The pathophysiology of coronavirus disease-2019 (COVID-19)-related acute respiratory distress syndrome (ARDS) varies from other pneumonia-related ARDS. We evaluated whether the mortality rates differed for COVID-19 and non-COVID-19-related ARDS in the Asian population in 2021. This single center retrospective observational cohort study included patients with COVID-19 and non-COVID-19-related ARDS that required invasive mechanical ventilation. The primary outcome was all-cause in-hospital mortality. The secondary outcomes included hospital length of stay, ICU length of stay, duration of mechanical ventilation, and ventilator-free days (VFDs) during the first 28 days. A 1:1 propensity score matching was performed to correct potential confounders by age, obesity or not, and ARDS severity. One-hundred-and-sixty-four patients fulfilled the inclusion criteria. After 1:1 propensity score matching, there were 50 patients in each group. The all-cause in-hospital mortality of all patients was 38 (38%), and no significant differences were found between COVID-19 and non-COVID-19-related ARDS (17 [34%) vs. 21 [42%], p = 0.410). Both groups had length of stay (30.0 [20.0-46.0] vs. 27.0 [13.0-45.0] days, p = 0.312), ICU length of stay (19.0 [13.0-35.0] vs. 16.0 [10.0-32.0] days, p = 0.249), length of mechanical ventilation (19.0 [10.0-36.0] vs. 14.0 [9.0-29.0] days, p = 0.488), and ventilator-free days during the first 28 days (5.5 [0.0-17.0] vs. 0.0 [0.0-14.0] days, p = 0.320). Immunocompromised status (Hazard ratio: 3.63; 95% CI: 1.51-8.74, p = 0.004) and progress to severe ARDS (Hazard ratio: 2.92; 95% CI: 1.18-7.22, p = 0.020) were significant in-hospital mortality-related confounders. There were no significant difference in mortality among both groups. Immunocompromised status and progression to severe ARDS are two possible risk factors for patients with ARDS; COVID-19 is not a mortality-related risk exposure.

During the early phase of the COVID-19 pandemic, reverse transcriptase-polymerase chain reaction (RT-PCR) testing faced limitations, prompting the exploration of machine learning (ML) alternatives for diagnosis and prognosis. Providing a comprehensive appraisal of such decision support systems and their use in COVID-19 management can aid the medical community in making informed decisions during the risk assessment of their patients, especially in low-resource settings. Therefore, the objective of this study was to systematically review the studies that predicted the diagnosis of COVID-19 or the severity of the disease using ML. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA), we conducted a literature search of MEDLINE (OVID), Scopus, EMBASE, and IEEE Xplore from January 1 to June 31, 2020. The outcomes were COVID-19 diagnosis or prognostic measures such as death, need for mechanical ventilation, admission, and acute respiratory distress syndrome. We included peer-reviewed observational studies, clinical trials, research letters, case series, and reports. We extracted data about the study's country, setting, sample size, data source, dataset, diagnostic or prognostic outcomes, prediction measures, type of ML model, and measures of diagnostic accuracy. Bias was assessed using the Prediction model Risk Of Bias ASsessment Tool (PROBAST). This study was registered in the International Prospective Register of Systematic Reviews (PROSPERO), with the number CRD42020197109. The final records included for data extraction were 66. Forty-three (64%) studies used secondary data. The majority of studies were from Chinese authors (30%). Most of the literature (79%) relied on chest imaging for prediction, while the remainder used various laboratory indicators, including hematological, biochemical, and immunological markers. Thirteen studies explored predicting COVID-19 severity, while the rest predicted diagnosis. Seventy percent of the articles used deep learning models, while 30% used traditional ML algorithms. Most studies reported high sensitivity, specificity, and accuracy for the ML models (exceeding 90%). The overall concern about the risk of bias was "unclear" in 56% of the studies. This was mainly due to concerns about selection bias. ML may help identify COVID-19 patients in the early phase of the pandemic, particularly in the context of chest imaging. Although these studies reflect that these ML models exhibit high accuracy, the novelty of these models and the biases in dataset selection make using them as a replacement for the clinicians' cognitive decision-making questionable. Continued research is needed to enhance the robustness and reliability of ML systems in COVID-19 diagnosis and prognosis.

