.002) and Hijdra ventricle score (p = 0.016). Multivariable regression analysis adjusted for age, H&H grade, modified Fisher and Hijdra scores showed that low CSF RBC counts predicted hospital survival (per 100,000 CSF RBCs: adjusted odds ratio [adjOR] = 0.74, 95% confidence interval [CI] = 0.61-0.89, p = 0.001) and good functional outcome after 3 months (per 100,000 CSF RBC: adjOR = 0.76, 95% CI = 0.60-0.96, p = 0.020). CSF RBC counts correlate with radiographic scores quantifying SAH volume and may serve as an early independent biomarker for hospital survival and good functional 3-month outcome in patients requiring ventriculostomy after SAH.

Circadian rhythm and aneurysmal subarachnoid hemorrhage: Is there an alarm clock for the rupture timing?

Data on the temporal distribution of the bleeding time of intracranial aneurysms are limited to a few small studies. With this study, the aim was to analyze time patterns of the occurrence of aneurysmal subarachnoid hemorrhage (SAH), particularly focusing on the impact of patients' socio-demographic and clinical characteristics on the ictus timing. The study is based on an institutional SAH cohort with 782 consecutive cases treated between January 2003 and June 2016. Data were collected on the ictus time, patients' socio-demographic and clinical characteristics, as well as the initial severity and outcome. Univariate and multivariate analyses were performed on the bleeding timeline. There were two peaks in the circadian rhythm of SAH, one in the morning (7-9 a.m.) and the other in the evening (7-9 p.m.). The strongest alterations in the bleeding time patterns were observed for weekdays, patients' age, sex and ethnicity. Individuals with chronic alcohol and painkiller consumption showed a higher bleeding peak between 1 and 3 p.m. Finally, the bleeding time showed no impact on the severity, clinically relevant complications and the outcome of SAH patients. This study is one of the very few detailed analyses of the impact of specific socio-demographic, ethnic, behavioral and clinical characteristics on the rupture timing of aneurysms. Our results point to the possible relevance of the circadian rhythm for the rupture event, and therefore might be useful in the elaboration of preventive measures against aneurysm rupture.

Substantially elevated serum glutamate and CSF GOT-1 levels associated with cerebral ischemia and poor neurological outcomes in subarachnoid hemorrhage patients

Brain injury and cerebral vasospasm during the 14 days after the subarachnoid hemorrhage (SAH) are considered the leading causes of poor outcomes. The primary injury induces a cascade of events, including increased intracranial pressure, cerebral vasospasm and ischemia, glutamate excitotoxicity, and neuronal cell death. The objective of this study was to monitor the time course of glutamate, and associated enzymes, such as glutamate–oxaloacetate transaminase (GOT1), glutamate-pyruvate transaminase (GPT) in cerebrospinal fluid (CSF) and serum, shortly after SAH, and to assess their prognostic value. A total of 74 participants participated in this study: 45 participants with SAH and 29 controls. Serum and CSF were sampled up to 14 days after SAH. SAH participants' clinical and neurological status were assessed at hospitalization, at discharge from the hospital, and 3 months after SAH. Furthermore, a logistic regression analysis was carried out to evaluate the ability of GOT1 and glutamate levels to predict neurological outcomes. Our results demonstrated consistently elevated serum and CSF glutamate levels after SAH. Furthermore, serum glutamate level was significantly higher in patients with cerebral ischemia and poor neurological outcome. CSF GOT1 was significantly higher in patients with uncontrolled intracranial hypertension and cerebral ischemia post-SAH, and independently predicted poor neurological outcomes.

Comparative Analyses of the Impact of Different Criteria for Sepsis Diagnosis on Outcome in Patients with Spontaneous Subarachnoid Hemorrhage.

