Critical Care最新文献

{"title":"An international observational study validating gene-expression sepsis immune subgroups","authors":"David B. Antcliffe, Estelle Peronnet, Frédéric Pène, Kristoffer Strålin, David Brealey, Sophie Blein, Richard Cleaver, Maria Cronhjort, Jean-Luc Diehl, Guillaume Voiriot, Aurore Fleurie, Claudia Lannsjö, Anne-Claire Lukaszewicz, Johan Mårtensson, Tài Pham, Nicolas De Prost, Jean-Damien Ricard, Mervyn Singer, Gabriel Terraz, Jean-François Timsit, Christian Unge, Antoine Vieillard-Baron, Rebecka Rubenson Wahlin, Jean-François Llitjos, Anthony C. Gordon","doi":"10.1186/s13054-025-05319-5","DOIUrl":"https://doi.org/10.1186/s13054-025-05319-5","url":null,"abstract":"Sepsis gene-expression sub-phenotypes with prognostic and theranostic potential have been discovered. These have been identified retrospectively and have not been translated to methods that could be deployed at the bedside. We aimed to identify subgroups of septic patients at high-risk of poor outcome, using a rapid, multiplex RNA-based test. Adults with sepsis, in the intensive care unit (ICU) were recruited from 17 sites in the United Kingdom, Sweden and France. Blood was collected at days 2–5 (S1), 6–8 (S2) and 13–15 (S3) after ICU admission and analyzed centrally. Patients were assigned into ‘high’ and ‘low’ risk groups using two models previously developed for the Immune-Profiling Panel prototype on the bioMérieux FilmArray® system. 357 patients were recruited (March 2021–November 2022). 69% were male with a median age of 67 years, APACHE II score of 21 and a 30% 90-day mortality rate. The proportions of high-risk patients decreased over the three sampling times (model 1: 53%, 40%, 15% and model 2: 81%, 74%, 37%). In model 1, 90-day mortality was higher in a high-risk group at each time (S1: 35% vs 24%, p = 0.04; S2: 43% vs 20%, p < 0.001; S3: 52% vs 24%, p = 0.007). In model 2, mortality was only significantly different at the second sampling time (S1: 30% vs 27%, p = 0.77; S2: 34% vs 14%, p = 0.002; S3: 35% vs 23%, p = 0.13). Gene-expression diagnostics can identify patients with sepsis at high-risk of poor outcomes and could be used to identify patients for precision medicine trials. ISRCTN11364482 Registered 24th September 2020.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"26 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Further considerations on the clinical applicability of time to positivity as a prognostic tool for catheter-related pseudomonas aeruginosa bloodstream infections","authors":"Yufan Liao, Xinmin Deng, Heng Xiao","doi":"10.1186/s13054-025-05322-w","DOIUrl":"https://doi.org/10.1186/s13054-025-05322-w","url":null,"abstract":"&lt;p&gt;To the Editor,&lt;/p&gt;&lt;p&gt;We carefully reviewed the article titled \"Time to positivity as a predictor of catheter-related bacteremia and mortality in adults with Pseudomonas aeruginosa bloodstream infection\" by Marco et al. [1]. This study provides valuable insights into the role of time to positivity (TTP) and differential time to positivity (DTP) as diagnostic and prognostic markers for catheter-related Pseudomonas aeruginosa (PAE) bloodstream infections (PAE-BSI). While the authors have made significant contributions, there are still several aspects worth further consideration to enhance the applicability of TTP as a diagnostic and prognostic tool in clinical settings.&lt;/p&gt;&lt;p&gt;One area that requires deeper exploration is the potential influence of the microbiological characteristics of Pseudomonas aeruginosa on TTP. Specifically, the resistance profiles of the strains in question could play a significant role in the dynamics of TTP. While the study suggests that TTP correlates with the presence of catheter-related infections, it does not address how different resistance mechanisms in PAE might affect this marker. Strains harboring extended-spectrum beta-lactamases (ESBLs), carbapenemases, or other multidrug-resistant mechanisms may demonstrate delayed or altered growth kinetics compared to susceptible strains [2, 3]. This delay in growth could