Airway hillocks are injury-resistant reservoirs of unique plastic stem cells.

Airway hillocks are stratified epithelial structures of unknown function1. Hillocks persist for months and have a unique population of basal stem cells that express genes associated with barrier function and cell adhesion. Hillock basal stem cells continually replenish overlying squamous barrier cells. They exhibit dramatically higher turnover than the abundant, largely quiescent classic pseudostratified airway epithelium. Hillocks resist a remarkably broad spectrum of injuries, including toxins, infection, acid and physical injury because hillock squamous cells shield underlying hillock basal stem cells from injury. Hillock basal stem cells are capable of massive clonal expansion that is sufficient to resurface denuded airway, and eventually regenerate normal airway epithelium with each of its six component cell types. Hillock basal stem cells preferentially stratify and keratinize in the setting of retinoic acid signalling inhibition, a known cause of squamous metaplasia2,3. Here we show that mouse hillock expansion is the cause of vitamin A deficiency-induced squamous metaplasia. Finally, we identify human hillocks whose basal stem cells generate functional squamous barrier structures in culture. The existence of hillocks reframes our understanding of airway epithelial regeneration. Furthermore, we show that hillocks are one origin of 'squamous metaplasia', which is long thought to be a precursor of lung cancer.

IL-17A and TNF-α as potential biomarkers for acute respiratory distress syndrome and mortality in patients with obesity and COVID-19.

Coronavirus disease 2019 (COVID-19) was declared a pandemic and international health emergency by the World Health Organization. Patients with obesity with COVID-19 are 7 times more likely to need invasive mechanical ventilation than are patients without obesity (OR 7.36; 95% CI: 1.63-33.14, p = 0.021). Acute respiratory distress syndrome (ARDS) is one of the main causes of death related to COVID-19 and is triggered by a cytokine storm that damages the respiratory epithelium. Interleukins that cause the chronic low-grade inflammatory state of obesity, such as interleukin (IL)-1ß, IL-6, monocyte chemoattractant peptide (MCP)-1, and, in particular, IL-17A and tumour necrosis factor alpha (TNF-α), also play very important roles in lung damage in ARDS. Therefore, obesity is associated with an immune state favourable to a cytokine storm. Our hypothesis is that serum concentrations of TNF-α and IL-17A are more elevated in patients with obesity and COVID-19, and consequently, they have a greater probability of developing ARDS and death. The immunobiology of IL-17A and TNF-α opens a new fascinating field of research for COVID-19.

A burned body with a gunshot wound in the mouth and a suicide note: A complex or complicated suicide?

The body of a 53-year-old man was found in a burning car. The ignition key was in start position and the accelerator pedal was held down by his right foot. Autopsy revealed a gunshot entrance wound in the hard palate, a bullet track through the anterior cranial fossa and a projectile lodged in the left frontal lobe. The brain stem was free of lesions and any signs of secondary brain injury, such as brain oedema and intracranial haemorrhage, were not significant. Soot deposits and thermal injury to the mucosa were observed in the airways below the glottis and carboxyhaemoglobin (COHb) saturation was 40%. A single bullet case and a handgun were recovered next to the driver's seat. Fire investigators identified the motor as the beginning of the burning: therefore, the conclusion was that the car had caught fire due to overheating of the engine. Differential diagnosis between complex and complicated suicide was essential. The cause of death was identified as carbon monoxide intoxication, and the injuries to the brain were not felt to be immediately fatal. The case has been classified as a complicated suicide. There are no other published cases of a complicated suicide involving exposure to fire or the use of firearms.

Burkholderia pseudomallei invades the olfactory nerve and bulb after epithelial injury in mice and causes the formation of multinucleated giant glial cells in vitro.