Data on sepsis in patients with a subarachnoid hemorrhage (SAH) are scarce. We assessed the impact of different sepsis criteria on the outcome in an SAH cohort. Adult patients admitted to our ICU with a spontaneous SAH between 11/2014 and 11/2018 were retrospectively included. In patients developing an infection, different criteria for sepsis diagnosis (Sepsis-1, Sepsis-3_original, Sepsis-3_modified accounting for SAH-specific therapy, alternative sepsis criteria compiled of consensus conferences) were applied and their impact on functional outcome using the modified Rankin Scale (mRS) on hospital discharge and in-hospital mortality was evaluated. Of 270 SAH patients, 129 (48%) developed an infection. Depending on the underlying criteria, the incidence of sepsis and septic shock ranged between 21–46% and 9–39%. In multivariate logistic regression, the Sepsis-1 criteria were not associated with the outcome. The Sepsis-3 criteria were not associated with the functional outcome, but in shock with mortality. Alternative sepsis criteria were associated with mortality for sepsis and in shock with mortality and the functional outcome. While Sepsis-1 criteria were irrelevant for the outcome in SAH patients, septic shock, according to the Sepsis-3 criteria, adversely impacted survival. This impact was higher for the modified Sepsis-3 criteria, accounting for SAH-specific treatment. Modified Sepsis-3 and alternative sepsis criteria diagnosed septic conditions of a higher relevance for outcomes in patients with an SAH.

Regional Variability in the Care and Outcomes of Subarachnoid Hemorrhage Patients in the United States.

Background and ObjectivesRegional variability in subarachnoid hemorrhage (SAH) care is reported in physician surveys. We aimed to describe variability in SAH care using patient-level data and identify factors impacting hospital outcomes and regional variability in outcomes.MethodsA retrospective multi-center cross-sectional cohort study of consecutive non-traumatic SAH patients in the Vizient Clinical Data Base, between January 1st, 2009 and December 30th, 2018 was performed. Participating hospitals were divided into US regions: Northeast, Midwest, South, West. Regional demographics, co-morbidities, severity-of-illness, complications, interventions and discharge outcomes were compared. Multivariable logistic regression was performed to identify factors independently associated with primary outcomes: hospital mortality and poor discharge outcome. Poor discharge outcome was defined by the Nationwide Inpatient Sample-SAH Outcome Measure, an externally-validated outcome measure combining death, discharge disposition, tracheostomy and/or gastrostomy. Regional variability in the associations between care and outcomes were assessed by introducing an interaction term for US region into the models.ResultsOf 109,034 patients included, 24.3% were from Northeast, 24.9% Midwest, 34.9% South, 15.9% West. Mean (SD) age was 58.6 (15.6) years and 64,245 (58.9%) were female. In-hospital mortality occurred in 21,991 (20.2%) and 44,159 (40.5%) had poor discharge outcome. There was significant variability in severity-of-illness, co-morbidities, complications and interventions across US regions. Notable findings were higher prevalence of surgical clipping (18.8 vs. 11.6%), delayed cerebral ischemia (4.3 vs. 3.1%), seizures (16.5 vs. 14.8%), infections (18 vs. 14.7%), length of stay (mean [SD] days; 15.7 [19.2] vs. 14.1 [16.7]) and health-care direct costs (mean [SD] USD; 80,379 [98,999]. vs. 58,264 [74,430]) in the West when compared to other regions (all p < 0.0001). Variability in care was also associated with modest variability in hospital mortality and discharge outcome. Aneurysm repair, nimodipine use, later admission-year, endovascular rescue therapies reduced the odds for poor outcome. Age, severity-of-illness, co-morbidities, hospital complications, and vasopressor use increased those odds (c-statistic; mortality: 0.77; discharge outcome: 0.81). Regional interaction effect was significant for admission severity-of-illness, aneurysm-repair and nimodipine-use.DiscussionMultiple hospital-care factors impact SAH outcomes and significant variability in hospital-care and modest variability in discharge-outcomes exists across the US. Variability in SAH-severity, nimodipine-use and aneurysm-repair may drive variability in outcomes.

