Objective Immune dysregulation influences outcome following acute ischemic stroke (AIS). Admission white blood cell (WBC) counts are routinely obtained, making the neutrophil–lymphocyte ratio (NLR) a readily available biomarker of the immune response to stroke. This study sought to identify the relationship between NLR and 90 day AIS outcome. Methods A retrospective analysis was performed on patients who underwent endovascular therapy for AIS at West Virginia University Hospitals, Morgantown, West Virginia. Admission WBC differentials were analyzed as the NLR. Stroke severity was measured by the National Institutes of Health Stroke Scale (NIHSS) score and outcome by the modified Rankin Scale (mRS) score at 90 days. Univariate relationships between NLR, age, NIHSS, and mRS were established by correlation coefficients; the t test was used to compare NLR with recanalization and stroke location (anterior vs posterior). Logistic regression models were developed to identify the ability of NLR to predict mRS when controlling for age, recanalization, and treatment with IV tissue plasminogen activator (tPA). Results 116 patients were reviewed from 2008 to 2011. Mean age of the sample was 67 years, and 54% were women. Mean baseline NIHSS score was 17 and 90 day mRS score was 4. There was a significant relationship between NLR and mRS (p=0.02) that remained when controlling for age, treatment with IV tPA, and recanalization. NLR ≥5.9 predicted poor outcome and death at 90 days. Conclusions This study shows that the NLR, a readily available biomarker, may be a clinically useful tool for risk stratification when evaluating AIS patients as candidates for endovascular therapies.

C-reactive protein (CRP) is an inflammatory biomarker of inflammation and may reflect progression of vascular disease. Conflicting evidence suggests CRP may be a prognostic biomarker of ischemic stroke outcome. Most studies that have examined the relationship between CRP and ischemic stroke outcome have used mortality or subsequent vascular event as the primary outcome measure. Given that nearly half of stroke patients experience moderate to severe functional impairments, using a biomarker like CRP to predict functional recovery rather than mortality may have clinical utility for guiding acute stroke treatments. The primary aim of this study was to systematically and critically review the relationship between CRP and long-term functional outcome in ischemic stroke patients to evaluate the current state of the literature. PubMed and MEDLINE databases were searched for original studies which assessed the relationship between acute CRP levels measured within 24 hours of symptom onset and long-term functional outcome. The search yielded articles published between 1989 and 2012. Included studies used neuroimaging to confirm ischemic stroke diagnosis, high-sensitivity CRP assay, and a functional outcome scale to assess prognosis beyond 30 days after stroke. Study quality was assessed using the REMARK recommendations. Five studies met all inclusion criteria. Results indicate a significant association between elevated baseline high sensitivity CRP and unfavorable long-term functional outcome. Our results emphasize the need for additional research to characterize the relationship between acute inflammatory markers and long-term functional outcome using well-defined diagnostic criteria. Additional studies are warranted to prospectively examine the relationship between high sensitivity CRP measures and long-term outcome.

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Introduction Acute respiratory distress syndrome (ARDS) is present in approximately 10% of ICU admissions and is associated with great morbidity and mortality. Prone ventilation has been shown to improve refractory hypoxemia and mortality in patients with ARDS. Methods In this simulation, a 70-year-old male had been transferred to the ICU for ARDS and was undergoing scheduled prone ventilation as part of his care when he experienced a cardiopulmonary arrest secondary to a tension pneumothorax. Learners demonstrated how to manage cardiac arrest in a prone patient and subsequently identified and treated the tension pneumothorax that was the cause of his initial arrest. This single-session simulation for internal medicine residents (PGY 1-PGY 4) utilized a prone mannequin connected to a ventilator in a high-fidelity simulation center. Following the simulation, facilitators led a team debriefing and reviewed key learning objectives. Results A total of 103 internal medicine residents participated in this simulation. Of those, 43 responded to a postsimulation survey. Forty-two of 43 agreed or strongly agreed that all learning objectives were met, that the simulation was appropriate for their level of training, and that their participation would be useful for their future practice. Discussion We designed this simulation to improve learners' familiarity with prone cardiopulmonary resuscitation and to enhance overall comfort with cardiac arrest management. Postsimulation survey results and debriefings revealed that the simulation was a valuable education opportunity, and learners felt that their participation in this simulation would be helpful in their future practice.

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Introduction: Reducing environmental noise has become a priority for many health systems. Following a 10-week preparation period, our health system transitioned from an overhead-activated to a silently activated in-hospital code team notification system. The goal of this initiative was to reduce environmental noise and support code team communication and function without adversely affecting response time, provider availability, or key quality metrics. Methods: Transitioning from overhead to silently activated events involved a three-step quality improvement approach. Input from key stakeholders and preimplementation education were of key importance. Multiple timed trials and a full in situ simulation were completed before going live with the new process. Results: Evaluation of 6-month pre- and postimplementation quality metrics showed no significant difference in compliance with defibrillating shockable rhythms within two minutes, event survival, or survival to discharge. Provider survey data and Hospital Consumer Assessment of Healthcare Providers and Systems “quiet at night” scores were not significantly different. Conclusion: By utilizing a multistep implementation approach, transitioning from overhead pages to a silently activated system for in-hospital code team activation was feasible and safe. Abandoning the overhead paging system did not lead to a decrease in key quality metrics nor impair team perception of code function.

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Objective: Stroke-induced immune suppression is common and clinically observed by the neutrophil- lymphocyte count ratio (NLR). The NLR can predict stroke recovery. The purpose of this study was to identify the relationships between the NLR and our previously established genomic profile for the characterization of immune pathways affecting stroke recovery. Methods: Patients with imaging confirmed ischemic stroke (IS) or transient ischemic attack (TIA) were recruited from West Virginia University Hospital (WVUH) in Morgantown, WV. White blood cell (WBC) differentials were performed on admission then analyzed as a ratio between the neutrophil and lymphocyte counts. Recovery was determined at 90 days for stroke patients only via the Modified Rankin Scale score (MRS). Peripheral blood samples were collected within 24 hours from symptom onset in Paxgene RNA tubes. Total RNA was extracted, amplified, and the expression of ARG1, CA4, CCR7, CSPG2, IQGAP, LY96, MMP9, ORM1, and S100a12 was quantified via Taqman PCR. The gene expression profile was compared to the NLR and MRS via Spearman rho correlation coefficient. Results: A total of 9 IS and 4 TIA patients were included in this study. The mean age of the IS patients was 72 years and TIA patients 70 years. Expression of ARG1 was significantly correlated with elevated NLR at baseline (r=.93, p=.001) for both IS and TIA and poor 90 day MRS (r=.86, p=.01) following IS. Elevated expression of S100A12 was correlated with higher neutrophil count (r=.67, p=.07) and total WBC (r= .78, p=.02) as well as with ARG1 expression (r=0.72; p=0.008) in both patient cohorts. Conclusion: We have identified a significant correlation between the expression of ARG1, S100a12 and the NLR for IS and TIA patients, as well as with ARG1 and outcome following IS. Elevated ARG1 decreases T-cell proliferation resulting in immune suppression. S100A12 modulates neutrophil activity. Our data suggests that ARG1 and S100A12 are interesting candidates for the study of the immune response following cerebral ischemia. Further studies are required to confirm this relationship when controlling for age, disease severity and comorbid conditions.