The Jafron series of sorbent cartridges provides a comprehensive array of coated, highly biocompatible sorbent beads made of styrene-divinylbenzene copolymers. Such beads carry a mean diameter of 0.8 mm with a range from 0.60 to 1.18 mm. The maximal pore size of these coated beads and the volume of the cartridge vary according to the type of cartridge ranging between 50 Da and 60 kDa. The sorbents, the size of the cartridge, the volume of sorbent, and the pore size (which reaches 60 kDa with the HA330 cartridge) aim to take advantage of the principles of molecular adsorption in a variety of diseases from uremic toxin retention to poisoning and drug overdose, from kidney disease to liver failure, from acute respiratory distress syndrome to sepsis, from toxic skin injury to COVID-19. The preliminary data from ex vivo studies, animal investigations, and human pilot work look promising and justify a program of systematic investigation of these products to advance our understanding of how they may be incorporated into our therapeutic arsenal.

Background Severe coronavirus disease 2019 (COVID -19) has led to severe pneumonia or acute respiratory distress syndrome (ARDS) worldwide. we have noted that many critically ill patients with COVID-19 present with typical sepsis-related clinical manifestations, including multiple organ dysfunction syndrome, coagulopathy, and septic shock. The molecular mechanisms that underlie COVID-19, ARDS and sepsis are not well understood. The objectives of this study were to analyze potential molecular mechanisms and identify potential drugs for the treatment of COVID-19, ARDS and sepsis using bioinformatics and a systems biology approach. Methods Three RNA-seq datasets (GSE171110, GSE76293 and GSE137342) from Gene Expression Omnibus (GEO) were employed to detect mutual differentially expressed genes (DEGs) for the patients with the COVID-19, ARDS and sepsis for functional enrichment, pathway analysis, and candidate drugs analysis. Results We obtained 110 common DEGs among COVID-19, ARDS and sepsis. ARG1, FCGR1A, MPO, and TLR5 are the most influential hub genes. The infection and immune-related pathways and functions are the main pathways and molecular functions of these three diseases. FOXC1, YY1, GATA2, FOXL, STAT1 and STAT3 are important TFs for COVID-19. mir-335-5p, miR-335-5p and hsa-mir-26a-5p were associated with COVID-19. Finally, the hub genes retrieved from the DSigDB database indicate multiple drug molecules and drug-targets interaction. Conclusion We performed a functional analysis under ontology terms and pathway analysis and found some common associations among COVID-19, ARDS and sepsis. Transcription factors-genes interaction, protein-drug interactions, and DEGs-miRNAs coregulatory network with common DEGs were also identified on the datasets. We believe that the candidate drugs obtained in this study may contribute to the effective treatment of COVID-19.

Cytokine adsorption using the CytoSorb® adsorber has been proposed in various clinical settings including sepsis, ARDS, hyperinflammatory syndromes, cardiac surgery or recovery after cardiac arrest. The aim of this analysis is to provide evidence for the efficacy of the CytoSorb® adsorber with regard to mortality in various settings.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological pathogen of coronavirus disease 2019 (COVID-19), a highly contagious disease, spreading quickly and threatening global public health. The symptoms of COVID-19 vary from mild reactions to severe respiratory distress or even fatal outcomes probably due to the different status of host immunity against the virus. Here in the study, we unveiled plasma proteomic signatures and transcriptional patterns of peripheral blood mononuclear cells (PBMCs) using blood samples of 10 COVID-19 patients with different severity. Through systemic analysis, α-defensin-1 (DEFA1) was identified to be elevated in both plasma and PBMCs, and correlated with disease severity and stages. In vitro study demonstrated that DEFA1 was secreted from immunocytes and suppressed SARS-CoV-2 infection of both original and mutated strains with dose dependency. By using sequencing data, we discovered that DEFA1 was activated in monocytes through NF-κB signaling pathway after infection, and secreted into circulation to perturb SARS-CoV-2 infection by interfering protein kinase C expression. It worked mainly during virus replication instead of entry in host cells. Together, the anti-SARS-CoV-2 mechanism of DEFA1 has unveiled a corner of how innate immunity is against SARS-CoV-2 and explored its clinical potential in disease prognosis and therapeutic intervention.

