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Due to the exponential growth of the number of subjects affected by coronavirus disease 2019 (COVID-19), the entire Italian health care system had to respond promptly and in a very short time with the need of semi-intensive and intensive care units. Moreover, trained dedicated COVID-19 teams consisting of physicians were coming from different specialties (intensivists or pneumologists and infectiologists), while respiratory therapists and nurses have been recruited to work on and on without rest. However, due to still limited and evolving knowledge of COVID-19, there are few recommendations concerning the need in respiratory rehabilitation and physiotherapy interventions. The presentation of this paper is the result of a consensus promoted by the Italian societies of respiratory health care professionals who contacted pulmonologists directly involved in the treatment and rehabilitation of COVID-19. The aim was to formulate the more proper and common suggestions to be applied in different hospital settings in offering rehabilitative programs and physiotherapy workforce planning for COVID-19 patients. Two main areas of intervention were identified: organization and treatment, which are described in this paper to face the emergency.

Patients with coronavirus disease 2019 (COVID-19) are reported to have a greater prevalence of hyperglycaemia. Cytokine release as a consequence of severe acute respiratory syndrome coronavirus 2 infection may precipitate the onset of metabolic alterations by affecting glucose homeostasis. Here we describe abnormalities in glycometabolic control, insulin resistance and beta cell function in patients with COVID-19 without any pre-existing history or diagnosis of diabetes, and document glycaemic abnormalities in recovered patients 2 months after onset of disease. In a cohort of 551 patients hospitalized for COVID-19 in Italy, we found that 46% of patients were hyperglycaemic, whereas 27% were normoglycaemic. Using clinical assays and continuous glucose monitoring in a subset of patients, we detected altered glycometabolic control, with insulin resistance and an abnormal cytokine profile, even in normoglycaemic patients. Glycaemic abnormalities can be detected for at least 2 months in patients who recovered from COVID-19. Our data demonstrate that COVID-19 is associated with aberrant glycometabolic control, which can persist even after recovery, suggesting that further investigation of metabolic abnormalities in the context of long COVID is warranted. Fiorina and colleagues document alterations in glucose metabolism in patients with COVID-19 and use continuous glucose monitoring to show that glycaemic abnormalities could still be detected 2 months after disease onset in patients who had recovered.

ObjectivesCOVID-19 causes lung parenchymal and endothelial damage that lead to hypoxic acute respiratory failure (hARF). The influence of hARF severity on patients’ outcomes is still poorly understood.DesignObservational, prospective, multicentre study.SettingThree academic hospitals in Milan (Italy) involving three respiratory high dependency units and three general wards.ParticipantsConsecutive adult hospitalised patients with a virologically confirmed diagnosis of COVID-19. Patients aged <18 years or unable to provide informed consent were excluded.InterventionsAnthropometrical, clinical characteristics and blood biomarkers were assessed within the first 24 hours from admission. hARF was graded as follows: severe (partial pressure of oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) <100 mm Hg); moderate (PaO2/FiO2 101–200 mm Hg); mild (PaO2/FiO2 201–300 mm Hg) and normal (PaO2/FiO2 >300 mm Hg).Primary and secondary outcome measuresThe primary outcome was the assessment of clinical characteristics and in-hospital mortality based on the severity of respiratory failure. Secondary outcomes were intubation rate and application of continuous positive airway pressure during hospital stay.Results412 patients were enrolled (280 males, 68%). Median (IQR) age was 66 (55–76) years with a PaO2/FiO2 at admission of 262 (140–343) mm Hg. 50.2% had a cardiovascular disease. Prevalence of mild, moderate and severe hARF was 24.4%, 21.9% and 15.5%, respectively. In-hospital mortality proportionally increased with increasing impairment of gas exchange (p<0.001). The only independent risk factors for mortality were age ≥65 years (HR 3.41; 95% CI 2.00 to 5.78, p<0.0001), PaO2/FiO2 ratio ≤200 mm Hg (HR 3.57; 95% CI 2.20 to 5.77, p<0.0001) and respiratory failure at admission (HR 3.58; 95% CI 1.05 to 12.18, p=0.04).ConclusionsA moderate-to-severe impairment in PaO2/FiO2 was independently associated with a threefold increase in risk of in-hospital mortality. Severity of respiratory failure is useful to identify patients at higher risk of mortality.Trial registration numberNCT04307459