Cerebral hypoperfusion after nimodipine administration is associated with worse functional outcomes in subarachnoid hemorrhage patients (P6-7.001)

Cerebral hypoperfusion after nimodipine administration is associated with worse functional outcomes in subarachnoid hemorrhage patients (P6-7.001)

Phosphatase alkaline levels are not associated with poor outcomes in subarachnoid hemorrhage patients

IntroductionAlkaline phosphatase (ALP) levels are often elevated in cerebrovascular and cardiovascular disease. Their prognostic role after subarachnoid hemorrhage (SAH) remains to be elucidated. MethodsWe performed a retrospective single center study of patients with non-traumatic SAH admitted to the intensive care unit (ICU) of Erasme Hospital (Brussels, Belgium) from 2006 to 2019. Exclusion criteria were previous history of liver cirrhosis or malignancies and early death (i.e. within 24 h from ICU admission). Baseline information, clinical data, radiologic data were collected, the occurrence of DCI as well as serum ALP levels during the first 12 days of ICU stay. Unfavorable neurological outcome (UO) at 3 months was defined as a Glasgow Outcome Scale of 1–3. ResultsSix hundred and fifty patients were included; ALP levels increased from baseline after day 6 from admission, in particular among patients with an initial poor clinical status. There was no difference in the ALP levels between patients with or without DCI over time. Patients with UO had higher ALP levels over time than others; however, in the multivariable analysis, nor ALP levels on admission or the highest ALP value during the ICU stay were independently associated with UO. ConclusionsThe results of this study suggested that ALP levels had no prognostic role in SAH patients. Other possible prognostic biomarkers should be evaluated in this setting.

Cerebrospinal fluid metabolic profiling reveals divergent modulation of pentose phosphate pathway by midazolam, propofol and dexmedetomidine in patients with subarachnoid hemorrhage: a cohort study

BackgroundAgitation is common in subarachnoid hemorrhage (SAH), and sedation with midazolam, propofol and dexmedetomidine is essential in agitation management. Previous research shows the tendency of dexmedetomidine and propofol in improving long-term outcome of SAH patients, whereas midazolam might be detrimental. Brain metabolism derangement after SAH might be interfered by sedatives. However, how sedatives work and whether the drugs interfere with patient outcome by altering cerebral metabolism is unclear, and the comprehensive view of how sedatives regulate brain metabolism remains to be elucidated.MethodsFor cerebrospinal fluid (CSF) and extracellular space of the brain exchange instantly, we performed a cohort study, applying CSF of SAH patients utilizing different sedatives or no sedation to metabolomics. Baseline CSF metabolome was corrected by selecting patients of the same SAH and agitation severity. CSF components were analyzed to identify the most affected metabolic pathways and sensitive biomarkers of each sedative. Markers might represent the outcome of the patients were also investigated.ResultsPentose phosphate pathway was the most significantly interfered (upregulated) pathway in midazolam (p = 0.0000107, impact = 0.35348) and propofol (p = 0.00000000000746, impact = 0.41604) groups. On the contrary, dexmedetomidine decreased levels of sedoheptulose 7-phosphate (p = 0.002) and NADP (p = 0.024), and NADP is the key metabolite and regulator in pentose phosphate pathway. Midazolam additionally augmented purine synthesis (p = 0.00175, impact = 0.13481) and propofol enhanced pyrimidine synthesis (p = 0.000203, impact = 0.20046), whereas dexmedetomidine weakened pyrimidine synthesis (p = 0.000000000594, impact = 0.24922). Reduced guanosine diphosphate (AUC of ROC 0.857, 95%CI 0.617–1, p = 0.00506) was the significant CSF biomarker for midazolam, and uridine diphosphate glucose (AUC of ROC 0.877, 95%CI 0.631–1, p = 0.00980) for propofol, and succinyl-CoA (AUC of ROC 0.923, 95%CI 0.785–1, p = 0.000810) plus adenosine triphosphate (AUC of ROC 0.908, 95%CI 0.6921, p = 0.00315) for dexmedetomidine. Down-regulated CSF succinyl-CoA was also associated with favorable outcome (AUC of ROC 0.708, 95% CI: 0.524–0.865, p = 0.029333).ConclusionPentose phosphate pathway was a crucial target for sedatives which alter brain metabolism. Midazolam and propofol enhanced the pentose phosphate pathway and nucleotide synthesis in poor-grade SAH patients, as presented in the CSF. The situation of dexmedetomidine was the opposite. The divergent modulation of cerebral metabolism might further explain sedative pharmacology and how sedatives affect the outcome of SAH patients.

