A large number of postoperative pulmonary outcome measures have been used, but most are poorly defined. Our four recommended outcome measures include a new definition of postoperative pulmonary complications, incorporating an assessment of severity. These definitions will meet the needs of most clinical effectiveness trials of treatments to improve postoperative pulmonary outcomes.

No abstract

Objective/Hypothesis: This prospective controlled human and murine study assessed the presence of inflammatory cells and cytokines to test the hypothesis that immune cells are associated with fibroproliferation in iatrogenic laryngotracheal stenosis (iLTS). Methods: Inflammation was assessed by histology and immunofluorescence (IF), quantitative real-time polymerase chain reaction (qRT-PCR), and flow cytometry of cricotracheal resections of iLTS patients compared to normal controls. An iLTS murine model assessed the temporal relationship between inflammation and fibrosis. Results: iLTS specimens showed increased inflammation versus normal controls (159/high power field [hpf] vs. 119/hpf, P = 0.038), and increased CD3 + T-cells, CD4 + cells, and CD3+/CD4 + T-helper (TH) cells (all P < 0.05). The inflammatory infiltrate was located immediately adjacent to the epithelial surface in the superficial aspect of the thickened lamina propria. Human flow cytometry and qRT-PCR showed a significant increase in interleukin (IL)-4 gene expression, indicating a TH2 phenotype. Murine IF revealed a dense CD4 + T-cell inflammatory infiltrate on day 4 to 7 postinjury, which preceded the development of fibrosis. Murine flow cytometry and qRT-PCR studies mirrored the human ones, with increased T-helper cells and IL-4 in iLTS versus normal controls. Conclusion: CD3/CD4 + T-helper lymphocytes and the proinflammatory cytokine IL-4 are associated with iLTS. The association of a TH2 immunophenotype with iLTS is consistent with findings in other fibroinflammatory disorders. The murine results reveal that the inflammatory infiltrate precedes the development of fibrosis. However, human iLTS specimens with well-developed fibrosis also contain a marked chronic inflammatory infiltrate, suggesting that the continued release of IL-4 by T-helper lymphocytes may continue to propagate iLTS.

In an earlier study, Bernard and Jara (1986) found that approximately 50% of clinical graduate students admitted that they would probably not do what the situation demanded when a peer was behaving unethically. In this study, we surveyed professional clinicians and found that significant numbers of them would also do less than they knew they should.

Objectives 1) Develop a novel method for serial assessment of gene and protein expression in laryngotracheal stenosis (LTS) 2) Assess cytokine expression and determine an immunophenotype in LTS. Study Design A matched comparison of endolaryngeal brush-biopsy samples from laryngotracheal scar and normal airway. Setting Tertiary care hospital, 2015–2016 Methods Brush-biopsy specimens of laryngotracheal scar and normal trachea were obtained from seventeen LTS patients at the time of OR dilation and were used for protein and RNA extraction. Gene expression of the TH1 cytokine Interferon-ϒ (INF-ϒ), TH2 cytokine Interleukin (IL) – 4, Transforming Growth Factor – β, and Collagen-1 (Coll1) was quantified using quantitative RT-PCR. Cytokine analysis was performed with flow cytometry using a cytometric bead array. Results LTS specimens demonstrated a 13.68 fold increase in Coll1 gene expression compared to normal (p<0.001, n=17). Additionally, IL-4 gene expression showed a 3.76-fold increase (p<0.001, n=17) in LTS scar. When stratified into iatrogenic LTS (iLTS) and idiopathic subglottic stenosis (iSGS) cohorts INF-ϒ gene expression was significantly increased in iSGS (p=0.011). Soluble cytokine measurements were below the limit of detection for reliable quantification and thus could not be assessed. Conclusions Brush biopsies from LTS samples can be successfully utilized for RNA extraction and demonstrate the expected increase in Coll1 gene expression associated with LTS. Preliminary gene expression suggests abnormal collagen production may be mediated by the TH2 cytokine IL-4, and that increased INF-ϒ expression may represent a key difference between iLTS and iSGS. Further analysis of soluble cytokines is needed to confirm these findings.