BackgroundThere is an emerging understanding that coronavirus disease 2019 (COVID-19) is associated with increased incidence of pneumomediastinum. We aimed to determine its incidence among patients hospitalised with COVID-19 in the United Kingdom and describe factors associated with outcome.MethodsA structured survey of pneumomediastinum and its incidence was conducted from September 2020 to February 2021. United Kingdom-wide participation was solicited via respiratory research networks. Identified patients had SARS-CoV-2 infection and radiologically proven pneumomediastinum. The primary outcomes were to determine incidence of pneumomediastinum in COVID-19 and to investigate risk factors associated with patient mortality.Results377 cases of pneumomediastinum in COVID-19 were identified from 58 484 inpatients with COVID-19 at 53 hospitals during the study period, giving an incidence of 0.64%. Overall 120-day mortality in COVID-19 pneumomediastinum was 195/377 (51.7%). Pneumomediastinum in COVID-19 was associated with high rates of mechanical ventilation. 172/377 patients (45.6%) were mechanically ventilated at the point of diagnosis. Mechanical ventilation was the most important predictor of mortality in COVID-19 pneumomediastinum at the time of diagnosis and thereafter (p<0.001) along with increasing age (p<0.01) and diabetes mellitus (p=0.08). Switching patients from continuous positive airways pressure support to oxygen or high flow nasal oxygen after the diagnosis of pneumomediastinum was not associated with difference in mortality.ConclusionsPneumomediastinum appears to be a marker of severe COVID-19 pneumonitis. The majority of patients in whom pneumomediastinum was identified had not been mechanically ventilated at the point of diagnosis.

Reduction of the risk of asthma attacks is a major goal of current asthma management. We propose to derive a risk scale predicting asthma attacks based on the blood eosinophil count and exhaled nitric oxide. Biomarker-stratified trial-level attack rates were extracted and pooled from the control arms of the Novel START, CAPTAIN, QUEST, Benralizumab Phase 2b, PATHWAY, STRATOS 1–2 and DREAM trials (n=3051). These were used to derive rate ratios and the predicted asthma attack rate for different patient groups. The resultant prototype risk scale shows potential to predict asthma attacks, which may be prevented by anti-inflammatory treatment.

Purpose of Review Subcutaneous emphysema is often observed by clinicians in the context of pneumothorax. It is usually clinically insignificant, but in a few cases can progress to threaten the patient’s vision or airway. A variety of approaches to management of such cases are described in the literature. There no controlled trials and no guidelines on management, other than that the cause should be identified and treated wherever possible. The goal of this article is to review the described approaches to subcutaneous emphysema in pneumothorax and provide a reference to the clinician. Summary Treatment can be directed primarily towards treating an underlying pneumothorax and / or towards the subcutaneous emphysema. These are not mutually exclusive approaches. Management of the underlying pneumothorax includes conservative management; use of negative suction; siting of wider bore intercostal drains and definitive surgical management. Management of subcutaneous emphysema may include decompression techniques such as: ‘blow hole’ incisions or subcutaneous angio-catheters or tunnelled drains. In the current absence of controlled trials is not possible to comment on the efficacy of these techniques: no recommendations on management of subcutaneous emphysema in pneumothorax can be made. Management will be significantly influenced by local technical expertise and patient factors for the foreseeable future.

No abstract

Reduction of the risk of asthma attacks is a major goal of current Global Initiative for Asthma (GINA) guidelines. OBJECTIVE: To develop a risk scale to predict asthma attacks based on the blood eosinophil count and exhaled nitric oxide. METHODS: Trial-level data were extracted from the Novel START, CAPTAIN, LIBERTY ASTHMA QUEST and DREAM trials. Attack rates for control or placebo-treated patients (n=1989) were stratified by blood eosinophils and exhaled nitric oxide in a 3×3 grid using cut-offs 0.15-0.30×10 9 cells/L and 25-50 ppb. Rate ratios and relative risks were used to derive biomarker-stratified multipliers for GINA treatment step attack rates derived from 222,817 patients. Other parameters included were a recent asthma attack history (≤1 year), ≥2 concurrent clinical risk factors*, and GINA treatment step. We compared predicted versus observed biomarker-stratified asthma attack rates in placebo-treated groups reported in 17 independent clinical trials. RESULTS: Biomarker-stratified asthma attack rates were multiplied by 0.64 in the lowest type 2 biomarker combination group and 1.96 in the highest. A previous asthma attack and/or having concurrent risk factors independently increased rates 2.8and/or 1.4-fold, respectively. Predicted annual attack rates ranged from 0.06 in the lowest biomarker step 1&2 patients to 2.4 in the highest biomarker step 5 patients. The resultant scale is shown in Figure 1. There was close agreement between observed and predicted asthma attack rates (intraclass correlation coefficient 0.80; 95% CI 0.56-0.90). CONCLUSION: Our prototype scale based on biomarkers of type 2 airway inflammation proves feasibility and shows potential to predict asthma attacks which can be prevented by anti-inflammatory treatment. FIGURE 1. Prototype Oxford Asthma Attack Risk ScaLE (ORACLE). Numbers in each cell are predicted annual asthma attack rates for patients over the age of 12. An asthma attack is an episode of acute asthma requiring treatment with systemic steroids ≥ 3 days. Blood eosinophil count is contemporaneous or the highest result in last 12 months; fractional exhaled nitric oxide level is contemporaneous. *Risk factors are GINA-defined: poor symptom control, low lung function, adherence issues, reliever overuse, intubation or intensive care unit admission for asthma previously, comorbidities (chronic rhinosinusitis, obesity, psychiatric disease), environmental exposures (smoking, allergen, pollution).

No abstract

No abstract