lead to longer TTP, potentially confounding the predictive value of TTP in diagnosing infections caused by resistant strains. In practice, this variation could be particularly important in settings with a high burden of multidrug-resistant organisms, where clinicians must be cautious in interpreting TTP as a reliable indicator for catheter-related infection. A more granular analysis that examines the relationship between TTP and different resistance patterns, or even molecular subtypes of PAE, would provide a more nuanced understanding of the predictive value of TTP and help optimize antibiotic stewardship strategies.&lt;/p&gt;&lt;p&gt;Another point of concern is the influence of patient factors, particularly comorbidities and immune status, on TTP and its prognostic value. The study acknowledges the role of underlying health conditions but stops short of exploring how specific immunocompromised states might affect TTP. For example, patients with neutropenia, as well as those receiving immunosuppressive therapy (e.g., corticosteroids, biologics, or chemotherapy), may exhibit a prolonged time to positivity due to impaired host immune responses[4]. Moreover, immunosuppressed individuals may also face higher mortality risks regardless of the promptness of diagnosis [5]. Therefore, stratifying the results by immune status or underlying comorbidities could significantly improve the interpretability of TTP as a prognostic marker. Understanding the interaction between these patient-specific factors and TTP could help clinicians better predict outcomes and make more informed decisions regarding treatment intensification or de-e","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"6 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143528237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Volume kinetics in a translational porcine model of stabilized sepsis with fluid accumulation","authors":"Son Ly Hong, Hugo Dumargne, Robert G. Hahn, Abdessalem Hammed, Romain Lac, Axel Guilpin, Charlotte Slek, Maxime Gerome, Bernard Allaouchiche, Vanessa Louzier, Auguste Dargent","doi":"10.1186/s13054-025-05308-8","DOIUrl":"https://doi.org/10.1186/s13054-025-05308-8","url":null,"abstract":"Fluid dynamics during and after a septic event is complex, but better knowledge could guide both fluid resuscitation and fluid removal. We aimed to compare fluid dynamics before and after sepsis in a clinically relevant mono-bacterial porcine model. Twelve sows with a mean body weight of 56 kg were anesthetized, mechanically ventilated, and invasively monitored. Sepsis was induced with an intravenous infusion of P. aeruginosa. Animals were resuscitated during the acute septic phase according to a protocolized algorithm. Volume kinetics was studied before the bacterial infusion (baseline) and 24 h later (late sepsis), and both consisted of an infusion of 1,500 mL of 0.9% saline over 20 min with repeated hemoglobin and albumin measurements and urine quantification. The kinetic analysis at baseline showed transient volume expansion of the central fluid compartment (the plasma) and a fast-exchange interstitial space, while gradually more fluid accumulated in the remote “third fluid space” with very slow turnover. In the late sepsis phase, hypoalbuminemia and slight hypovolemia was observed. As compared with baseline, fluid kinetics showed improved plasma expansion, and more expansion of the fast-exchange interstitial space rather than the slow-exchange space. The rate constant k21 describing return flow to the circulation was increased during the late sepsis phase, and hemoglobin-albumin dilution difference suggested that interstitial albumin recruitment occurred with the fluid infusion. The model predicted that high cardiac index and sepsis-induced weight gain were associated with greater fast-exchange compartment expansion. After sepsis, fluid was accumulated in the slow-exchange compartment, and further fluid administration distributed preferentially to the fast-exchange compartment with acceleration of lymph flow, improved plasma expansion, and recruitment of interstitial albumin.