Background High-flow nasal oxygen therapy (HFOT) is a promising first-line therapy for acute respiratory failure. However, its weaning has never been investigated and could lead to unnecessary prolonged intensive-care unit (ICU) stay. The aim of this study is to assess predictors of successful separation from HFOT in critically ill patients. We performed a retrospective monocenter observational study over a 2-year period including all patients treated with HFOT for acute respiratory failure in the ICU. Those who died or were intubated without prior HFOT separation attempt, who were treated with non-invasive ventilation at the time of HFOT separation, or who received HFOT as a preventive treatment during the post-extubation period were excluded. Results From the 190 patients analyzed, 168 (88%) were successfully separated from HFOT at the first attempt. Patients who failed separation from HFOT at the first attempt had longer ICU length of stay than those who succeeded: 10 days (7–12) vs. 5 (4–8), p < 0.0001. Fraction of inspired oxygen (FiO2) ≤ 40% and a respiratory rate-oxygenation (ROX) index (calculated as the ratio of SpO2/FiO2 to the respiratory rate) ≥ 9.2 predicted successful separation from HFOT with sensitivity of 85% and 84%, respectively. Conclusions FiO2 ≤ 40% and ROX index ≥ 9.2 were two predictors of successful separation from HFOT at the bedside. Prospective multicenter studies are needed to confirm these results.
BackgroundIschemia reperfusion injury (IRI) induced immune response is a critical issue in transplantation. Complement and contact system activation are among its key mechanisms.Study designWe investigated the benefits of pre-reperfusion treatment with recombinant human C1INH (rhC1INH), inhibitor of both complement and contact activation, in a pig model of kidney autotransplantation, subjecting the organ to 60 min warm ischemia prior to 24 h static preservation to maximize damage.ResultsSerum creatinine measurement showed that treated animals recovered glomerular function quicker than the Vehicle group. However, no difference was observed in tubular function recovery, and elevated level of urinary NGal (Neutrophil gelatinase-associated lipocalin) and plasma AST (Aspartate Aminotransferase) were detected, indicating that treatment did not influence IRI-mediated tubular cell necrosis. Regarding chronic graft outcome, rhC1INH significantly prevented fibrosis development and improved function. Immunohistochemistry and western blot showed decreased invasion by macrophages and T lymphocytes, and reduction of epithelial to mesenchymal transition. We determined the effect of treatment on complement activation with immunofluorescence analyses at 30 min post reperfusion, showing an inhibition of C4d deposition and MBL staining in treated animals.ConclusionsIn this model, the inhibition of complement activation by rhC1INH at reperfusion, while not completely counteracting IRI, limited immune system activation, significantly improving graft outcome on the short and long term.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1013-7) contains supplementary material, which is available to authorized users.
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