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. 2026 May 5;12(3):01733-2025. doi: 10.1183/23120541.01733-2025

ERS Congress 2025: highlights from the Respiratory Intensive Care Assembly

Miguel Jiménez-Gómez 1, Giancarlo De Leo 2, Maria João Oliveira 3, Luk-Ping Lam 4, Daniel Lopez Padilla 5, Teresa Machado 3, Mafalda Pais 3, Vaia Stamatopoulou 6, Rudolfs Vilde 7,8, Christoph Fisser 9,10, João Winck 11, Rebecca F D'Cruz 12,13,✉
PMCID: PMC13139921  PMID: 42094227

Shareable abstract

Assembly 2 members attended sessions relevant to respiratory critical care, including ERS guidelines on telemonitoring in home ventilation, high-flow therapy applications, infections, precision medicine and treatment of acute respiratory failure https://bit.ly/3MLXZsT

Introduction

Early career members of Assembly 2 (Respiratory Intensive Care) attended the 2025 European Respiratory Society (ERS) Congress held in Amsterdam, the Netherlands. In this article, we provide an overview of the Congress sessions relevant to Assembly 2 members, including the evidence reviewed and panel discussions. The sessions included ERS Clinical Practice Guidelines on telemonitoring, infections in severe respiratory failure, developments in the application of nasal high-flow (NHF) therapy, precision medicine in acute respiratory failure (ARF) and state of the art treatment of acute respiratory distress syndrome (ARDS).

Guidelines session: Telemedicine in home mechanical ventilation

The success of long-term home noninvasive ventilation (NIV) depends on close monitoring, training, and multidisciplinary support. Telemonitoring permits longitudinal data on patients’ NIV usage and technical data with opportunities available during the early initiation period and subsequent follow-up. The 2025 ERS Clinical Practice Guideline on telemonitoring in home mechanical ventilation (HMV) provide recommendations on initiation, follow-up, and future directions [1].

Claudia Crimi (Catania, Italy) reported that, at HMV initiation, telemedicine offers several potential advantages including feasibility, effectiveness, and the potential for personalised care. The panel issued a conditional recommendation for telemonitoring in patients with neuromuscular diseases and COPD, based on data that demonstrate non-inferiority to in-hospital initiation regarding adherence, efficacy, and quality of life. No recommendation could be made for patients with obesity hypoventilation syndrome based on the lack of randomised trial data. Of note, most studies have been conducted within a single healthcare system equipped with specialised infrastructure, which limits the generalisability of these findings.

For HMV follow-up, a conditional recommendation for telemonitoring was provided, as meta-analyses demonstrate equivalence between telemedicine and standard care. No consensus was reached on which parameters should be prioritised for monitoring. Current recommendations are based on theoretical benefits and patient/caregiver preferences, rather than high-quality evidence. Crucially, direct comparisons of comprehensive physiological monitoring (gas exchange, sleep quality and patient–ventilator synchrony) with ventilator telemonitoring data are still lacking.

Narrative questions underscored the generally positive views of patients and caregivers, while also highlighting barriers such as digital literacy, healthcare organisation, and reimbursement policies. One patient provided online testimony, noting the reassurance offered by telemonitoring and describing how NIV setup was felt to be safe and comfortable.

Maxime Patout (Paris, France) emphasised that a key question for the future is how telemonitoring will reshape our interaction with patients and transform clinical practice in the coming years. Priorities include incorporating patient and caregiver perspectives, developing artificial intelligence (AI)-powered analytics, standardising monitoring parameters, and integrating these innovations to enhance care quality and personalise treatment during HMV setup and follow-up.

Telemonitoring provides an opportunity to identify patients who need medical intervention, as demonstrated by the association between increasing respiratory rate of patients using home NIV and hospitalisation rate [2]. However, managing telemonitoring data requires optimisation and data are conflicting regarding how it influences clinical outcomes. Current data indicate that there is a risk of alerts driving increased healthcare contact and reduced self-efficacy [3], although more frequent clinical contact may improve adherence and outcomes [4]. The discussion emphasised that telemonitoring should not overlook key behavioural and social factors. For example, obstructive sleep apnoea severity may worsen on weekends, highlighting the influence of human behaviour beyond physiological data [5].