In spite of various reports on perinatal outcomes of coronavirus disease 2019 (COVID-19) during pregnancies, the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on unborn babies and pregnant mothers are still mysterious. The goal of our research is to examine the perceived fetomaternal outcomes of COVID-19 during pregnancy. A total of 396 pregnant women were admitted to the Department of Gynaecology and Obstetrics, Pt. JNM Medical College, Raipur, Chhattisgarh, India, during the period from July 20, 2020 to January 6, 2021. The presence of SARS-CoV-2 in different biological samples was recorded via positive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) test results. All the newborns delivered from the infected pregnant mothers were tested as RT-PCR negative. Negative findings of RT-PCR for respiratory swabs of newborns, amniotic fluid, placental tissue, breast milk, vaginal swabs, and cord blood indicated no transmission of the virus from mother to baby. However, maternal outcomes, such as hospitalization (46.96%), preeclampsia (13.88%), pre-term birth (14.39%), prelabor rupture of membranes (PROM) before 34 weeks (3.78%), PROM before 37 weeks (2.77%), vaginal bleeding (4.29%), postpartum hemorrhage (2.52%), pregnancy-induced hypertension (1.51%), and neonatal outcomes such as low birth weight ≤1.5 kg (6.59) and 1.6-2.4 kg (39.34%), intrauterine deaths (IUD) (0.50%), fetal distress (22.33%), NICU admission (5.58%), meconium-stained liquor (14.46%), diarrhea (0.25%), and low APGAR score 4-6 at 1 min (20.54%), were observed. The results of the present study indicate that SARS-CoV-2-induced complications during pregnancy must be taken seriously. Intrauterine fetal deaths occurred at lower rates. There is no substantial proof of vertical perinatal transmission of the virus, as none of the neonates had tested positive for COVID-19.

Long non-coding RNAs (lncRNAs) are endogenously expressed RNAs longer than 200 nt that are not translated into proteins. In general, lncRNAs bind to mRNA, miRNA, DNA, and proteins and regulate gene expression at various cellular and molecular levels, including epigenetics, transcription, post-transcription, translation, and post-translation. LncRNAs play important roles in many biological processes, such as cell proliferation, apoptosis, cell metabolism, angiogenesis, migration, endothelial dysfunction, endothelial-mesenchymal transition, regulation of cell cycle, and cellular differentiation, and have become an important topic of study in genetic research in health and disease due to their close link with the development of various diseases. The exceptional stability, conservation, and abundance of lncRNAs in body fluids, have made them potential biomarkers for a wide range of diseases. LncRNA MALAT1 is one of the best-studied lncRNAs in the pathogenesis of various diseases, including cancers and cardiovascular diseases. A growing body of evidence suggests that aberrant expression of MALAT1 plays a key role in the pathogenesis of lung diseases, including asthma, chronic obstructive pulmonary diseases (COPD), Coronavirus Disease 2019 (COVID-19), acute respiratory distress syndrome (ARDS), lung cancers, and pulmonary hypertension through different mechanisms. Here we discuss the roles and molecular mechanisms of MALAT1 in the pathogenesis of these lung diseases.

The novel coronavirus 2019 (COVID-19) which is caused by severe acute respiratory syndrome coronavirus-2 was first reported from Wuhan, China in December 2019. Since then, it has caused global crisis and it still continues to be a Public Health Emergency of International Concern. Although it primarily involves respiratory system with symptoms ranging from mild to severe acute respiratory distress syndrome, extrapulmonary involvement including gastrointestinal manifestations is increasingly reported. There are few reported cases of acute pancreatitis following severe acute respiratory syndrome coronavirus-2 infection; however, little is known on true prevalence of acute pancreatitis or other extrapulmonary manifestations. More data and research on pathophysiology and organ-specific extrapulmonary manifestations would aid clinicians to monitor and recognise these wide spectra of manifestations so that organ-specific therapeutic strategies and management pathways could be developed. We report a case of acute pancreatitis in an otherwise asymptomatic severe acute respiratory syndrome coronavirus-2 infection. He developed acute upper abdominal pain on day 13th of severe acute respiratory syndrome coronavirus-2 infection detection. Diagnosis of acute pancreatitis was made after his serum amylase level was raised by more than five times the normal and the computed tomography abdomen showed oedematous pancreas. He was successfully managed and discharged after 12 days of diagnosis of acute pancreatitis. On follow-up after 1 year, there were no recurrent attacks of pancreatitis. Our case highlights that acute pancreatitis can occur even in asymptomatic and milder form of COVID-19 and the onset of such complications could be delayed. Abdominal pain in COVID-19 should be carefully assessed because prompt diagnosis and management of acute pancreatitis in COVID-19 patient is crucial in preventing multi-organ dysfunction leading to subsequent morbidity and mortality.

