Exacerbation of COPD Treatment Combination Therapy NIV with Thermal Helium- Oxygen Plus Nitric Oxide: A Case Report

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide despite increased health care efforts, financial costs, and research concerning its early diagnosis and proper management [1]. The most relevant event affecting COPD mortality is the acute exacerbation of COPD (AECOPD), a catastrophic event during the clinical course of the disease [2]. In cases of acute respiratory acidosis, noninvasive mechanical ventilation (NIV) is considered. Nevertheless, in 30% of patients with severe exacerbation of COPD, NIV does not lead to the desired results [3]. However, there have been cases of NIV failure in patients with severe respiratory acidosis, and associated pulmonary arterial hypertension. Many studies have shown that thermal helium-oxygen and nitric oxide gas heat treatment has many effects. Here we are reporting a case of severe exacerbation COPD, 67 years old male patient, who came to us with shortness of breath, fever, wheezing and a cough with yellow phlegm. He had a history of smoking 30 pack-year smoker many years. He was given NIV treatment with a combination of helium and nitric oxide heat. And we have had very good results.

The Clinical Utility of Forced Oscillation Technique (FOT) during Hospitalisation in patients with exacerbation of COPD

BackgroundForced Oscillation Technique (FOT) is an innovative tool to measure within-breath reactance at 5 Hz (ΔXrs5Hz) but its feasibility and utility in acute exacerbations of COPD (AECOPD) is understudied.MethodsA prospective observational study was conducted in 82 COPD patients admitted due to AECOPD. FOT indices were measured and the association between these indices and spirometry, peak inspiratory flow rate, blood inflammatory biomarkers and patient-reported outcomes including assessment of dyspnoea, quality of life; anxiety and depression and frailty at admission and discharge were explored.ResultsAll patients were able to perform FOT in both sitting and supine position. The prevalence of expiratory flow limitation (EFL) in the upright position was 39% (32/82) and increased to 50% (41/82) in the supine position. EFL (measured by ΔXrs5Hz) and resistance at 5 Hz (Rrs5Hz) negatively correlated with FEV1; those with EFL had lower FEV1 (0.74±0.30 versus 0.94±0.36 L, p=0.01) and FVC (1.7 ±0.55 versus 2.1 ±0.63 L, p= 0.009) and higher BMI [27 (21–36) versus 23 (19–26) kg/m2, p=0.03] compared to those without EFL. During recovery from AECOPD, changes in EFL was observed in association with improvement in breathlessness.ConclusionFOT was easily used to detect EFL during hospitalisation due to AECOPD. The prevalence of EFL increased when patients moved from a seated to a supine position and EFL was negatively correlated with airflow limitation. Improvements in EFL were associated with a reduction in breathlessness. FOT is of potential clinical value by providing a non-invasive, objective, and effort-independent technique to measure lung function parameters during AECOPD requiring hospital admission.

Microalbuminuria on admission for acute exacerbation of COPD as a predictor of all-cause mortality and future exacerbations

ObjectivesMicroalbuminuria (MAB) is a sensitive biomarker of cardiovascular risk that is directly associated with cardiovascular events and mortality. Recent studies have evaluated the presence of MAB in patients with stable chronic obstructive pulmonary disease (COPD) or hospitalised for acute exacerbation of COPD (AECOPD).MethodsWe evaluated 320 patients admitted for AECOPD in respiratory medicine departments of two tertiary hospitals. On admission, demographic, clinical and laboratory values and COPD severity were assessed. Patients were evaluated monthly for 1 year, recording new AECOPD and death from any cause.ResultsPatients with documented MAB (urinary albumin excretion of 30–300 mg/24 hours) on admission had worse lung function (forced expiratory volume in 1 s, %) (mean (SD) 34.2 (13.6)% vs 61.5 (16.7)%), higher modified Medical Research Council (3.6 (1.2) vs 2.1 (0.8)), lower 6 min walk test (171 (63) vs 366 (104)) and more hospitalisation days (9 (2.8) vs 4.7 (1.9)) (p<0.001 for all comparisons). MAB was also correlated with Global Initiative for Chronic Obstructive Lung Disease 2020 COPD stages (p<0.001). In multivariate regression analysis, MAB was a significant predictor of longer hospitalisation duration (OR 6.847, 95% CI 3.050 to 15.370, p<0.0001). Twelve-month follow-up revealed that patients with MAB experienced more AECOPDs (4.6 (3.6) vs 2.2 (3.5), p<0.0001) and deaths, n (%) (52 (36.6) vs 14 (7.8), p<0.001). Kaplan-Meier survival curves demonstrated that patients with MAB presented with increased mortality, AECOPD and hospitalisation for AECOPD risk at 1 year (p<0.001 for all comparisons).ConclusionsThe presence of MAB on admission for AECOPD was associated with more severe COPD and prolonged hospitalisation, as well as with higher rates of AECOPD and mortality risk at 1-year follow-up.

