Impact of simulation training on a telestroke network.

BACKGROUND: Stroke is a leading cause of morbidity and mortality in Brazil, where there are significant imbalances in access to specialized stroke care. Telemedicine networks allow patients to receive neurological evaluation and intravenous thrombolysis in underserved areas, where performance measures are challenging. AIMS: To describe the impact caused by adequate stroke care training, using realistic simulation, in a developing country telestroke network. METHODS: Retrospective observational study comparing the number of all stroke diagnoses, thrombolysis rate, door-to-needle time and symptomatic intracranial hemorrhage after intravenous thrombolysis, during one year providing just algorithms and orientation in stroke care to spoke facilities (phase 1), with the results achieved along one year after the beginning of ongoing live training sessions (phase 2). RESULTS: The mean number of patients diagnosed with stroke increased from 7.5 to 16.58 per month (P = 0.019) rising from 90 patients during phase 1 to 199 in phase 2. There was a reduction in the mean door-to-needle time from 137.1 to 95.5 min (-41.58; 95% CI -62.77 to -20.40). The thrombolysis and symptomatic intracranial hemorrhage rates had a non-significant decrease from 21.31% to 18.18% (OR 0.82; 95% CI 0.39 to 1.71) and 12.5% to 7.69% (OR 0.58; 95% CI 0.046 to 7.425), respectively. CONCLUSIONS: Realistic simulation stroke care training provided by stroke centers to spoke facilities seems to significantly reduce door-to-needle time and enhance adherence in a telestroke network.

Reperfusion after 4.5 hours reduces infarct growth and improves clinical outcomes.

BACKGROUND: The currently proven time window for thrombolysis in ischemic stroke is 4.5 h. Beyond this, the risks and benefits of thrombolysis are uncertain. AIMS: To determine whether thrombolysis and reperfusion were beneficial after 4.5 h, we examined clinical and radiological outcomes in patients treated with tissue plasminogen activator or placebo within 4.5-6 h, using data from the Echoplanar Imaging Thrombolytic Evaluation Trial. METHODS: In the Echoplanar Imaging Thrombolytic Evaluation Trial, ischemic stroke patients presenting three to six-hours after stroke onset were randomized to tissue plasminogen activator or placebo, without knowledge of magnetic resonance imaging results. This analysis was restricted to patients treated between 4.5 and 6 h. The effect of tissue plasminogen activator and reperfusion on infarct growth between baseline diffusion-weighted imaging and day 90 T2 imaging was assessed, along with good neurological outcome (≥8 point reduction or reaching 0-1 at 90 days on National Institutes of Health Stroke Scale) and functional outcome (modified Rankin scale). The effect of tissue plasminogen activator on reperfusion was also analyzed. RESULTS: Sixty-nine patients were treated 4.5-6 h after onset, and infarct growth was assessed in 63. Tissue plasminogen activator was associated with lower relative growth (94% vs. 168%, P = 0.03) and a trend to lower absolute growth (-0.17 ml versus 9.6 ml, P = 0.07). Reperfusion was increased in the tissue plasminogen activator group (58% versus 25%, P = 0.03) and was associated with increased rates of good neurological (86% versus 28% P < 0.001) and functional (modified Rankin scale 0-2 73% versus 34%, P = 0.01) outcomes. Reperfusion was strongly associated with lower relative (80% versus 189%, P < 0.001) and absolute (-2.5 ml versus 40 ml, P < 0.001) infarct growth. CONCLUSIONS: Thrombolysis 4.5-6 h after stroke onset reduced infarct growth and increased the rate of reperfusion, which was associated with good neurological and functional outcome.

Lung parenchyma remodeling in a murine model of chronic allergic inflammation.

This study tested the hypotheses that chronic allergic inflammation induces not only bronchial but also lung parenchyma remodeling, and that these histologic changes are associated with concurrent changes in respiratory mechanics. For this purpose, airway and lung parenchyma remodeling were evaluated by quantitative analysis of collagen and elastin, immunohistochemistry (smooth-muscle actin expression, eosinophil, and dendritic cell densities), and electron microscopy. In vivo (airway resistance, viscoelastic pressure, and static elastance) and in vitro (tissue elastance, resistance, and hysteresivity) respiratory mechanics were also analyzed. BALB/c mice were sensitized with ovalbumin and exposed to repeated ovalbumin challenges. A marked eosinophilic infiltration was seen in lung parenchyma and in large and distal airways. Neutrophils, lymphocytes, and dendritic cells also infiltrated the lungs. There was subepithelial fibrosis, myocyte hypertrophy and hyperplasia, elastic fiber fragmentation, and increased numbers of myofibroblasts in airways and lung parenchyma. Collagen fiber content was increased in the alveolar walls. The volume proportion of smooth muscle-specific actin was augmented in distal airways and alveolar duct walls. Airway resistance, viscoelastic pressure, static elastance, and tissue elastance and resistance were significantly increased. In conclusion, prolonged allergen exposure induced remodeling not only of the airway wall but also of the lung parenchyma, leading to in vivo and in vitro mechanical changes.