Background Epidemiology of dysphagia and its drivers in obstructive sleep apnea (OSA) are poorly understood. The study aims to investigate the prevalence of dysphagia symptoms and their association with demographic and clinical factors in patients with OSA. Methods Patients with OSA referring to an Academic Sleep Outpatient Clinic were enrolled in a prospective study. Demographic, clinical characteristics, and OSA symptoms were collected. All patients underwent home sleep cardiorespiratory polygraphy and the Eating-Assessment Tool questionnaire (EAT-10) to investigate dysphagia symptoms. Patients with a positive EAT-10 were offered to undergo a fiberoptic endoscopic evaluation of swallowing (FEES) to confirm the presence of dysphagia. FEES findings were compared with a healthy control group. Univariate and multivariate analyses were performed to assess predictors of dysphagia. Results 951 patients with OSA (70% males, age 62 IQR51-71) completed the EAT-10, and 141 (15%) reported symptoms of dysphagia. Female gender (OR = 2.31), excessive daily sleepiness (OR = 2.24), number of OSA symptoms (OR = 1.25), anxiety/depression (OR = 1.89), and symptoms of gastroesophageal reflux (OR = 2.75) were significantly (p < 0.05) associated with dysphagia symptoms. Dysphagia was confirmed in 34 out of 35 symptomatic patients that accepted to undergo FEES. Patients with OSA exhibited lower bolus location at swallow onset, greater pharyngeal residue, and higher frequency and severity of penetration and aspiration events than healthy subjects (p < 0.05). Conclusion A consistent number of patients with OSA show symptoms of dysphagia, which are increased in females and patients with a greater OSA symptomatology, anxiety and depression, and gastroesophageal reflux. The EAT-10 appears a useful tool to guide the selection of patients at high risk of dysphagia. In clinical practice, the integration of screening for dysphagia in patients with OSA appears advisable.

[...]timely CPAP removal appears desirable [1, 2]. [...]predictors should be sequentially measured at different time-points during zero-PEEP, to assess their performance variability during the weaning trial and unassisted breathing [2, 6]. [...]the mROX threshold of 8.4 mmHg/bpm appears a sensitive and robust predictor of weaning success from helmet CPAP in patients with COVID-19.

Introduction COPD is a leading cause of death and significant healthcare burden in Italy. The ETHOS (NCT02465567||5/2015) and IMPACT (NCT02164513||6/2014) randomized controlled trials (RCTs) have evaluated single-inhaler triple therapy (SITT) and have shown SITT efficacy and safety in reducing exacerbations and all-cause mortality in COPD patients. Despite benefits seen in RCTs, there are currently no studies that evaluate the long-term implications of broader and appropriate SITT use in Italy. We therefore evaluated the potential impact of broader SITT adoption on mortality, exacerbations, and related medical costs in Italy. Methods We developed a 10-year (2025–2034) microsimulation model using literature-based patient demographic and clinical characteristics, incidence, therapy distribution and changes, COPD severity changes, mortality, and exacerbations to simulate the Italian COPD population. We modeled two scenarios: “status quo” and “increased SITT,” and used patients’ airflow limitation and exacerbation history (per GOLD guidelines) to choose patients for SITT. The model simulated annual changes in patient characteristics and related changes in medication therapy over 10-years. Patients’ progression reflected reductions in % of FEV1 predicted and annual clinical characteristics. Flagged patients were those that qualified for SITT. Results A starting population of approximately 1,550,000 diagnosed prevalent and incident COPD patients were included in the analysis. Based on our modeled “increased SITT” simulation and medication transition algorithm, at the end of the 10-year projection, the prevalent and incident COPD population in Italy increased to 1,881,000 patients, of which 45.4% received SITT. Over 10 years, modeled increased SITT treatment reduced severe and moderate Exacerbations by 12% and 13%, respectively, and all-cause mortality by 14%, avoiding 40,000 deaths, compared to status quo treatment for flagged COPD patients. Consequently, higher than current SITT adoption could reduce associated medical costs by €646 million for flagged COPD patients. Conclusion Assuming RCTs effects and adherence translate to clinical practice, our model shows that higher than current SITT use in the Italian COPD population may lead to lower mortality rates and exacerbations, ensuring a substantial savings in associated medical costs. The results of this modeling study could provide rationale to modify existing practices on SITT prescribing with the aim of alleviating the burden of COPD.