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"15 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of trunk upward verticalization on pulmonary vascular resistance in ARDS","authors":"Martín H. Benites, Jaime Retamal","doi":"10.1186/s13054-025-05313-x","DOIUrl":"https://doi.org/10.1186/s13054-025-05313-x","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;&lt;p&gt;Bouchant et al. examined the effects of progressive verticalization on lung mechanics and hemodynamics in patients with Acute Respiratory Distress Syndrome (ARDS) [1]. We commended the authors for this high-quality research. Several of their findings are particularly noteworthy and warrant further discussion.&lt;/p&gt;&lt;p&gt;Changes in trunk inclination affect respiratory mechanics, oxygenation, ventilation distribution, and ventilatory efficiency in patients with acute respiratory failure [2]. When patients are transitioned from a flat supine position to a semi-recumbent position, the driving pressure increases, respiratory system compliance decreases, and ventilatory efficiency for carbon dioxide (CO&lt;sub&gt;2&lt;/sub&gt;) removal decreases [3,4,5,6].&lt;/p&gt;&lt;p&gt;Marrazzo et al. observed that the PEEP level optimized in the flat supine position led to overdistension when patients were moved to a semi-recumbent position [7]. Therefore, the change in trunk inclination from a flat supine position to a semi-recumbent position could generate a similar effect as an increase in PEEP levels.&lt;/p&gt;&lt;p&gt;In this way, both the effect of PEEP setting and trunk inclination on respiratory mechanics could depend on lung recruitment potential [8]. These studies revealed that in patients with low recruitment potential, an increase in PEEP results in minimal lung volume expansion, elevated airway pressure, increased pulmonary vascular resistance, and impaired right ventricular function [8, 9].&lt;/p&gt;&lt;p&gt;In a comprehensive hemodynamic assessment using pulmonary artery catheterization, Bouchant et al. investigated the effects of progressive verticalization in 30 ARDS patients by optimizing the PEEP level in a 30° semi-recumbent position and maintaining it unchanged throughout the study [1]. The study demonstrated a consistent increase in pulmonary vascular resistance as the verticalization angle progressed from supine (0°) to upright (90°). Specifically, the pulmonary vascular resistance increased from 181 (143–266) dyn·s·cm⁻&lt;sup&gt;5&lt;/sup&gt; at 0° to 287 (241–429) dyn·s·cm⁻&lt;sup&gt;5&lt;/sup&gt; at 90°, indicating a clear association between vertical positioning and vascular resistance. Likewise, cardiac output steadily declined from 6.5 (4.8–8.0) L/min at 0° to 4.8 (3.2–5.8) L/min at 90°, requiring increasing vasopressor support to maintain adequate perfusion. Interestingly, the end-expiratory lung volume (EELV) increased from 24 mL/kg (15–30 mL/kg) at 0° to 34 mL/kg (27–37 mL/kg) at 90°, while respiratory system compliance decreased from 43 mL/cmH₂O (32–49 mL/cmH₂O) at 0° to 25 mL/cmH₂O (21–37 mL/cmH₂O) at 90°, being the elasticity of the chest wall the most affected component of postural changes. Likewise, PaCO₂ levels progressively increased from 45 (37–50) mm Hg at 0° to 51 (42–60) mm Hg at 90°, reflecting a concurrent deterioration in gas exchange. In summary, upward verticalization without modification of the PEEP level was associated with increased pulmonary vascular resistance, red","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"33 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to “Relationships between dyspnea, oxygenation and prognosis in hypoxemic respiratory failure”","authors":"Alexandre Demoule, Amandine Baptiste, Maxens Decavèle, Lisa Belin, Jean-Pierre Frat","doi":"10.1186/s13054-025-05280-3","DOIUrl":"https://doi.org/10.1186/s13054-025-05280-3","url":null,"abstract":"&lt;p&gt;We thank Dr Shen and Dr Ding [1] for their thorough reading of our manuscript [2] and for having pointed out mistakes in Tables 1 and 2 regarding the ratio of arterial oxygen