Certain stimuli, such as microorganisms, cause neutrophils to release neutrophil extracellular traps (NETs), which are basically web-like structures composed of DNA with granule proteins, such as myeloperoxidase (MPO) and neutrophil elastase (NE), and cytoplasmic and cytoskeletal proteins. Although interest in NETs has increased recently, no sensitive, reliable assay method is available for measuring NETs in clinical settings. This article describes a modified sandwich enzyme-linked immunosorbent assay to quantitatively measure two components of circulating NETs, MPO-DNA and NE-DNA complexes, which are specific components of NETs and are released into the extracellular space as breakdown products of NETs. The assay uses specific monoclonal antibodies for MPO or NE as the capture antibodies and a DNA-specific detection antibody. MPO or NE binds to one site of the capture antibody during the initial incubation of samples containing MPO-DNA or NE-DNA complexes. This assay shows good linearity and high inter-assay and intra-assay precision. We used it in 16 patients with COVID-19 with accompanying acute respiratory distress syndrome and found that the plasma concentrations of MPO-DNA and NE-DNA were significantly higher than in the plasma obtained from healthy controls. This detection assay is a reliable, highly sensitive, and useful method for investigating the characteristics of NETs in human plasma and culture supernatants.

The potential antimicrobial and anti-inflammatory effectiveness of azithromycin against severe influenza is yet unclear. We retrospectively investigated the effect of intravenous azithromycin administration within 7 days of hospitalization in patients with influenza virus pneumonia and respiratory failure. Using Japan's national administrative database, we enrolled and classified 5066 patients with influenza virus pneumonia into severe, moderate, and mild groups based on their respiratory status within 7 days of hospitalization. The primary endpoints were total, 30-day, and 90-day mortality rates. The secondary endpoints were the duration of intensive-care unit management, invasive mechanical ventilation, and hospital stay. The inverse probability of the treatment weighting method with estimated propensity scores was used to minimize data collection bias. Use of intravenous azithromycin was proportional to the severity of respiratory failure (mild: 1.0%, moderate: 3.1%, severe: 14.8%). In the severe group, the 30-day mortality rate was significantly lower with azithromycin (26.49% vs. 36.65%, p = 0.038). In the moderate group, the mean duration of invasive mechanical ventilation after day 8 was shorter with azithromycin; there were no significant differences in other endpoints between the severe and moderate groups. These results suggest that intravenous azithromycin has favorable effects in patients with influenza virus pneumonia using mechanical ventilation or oxygen.

Ventilation in a prone position (PP) for 12 to 16 h per day improves survival in ARDS. However, the optimal duration of the intervention is unknown. We performed a prospective observational study to compare the efficacy and safety of a prolonged PP protocol with conventional prone ventilation in COVID-19-associated ARDS. Prone position was undertaken if P/F < 150 with FiO2 > 0.6 and PEEP > 10 cm H2O. Oxygenation parameters and respiratory mechanics were recorded before the first PP cycle, at the end of the PP cycle and 4 h after supination. We included 63 consecutive intubated patients with a mean age of 63.5 years. Of them, 37 (58.7%) underwent prolonged prone position (PPP group) and 26 (41.3%) standard prone position (SPP group). The median cycle duration for the SPP group was 20 h and for the PPP group 46 h (p < 0.001). No significant differences in oxygenation, respiratory mechanics, number of PP cycles and rate of complications were observed between groups. The 28-day survival was 78.4% in the PPP group versus 65.4% in the SPP group (p = 0.253). Extending the duration of PP was as safe and efficacious as conventional PP, but did not confer any survival benefit in a cohort of patients with severe ARDS due to COVID-19.