BackgroundPsoriatic arthritis (PsA) patients are often affected by numerous comorbidities. However, contrasting results have been reported with regard to the respiratory involvement in PsA patients. The aim of this study was to evaluate the presence of subclinical airway inflammation in non-smoking PsA patients compared to patients with only psoriasis using the fraction of exhaled nitric oxide (FeNO) as an indirect marker of airway inflammation.MethodsThe study included 164 non-smoking psoriatic patients (Psoriasis Area of Severity Index or PASI score > 10): 82 with and 82 without PsA, who underwent FeNO tests at different flow rates (30, 50, 100, 200 mL/s). PsA patients were evaluated with Disease Activity in PSoriatic Arthritis Score (DAPSA). Both study groups were compared in terms of FeNO values and its association with the PASI score. The correlations between the variables were evaluated by means of Pearson’s coefficient.ResultsPatient with PsA had higher levels of FeNO than those with psoriasis but without arthritis (at 30 mL/s, 71.09 ± 18.40 ppb vs 66.88 ± 19.12 ppb (NS); at 50 mL/s, 36.61 ± 9.30 ppb vs 30.88 ± 9.73 ppb (p < 0.001); at 100 mL/s, 19.09 ± 4.66 ppb vs 16.63 ± 4.90 ppb (p < 0.001); and at 200 mL/s, 10.88 ± 2.53 ppb vs 9.43 ± 2.55 ppb (p < 0.001), respectively). PASI score correlated to FeNO only in psoriatic patients without arthritis. However, CASPAR index correlated with FeNO (FeNO30: r = 0.81, p < 0.001; FeNO50: r = 0.84, p < 0.001; FeNO100: r = 0.71, p < 0.001; FeNO200: r = 0.58, p < 0.001). DAPSA was also correlated with FeNO to all flows (FeNO30: r = 0.43, p < 0.001; FeNO50: r = 0.33, p < 0.001; FeNO100: r = 0.34, p < 0.001; FeNO200: r = 0.25, p < 0.001).ConclusionsPsA patients seem to have more commonly subclinical airway inflammation than those with only psoriasis. Further studies are needed to replicate these findings.Key Points• Fraction of exhaled nitric oxide (FeNO) is a useful device to detect and monitor airway inflammation not only in asthma but also in systemic inflammatory diseases such as psoriatic arthritis and psoriasis.• Clinicians should be aware to check respiratory diseases in patients with psoriatic arthritis.

The topic of 24-hour management of COPD is related to day-to-night symptoms management, specific follow-up and patients' adherence to therapy. COPD symptoms strongly vary during day and night, being worse in the night and early morning. This variability is not always adequately considered in the trials. Night-time symptoms are predictive of higher mortality and more frequent exacerbations; therefore, they should be a target of therapy. During night-time, in COPD patients the supine position is responsible for a different thoracic physiology; moreover, during some sleep phases the vagal stimulation determines increased bronchial secretions, increased blood flow in the bronchial circulation (enhancing inflammation) and increased airway resistance (broncho-motor tone). Moreover, in COPD patients the circadian rhythm may be impaired. The role of pharmacotherapy in this regard is still poorly investigated. Symptoms can be grossly differentiated according to the different phenotypes of the disease: wheezing recalls asthma, while dyspnea is strongly related to emphysema (dynamic hyperinflation) or obstructive bronchiolitis (secretions). Those symptoms may be different targets of therapy. In this regard, GOLD recommendations for the first time introduced the concept of phenotype distinction suggesting the use of inhaled corticosteroids (ICS) particularly when an asthmatic pattern or eosiophilic inflammations are present, and hypothesized different approaches to target symptoms (ie, dyspnea) or exacerbations. Pharmacotherapy should be evaluated and possibly directed on the basis of circadian variations, for instance, supporting the use of twice-daily rapid-action bronchodilators and evening dose of ICS. Recommendations on day and night symptoms monitoring strategies and choice of the specific drug according to patient's profile are still not systematically investigated or established. This review is the summary of an advisory board on the topic \"24-hour control of COPD and role of pharmacotherapy\", held by five pulmonologists, experts in respiratory pathophysiology, pharmacology and sleep medicine.

Background Environmental pollution is a known risk factor for multiple diseases and furthermore increases rate of hospitalisations. We investigated the correlation between emergency room admissions (ERAs) of the general population for respiratory diseases and the environmental pollutant levels in Milan, a metropolis in northern Italy. Methods We collected data from 45770 ERAs for respiratory diseases. A time-stratified case-crossover design was used to investigate the association between air pollution levels and ERAs for acute respiratory conditions. The effects of air pollutants were investigated at lag 0 to lag 5, lag 0–2 and lag 3–5 in both single and multi-pollutant models, adjusted for daily weather variables. Results An increase in ozone (O 3 ) levels at lag 3–5 was associated with a 78% increase in the number of ERAs for asthma, especially during the warm season. Exposure to carbon monoxide (CO) proved to be a risk factor for pneumonia at lag 0–2 and in the warm season increased the risk of ERA by 66%. A significant association was found between ERAs for COPD exacerbation and levels of sulphur dioxide (SO 2 ), CO, nitrate dioxide (NO 2 ), and particulate matter (PM 10 and PM 2.5 ). The multipollutant model that includes all pollutants showed a significant association between CO (26%) and ERA for upper respiratory tract diseases at lag 0–2. For chronic obstructive pulmonary disease (COPD) exacerbations, only CO (OR 1.19) showed a significant association. Conclusions Exposure to environmental pollution, even at typical low levels, can increase the risk of ERA for acute respiratory diseases and exacerbation of obstructive lung diseases in the general population.