IL-20 Cytokines Are Involved in Epithelial Lesions Associated with Virus-Induced COPD Exacerbation in Mice

(1) Background: viral infections are a frequent cause of chronic obstructive pulmonary disease (COPD) exacerbations, which are responsible for disease progression and mortality. Previous reports showed that IL-20 cytokines facilitate bacterial lung infection, but their production and their role in COPD and viral infection has not yet been investigated. (2) Methods: C57BL/6 WT and IL-20 Rb KO mice were chronically exposed to air or cigarette smoke (CS) to mimic COPD. Cytokine production, antiviral response, inflammation and tissue damages were analyzed after PVM infection. (3) Results: CS exposure was associated with an increase in viral burden and antiviral response. PVM infection in CS mice enhanced IFN-γ, inflammation and tissue damage compared to Air mice. PVM infection and CS exposure induced, in an additive manner, IL-20 cytokines expression and the deletion of IL-20 Rb subunit decreased the expression of interferon-stimulated genes and the production of IFN-λ2/3, without an impact on PVM replication. Epithelial cell damages and inflammation were also reduced in IL-20 Rb-/- mice, and this was associated with reduced lung permeability and the maintenance of intercellular junctions. (4) Conclusions: PVM infection and CS exposure additively upregulates the IL-20 pathway, leading to the promotion of epithelial damages. Our data in our model of viral exacerbation of COPD identify IL-20 cytokine as a potential therapeutic target.

Silent Hypoxia in COVID-19: A Case Series

<b><i>Background:</i></b> The coronavirus disease 2019 (COVID-19) pandemic is an ongoing global crisis challenging the worldwide healthcare systems. Many patients present with a mismatch of profound hypoxemia and few signs of respiratory distress (i.e., silent hypoxemia). This particular clinical presentation is often cited, but data are limited. <b><i>Main Body:</i></b> We describe dyspnea sensation as assessed by using the BORG scale in pulmonary patients admitted to the emergency room during a 4-week period and transferred to the respiratory department of Siloah Hospital, Hannover, Germany. From October 1 to November 1, 2020, 82 patients with hypoxemia defined as oxygen demand to achieve an oxygen saturation (SpO₂) ≥92% were included. In 45/82 (55%) patients, SARS-CoV-2 was detected by PCR on admission. Among non-COVID patients, exacerbation of COPD was the main diagnosis (15/37, 41%). All subjects rated their perceived dyspnea using the modified Borg CR10 scale. Patients in the non-COVID group suffered from more dyspnea on the modified Borg CR10 scale (median 1, IQR: 0–2 vs. median 5, IQR: 3–6, <i>p</i> &#x3c; 0.001). In multivariate analysis, “silent hypoxemia” as defined by the dyspnea Borg CR10 scale ≥5 was independently associated with COVID-19 and presence of severe hypocapnia with an odds ratio of 0.221 (95% confidence interval 0.054, 0.907, <i>p</i> 0.036). <b><i>Conclusion:</i></b> Among pulmonary patients with acute hypoxemia defined as oxygen demand, patients suffering from COVID-19 experience less dyspnea compared to non-COVID patients. “Silent” hypoxemia was more common in COVID-19 patients.