Sıçan Subaraknoid Kanama Modelinde Bilateral Superior Servikal Ganglionektomi ve Melatonin Seviyeleri: Basit Önlemler Melatonin Düzeylerini Koruyabilir

Aim: Subarachnoid hemorrhage (SAH) is a serious disease, and it is thought that melatonin may have positive effects after SAH. Bilateral resection or blockage of superior cervical ganglions has constant effects on melatonin levels. Animal models with bilateral superior cervical ganglionectomy (SCG) show the role of superior cervical ganglion on melatonin and give clues about simple precautions which may help to prevent unfavorable outcomes in SAH patients. The aim of this study is to examine how melatonin levels change in SAH and SCG models. Material and Methods: Forty-two Sprague Dawley male rats weighing 200-250 g were used in the study and randomly divided into six groups. Arterial blood samples were collected 24 hours after the procedure in all groups. Serum melatonin levels of the groups were studied. Results: A significant difference in blood melatonin levels was observed between SAH and SCG groups, and against the control group. There was no significant difference between the melatonin levels in SCG group and SAH+SCG group (p=0.983). The mean blood melatonin level of the SAH group was higher than the SCG (p&amp;lt;0.001), SAH+SCG (p&amp;lt;0.001) and control groups (p=0.001). The mean blood melatonin levels of SAH+SCG and SCG groups were lower than the mean blood melatonin levels of the other groups and also the SAH group (p&amp;lt;0.001). Conclusion: Bilateral SCG significantly inhibited the abrupt increase of serum melatonin levels after SAH model in rats. Future studies aiming to address melatonin’s complex outcomes should take into account that minor exogenous factors may affect serum melatonin levels.

Time course of outcome in poor grade subarachnoid hemorrhage patients: a longitudinal retrospective study

BackgroundNeurological outcome and mortality of patients suffering from poor grade subarachnoid hemorrhage (SAH) may have changed over time. Several factors, including patients’ characteristics, the presence of hydrocephalus and intraparenchymal hematoma, might also contribute to this effect. The aim of this study was to assess the temporal changes in mortality and neurologic outcome in SAH patients and identify their predictors.MethodsWe performed a single center retrospective cohort study from 2004 to 2018. All non-traumatic SAH patients with poor grade on admission (WFNS score of 4 or 5) who remained at least 24 h in the hospital were included. Time course was analyzed into four groups according to the years of admission (2004–2007; 2008–2011; 2012–2015 and 2016–2018).ResultsA total of 353 patients were included in this study: 202 patients died (57 %) and 260 (74 %) had unfavorable neurological outcome (UO) at 3 months. Mortality tended to decrease in in 2008–2011 and 2016–2018 periods (HR 0.55 [0.34–0.89] and HR 0.33 [0.20–0.53], respectively, when compared to 2004–2007). The proportion of patients with UO remained high and did not vary significantly over time. Patients with WFNS 5 had higher mortality (68 % vs. 34 %, p = 0.001) and more frequent UO (83 % vs. 54 %, p = 0.001) than those with WFNS 4. In the multivariable analysis, WFNS 5 was independently associated with mortality (HR 2.12 [1.43–3.14]) and UO (OR 3.23 [1.67–6.25]). The presence of hydrocephalus was associated with a lower risk of mortality (HR 0.60 [0.43–0.84]).ConclusionsBoth hospital mortality and UO remained high in poor grade SAH patients. Patients with WFNS 5 on admission had worse prognosis than others; this should be taken into consideration for future clinical studies.

Size does matter: The role of decompressive craniectomy extent for outcome after aneurysmal subarachnoid hemorrhage.