The infectious disease melioidosis is caused by the bacterium Burkholderia pseudomallei. Melioidosis is characterised by high mortality and morbidity and can involve the central nervous system (CNS). We have previously discovered that B. pseudomallei can infect the CNS via the olfactory and trigeminal nerves in mice. We have shown that the nerve path is dependent on mouse strain, with outbred mice showing resistance to olfactory nerve infection. Damage to the nasal epithelium by environmental factors is common, and we hypothesised that injury to the olfactory epithelium may increase the vulnerability of the olfactory nerve to microbial insult. We therefore investigated this, using outbred mice that were intranasally inoculated with B. pseudomallei, with or without methimazole-induced injury to the olfactory neuroepithelium. Methimazole-mediated injury resulted in increased B. pseudomallei invasion of the olfactory epithelium, and only in pre-injured animals were bacteria found in the olfactory nerve and bulb. In vitro assays demonstrated that B. pseudomallei readily infected glial cells isolated from the olfactory and trigeminal nerves (olfactory ensheathing cells and trigeminal Schwann cells, respectively). Bacteria were degraded by some cells but persisted in other cells, which led to the formation of multinucleated giant cells (MNGCs), with olfactory ensheathing cells less likely to form MNGCs than Schwann cells. Double Cap mutant bacteria, lacking the protein BimA, did not form MNGCs. These data suggest that injuries to the olfactory epithelium expose the primary olfactory nervous system to bacterial invasion, which can then result in CNS infection with potential pathogenic consequences for the glial cells.

A novel rat model for tracheal mucosal damage assessment of following long term intubation.

OBJECTIVE: Tracheal mucosal damage is a well-known complication of endo-tracheal intubation and animal models are essential for studying the underlying cellular injury cascade. The novel rat model described here is based on retrograde intubation via tracheotomy and suture fixation of the tube. It aims to simulate the common clinical scenario of tube-related airway damage due to long term intubation. STUDY DESIGN: Prospective randomized control pilot study. METHODS: Male Sprague-Dawley were randomly assigned into two groups: control (no intubation, n = 10), one week of intubation (n = 13). The animals were then euthanized and the trachea was sent for histological analysis. Epithelial damage, mucosal thickness, mucosal gland hypertrophy and fibrosis were reviewed. RESULTS: Intubation procedure survival rate was 84.6% (11/13) and 100% in the control (10/10). The damaged ciliary mechanism was a common finding in the intubated group compared to the preserved normal ciliary architecture in almost all control rats. Average tracheal mucosal thickness was 119.0 ±â€¯21.8 µm for the control group and 254.6 ±â€¯22.8 µm for the intubated group, (p < 0.001). The ciliary damage score was 1.00 ±â€¯0.02 in the intubated group, and 0 ±â€¯0.02 in the control group. (p < 0.001). The (objective) average total tracheal mucosal gland area was 19,530 ±â€¯24,606 in the intubated group and 10,031 ±â€¯23,461 in the control group (p < 0,05). Collagen deposition seems higher in the intubated trachea compared to the control. CONCLUSIONS: We describe a novel rat-based animal model for simulating tracheal mucosal damage following long term intubation. This animal model is easy to carry out, reproducible and involves containable animal mortality rates. LEVEL OF EVIDENCE: I.

Collagen sponge scaffolds containing growth factors for the functional regeneration of tracheal epithelium.

Tracheal epithelia have barrier and mucociliary clearance functions that prevent invasion of extraneous particles and infectious materials. Hence, following tracheal reconstructions, functional and morphological regeneration of epithelia is required to prevent respiratory declines and infectious diseases. Although growth factors (GFs) promote the regeneration of tracheal epithelial morphologies, it remains unclear whether tracheal grafts containing GFs are beneficial for regeneration of tracheal epithelial functions. Thus, we fabricated collagen sponge scaffolds containing insulin-like GF-1 (IGF-1) and the basic fibroblast, hepatocyte, and epidermal GFs (bFGFs, HGFs, and EGFs, respectively), and we evaluated the effects of the grafts on the functional regeneration of tracheal epithelia. Partial tracheal defects were imposed surgically, and collagen sponges containing IGF-1, bFGF, HGF, or EGF were then transplanted to defect sites. Subsequent immunofluorescence studies suggested that EGF and bFGF contribute to regular distributions of tight junction molecules, and tracer permeability assays suggested that EGF and bFGF promote regeneration of barrier function. Increased ciliogenesis was also observed using scanning electron microscopy in reconstructed regions treated with EGF- and bFGF-supplemented collagen sponges. However, bFGF-supplemented collagen sponges led to greater microsphere transport than did EGF-supplemented sponges. The present data suggested that collagen sponge scaffold containing bFGF promotes functional regeneration of tracheal epithelial tissues.