COVID-19-associated ARDS (C-ARDS) is mentioned to express higher analgosedation needs, in comparison to ARDS of other etiologies. The objective of this monocentric retrospective cohort study was to compare the analgosedation needs between C-ARDS and non-COVID-19 ARDS (non-C-ARDS) on veno-venous extracorporeal membrane oxygenation (VV-ECMO). Data were collected from the electronic medical records of all adult patients treated with C-ARDS in our Department of Intensive Care Medicine between March 2020 and April 2022. The control group included patients treated with non-C-ARDS between the years 2009 and 2020. A sedation sum score was created in order to describe the overall analgosedation needs. A total of 115 (31.5%) patients with C-ARDS and 250 (68.5%) with non-C-ARDS requiring VV-ECMO therapy were included in the study. The sedation sum score was significantly higher in the C-ARDS group (p < 0.001). COVID-19 was significantly associated with analgosedation in the univariable analysis. By contrast, the multivariable model did not show a significant association between COVID-19 and the sum score. The year of VV-ECMO support, BMI, SAPS II and prone positioning were significantly associated with sedation needs. The potential impact of COVID-19 remains unclear, and further studies are warranted in order to evaluate specific disease characteristics linked with analgesia and sedation.

Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.

The clinical manifestations of SARS-CoV-2 infection vary widely, from asymptomatic infection to the development of acute respiratory distress syndrome (ARDS) and death. The host response elicited by SARS-CoV-2 plays a key role in determining the clinical outcome. We hypothesized that determining the dynamic whole blood transcriptomic profile of hospitalized adult COVID-19 patients and characterizing the subgroup that develops severe disease and ARDS would broaden our understanding of the heterogeneity in clinical outcomes. We recruited 60 hospitalized patients with RT-PCR-confirmed SARS-CoV-2 infection, among whom 19 developed ARDS. Peripheral blood was collected using PAXGene RNA tubes within 24 h of admission and on day 7. There were 2572 differently expressed genes in patients with ARDS at baseline and 1149 at day 7. We found a dysregulated inflammatory response in COVID-19 ARDS patients, with an increased expression of genes related to pro-inflammatory molecules and neutrophil and macrophage activation at admission, in addition to an immune regulation loss. This led, in turn, to a higher expression of genes related to reactive oxygen species, protein polyubiquitination, and metalloproteinases in the latter stages. Some of the most significant differences in gene expression found between patients with and without ARDS corresponded to long non-coding RNA involved in epigenetic control.

Critical care and mechanical ventilation have a relatively brief history in medicine. Premises existed through the seventeenth to nineteenth centuries but modern mechanical ventilation started in the twentieth century. Noninvasive ventilation techniques had started both in the intensive care unit and for home ventilation at the end of the 1980s and the 1990s. The need for mechanical ventilation is increasingly influenced worldwide by the spread of respiratory viruses, and the last coronavirus disease 2019 pandemic has seen a massive successful use of noninvasive ventilation.

The Cooling to Help Injured Lungs (CHILL) trial is an open label, two group, parallel design multicenter, randomized phase IIB clinical trial assessing the efficacy and safety of targeted temperature management with combined external cooling and neuromuscular blockade to block shivering in patients with early moderate-severe acute respiratory distress syndrome (ARDS). This report provides the background and rationale for the clinical trial and outlines the methods using the Consolidated Standards of Reporting Trials guidelines. Key design challenges include: [1] protocolizing important co-interventions; [2] incorporation of patients with COVID-19 as the cause of ARDS; [3] inability to blind the investigators; and [4] ability to obtain timely informed consent from patients or legally authorized representatives early in the disease process. Results of the Reevaluation of Systemic Early Neuromuscular Blockade (ROSE) trial informed the decision to mandate sedation and neuromuscular blockade only in the group assigned to therapeutic hypothermia and proceed without this mandate in the control group assigned to a usual temperature management protocol. Previous trials conducted in National Heart, Lung, and Blood Institute ARDS Clinical Trials (ARDSNet) and Prevention and Early Treatment of Acute Lung Injury (PETAL) Networks informed ventilator management, ventilation liberation and fluid management protocols. Since ARDS due to COVID-19 is a common cause of ARDS during pandemic surges and shares many features with ARDS from other causes, patients with ARDS due to COVID-19 are included. Finally, a stepwise approach to obtaining informed consent prior to documenting critical hypoxemia was adopted to facilitate enrollment and reduce the number of candidates excluded because eligibility time window expiration.