In previous studies in patients with traumatic brain injury and ischemic stroke, the size of decompressive craniectomy (DC) was reported to be paramount with regard to patient outcomes. We aimed to identify the impact of DC size on treatment results in individuals with aneurysmal subarachnoid hemorrhage (SAH). The extent of DC in 232 patients with SAH who underwent bifrontal or hemicraniectomy between January 2003 and December 2015 was analyzed using semi-automated surface measurements. The study endpoints were course of intracranial pressure (ICP) treatment after DC, occurrence of cerebral infarcts, in-hospital mortality, and unfavorable outcome at 6months (defined as modified Rankin scale score >3). The associations of DC size with the study endpoints were adjusted for DC timing, patient age, clinical and radiographic severity of SAH, aneurysm location, and treatment modality. The mean DC surface area was 100.9 (±45.8) cm2 . In multivariate analysis, a large DC (>105cm2 ) was independently associated with a lower risk of cerebral infarcts (adjusted odds ratio [aOR]0.30, 95% confidence interval [CI]0.16-0.56), in-hospital mortality (aOR 0.28, 95%CI0.14-0.56) and unfavorable outcome (aOR 0.51, 95% CI0.27-0.98). Moreover, SAH patients with a small DC size (<75cm2 ) were more likely to require prolonged (>3days, aOR 3.60, 95% CI1.37-9.42) and enhanced (aOR2.31, 95% CI1.12-4.74) postoperative ICP treatment. This is the first study showing the impact of DC size on postoperative ICP control and patient outcome in the context of SAH; specifically, a large craniectomy flap (>105cm2 ) might lead to better outcomes in SAH patients requiring decompressive surgery.

Prognostic value of albumin-fibrinogen ratio in subarachnoid hemorrhage patients.

Inflammation plays an important role in the pathophysiology of subarachnoid hemorrhage (SAH). Recent studies have indicated that the albumin to fibrinogen ratio (AFR) is a useful biomarker of inflammation.This research aimed to determine the ability of AFR to predict the prognosis of patients with SAH.A total of 440 patients with SAH who had been diagnosed within 72 hours of symptom onset were retrospectively reviewed. Clinical findings and laboratory data were retrieved from the hospital database. Functional outcome was measured according to the modified Rankin scale at 30 days. Logistic regression analysis was used to evaluate the correlation between AFR and the prognosis of patients with SAH. Receiver operating characteristic (ROC) analysis was performed to determine the prognostic ability of AFR at admission to predict the 30-day outcomes.The average age of all 440 patients with SAH was 56.75 ± 11.19 years and 31.4% (138) were male. Of these patients, 161 exhibited unfavorable outcomes at 30 days. According to the multivariate logistic regression analysis, the AFR was positively correlated with the outcome of patients with SAH (odds ratio 0.939, 95% confidence interval 0.885–0.996, P = .038). The ROC analysis revealed an area under the curve of 0.713 for AFR's ability to predict the 30-day outcomes.AFR is independently associated with the outcome of SAH patients. As a parameter that can be easily assessed at admission, AFR could be used to help the decision-making of clinical treatment.

Multidrug-resistant organisms (MDROs) in patients with subarachnoid hemorrhage (SAH)

Patient care in a neurointensive care unit (neuro-ICU) is challenging. Multidrug-resistant organisms (MDROs) are increasingly common in the routine clinical practice. We evaluated the impact of infection with MDROs on outcomes in patients with subarachnoid hemorrhage (SAH). A single-center retrospective analysis of SAH cases involving patients treated in the neuro-ICU was performed. The outcome was assessed 6 months after SAH using the modified Rankin Scale [mRS, favorable (0–2) and unfavorable (3–6)]. Data were compared by matched-pair analysis. Patient characteristics were well matched in the MDRO (n = 61) and control (n = 61) groups. In this center, one nurse was assigned to a two-bed room. If a MDRO was detected, the patient was isolated, and the nurse was assigned to the patient infected with the MDRO. In the MDRO group, 29 patients (48%) had a favorable outcome, while 25 patients (41%) in the control group had a favorable outcome; the difference was not significant (p > 0.05). Independent prognostic factors for unfavorable outcomes were worse status at admission (OR = 3.1), concomitant intracerebral hematoma (ICH) (OR = 3.7), and delayed cerebral ischemia (DCI) (OR = 6.8). Infection with MRDOs did not have a negative impact on the outcome in SAH patients. Slightly better outcomes were observed in SAH patients infected with MDROs, suggesting the benefit of individual care.