A Fatal Mediastinitis Due to a Neck Trauma from an Undeclared Assault.

History of neck trauma should be promptly investigated in patients with severe infections of the chest as mediastinitis. We present a forensic case of a death due to a mediastinitis in a patient with an undetected fracture of the superior horn of the thyroid cartilage that was exclusively revealed at autopsy examination. Histological analyses of the neck tissues showed signs of pharyngeal mucosal microperforation caused by the fracture and surrounded by an inflammatory reaction. The fracture was caused by a not declared manual strangulation attempt, happened several days before medical evaluations. We share our experience to emphasize the importance of revealing the etiologies of fatal infections of the mediastinum both for clinical and forensic purposes.

Tissue Factor Facilitates Wound Healing in Human Airway Epithelial Cells.

BACKGROUND: Tissue factor (TF) canonically functions as the initiator of the coagulation cascade. TF levels are increased in inflamed airways and seem to be important for tumor growth and metastasis. We hypothesized that airway epithelia release TF as part of a wound repair program. OBJECTIVES: The goal of this study was to evaluate whether airway epithelia release TF in response to pro-inflammatory stimuli and to investigate roles of TF in cell growth and repair. METHODS: Airway epithelial cells were exposed to 10 µg/mL of lipopolysaccharide or 1 ng/mL of transforming growth factor ß (TGF-ß). TF and TGF-ß messenger RNA and protein were measured in cell lysate and culture media, respectively. Signaling pathways were evaluated by using selective agonists and inhibitors. Airway epithelia were mechanically injured in the presence of TF and tissue factor pathway inhibitor to investigate their roles in wound repair. RESULTS: TF protein levels increased in cell media after exposure to lipopolysaccharide (P < .01) but only in growing cells, and this action was blocked when exposed to an extracellular signal-regulated kinase inhibitor or a "small" worm phenotype and mothers against Decapentaplegic inhibitor. TF protein also increased in the presence of TGF-ß (P < .05). Exposure to TF pathway inhibitor decreased the rate of cell growth by 60% (P < .05), and exposure to TF increased the rate of airway healing after injury by 19% (P < .05). CONCLUSIONS: Growing airway epithelia release TF when exposed to lipopolysaccharide or TGF-ß. TF reduces wound-healing time in airway epithelia and therefore may be important to airway recovery after injury.

Electrospun mucosal wound dressings containing styptics for bleeding control.

Two major aspects need to be focused to accelerate wound healing of mucosal damages especially in the field of otorhinolaryngology. (i) The problem of application due to the small access during surgery, (ii) the fixation of the wound dressing to reveal a stable healing process. In the present work the high request to a mucosal wound dressing which additionally support hemostasis was addressed. We developed an electrospun fabric made of poly(l-lactide-co-d/l-lactide) (PLA) which can be loaded with the hemostatic agents adrenaline and tranexamic acid to cover mucosal lesions analogues to common skin patches. These loaded electrospun fabrics were demonstrated to be biocompatible, thin and flexible, and thus could be adapted individually to the mucosal defect with respect to localization and size of the lesion. The treatment of mucosal defects with these loaded PLA wound dressings induced a faster and time controlled hemostatic reaction, which significantly improved the healing process.

Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells.