Ultimately, data are only valuable if healthcare systems can act on them. The key challenge is to determine thresholds for changes in monitored parameters that predict or impact outcomes and what interventions they require. The way forward lies in strengthening the evidence base through randomised controlled trials (RCTs) and including patient-reported outcomes, ensuring that technological progress translates into meaningful clinical benefit.

Take-home messages

  •  Telemonitoring is feasible and non-inferior to in-hospital initiation for neuromuscular and COPD patients. Evidence remains insufficient for obesity hypoventilation syndrome. For follow-up, telemonitoring is equivalent to standard care.

  •  The benefits of telemonitoring depend on healthcare system capacity, and require structured alarm-management.

  •  Future priorities include standardising monitored parameters, integrating patient and caregiver perspectives, and validating AI-driven analytics through robust RCTs.

Mini symposium: Infections in severe respiratory failure

Alveolar host–pathogen interactions

Interactions between pathogens and pulmonary host cells are key determinants of respiratory infection severity. The alveolar epithelial glycocalyx is critical for preserving the haemato–alveolar barrier; its pathogen-induced degradation and increased fucosylation heighten infection susceptibility, whereas inhibition with 2-deoxy-galactose reduces bacterial burden and improves outcomes [6]. Beyond structural components, the phenotype and functional state of immune cells play a crucial role in the host response. A CD163+ macrophage subpopulation with a profibrotic phenotype has been identified, predominating during the fibrotic phase of ARDS [7]. In contrast, microRNA-223 modulates polymorphonuclear activation, reducing mortality in Streptococcus pneumoniae infection [8]. In parallel, monoclonal antibodies targeting C5a have emerged as promising host-directed therapy, underscoring the potential of immune modulation to improve outcomes [9].

Bacterial superinfections and diagnosis

Recent evidence highlights the prevalence of co-infections in severe respiratory diseases, with up to 50% of community-acquired pneumonia cases having an unknown aetiology. Co-infection has been independently associated with increased mortality, particularly among patients admitted to intensive care with Pseudomonas aeruginosa or Aspergillus spp. infections [10]. Therefore, the integration of molecular diagnostic tools and metagenomic DNA sequencing is essential to achieve precise aetiological diagnoses (figure 1).

FIGURE 1.

FIGURE 1

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Diagnosing the aetiology of co-infections by integrating molecular diagnostic tools and metagenomic DNA sequencing. BAL: bronchoalveolar lavage; NPV: negative predictive value; VAPA: viral-associated pulmonary aspergillosis.

Procalcitonin has become an important biomarker in clinical decision-making. It is increasingly used to guide both the initiation and discontinuation of antibiotic therapy. Low procalcitonin levels have demonstrated a high negative predictive value for excluding bacterial infection in patients without septic shock [11].

Invasive aspergillosis in viral pneumonia

Invasive pulmonary aspergillosis is not confined to neutropenic or profoundly immunosuppressed hosts. Over the past decade, it has increasingly affected critically ill patients, particularly those with severe influenza or COVID-19, as well as recipients of CAR-T immunotherapy or kinase inhibitor therapies. Viral-associated pulmonary aspergillosis (VAPA) has been reported in up to 60% of influenza-associated cases and 20% of COVID-19-associated cases [12], with mortality approaching 50%. Virus-induced epithelial injury and immune dysregulation facilitate Aspergillus invasion. Diagnosis remains challenging due to nonspecific clinical and radiological features [13]. Failure to actively search for VAPA often leads to underdiagnosis, underscoring the need for a high index of suspicion, particularly in high-risk patients [14]. Bronchoalveolar lavage remains the diagnostic gold standard, with galactomannan providing the best sensitivity–specificity balance (PCR assays are less validated, culture and cytology show lower sensitivity) [15]. Histopathological examination may confirm angioinvasion, when available. Serum galactomannan has lower sensitivity than bronchoalveolar lavage, as detection requires angioinvasive disease. The role of antifungal prophylaxis remains uncertain. First-line therapy relies on azoles, often combined with echinocandins in regions with azole resistance. Treatment duration should be individualised, typically lasting 6–12 weeks.

Take-home messages

  •  Integration of molecular assays and biomarkers, such as procalcitonin and galactomannan, may improve diagnostic precision and guide personalised therapy.