Clinical Significance of Cytotoxic Lesions of the Corpus Callosum in Subarachnoid Hemorrhage Patients: A Retrospective Analysis

Introduction: Cytotoxic lesions of the corpus callosum are secondary lesions induced by significant increases in cytokine levels in the brain and are associated with subarachnoid hemorrhage (SAH). However, their clinical significance in SAH patients remains unclear. Methods: We retrospectively analyzed SAH patients who were treated in our hospital and evaluated between-group differences in the backgrounds, clinical findings, and outcomes between SAH patients who developed cytotoxic lesions of the corpus callosum and those who did not. We further compared patients who achieved good outcomes with those who had poor outcomes. Multivariate logistic regression analysis was used to identify risk factors for poor clinical outcomes. Results: We analyzed 159 SAH patients; 17 patients (10.7%) had cytotoxic lesions of the corpus callosum. Patients with cytotoxic lesions of the corpus callosum were more likely to be in a severe condition (World Federation of Neurosurgical Societies grading IV-V: odds ratio [OR], 4.53; 95% confidence interval [95% CI]: 1.60–12.84; p = 0.0042) and have an intraventricular (OR, 5.98; 95% CI: 1.32–27.13; p = 0.0054) or an intraparenchymal hematoma (OR, 3.62; 95% CI: 1.25–10.45; p = 0.023). Patients with cytotoxic lesions of the corpus callosum had a greater propensity of a poor outcome 3 months after onset (modified Rankin Scale score 0–2: OR, 0.22; 95% CI: 0.07–0.66; p = 0.0043). Multivariate analysis confirmed that cytotoxic lesions of the corpus callosum increased the risk of a poor outcome (OR, 4.39; 95% CI: 1.06–18.1; p = 0.037). Discussion/Conclusions: The development of cytotoxic lesions of the corpus callosum may be related to the extent of hematomas in SAH patients. Although they are usually reversible lesions, the development of cytotoxic lesions of the corpus callosum may be a predictor of poor outcomes in SAH patients.

Abstract P453: Histamine 2 Blockers and Nimodipine in Aneurysmal Subarachnoid Hemorrhage Patients

Background: Histamine (H) 2 blockers led to a significant increase of the relative bioavailability of nimodipine and therefore may change tolerability of nimodipine in patients with aneurysmal subarachnoid hemorrhage (SAH). Objective: To determine the effect of H2 blockers on outcome of SAH patients being treated with nimodipine on outcomes. Methods: We analyzed data from Cerner Health Facts® which collected data from participating facilities from January 1st, 2000 to July 1st, 2018. We identified SAH patients who underwent endovascular or surgical treatment for intracranial aneurysm and received nimodipine with or without H2 blockers. Outcome was defined by discharge destination and classified into none to minimal disability, moderate to severe disability, or death. Results: A total of 815 (54.8%) of 1488 SAH patients received H2 blockers in addition to nimodipine. There were no differences in rates of cerebral ischemia (8.8% versus 9.8%) or performance of angioplasty (3.8% versus 3.7%) between patients who did or did not receive H2 blockers. There were no differences in rates of intubation/mechanical ventilation (26.0% versus 29.3%) or intra-procedural cerebral infarction (3.4% versus 2.8%) between the two groups. There was no difference in in hospital mortality rates (10.9% versus 10.2%) or none to minimal disability (41.8% versus 38.2%) between patients who did or did not receive H2 blockers. Conclusions: H2 blockers are frequently used with nimodipine in SAH patients and did not appear to adversely affect rates of death or disability. The finding does not support any clinically significant interaction between H2 blockers and nimodipine in SAH patients.