Since its emergence, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a public health threat worldwide. While the majority of patients recover in 3-4 weeks, complications in severely ill patients, including acute respiratory distress syndrome, cardiac injury, thrombosis, and sepsis, can lead to death. Several biomarkers, in addition to cytokine release syndrome (CRS), have been associated with severe and fatal outcomes in coronavirus disease 2019 (COVID-19) patients. The aim of this study is to assess clinical characteristics and cytokines profiles in hospitalized COVID-19 patients in Lebanon. A total of 51 hospitalized COVID-19 patients were recruited between February 2021 and May 2022. Clinical data and sera were collected at two time points: at hospital presentation (T0) and last collected results during hospitalization (T1). Our results showed that 49% of participants were >60 years with males accounting for the majority (72.5%). Hypertension, followed by diabetes and dyslipidemia, were the most frequent comorbid conditions among study participants accounting for 56.9% and 31.4%, respectively. Chronic obstructive pulmonary disease (COPD) was the only significantly different comorbid condition between intensive care unit (ICU) and non-ICU patients. Our results also showed that the median level of D-dimer was significantly elevated among patients in ICU and those who died compared to non-ICU patients and those who survived. Moreover, C-reactive protein (CRP) levels were significantly higher at T0 compared to T1 in ICU and non-ICU patients. The median level of IL-12p70 was significantly higher in patients >60 years compared to those ≤60 years (p = 0.0209). Our data are in agreement with previous reports suggesting the importance of IL-6, CRP, and IL-12p70 in the assessment of risk of severe disease and mortality.

Diagnosis and management of SARS-CoV-2 infection in immunocompromised patients are extremely challenging. These patients can have atypical clinical courses, and there is a paucity of data regarding clinical features, diagnostic findings, and the safety and efficacy of available therapeutic agents used to treat COVID-19 in these patients. In this case series, we report atypical COVID-19 presentations in 4 immunocompromised pediatric patients who were admitted with acute respiratory failure after an initial diagnosis of COVID-19 a few weeks earlier. All patients included in this cohort showed persistent worsening respiratory symptoms for several weeks before hospital presentation. While they manifested common COVID-19 sequelae, they also had rare COVID-19-related pathognomonic and radiographic features developed along their hospital course. Multiple therapeutic agents were used in their COVID-19 management, including corticosteroids, remdesivir, and monoclonal antibodies. All three patients who have received concurrent therapy with remdesivir, hydrocortisone, and monoclonal antibodies survived, and only one patient died as a direct complication of COVID-19 ARDS with secondary pulmonary mucormycosis. Our outcomes suggest the potential benefit of remdesivir use in combination with hydrocortisone and monoclonal antibodies in the management of severe COVID-19 ARDS in this group, as well as the importance of close surveillance and early administration of broad empirical antimicrobial and antifungal coverage if clinically indicated in this high-risk population.

Early Career Members of Assembly 2 (Respiratory Intensive Care) attended the 2022 European Respiratory Society (ERS) International Congress in Barcelona, Spain. The conference covered acute and chronic respiratory failure. Sessions of interest to our Assembly members and to those interested in respiratory critical care included the state-of-the-art session on respiratory critical care, the journal session (ERS/Lancet) on acute respiratory distress syndrome (ARDS) phenotyping into precision medicine, and sessions on specificity of coronavirus disease 2019 ARDS and its post-critical care. A symposium on treatment of acute respiratory failure in patients with COPD and innovations in mechanical ventilation either in the intensive care unit or at home were also reported upon. These sessions are summarised in this article.