  •  Antimicrobial stewardship is crucial to reduce confounders and resistance. Future research should focus on personalised host interventions and novel therapies.

Symposium: Nasal high-flow: quo vadis?

Physiological benefits of NHF

Marieke Duiverman (Groningen, the Netherlands) outlined the principal physiological advantages of NHF, noting that delivery of heated, humidified gas at high flow rates provides a stable and predictable inspiratory oxygen fraction (FIO2). Increasing flow rate promotes dead space washout of the upper airway, reduces rebreathing, improves ventilatory efficiency, and can lower arterial carbon dioxide tension (PaCO2), effects that are accentuated with asymmetrical nasal prongs [16]. NHF can generate low-level positive end-expiratory pressure (PEEP), increasing end-expiratory lung volume and promoting alveolar recruitment [17]. In providing a stable FIO2, providing modest PEEP, and optimising pulmonary mechanics, NHF reduces respiratory rate and work of breathing [17]. Heated humidification improves patient comfort and mucociliary clearance, facilitating secretion removal and enhancing tolerance of therapy [18].

NHF in ARF

Oriol Roca Gas (Barcelona, Spain) presented an evidence-driven appraisal of NHF in acute hypoxaemic respiratory failure, detailing physiological benefits including accurate FIO2 delivery, flow-dependent PEEP, dead-space washout, and superior tolerance compared to conventional oxygen therapy (COT), alongside key limitations and comparative trial findings. Meta-analyses indicate that NHF lowers intubation rate compared to COT without a consistent mortality impact in patients. This effect is most evident in de novo hypoxaemic respiratory failure cohorts [19], and patients at high and low risk of post-extubation respiratory failure [20, 21]. Comparisons with continuous positive airway pressure (CPAP) and NIV are heterogeneous and context-dependent. During severe COVID-19 infection, evidence suggests CPAP/NIV may reduce intubation risk compared to NHF, but mortality outcomes are inconclusive [22]. Mechanisms of patient self-inflicted lung injury from excessive inspiratory effort and occult pendelluft which can be exacerbated by NIV were highlighted [23]. It was emphasised that delayed intubation worsens outcomes, and protocolised monitoring tools, such as the ROX index (the ratio of oxygen saturation to FIO2 to respiratory rate) [24], HACOR (heart rate, acidosis, level of consciousness, oxygenation, respiratory rate) score [25], and inspiratory effort measured using oesophageal manometry [26] can guide timely escalation [27].

NHF in chronic hypercapnic respiratory failure

Jens Bräunlich (Leipzig, Germany) reviewed emerging data evaluating NHF in patients with chronic hypercapnia. Randomised and observational studies indicate that NHF used with long-term oxygen therapy reduces moderate/severe exacerbation rate in stable COPD patients with mild hypercapnia (<53 mmHg) compared with long-term oxygen therapy alone, but was not associated with sustained improvements in quality of life and exercise capacity [28]. Effects of NHF on PaCO2 in chronic hypercapnia are heterogeneous. In short-term randomised trials evaluating stable COPD patients with mild hypercapnia, NHF has been identified as non-inferior to NIV in reducing PaCO2 and increasing time to first COPD exacerbation [28, 29]. However, multicentre randomised clinical trials evaluating long-term physiological and clinical outcomes in patients with significant hypercapnia (PaCO2 >53 mmHg per 7 kPa) are currently lacking. The most significant PaCO2 decreases are observed at higher flow rates [29]. It was concluded that individualised, case-by-case decision-making is essential, recommending a trial of NHF when first-line NIV therapy is not tolerated and continued prescription only if predefined clinical goals are achieved.

Quo vadis: what comes next?

Stefano Nava (Bologna, Italy) reviewed evidence and practical guidance on NHF, highlighting its expanding clinical roles. The RENOVATE trial found no consistent superiority of NHF over NIV for preventing intubation and reducing 7-day mortality across heterogeneous disease subgroups, emphasising the importance of patient selection [30]. Data indicate that NHF can safely be used to prevent desaturation during airway procedures: PROSA 2 showed that NHF reduces oxygen desaturation during bronchoscopy in COPD patients compared with COT [31]. It can additionally maintain oxygenation during transport and aeromedical transfer: prospective observational data indicate that NHF can stabilise oxygenation during intra-hospital transport of critically ill adults [32], and retrospective cohort studies from aeromedical retrieval services indicate that NHF is safe and feasible in paediatric transfers during long-distance flights [33].

