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BACKGROUND: Bronchiectasis is the consequence of chronic bronchial inflammation, inappropriate mucus clearance, bacterial colonization, and recurrent or chronic infection. High flow therapy (HFT) is a type of non-invasive respiratory therapy, usually delivered through a nasal cannula interface (HFNC). It delivers heated and humidified air with a stable fraction of inspired oxygen and a wide range of possible flow rates. AIM OF THE STUDY: Determine the effectiveness of HFNC as add-on therapy in adult primary and secondary bronchiectasis with frequent acute exacerbations (AEs) and/or hospitalizations. METHODS: This is a single-center crossover study on long-term home therapy with HFNC in adult bronchiectasis. Pharmacological therapy included pulse therapy with mucolytics and bronchodilators. After one year, all patients were switched to additional HFNC. The temperature range was 31-37 °C. The flow range was 35-60 L/m. FiO2 was 0.21. RESULTS: Seventy-eight patients completed the follow-up; 54% were females; the median age was 70 years (IQR 60-76). The etiology of bronchiectasis was mainly post-infective (51%), COPD related (26%), and congenital (11%). AEs at baseline were 2.81 (±2.15). A significant reduction in AEs was observed after 24 months with a mean of 0.45 (±0.66) (f-ratio value 79.703. p-value < 0.00001). No significant difference was observed after HFNC therapy on FEV1 (2.39 ± 0.87 vs. 2.55 ± 0.82; f-ratio 0.79. p-value 0.45) and FVC (2.73 ± 0.88 vs. 2.84 ± 0.90; f-ratio 0.411. p-value 0.66). A significant reduction in mMRC score was observed after HFNC therapy (2.40 ± 0.81 vs. 0.97 ± 0.97 at 2 months vs. 0.60 ± 0.78 at 24 months; f-ratio value 95.512. p-value < 0.00001). CONCLUSIONS: HFNC is a well-tolerated add-on therapy for adult bronchiectasis. Dyspnea improved after 2 months and further after 2 years. The exacerbation rate decreased during the 2 years follow-up. No significant difference was observed in lung function.
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Mechanical ventilation started with negative-pressure ventilation (NPV) during the 1950s to assist patients with respiratory failure, secondary to poliomyelitis. Over the years, technological evolution has allowed for the development of more comfortable devices, leading to an increased interest in NPV. The patients affected by neuromuscular diseases (NMD) with chronic and acute respiratory failure (ARF) may benefit from NPV. The knowledge of the available respiratory-support techniques, indications, contraindications, and adverse effects is necessary to offer the patient a personalized treatment that considers the pathology's complexity.
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A 59-year-old female ex-smoker with 40 pack year smoking history and a 5-year current e-cigarette (EC) use history, presented with progressive dyspnea on exertion and daily cough for 2 months. A CT scan showed a consolidation area with air bronchogram in the middle lobe and non-calcific bilateral nodules, which could be attributed to community-acquired pneumonia. The patient was treated with empiric antibiotics and systemic steroids for 10 days. Infectious, neoplastic and autoimmune pathologies were excluded, whereas a broncho-alveolar lavage revealed an accumulation of lipids in the cytoplasm of the alveolar macrophages. Despite the recommendation of vaping cessation, the patient continued to use EC. A new CT exam, carried out after 18 months, showed reversed halo sign (RHS), patchy ground-glass opacity (GGO), pleuro-parenchymal bands, and indeed perilobular pattern, suggestive of organizing pneumonia (OP). The final diagnosis was E-cigarette, or vaping, product use Associated Lung Injury (EVALI)- related OP.