BACKGROUND: Impaired regeneration of airway epithelium may lead to persistence of inflammation and remodelling. Regeneration of injured epithelium is a complex phenomenon and the role of toll-like receptors (TLRs) in the stimulation of respiratory virus products in this process has not been established. OBJECTIVE: This study was undertaken to test the hypothesis that the wound repair process in airway epithelium is modulated by microbial products via toll-like receptors. METHODS: Injured and not-injured bronchial epithelial cells (ECs) (BEAS-2B line) were incubated with the TLR agonists poly(I:C), lipopolisacharide (LPS), allergen Der p1, and supernatants from virus-infected epithelial cells, either alone or in combination with TLR inhibitors. Regeneration and immune response in injured and not-injured cells were studied. RESULTS: Addition of either poly(I:C) or LPS to ECs induced a marked inhibition of wound repair. Supernatants from RV1b-infected cells also decreased regeneration. Preincubation of injured and not-injured ECs with TLR inhibitors decreased LPS and poly(I:C)-induced repair inhibition. TGF-ß and RANTES mRNA expression was higher in injured ECs and IFN-α, IFN-ß, IL-8, and VEGF mRNA expression was lower in damaged epithelium as compared to not-injured. Stimulation with poly(I:C) increased IFN-α and IFN-ß mRNA expression in injured cells, and LPS stimulation decreased interferons mRNA expression both in not-injured and injured ECs. CONCLUSION: Regeneration of the airway epithelium is modulated by microbial products via toll-like receptors.

Nasal symptoms, epithelial injury and neurogenic inflammation in elite swimmers.

BACKGROUND: A high burden of lower airway symptoms is found in elite swimmers. To what extent elite swimmers suffer from upper airway symptoms and how these associate with nasal inflammation is less clear. We here aimed to evaluate upper airway symptoms and nasal inflammation in elite athletes. METHODOLOGY: Elite swimmers, indoor athletes and age-matched controls were recruited. Upper airway symptoms were assessed by sino-nasal outcome test (SNOT)-22 questionnaire. Visual Analogue score (VAS) for nasal symptoms as well as neurogenic and inflammatory mediators in nasal fluid were assessed at baseline, immediately and 24-hours after sport-specific training. The effect of hypochlorite on nasal epithelial cells was evaluated in vitro. RESULTS: Baseline SNOT-22 and VAS for nasal itch and impaired smell were significantly higher in swimmers compared to controls. Nasal substance P and uric acid levels were increased in elite swimmers 24-hours after swimming compared to baseline. In elite swimmers, uric acid levels 24-hours post-exercise correlated with baseline SNOT-22. As increased symptoms and inflammation were found in swimmers but not in indoor athletes, we hypothesized that hypochlorite exposure might be the underlying mechanism. In vitro, the highest dose of hypochlorite decreased nasal epithelial cell integrity and induced release of uric acid. CONCLUSION: Upper airway symptoms are frequently reported in elite swimmers. Intensive swimming resulted in a delayed increase of epithelial injury and neurogenic inflammation.

Exendin-4 partly ameliorates - hyperglycemia-mediated tissue damage in lungs of streptozotocin-induced diabetic mice.

Glucagon-like peptide-1 (GLP-1) stimulates insulin secretion, - plays anti-inflammatory role in atherosclerosis, and has surfactant-releasing effects in lungs. GLP-1 analogues are used in diabetes therapy. This is the first study to investigate the effects of exendin-4, a GLP-1 receptor agonist, on lung injury in diabetic mice. BALB/c male mice were divided into four groups. The first group was given only citrate buffer, the second group was given only exendin-4, the third group was given only streptozotocin (STZ), and the fourth group was given both exendin-4 and STZ. Exendin-4 (3µg/kg) was administered daily by subcutaneous injection for 30days after mice were rendered diabetic with a single dose of STZ (200mg/kg). Structural alterations, oxidative stress, apoptosis, insulin signaling and expressions of prosurfactant-C, alpha-smooth muscle actin, collagen-I and fibronectin were evaluated in lung tissue. Diabetic mice lungs were characterized by induced oxidative stress, apoptosis, edema, and cell proliferation. They had honeycomb-like alveoli, thicker alveolar walls, and hypertrophic pneumocytes. Although exendin-4 treatment improved pulmonary edema, apoptosis, oxidative stress, and lung injury, it led to the disrupted insulin signaling and interstitial collagen accumulation in the lungs of diabetic mice. Exendin-4 ameliorates hyperglycemia-mediated lung damage by reducing glucose, -oxidative stress and stimulating cell proliferation. However, exendin-4 led to increased lung injury partly by reducing insulin signaling - and collagen accumulation around pulmonary vasculature in diabetic mice.