tension to inspired oxygen fraction (PaO&lt;sub&gt;2&lt;/sub&gt;/FiO&lt;sub&gt;2&lt;/sub&gt;). These mistakes have been corrected [3]. Although there was a trend toward a lower PaO&lt;sub&gt;2&lt;/sub&gt;/FiO&lt;sub&gt;2&lt;/sub&gt; in the most dyspneic patients, the association between dyspnea and PaO&lt;sub&gt;2&lt;/sub&gt;/FiO&lt;sub&gt;2&lt;/sub&gt; was not significant. This is not surprising since this absence of significant link between PaO&lt;sub&gt;2&lt;/sub&gt;/FiO&lt;sub&gt;2&lt;/sub&gt; has been previously reported in intubated patients [4, 5] and in patients receiving non-invasive ventilation for acute respiratory failure [6].&lt;/p&gt;&lt;p&gt;As pointed by Dr Shen and Dr Deng, many inputs and factors contribute to the pathogenesis of dyspnea [7], including respiratory system mechanics and low tidal volume or low level of inspiratory assist in mechanically ventilated patients [4, 5, 8]. There is also a strong association between anxiety and dyspnea [4, 5]. A high inspiratory dive is also associated with dyspnea [9]. Unfortunately, none of these factors has an excellent performance to predict dyspnea in non-communicative patients who cannot self-report dyspnea, reason why observational scales such as the mechanical ventilation—respiratory distress observation scale (MV-RDOS) have been developed to detect dyspnea in this population [10].&lt;/p&gt;&lt;p&gt;Finally, that moderate to severe dyspnea is associated with a higher rate of intubation is a fact [6]. The intubation making decision is complex and relies on many factors. As suggested by Dr Shen and Dr Deng, this decision should not been based on the sole level of dyspnea. However, it might be valuable to integrate the intensity of dyspnea in this decision making process. Future prospective trials may help addressing this important question.&lt;/p&gt;&lt;p&gt;No datasets were generated or analysed during the current study.&lt;/p&gt;&lt;ol data-track-component=\"outbound reference\" data-track-context=\"references section\"&gt;&lt;li data-counter=\"1.\"&gt;&lt;p&gt;Shen Y, Ding X. Relationships between dyspnea, oxygenation and prognosis in hypoxemic respiratory failure. Crit Care. 2024;28:417. https://doi.org/10.1186/s13054-024-05207-4.&lt;/p&gt;&lt;p&gt;Article PubMed PubMed Central Google Scholar &lt;/p&gt;&lt;/li&gt;&lt;li data-counter=\"2.\"&gt;&lt;p&gt;Demoule A, Baptiste A, Thille AW, et al. Dyspnea is severe and associated with a higher intubation rate in de novo acute hypoxemic respiratory failure. Crit Care. 2024;28:174. https://doi.org/10.1186/s13054-024-04903-5.&lt;/p&gt;&lt;p&gt;Article PubMed PubMed Central Google Scholar &lt;/p&gt;&lt;/li&gt;&lt;li data-counter=\"3.\"&gt;&lt;p&gt;Demoule A, Baptiste A, Thille AW et al. Correction to: dyspnea is severe and associated with a higher intubation rate in de novo acute hypoxemic respiratory failure. Crit Care. 2024;29. https://doi.org/10.1186/s13054-025-05314-w&lt;/p&gt;&lt;/li&gt;&lt;li data-counter=\"4.\"&gt;&lt;p&gt;Demoule A, Hajage D, Messika J, Jaber S, Diallo H, Coutrot M, et al. Prevalence, intensity, a","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"26 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143507496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of gut failure as a cause and consequence of critical illness","authors":"Danielle E. Soranno, Craig M. Coopersmith, Jessica F. Brinkworth, Faith N. F. Factora, Julia H. Muntean, Monty G. Mythen, Jacob Raphael, Andrew D. Shaw, Vidula Vachharajani, Jeannette S. Messer","doi":"10.1186/s13054-025-05309-7","DOIUrl":"https://doi.org/10.1186/s13054-025-05309-7","url":null,"abstract":"In critical illness, all elements of gut function are perturbed. Dysbiosis develops as the gut microbial community loses taxonomic diversity and new virulence factors appear. Intestinal permeability increases, allowing for translocation of bacteria and/or bacterial products. Epithelial function is altered at a cellular level and homeostasis of the epithelial monolayer is compromised by increased intestinal epithelial cell death and decreased