NHF can also provide dyspnoea relief for ventilated patients during spontaneous breathing trials or breaks from acute NIV/CPAP [34]. It has been utilised in the palliative care setting, with guidelines from the American Society of Clinical Oncology and observational studies in terminal cancer patients supporting its role as a time-limited intervention for symptom relief [35, 36]. In the acute setting, NHF implementation should prioritise hypoxaemic patients, involve establishing the goals of care, including symptom management, and utilise frequent physiological monitoring to avoid delayed intubation. Operational needs include trained staff, standardised device settings and escalation pathways. Emerging strategies such as biomarker-driven sub-phenotyping and machine learning models to predict failure are promising but require prospective validation. Future research should focus on pragmatic randomised studies in defined phenotypes, immunocompromised patients, and cardiogenic pulmonary oedema, alongside implementation research in transport and peri-procedural settings, and rigorous validation of predictive machine learning models to guide clinical decision-making.

Take-home messages

  •  NHF therapy can provide a stable FIO2 and optimise pulmonary mechanics to improve work of breathing.

  •  In an acute setting, NHF therapy can reduce the risk of intubation in moderate/severe hypoxaemia and early reintubation compared to COT and NIV. Close monitoring is required to avoid delayed intubation.

  •  More randomised trials are required to understand the safety and efficacy of NHF in chronic hypercapnic respiratory failure.

Hot topics: Precision medicine in acute respiratory failure: a global challenge

The session provided an overview of current knowledge and future research directions in the field of ARF and ARDS. Juliana Carvalho Ferreira (São Paulo, Brazil) highlighted that, despite being a global health challenge, the incidence and outcomes of ARF are unknown. New diagnostic criteria for ARDS are emerging, responding to real-world clinical scenarios in the management of ARF and ARDS, such as use of NHF [37]. The appropriate treatment for the patient, based on recent guidelines [38] and clinical trials [30], and individualised patient care is crucial for optimising clinical outcomes. Significant global disparities persist, especially for low- and middle-income countries. For this reason, international networks and collaborations are required to promote equitable access to optimal ARF management.

Lorraine Ware (Nashville, TN, USA) emphasised the need to modify clinical approaches to ARDS. Currently, management relies primarily on supportive therapy guided by physiological principles, rather than underlying biological mechanisms. Preliminary literature on ARDS phenotyping (hypoinflammatory versus hyperinflammatory [39]) has shown promising results in improving prognostic accuracy [40] (figure 2) and response to specific therapeutic interventions such as simvastatin and recombinant activated protein C [41, 42]. Further research is needed to advance our understanding of the biological mechanisms driving distinct ARDS phenotypes, although interesting hypotheses continue to emerge, such as different gene pattern expression and the infection-driving pathogen [43].

FIGURE 2.

FIGURE 2

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A comparative analysis of mortality rates in hypo-inflammatory versus hyper-inflammatory acute respiratory distress syndrome phenotypes, as reported in different clinical trials. Reproduced from [40] with permission.

Lieuwe Bos (Amsterdam, the Netherlands) stressed the importance of RCTs focused on predictive enrichment [44] through precision medicine [45]. Currently, most evidence on the pharmacological treatment of ARDS is limited to observational studies or secondary RCT analyses. Recent studies have highlighted significant differences between ARDS phenotypes and treatment response. For example, post hoc RCT analyses indicate that corticosteroids may be harmful in the hypoinflammatory phenotype [46]. Prospective data are warranted to validate this observation. It has also been reported that therapy can influence ARDS phenotype [46], introducing the concept of dynamic ARDS phenotyping over time. In this context, the adaptive platform design of the PANTHER trial (https://panthertrial.org/), an ERS Clinical Research Collaboration, was highlighted. This enables rapid identification of ARDS phenotypes and allows for a tailored therapeutic approach. Among promising treatments, baricitinib (Janus kinase 1/2 inhibitor) was shown in a small single-centre observational study of 20 patients to show beneficial immunomodulatory effects in patients with hyper-inflammatory COVID-19 [47]. Rapid classification combining biomarkers (interleukin-6, soluble tumour necrosis factor receptor 1, bicarbonate) and clinical features is feasible, though biomarker testing remains costly and clinical tools require further validation [48].