[Effect of conditioned medium from mesenchymal stem cells on regeneration of endothelium at HCl-induced damage trachea in rats].

The purpose. Respiratory epithelium regeneration is studied in rats with tracheal damage induced by inhaling hydrochloric acid vapor. Method. Regeneration process after the chemical burn was activated by intratracheal administration of preparations obtained from the same-species mesenchymal stem cells (MSC). Results. Tracheal epithelium is shown to recover almost completely on day 3-7 after applying MSC compositions (MSCs). Closed structures containing ciliated cells similar to ciliated cells of the respiratory epithelium lining the trachea are formed in the submucosal epithelium during regeneration. These structures migrate towards epithelium and get incorporated into the damaged epithelium. This phenomenon is apparently indicative of the special mechanism of respiratory epithelium regeneration after HCl-induced injury. Conclusion. It is demonstrated in this study that cell-free MSCs instilled intratracheally promote the recovery of normal submucosal epithelium by either preventing or reducing necrosis and inflammation. Such topical MSCs administration significantly accelerates migration of ciliated cell towards the surface and de novo formation of the ciliary epithelium.

Heparin cross-linked collagen sponge scaffolds improve functional regeneration of rat tracheal epithelium.

Tracheal epithelial cells maintain airway homeostasis by mediating mucociliary clearance. Following tracheal reconstruction, timely epithelial regeneration is required to prevent respiratory compromise and infectious diseases. To achieve rapid tracheal epithelial regeneration, a heparin cross-linked collagen sponge containing fibroblast growth factor-2 (FGF-2) was prepared as a graft for tracheal reconstruction. The heparin cross-linked sponge exhibited a high FGF-2 retaining capacity, and tracheal epithelial and mesenchymal cells cultured in this sponge containing FGF-2 showed high proliferative capacities. Subsequently, heparin-free collagen sponge scaffolds (C/F scaffold) and collagen sponge scaffolds cross-linked with 10 µg/ml heparin retained FGF-2 (C/H10/F scaffold), and were transplanted into rats with tracheal defects. Invasion of both epithelial and non-epithelial cells was greater in rats treated with the C/H10/F scaffold at 1 week post-transplantation than in rats treated with the C/F scaffold. Moreover, at 2 weeks after transplantation, improved cilia formation was observed in the C/H10/F scaffold group, with higher motility and more potent posterior-anterior flow generation than in the C/F scaffold group. These results suggest that heparin improves functional regeneration of tracheal epithelium. Copyright © 2017 John Wiley & Sons, Ltd.

Simvastatin Treatment Modulates Mechanically-Induced Injury and Inflammation in Respiratory Epithelial Cells.