proliferation. Gut immunity is impaired with simultaneous activation of maladaptive pro- and anti-inflammatory signals leading to both tissue damage and susceptibility to infections. Additionally, splanchnic vasoconstriction leads to decreased blood flow with local ischemic changes. Together, these interrelated elements of gastrointestinal dysfunction drive and then perpetuate multi-organ dysfunction syndrome. Despite the clear importance of maintaining gut homeostasis, there are very few reliable measures of gut function in critical illness. Further, while multiple therapeutic strategies have been proposed, most have not been shown to conclusively demonstrate benefit, and care is still largely supportive. The key role of the gut in critical illness was the subject of the tenth Perioperative Quality Initiative meeting, a conference to summarize the current state of the literature and identify key knowledge gaps for future study. This review is the product of that conference. ","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"66 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143507128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Dyspnea is severe and associated with a higher intubation rate in de novo acute hypoxemic respiratory failure","authors":"Alexandre Demoule, Amandine Baptiste, Arnaud W. Thille, Thomas Similowski, Stephanie Ragot, Gwénael Prat, Alain Mercat, Christophe Girault, Guillaume Carteaux, Thierry Boulain, Sébastien Perbet, Maxens Decavèle, Lisa Belin, Jean-Pierre Frat","doi":"10.1186/s13054-025-05314-w","DOIUrl":"https://doi.org/10.1186/s13054-025-05314-w","url":null,"abstract":"&lt;p&gt;&lt;b&gt;Correction: Critical Care (2024) 28:174&lt;/b&gt; &lt;b&gt;https://doi.org/10.1186/s13054-024-04903-5&lt;/b&gt;&lt;/p&gt;&lt;p&gt;Following publication of the original article [1], the authors identified errors in Tables 1, 2 and 3.&lt;/p&gt;&lt;p&gt;On Table 1, the ratio of arterial oxygen tension to inspired oxygen fraction at inclusion was 135 (103–182) mmHg instead of 129 (98–171) mmHg in the No dyspnea group of patients (dyspnea visual analog scale [VAS] &lt; 16 mmHg), 154 (92–197) mmHg instead of 135 (103–182) mmHg in the Mild dyspnea group (dyspnea VAS between 16 and 39 mm), 133 (105–165) mmHg instead of 154 (92–197) mmHg in the Moderate dyspnea group (dyspnea VAS 40 to 64 mm) and 115 (96–156) mmHg instead of 133 (105–165) mmHg in the Severe dyspnea group (dyspnea VAS &gt; 65 mm). The &lt;i&gt;p&lt;/i&gt; value was unaffected by these copy paste mistakes (&lt;i&gt;p&lt;/i&gt; = 0.231). We also noticed that some values were not rounded.&lt;/p&gt;&lt;p&gt;On Table 2, the ratio of arterial oxygen tension to inspired oxygen fraction at inclusion was 133 (103–173) mmHg in the whole population instead of 146 (97–199) mmHg, 145 (104–187) instead of 133 (103–173) mmHg in the No dyspnea group of patients, 147 (105–179) mmHg instead of in the Mild dyspnea group, 131 (96–165) mmHg instead of 147 (105–179) mmHg in the Moderate dyspnea group and 118 (100–157) mmHg instead of 131 (96–165) mmHg in the Severe dyspnea group. The &lt;i&gt;p&lt;/i&gt; value was unaffected by these copy paste mistakes (&lt;i&gt;p&lt;/i&gt; = 0.296).&lt;/p&gt;&lt;p&gt;Finally, on Table 3 the authors have noted that two &lt;i&gt;p&lt;/i&gt; values have moved from one line to another and that one Odds ratio value was misplaced.&lt;/p&gt;&lt;p&gt;In addition to these errors, there are some values that were not rounded, with decimals lefts.&lt;/p&gt;&lt;p&gt;None of these errors changes the original message and accuracy of the analysis.