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Sistemas Electrónicos de Liberación de Nicotina , Lesión Pulmonar , Médicos , Neumonía , Vapeo , Femenino , Humanos , Lesión Pulmonar/inducido químicamente , Lesión Pulmonar/diagnóstico por imagen , Persona de Mediana Edad , Neumonía/diagnóstico por imagen , Neumonía/etiología , Radiólogos , Vapeo/efectos adversosRESUMEN
Background and objective: Insertion/deletion polymorphisms of angiotensin-converting enzyme (ACE) have been previously described in association with adult respiratory distress syndrome (ARDS) and correlated to outcome. The ACE deletion/deletion(D/D)genotype represents a marker of thrombosis in subjects apparently without predisposing factors and/or traditional thrombophilic alterations and increases the risk of venous thromboembolism in subjects in whom a thrombogenic condition occurs. Thrombosis seems to play a role very early in the disease caused by SARS-CoV-2, in particular in those with severe COVID-19 pneumonia. The counterbalance between angiotensin-converting enzyme (ACE) and ACE2 activities in COVID-19 disease may play a crucial role in the thrombo-inflammatory process. We hypothesised that a genetic predisposition could condition the severity and complications of SARS-CoV-2 infection. Materials and methods: We conducted a spontaneous, single centre observational study in the Sub-Intensive Care Unit of A.O.R.N. Ospedali dei Colli, Cotugno Hospital, Naples (Italy). In this study, we performed genetic screening for ACE D/D genotype and other thrombophilic mutations in 20 patients affected by ARDS related to COVID-19 pneumonia, compared to 19 age- and sex-matched healthy controls. Results: All tested patients had multiple polymorphisms and, in particular, a significantly higher prevalence of ACE D/D polymorphism in severe COVID-19 patients Conclusion: We found that the majority of patients who tested positive for ACE D-D genotype and who were not associated with other risk factors for VTE showed an evolution to ARDS. This finding could have a predicting role in the selection of patients more prone to developing severe COVID-19 during clinical observation in emergency department.
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COVID-19 , Peptidil-Dipeptidasa A , Adulto , Servicio de Urgencia en Hospital , Genotipo , Humanos , Peptidil-Dipeptidasa A/genética , Factores de Riesgo , SARS-CoV-2RESUMEN
BACKGROUND: Pneumomediastinum, subcutaneous emphysema and pneumothorax are not rarely observed during the COVID-19 pandemic. Such complications can worsen gas exchange and the overall prognosis in critical patients. The aim of this study is to investigate what predisposing factors are related to pneumomediastinum and pneumothorax in SARS-CoV2-Acute Respiratory Distress Syndrome (ARDS), what symptoms may predict a severe and potentially fatal complication and what therapeutical approach may provide a better outcome. METHODS: In this single center cohort study, we recorded data from 45 critically ill COVID-19 patients who developed one or more complicating events among pneumomediastinum, subcutaneous emphysema and pneumothorax. All patients showed ARDS and underwent non-invasive ventilation (NIV) at baseline. Patients with mild to moderate ARDS and pneumomediastinum/pneumothorax (n = 25) received High Flow Nasal Cannula (HFNC), while patients with severe ARDS and pneumomediastinum/pneumothorax underwent HFNC (n = 10) or invasive mechanical ventilation (IMV) (n = 10). RESULTS: Pneumomediastinum/pneumothorax developed in 10.5% of subjects affected by SARS-coV2-ARDS. Dyspnea affected 40% and cough affected 37% of subjects. High resolution computed tomography of the chest showed bilateral diffuse ground glass opacities (GGO) in 100% of subjects. Traction bronchiolectasis, reticulation, crazy paving and distortion were observed in 64%. Furthermore, 36% showed subcutaneous emphysema. Non-severe ARDS cases received HFNC, and 76% patients recovered from pneumomediastinum/pneumothorax over a median follow up of 5 days. Among severe ARDS cases the recovery rate of pneumomediastinum/pneumothorax was 70% with the HFNC approach, and 10% with IMV. CONCLUSION: HFNC is a safe and effective ventilatory approach for critical COVID-19 and has a positive role in associated complications such as pneumomediastinum and pneumothorax.