Mechanical forces in the respiratory system, including surface tension forces during airway reopening and high transmural pressures, can result in epithelial cell injury, barrier disruption and inflammation. In this study, we investigated if a clinically relevant pharmaceutical agent, Simvastatin, could mitigate mechanically induced injury and inflammation in respiratory epithelia. Pulmonary alveolar epithelial cells (A549) were exposed to either cyclic airway reopening forces or oscillatory transmural pressure in vitro and treated with a wide range of Simvastatin concentrations. Simvastatin induced reversible depolymerization of the actin cytoskeleton and a statistically significant reduction the cell's elastic modulus. However, Simvastatin treatment did not result in an appreciable change in the cell's viscoelastic properties. Simvastatin treated cells did exhibit a reduced height-to-width aspect ratio and these changes in cell morphology resulted in a significant decrease in epithelial cell injury during airway reopening. Interestingly, although very high concentrations (25-50 µM) of Simvastatin resulted in dramatically less IL-6 and IL-8 pro-inflammatory cytokine secretion, 2.5 µM Simvastatin did not reduce the total amount of pro-inflammatory cytokines secreted during mechanical stimulation. These results indicate that although Simvastatin treatment may be useful in reducing cell injury during airway reopening, elevated local concentrations of Simvastatin might be needed to reduce mechanically-induced injury and inflammation in respiratory epithelia.

Impact of Pulmonary Vein Cryoballoon Ablation on Bronchial Injury.

INTRODUCTION: There is a paucity of data on the mechanisms of cough and hemoptysis that sometimes ensue from cryoballoon ablation of pulmonary veins (Cryo-PV). This study specifically examined the impact of ultra-cold (≤-60 °C, 3 minutes), prolonged (>-55 °C, 6 minutes), and conventional (>-55 °C, 3 minutes) Cryo-PV on lung/bronchial injury. METHODS AND RESULTS: Four healthy adult swine underwent Cryo-PV. Each animal received Cryo-PV to the inferior common trunk and the right superior PV. In 2 animals, 1 PV was treated with 2 ultra-cold (Cryo-AUltra-cold ) and the other with 2 conventional (Cryo-AConventional ) cryoapplications. In the other 2 animals, 1 PV was ablated using 2 prolonged (Cryo-BProlonged ) and the other with 2 conventional (Cryo-BConventional ) applications. The nadir cryoballoon temperatures were lower in Cryo-AUltra-cold versus Cryo-AConventional (-66 ± 6 °C vs. -45 ± 5 °C; P = 0.001), but did not differ between Cryo-BProlonged and Cryo-BConventional (-46 ± 3 °C vs. -49 ± 3 °C; P = 0.123). Post-ablation bronchoscopy revealed immediate mucosal edema and erythema with/without bleeding in the adjacent bronchi in 100% of Cryo-AUltra-cold and 50% of Cryo-AConventional /Cryo-BConventional and Cryo-BProlonged . At 4 hours post-ablation, there were marked increases in bronchoalveolar macrophages (P <0.001), lymphocytes (P = 0.035) and neutrophils (P = 0.001). Furthermore, Cryo-AUltra-cold yielded the largest increase in the macrophage (P = 0.005) and neutrophil (P = 0.034) cell counts. While similar trends were seen in Cryo-BProlonged , these did not reach statistical significance. CONCLUSION: Cryo-PV can elicit acute bronchial inflammation, bleeding, and mucosal injury. While this was further augmented by ultra-cold cryoapplications, it was also evident to a lesser degree with prolonged and even conventional cryoapplications. The mechanism for this appears to be direct collateral injury.

Inhibition of endotoxin-induced airway epithelial cell injury by a novel family of pyrrol derivates.

