Lesion size is a significant factor predicting visualization of EBUS for PPL. The location of PPL on CT scans and position of the probe are significantly related to a higher diagnostic yield with EBUS-guided TBB.
IntroductionThe effectiveness of corticosteroid therapy on the mortality of acute respiratory distress syndrome (ARDS) remains under debate. We aimed to explore the grounds for the inconsistent results in previous studies and update the evidence.MethodsWe searched MEDLINE, Cochrane Central Register of Controlled Trials and Web of Science up to December 2013. Eligible studies included randomized clinical trials (RCTs) and cohort studies that reported mortality and that had corticosteroid nonusers for comparison. The effect of corticosteroids on ARDS mortality was assessed by relative risk (RR) and risk difference (RD) for ICU, hospital, and 60-day mortality using a random-effects model.ResultsEight RCTs and 10 cohort studies were included for analysis. In RCTs, corticosteroids had a possible but statistically insignificant effect on ICU mortality (RD, −0.28; 95% confidence interval (CI), −0.53 to −0.03 and RR, 0.55; 95% CI, 0.24 to 1.25) but no effect on 60-day mortality (RD, −0.01; 95% CI, −0.12 to 0.10 and RR, 0.97; 95% CI, 0.75 to 1.26). In cohort studies, corticosteroids had no effect on ICU mortality (RR, 1.05; 95% CI, 0.74 to 1.49) but non-significantly increased 60-day mortality (RR, 1.30; 95% CI, 0.96 to 1.78). In the subgroup analysis by ARDS etiology, corticosteroids significantly increased mortality in influenza-related ARDS (three cohort studies, RR, 2.45, 95% CI, 1.40 to 4.27).ConclusionsThe effects of corticosteroids on the mortality of ARDS differed by duration of outcome measures and etiologies. Corticosteroids did not improve longer-term outcomes and may cause harm in certain subgroups. Current data do not support routine use of corticosteroids in ARDS. More clinical trials are needed to specify the favorable and unfavorable subgroups for corticosteroid therapy.
Chronic obstructive pulmonary disease (COPD) is the leading cause of death worldwide, and poses a substantial economic and social burden. Telemonitoring has been proposed as a solution to this growing problem, but its impact on patient outcome is equivocal. This randomized controlled trial aimed to investigate effectiveness of telemonitoring in improving COPD patient outcome. In total, 106 subjects were randomly assigned to the telemonitoring (n = 53) or usual care (n = 53) group. During the two months following discharge, telemonitoring group patients had to report their symptoms daily using an electronic diary. The primary outcome measure was time to first re-admission for COPD exacerbation within six months of discharge. During the follow-up period, time to first re-admission for COPD exacerbation was significantly increased in the telemonitoring group than in the usual care group (p = 0.026). Telemonitoring was also associated with a reduced number of all-cause re-admissions (0.23 vs. 0.68/patient; p = 0.002) and emergency room visits (0.36 vs. 0.91/patient; p = 0.006). In conclusion, telemonitoring intervention was associated with improved outcomes among COPD patients admitted for exacerbation in a country characterized by a small territory and high accessibility to medical services. The findings are encouraging and add further support to implementation of telemonitoring as part of COPD care.
Objectives: Experience with extracorporeal membrane oxygenation for adult patients with refractory septic shock remains limited. We aimed to study the clinical features and outcomes of this patient group in an extracorporeal membrane oxygenation referral center in Taiwan.Methods: From January 2005 to December 2010, all adult patients in refractory septic shock and requiring venoarterial extracorporeal membrane oxygenation for circulatory support were included in the present study. The variables analyzed included patient demographics; comorbidities; smoking status; hemodynamic, ventilatory, and laboratory parameters just before extracorporeal membrane oxygenation support; clinical course; extracorporeal membrane oxygenation details; complications; microbiology results; and outcomes. The primary endpoint was survival to hospital discharge.Results: A total of 52 patients, 39 men and 13 women, were included during a 6-year period. Their median age and body mass index was 56.8 years and 24.1 kg/m 2 , respectively. Of the 52 patients, 39 (75%) had failure of at least 3 organ systems and 21 (40%) had developed cardiac arrest and received cardiopulmonary resuscitation at extracorporeal membrane oxygenation implantation. Of these 52 patients, 8 (15%) survived to hospital discharge. The nonsurvivors were significantly older than the survivors (59.3 vs 43.8 years; P ¼ .009), and all 20 patients (38%) aged 60 years or older died.
IntroductionNatural history of chronic obstructive pulmonary disease (COPD) is punctuated by exacerbations; however, little is known about prognosis of the first-ever COPD exacerbation and variables predicting its outcomes.Materials and MethodsA population-based cohort study among COPD patients with their first-ever exacerbations requiring hospitalizations was conducted. Main outcomes were in-hospital mortality and one-year mortality after discharge. Demographics, comorbidities, medications and in-hospital events were obtained to explore outcome predictors.ResultsThe cohort comprised 4204 hospitalized COPD patients, of whom 175 (4%) died during the hospitalization. In-hospital mortality was related to higher age (odds ratio [OR]: 1.05 per year; 95% confidence interval [CI]: 1.03–1.06) and Charlson comorbidity index score (OR: 1.08 per point; 95% CI: 1.01–1.15); angiotensin II receptor blockers (OR: 0.61; 95% CI: 0.38–0.98) and β blockers (OR: 0.63; 95% CI: 0.41–0.95) conferred a survival benefit. At one year after discharge, 22% (871/4029) of hospital survivors were dead. On multivariate Cox regression analysis, age and Charlson comorbidity index remained independent predictors of one-year mortality. Longer hospital stay (hazard ratio [HR] 1.01 per day; 95% CI: 1.01–1.01) and ICU admission (HR: 1.33; 95% CI: 1.03–1.73) during the hospitalization were associated with higher mortality risks. Prescription of β blockers (HR: 0.79; 95% CI: 0.67–0.93) and statins (HR: 0.66; 95% CI: 0.47–0.91) on hospital discharge were protective against one-year mortality.ConclusionsEven the first-ever severe COPD exacerbation signifies poor prognosis in COPD patients. Comorbidities play a crucial role in determining outcomes and should be carefully assessed. Angiotensin II receptor blockers, β blockers and statins may, in theory, have dual cardiopulmonary protective properties and probably alter prognosis of COPD patients. Nevertheless, the limitations inherent to a claims database study, such as the diagnostic accuracy of COPD and its exacerbation, should be born in mind.
This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1 mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0 mA and 10 mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1 mA compared to those stimulated with 1.0 mA or 10 mA. These results suggest that more NPY was released following low-intensity stimulation, and consequently fewer NPY-LI fibers and more c-Fos-LI cells were identified in the CN. Furthermore, the number of c-Fos-LI cells as well as the percentage of c-Fos-LI cuneothalamic projection neurons (CTNs) in the CN was markedly decreased after injection of NPY receptor antagonist along with retrograde tract-tracing method, indicating that NPY regulated c-Fos expression. In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.
STANDARDIZED and functional virally inactivated HPGF can be prepared from human PC for possible applications in cell therapy and regenerative medicine.
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