Leanna Hays (Dublin, Ireland) underscored the need for a more active role for patients in research. The Public and Patient Involvement (PPI) Programme for Respiratory Adaptive Platform Trials, inspired by the Irish Critical Care PPI Group, represents a collaborative model between researchers and patients aimed at advancing critical care research. Understanding patients’ and relatives’ experiences is essential for improving ethical and patient-centred research design. The results from the ERS Clinical Research Collaboration were presented, describing public perceptions regarding participation in critical care research. Despite regional differences, the survey revealed a broad consensus on the importance of participating and the need for patient-tailored research protocols [49].

Take-home messages

  •  Despite being a global health challenge, the incidence and outcomes of ARF are unknown. Diagnostic criteria for ARDS are emerging, responding to real-world clinical scenarios in the management of ARF and ARDS.

  •  ARDS phenotyping demonstrates promising results in improving prognostic accuracy, reducing mortality, and guiding therapeutic responses.

  •  Patient collaboration in intensive care unit trials is necessary for designing and delivering critical care research.

State of the art: Treatment of ARDS

ARDS phenotyping and outcomes

Lieuwe Bos outlined a phenotype-guided approach to treating ARDS, noting that lung shape should steer ventilator settings. By categorising lungs into focal (dorso-inferior consolidation) or non-focal (diffuse or patchy loss of aeration) patterns based on computed tomography imaging, clinicians can anticipate how patients will react to therapeutic interventions. Focal ARDS responds better to prone positioning and non-focal ARDS responds well to recruitment manoeuvres [50]. The LIVE trial, which tested this approach, found no survival benefit and showed misclassifying patients could negate any potential advantage [51]. The findings sharpened the call for bedside imaging tools. Lung ultrasound has emerged as a radiation-free alternative with impressive diagnostic accuracy in ARDS [50]. The PEGASUS trial (NCT05492344) is an ongoing study investigating explores whether ventilation guided by lung ultrasound and adapted to morphological patterns can reduce lung injury and improve outcomes, refining phenotype-based strategies for ARDS.

The role of pathophysiology of severe infections in ARDS

Ignacio Martin-Loeches (Dublin, Ireland) highlighted how infection-driven immune chaos and a disturbed respiratory-tract microbiome shape ARDS pathophysiology. Airway microbiome surveys reveal that when commensal diversity thins and opportunistic species proliferate, patients are at greater risk of pneumonia and require prolonged mechanical ventilation [52]. Systemic inflammation, coupled with endothelial activation, is now recognised as a key driver of multi-organ failure and infection-related ARDS [53]. The discussion also highlighted that transcriptomic data indicate that the lingering nature of infection in ventilator-associated respiratory tract infections may be driven more by a fatigued host immune system than by pathogen virulence alone [54]. Metabolomic profiling supports this view by revealing metabolic patterns that mirror ARDS sub-phenotypes and highlight its biological heterogeneity [55].

How to set the ventilator

ARDS is a complex disease characterised by lung inhomogeneity and high mortality. Although conventional lung-protective ventilation focuses on low tidal volume (VT) and plateau pressure, Annemijn Jonkman (Rotterdam, the Netherlands) stressed the importance of an individualised approach in determining ventilator settings. Lung-protective ventilation should target a safe driving pressure (ΔPrs <15 cmH2O) and consider respiratory system elastance [56]. Optimal PEEP selection, aiming to balance overdistension and atelectrauma, requires input from advanced respiratory monitoring tools, such as oesophageal pressure measurement and electrical impedance tomography [57]. Mechanical power appears propitious as it incorporates respiratory rate and PEEP, constituting a reliable measure of the energy delivered from the ventilator to the lungs. Additionally, the plan should include diaphragm protection by avoiding high respiratory drive, excessive or insufficient respiratory effort, and asynchrony [58].