Inflammation and apoptosis are crucial mechanisms for the development of the acute respiratory distress syndrome (ARDS). Currently, there is no specific pharmacological therapy for ARDS. We have evaluated the ability of a new family of 1,2,3,5-tetrasubstituted pyrrol compounds for attenuating lipopolysaccharide (LPS)-induced inflammation and apoptosis in an in vitro LPS-induced airway epithelial cell injury model based on the first steps of the development of sepsis-induced ARDS. Human alveolar A549 and human bronchial BEAS-2B cells were exposed to LPS, either alone or in combination with the pyrrol derivatives. Rhein and emodin, two representative compounds with proven activity against the effects of LPS, were used as reference compounds. The pyrrol compound that was termed DTA0118 had the strongest inhibitory activity and was selected as the lead compound to further explore its properties. Exposure to LPS caused an intense inflammatory response and apoptosis in both A549 and BEAS-2B cells. DTA0118 treatment downregulated Toll-like receptor-4 expression and upregulated nuclear factor-κB inhibitor-α expression in cells exposed to LPS. These anti-inflammatory effects were accompanied by a significantly lower secretion of interleukin-6 (IL-6), IL-8, and IL-1ß. The observed antiapoptotic effect of DTA0118 was associated with the upregulation of antiapoptotic Bcl-2 and downregulation of proapoptotic Bax and active caspase-3 protein levels. Our findings demonstrate the potent anti-inflammatory and antiapoptotic properties of the pyrrol DTA0118 compound and suggest that it could be considered as a potential drug therapy for the acute phase of sepsis and septic ARDS. Further investigations are needed to examine and validate these mechanisms and effects in a clinically relevant animal model of sepsis and sepsis-induced ARDS.

Tolerability and performance of BIP endotracheal tubes with noble metal alloy coating--a randomized clinical evaluation study.

BACKGROUND: Hospital acquired infections worsen the outcome of patients treated in intensive care units and are costly. Coatings with silver or metal alloys may reduce or alter the formation of biofilm on invasive medical devices. An endotracheal tube (ETT) is used to connect the patient to a ventilator and coated tubes have been tested in relation to bacterial colonization and respiratory infection. In the present study, we aimed to evaluate and compare a coated and uncoated ETT for patient symptoms and local tracheal tolerability during short term clinical use. Degree of bacterial colonization was also described. METHODS: A silver-palladium-gold alloy coating ('Bactiguard®'Infection Protection, BIP) has been extensively used on urinary tract catheters and lately also on central venous catheters. We performed a randomised, single-blinded, controlled, first in man, post Conformité Européenne (EC) certification and CE marking study, focused on Bactiguard® coated ETTs (BIP ETT). Thirty patients at a tertiary university hospital scheduled for upper abdominal elective surgery with an expected duration of anaesthesia of at least 3 h were randomised; BIP ETT (n = 20) or standard ETT (n = 10). The tolerability was assessed with a modified version of Quality of Life Head and Neck Module, QLQ-H&N35 and by inspection of the tracheal mucosa with a fibre-optic bronchoscope before intubation and at extubation. Adverse Events (AE) and bacterial adherence were also studied. Statistical evaluations were carried out with the Fisher's Exact Test, the Clopper-Pearson method, as well as a Proportional Odds Model. RESULTS: Differences between groups were identified in 2 of 8 patient related symptoms with regard to tolerability by QLQ-H&N35 (cough, p = 0.022 and dry mouth, p = 0.014 in the treatment group.). No mucosal damage was identified with bronchoscopy. A low level of bacterial colonization with normal flora, equal between groups, was seen after short-term of intubation (median 5 h). No serious Adverse Events related to the use of an ETT were observed. The results should be treated with caution due to statistical confounders, a small study size and large inter-individual variability in bacterial adhesion. CONCLUSIONS: The new device BIP ETT is well tolerated and has good clinical performance during short-term intubation. Studies with larger sample sizes and longer intubation periods (>24 h) in the ICU-setting are needed and can now be planned in order to identify possible differences in clinical outcomes. TRIAL REGISTRATION: Registered in ClinicalTrials.gov, REGISTRATION NUMBER: NCT01682486 , Date of Registration: August, 30, 2012.

[Patient safety and the prevention of skin and mucosal lesions associated with airway invasive devices]. / Segurança do paciente e a prevenção de lesões cutâneo-mucosas associadas aos dispositivos invasivos nas vias aéreas.