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SARS-CoV-2 is a betacoronavirus that belongs to the family Coronaviridae and the order Nidovirales (1). During December 2019, a series of pneumonia cases caused by a SARS-CoV-2 outbreak was identified in Wuhan, Hubei, China, and rapidly spread across the world. The spectrum of SARS-CoV-2 disease (COVID 19) varies from asymptomatic or paucisymptomatic forms to clinical conditions characterized by respiratory failure that necessitate mechanical ventilation and support in an intensive care unit (ICU), multiorgan and systemic manifestations, and, in terms of sepsis, septic shock, and multiple organ dysfunction syndromes (MODS) (2). Whilst many reports have characterized the clinical, epidemiological, laboratory, and radiological features, as well as treatment and clinical outcomes of patients with COVID-19 pneumonia, information on SARS-CoV-2 reactivation remains unreported. Curative and eradicative therapy for COVID-19 is not currently available (3). We report a case of a patient with PCR-confirmed COVID-19 pneumonia who experienced reactivation after 43 days and negative PCR sampling.
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We describe a 42-year old woman, admitted to our Department after 15 days of persistence of respiratory failure and treated with infusion of intravenous immunoglobulin with a successful outcome.
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Most recent studies have stressed a high risk of thromboembolism in patients with SARS-CoV-2 infection, particularly in those with severe COVID-19 pneumonia. Counterbalance between angiotensin-converting-enzyme (ACE) and ACE2 activities in COVID-19 disease may be crucially involved in the thrombo-inflammatory process. Currently, no study has investigated ACE I/D polymorphism involvement in COVID-19 disease complicated by pulmonary embolism, hence the aim of the present pilot study. This is a retrospective, single-center observational case-control study, conducted at the Sub-Intensive Care Unit of A.O.R.N. Ospedali dei Colli, Cotugno Hospital, Naples (Italy). We included 68 subjects with severe/critical COVID-19 pneumonia. COVID-19 patients were divided according to occurrence of PE (PE+, n = 25) or absence of thromboembolic complications (PE-, n = 43). Assessment of ACE I/D polymorphisms showed a statistically significant difference between PE+ and PE- patients (p = 0.029). Particularly, prevalence of D/D homozygous polymorphism was significantly higher in PE+ COVID-19 patients than in PE- (72 vs. 46.5%; p = 0.048), while heterozygote I/D polymorphism was significantly lower expressed in PE+ patients than in PE- (16 vs. 48.8%; p = 0.009). Computed tomographic pulmonary angiography showed predominantly mono/bilateral sub-segmental embolisms. In conclusion, our findings let us hypothesize a genetic susceptibility to thromboembolism in COVID-19 disease. ACE D/D polymorphism might represent a genetic risk factor, although studies on larger populations are needed.
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A young woman with a clinical history characterized by recurrent respiratory infections, occurring since early infancy, was referred to our hospital. When the patient was a young girl, she underwent sweat chloride test, serum analysis of immunoglobulins, and evaluation of blood lymphocyte subsets; all these diagnostic tests were normal, as well as chest X ray aside from pneumonia episodes. Skin prick tests were positive for several different allergens, and a diagnosis of allergic rhinitis was made. At the age of 11 years, she started to complain of gastroesophageal reflux disease (GERD) symptoms, and a gastroscopy detected a hiatal hernia with esophagitis. Despite pharmacologic treatments for allergic rhinitis and GERD, the patient continued to complain of chronic cough, associated with choking and recurrent respiratory infections treated with antibiotic therapy. For the first time in her life, we performed a spirometry that showed a flow-volume curve characterized by a plateau in the expiratory phase, suggestive of an central airway obstruction. Bronchoscopy demonstrated a compression of the distal portion of trachea. Computed tomography (CT) angiogram revealed a double aortic arch. Barium enhancement evidenced an esophageal compression. A surgical division of the smaller of the two arches was then performed. Therefore, we strongly suggest to perform lung function tests in all cases of unexplained respiratory complaints.