Evidence-based treatment of severe ARDS: prone positioning and extracorporeal membrane oxygenation

Prone positioning increases lung homogeneity, improves ventilation–perfusion match, reduces lung stress and strain (stress refers to transpulmonary pressure, strain refers to change in lung volume relative to resting volume (VT/functional residual capacity)), and improves outcomes [59]. Christian Karagiannidis (Cologne, Germany) highlighted the recommendation for prolonged prone positioning in patients with moderate/severe ARDS in recent guidelines [38]. In non-intubated patients with COVID-19, awake prone positioning may reduce intubation rate [38]. In severe ARDS with refractory gas exchange failure, guidelines support the use of veno-venous extracorporeal membrane oxygenation (VV-ECMO), which permits ultra-lung-protective ventilation, improves gas exchange and unloads the right ventricle [38]. Considering its complications and real-world data that suggest worse outcomes in older patients [60], it was underlined that ECMO should be initiated after careful consideration of selection criteria, in experienced centres, after conventional measures of lung-protective ventilation, recruitment and prone positioning have failed.

Take-home messages

  •  It is important to phenotype ARDS to guide individualised therapeutic strategies. Current studies are evaluating novel phenotyping methods, including lung ultrasound.

  •  Dysregulated host immunity and microbiome disruption are central to infection-related ARDS, and transcriptomic and metabolomic data provide evidence of biological heterogeneity in ARDS.

  •  Ventilation strategies in ARDS require an individualised approach that emphasises lung protection (figure 3). This includes safe driving pressure, monitoring to optimise PEEP selection, safe mechanical power, and preservation of diaphragm function.

  •  Prolonged prone positioning in severe ARDS improves outcomes. VV-ECMO may be considered with refractory gas exchange impairment following careful patient selection.

FIGURE 3.

FIGURE 3

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Illustration of individualised lung-protective ventilation strategies in acute respiratory distress syndrome (ARDS). A comprehensive approach to personalised ventilatory settings is demonstrated, in which initial settings of tidal volume (VT) and positive end-expiratory pressure (PEEP) are not based on the conventional strategy of 6 mL·kg−1 predicted body weight (PBW) and PEEP–FIO2 (inspiratory oxygen fraction) tables, but are guided by respiratory system elastance (Ers), targeting a safe distending pressure (ΔPrs <15 cmH2O). Ventilator settings are adjusted to achieve balance between atelectasis and overdistension, based on respiratory system driving pressure. Advanced ventilatory monitoring techniques, including transpulmonary pressure assessment using oesophageal manometry and electrical impedance tomography (EIT), may be used to support clinical evaluation, if available. This continuum is complemented with patient phenotyping and with additional interventions which aim to reduce lung stress and strain. Interventions include recruitment manoeuvres, prolonged prone positioning and neuromuscular blockade. Patient response should be monitored continuously and after each intervention; in case of improvement, the ventilation strategy should focus on preserving the diaphragmatic function, whereas in severe refractory ARDS, when noninvasive measures have failed to restore gas exchange, extracorporeal membrane oxygenation (ECMO) should be considered. PL: transpulmonary pressure; Poes: oesophageal pressure; VV: veno-venous. Figure created with BioRender.com.

Conclusions

Assembly 2 members attended sessions relevant to respiratory critical care, which covered recently published ERS Clinical Practice Guidelines on telemonitoring in HMV, applications of NHF therapy, infections, precision medicine and treatment of ARF. The ERS Congress and the Respiratory Failure and Mechanical Ventilation Conference held in Rotterdam in February 2026 (https://channel.ersnet.org/event-334-respiratory-failure-and-mechanical-ventilation-conference-2026) provided an excellent opportunity for Assembly 2 early career members to advance and consolidate their knowledge in their areas of interest, engage with experts, extend their professional networks and form new clinical and academic collaborations.

Acknowledgements

Use of generative AI model was not involved in the planning, conduct or writing of this manuscript.

Footnotes

Provenance: Commissioned article, peer reviewed.

Conflicts of interest: G. De Leo, M.J. Oliveira, L-P. Lam, D. Lopez Padilla, T. Machado, M. Pais, V. Stamatopoulou, C. Fisser and J. Winck report no conflicts of interest to disclose. M. Jiménez-Gómez reports honoraria from GlaxoSmithKline and Chiesi and support for attending meetings from FAES Farma, Sanofi and Chiesi. R. Vilde reports support for attending meetings from Norameda and Hipnos. R.F. D'Cruz reports honoraria and support for attending meetings from Fisher & Paykel, Astra Zeneca and Aerogen.

Support statement: No funding declared.

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