OBJECTIVE: To analyze the care implemented by the nursing team to promote the safety of adult patients and prevention of skin and mucosal lesions associated with the presence of lower airways invasive devices. METHOD: Study with qualitative and quantitative approach, descriptive and exploratory type, whose investigative scenarios were adult inpatient units of a hospital in the West Frontier of Rio Grande do Sul. The study subjects consisted of nurses, nursing technicians and nursing assistants. RESULTS: A total of 118 professionals were interviewed. We highlight the observed specific care with endotracheal tube and tracheostomy, management and assessment of the cuff and the criteria used to secretion aspiration. CONCLUSION: There is a superficial nursing work in the patient direct care and a differentiation in relation to the perception of nurse technicians, especially those working in the intensive care unit, who presented major property and view of the patient's clinical status.

Patient safety and the prevention of skin and mucosal lesions associated with airway invasive devices / La seguridad del paciente y la prevención de lesiones cutáneo-mucosas asociadas con los dispositivos invasivos en las vías aéreas / Segurança do paciente e a prevenção de lesões cutâneo-mucosas associadas aos dispositivos invasivos nas vias aéreas

AbstractOBJECTIVETo analyze the care implemented by the nursing team to promote the safety of adult patients and prevention of skin and mucosal lesions associated with the presence of lower airways invasive devices.METHODStudy with qualitative and quantitative approach, descriptive and exploratory type, whose investigative scenarios were adult inpatient units of a hospital in the West Frontier of Rio Grande do Sul. The study subjects consisted of nurses, nursing technicians and nursing assistants.RESULTSA total of 118 professionals were interviewed. We highlight the observed specific care with endotracheal tube and tracheostomy, management and assessment of the cuff and the criteria used to secretion aspiration.CONCLUSIONThere is a superficial nursing work in the patient direct care and a differentiation in relation to the perception of nurse technicians, especially those working in the intensive care unit, who presented major property and view of the patient's clinical status.

ResumenOBJETIVOAnalizar los cuidados implantados por el equipo de Enfermería para la promoción de la seguridad del paciente adulto y la prevención de lesiones cutáneo-mucosas asociadas con la presencia de dispositivos invasivos en las vías aéreas inferiores.MÉTODOEstudio con abordaje cualitativo y cuantitativo, del tipo descriptivo y exploratorio, cuyos escenarios investigativos fueron las unidades de estancia hospitalaria de adultos en un hospital de Fronteira Oeste, Rio Grande do Sul. Los sujetos investigados se constituyeron de enfermeros, técnicos y auxiliares de Enfermería.RESULTADOSFueron entrevistados 118 profesionales. Se evidenciaron los cuidados específicos con el tubo orotraqueal y la traqueotomía, con el manejo y la evaluación del cuff y los criterios utilizados para la aspiración de secreciones.ConclusiónExiste una superficialidad de la actuación del enfermero en el cuidado directo al paciente y una diferenciación con respecto a la percepción de los técnicos de Enfermería, en especial los actuantes en la unidad de terapia intensiva, que presentaron mayor propiedad y visión clínica del paciente.

ResumoOBJETIVOAnalisar os cuidados implementados pela equipe de Enfermagem para a promoção da segurança do paciente adulto e a prevenção de lesões cutâneo-mucosas associadas à presença de dispositivos invasivos nas vias aéreas inferiores.MÉTODOEstudo com abordagem qualitativa e quantitativa, do tipo descritivo e exploratório, cujos cenários investigativos foram as unidades de internação adulto de um hospital da Fronteira Oeste do Rio Grande do Sul. Os sujeitos pesquisados constituíram-se de enfermeiros, técnicos e auxiliares de Enfermagem.RESULTADOSForam entrevistados 118 profissionais. Evidenciaram-se os cuidados específicos com o tubo orotraqueal e traqueostomia, com o manejo e avaliação do cuff e os critérios utilizados para a aspiração de secreções.CONCLUSÃOHá uma superficialidade da atuação do enfermeiro no cuidado direto ao paciente e uma diferenciação em relação à percepção dos técnicos de Enfermagem, em especial os atuantes na unidade de terapia intensiva, que apresentaram maior propriedade e visão da clínica do paciente.