&lt;/p&gt;&lt;p&gt;The incorrect Table 1:&lt;/p&gt;&lt;figure&gt;&lt;figcaption&gt;&lt;b data-test=\"table-caption\"&gt;Table 1 Univariate analysis: factors associated with moderate-to-severe dyspnea at baseline&lt;/b&gt;&lt;/figcaption&gt;&lt;span&gt;Full size table&lt;/span&gt;&lt;svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"&gt;&lt;use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;/use&gt;&lt;/svg&gt;&lt;/figure&gt;&lt;p&gt;The correct Table 1:&lt;/p&gt;&lt;figure&gt;&lt;figcaption&gt;&lt;b data-test=\"table-caption\"&gt;Table 1 Univariate analysis: factors associated with moderate-to-severe dyspnea at baseline&lt;/b&gt;&lt;/figcaption&gt;&lt;span&gt;Full size table&lt;/span&gt;&lt;svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"&gt;&lt;use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;/use&gt;&lt;/svg&gt;&lt;/figure&gt;&lt;p&gt;The incorrect Table 2:&lt;/p&gt;&lt;figure&gt;&lt;figcaption&gt;&lt;b data-test=\"table-caption\"&gt;Table 2 Univariate analysis: factors associated with moderate to severe dyspnea 1 h after treatment initiation&lt;/b&gt;&lt;/figcaption&gt;&lt;span&gt;Full size table&lt;/span&gt;&lt;svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"&gt;&lt;use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlin","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"32 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143507253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human judgment error in the intensive care unit: a perspective on bias and noise","authors":"I. P. Peringa, E. G. M. Cox, R. Wiersema, I. C. C. van der Horst, R. R. Meijer, J. Koeze","doi":"10.1186/s13054-025-05315-9","DOIUrl":"https://doi.org/10.1186/s13054-025-05315-9","url":null,"abstract":"In the Intensive Care Unit (ICU), clinicians frequently make complex, high-stakes judgments, where inaccuracies can profoundly affect patient outcomes. This perspective examines human judgment error in ICU settings, specifically bias (systematic error) and noise (random error). While past research has emphasized bias, we explore the role of noise in clinical decision making and its mitigation. System noise refers to unwanted variability in judgments that should ideally be identical. This variability stems from level noise (variability in clinicians’ average judgments), stable pattern noise (variability in clinicians’ responses to specific patient characteristics), and occasion noise (random, within-clinician variability). Two strategies to reduce noise are the use of algorithms and the averaging of independent judgments. Recognizing and addressing noise in clinical decision making is essential to enhancing judgment accuracy in critical care. By implementing effective noise reduction strategies, clinicians can reduce errors and improve patient outcomes, ultimately advancing the quality of care delivered in ICU settings.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"50 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A narrative review on the future of ARDS: evolving definitions, pathophysiology, and tailored management","authors":"Lou’i Al-Husinat, Saif Azzam, Sarah Al Sharie, Mohammad Araydah, Denise Battaglini, Suhib Abushehab, Gustavo A. Cortes-Puentes, Marcus J. Schultz, Patricia R. M. Rocco","doi":"10.1186/s13054-025-05291-0","DOIUrl":"https://doi.org/10.1186/s13054-025-05291-0","url":null,"abstract":"Acute respiratory distress syndrome (ARDS) is a severe complication of critical illness, characterized by bilateral lung infiltrates and hypoxemia. Its clinical and pathophysiological heterogeneity poses challenges for both diagnosis and treatment. This review outlines the evolution of ARDS definitions, discusses the underlying pathophysiology of ARDS, and examines the clinical implications of its heterogeneity. Traditional ARDS definitions required invasive mechanical ventilation and relied on arterial blood gas measurements to calculate the PaO2/FiO2 ratio. Recent updates have expanded these criteria to include patients receiving noninvasive respiratory support, such as high-flow nasal oxygen, and the adoption of the SpO2/FiO2 ratio as an alternative to the PaO2/FiO2 ratio. While these changes broaden the diagnostic criteria, they also introduce additional complexity. ARDS heterogeneity—driven by varying etiologies, clinical subphenotypes, and underlying biological mechanisms—highlights the limitations of a uniform management approach. Emerging evidence highlights the presence of distinct ARDS subphenotypes, each defined by unique molecular and clinical characteristics, offering a pathway to more precise therapeutic targeting. Advances in omics technologies—encompassing genomics, proteomics, and metabolomics—are paving the way for precision-medicine approaches with the potential to revolutionize ARDS management by tailoring interventions to individual patient profiles. This paradigm shift from broad diagnostic categories to precise, subphenotype-driven care holds promise for redefining the landscape of treatment for ARDS and, ultimately, improving outcomes in this complex, multifaceted syndrome.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"65 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tocilizumab in treating children with refractory septic shock","authors":"En-Pei Lee, Shih-Hsiang Chen, Han-Ping Wu","doi":"10.1186/s13054-025-05318-6","DOIUrl":"https://doi.org/10.1186/s13054-025-05318-6","url":null,"abstract":"&lt;p&gt;Pediatric septic shock causes significant morbidity and mortality, contributing to over 4.5 million deaths annually worldwide [1]. It stems from a dysregulated host immune response to infection, characterized by high levels of cytokines, including interleukin-6 (IL-6). Tocilizumab, an IL-6 receptor antagonist, has shown promise in managing cytokine storms in adult sepsis and COVID-19 cases [2]. However, its efficacy in pediatric septic shock remains underexplored.&lt;/p&gt;&lt;p&gt;A total of 13 pediatric patients (aged 1–19 years) treated at a pediatric intensive care unit (PICU) from April 2023 to February 2024 were recorded. Participants were categorized based on underlying conditions: hematological malignancy (n = 7) or other diseases (n = 6). Following diagnosis and confirmation of elevated IL-6 levels, all patients received a single dose of tocilizumab within 24 h. Outcomes were assessed in terms of 28-day mortality, shock duration, and morbidity.&lt;/p&gt;&lt;p&gt;Among the 13 patients, seven had hematological malignancies, primarily presenting with bacteremia or neutropenic fever, and six had other underlying diseases (Table 1).&lt;/p&gt;&lt;figure&gt;&lt;figcaption&gt;&lt;b data-test=\"table-caption\"&gt;Table 1 Clinical characteristics of the patients with septic shock&lt;/b&gt;&lt;/figcaption&gt;&lt;span&gt;Full size table&lt;/span&gt;&lt;svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"&gt;&lt;use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;/use&gt;&lt;/svg&gt;&lt;/figure&gt;&lt;p&gt;Tocilizumab administration resulted in significant reductions in IL-6 levels for all patients, accompanied by improved hemodynamics and survival in 12 patients (92.3%). The median shock duration was approximately 5.5 days, and the 28-day mortality rate was 7.6%. Patients with malignancies showed a reduced shock duration (median 82 h) compared to previous reports (96 h).&lt;/p&gt;&lt;p&gt;No complications, such as secondary infections or long-term liver impairment, were observed.&lt;/p&gt;&lt;p&gt;One of the main pathophysiologies of sepsis is the upregulation of both pro- and anti-inflammatory pathways. Many proinflammatory cytokines, such as IL-1, IL-6, IL-8, IL-12, IL-18, TNF-a, and IFN-r, are highly expressed, leading to cytokine storms after sepsis develops [3]. Excessive cytokine levels result in progressive tissue damage, resulting in multiorgan impairment. A previous study reported that among the various cytokines, IL-6 was the most valuable cytokine associated with sepsis severity and outcome prediction [4]. Among patients with septic shock, survivors usually show a decreasing trend of IL-6 levels and non-survivors usually show increasing IL-6 levels [4]. By targeting the IL-6 signaling pathway, tocilizumab may suppress cytokine storms and reduce the risk of multiorgan dysfunction. The observed 28-day mortality rate (7.6%) and reduced shock duration align with findings from studies in adult populations, emphasizing the potential of tocilizumab as an adjunctive therapy [5].&lt;/p&gt;&lt;p&gt;Tocilizumab appears to","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"27 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}