Critical CarePub Date : 2025-08-21DOI: 10.1186/s13054-025-05618-x
Sylvain Diop, Maxime Aparicio, Hatem Kallel, Roman Mounier
{"title":"Hyperoxia and acute brain injury","authors":"Sylvain Diop, Maxime Aparicio, Hatem Kallel, Roman Mounier","doi":"10.1186/s13054-025-05618-x","DOIUrl":"https://doi.org/10.1186/s13054-025-05618-x","url":null,"abstract":"<p>Dear editor,</p><p>We read the interesting work of Romero‑Garcia and colleagues on the association between partial pressure of O<sub>2</sub> in arterial blood (P<sub>a</sub>O<sub>2</sub>) and neurological outcomes in a context of acute brain injury (ABI) [1]. This is a particularly relevant topic as the brain is highly vulnerable to excessive oxidative stress and reactive oxygen species (ROS) due to its huge dioxygen (O<sub>2</sub>) consumption and its high polyunsaturated fatty acid and iron content. The authors showed that high P<sub>a</sub>O<sub>2</sub> (hyperoxemia) was associated with poor neurological outcomes and mortality and conclude that it is important to adjust oxygenation strategies in this population [1]. It gives us the opportunity to explore the physiological effect of O<sub>2</sub>, hyperoxemia and hyperoxia on cerebral blood flow and metabolism beyond the sole results of the present meta-analysis.</p><p>Oxidative stress via the generation of reactive oxygen species (ROS) is one of the suggested mechanisms to explain the worsened outcomes associated with hyperoxemia [1, 2]. To properly understand how O<sub>2</sub> affects the generation of ROS, it seems important to recall some fundamental of physiology. ROS are a normal product of aerobic metabolism and are generated inside the cells, mainly in the mitochondria [2, 3]. Their excessive production is observed in various conditions, but mostly when the O<sub>2</sub> concentration reaching the cells abruptly changes as it happens during ischemia-reperfusion phenomenon (i.e., generation of superoxyde anion by the degradation of the accumulated hypoxanthine during ischemic phase by the xanthine oxidase following reestablishment of O<sub>2</sub> supply) [4, 5].</p><p>However, to hypothesize that hyperoxemia leads to increase ROS is an oversimplified statement [6]. Hyperoxemia refers by definition to a supranormal quantity of O<sub>2</sub> in the blood (assuming that a normal quantity is observed in a healthy person breathing air at sea level). It usually refers to either the partial pressure of dissolved O<sub>2</sub> (the P<sub>a</sub>O<sub>2</sub> in clinical practice) or the arterial content in O<sub>2</sub> (pooling both the dissolved O<sub>2</sub> and the O<sub>2</sub> carried by hemoglobin). Hyperoxia refers to a supranormal concentration of O<sub>2</sub> reaching the intracellular compartment. In normobaric (and normothermic) conditions, the absolute quantity of O<sub>2</sub> transported in its dissolved form is very low due to the low solubility coefficient of O<sub>2</sub> in blood (Fig. 1). This is why a carrier system (the hemoglobin) is needed to supply the global demand in O<sub>2</sub> [7]. However, only dissolved O<sub>2</sub> molecules can diffuse through the tissue to reach their effect site [7].</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 1</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.11","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"13 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899584","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}
Critical CarePub Date : 2025-08-21DOI: 10.1186/s13054-025-05625-y
Sasa Rajsic, Robert Breitkopf
{"title":"eCPR challenge: navigating the fine line between life and burden","authors":"Sasa Rajsic, Robert Breitkopf","doi":"10.1186/s13054-025-05625-y","DOIUrl":"https://doi.org/10.1186/s13054-025-05625-y","url":null,"abstract":"<p>To the Editor,</p><p>We read with great interest the retrospective analysis of sub-phenotypes in patients with out-of-hospital cardiac arrest (OHCA) who received extracorporeal cardiopulmonary resuscitation (eCPR) [1]. This methodologically robust, multicentre observational study included data from 83 hospitals and a total of 1,528 patients. The reported 30-day survival rate was 20.9% and a favourable neurological outcome, defined as cerebral performance category (CPC) score of 1 or 2 (good neurological recovery or moderate cerebral disability), was reported in 9.4%.</p><p>The highest survival was observed in the “standard eCPR” subgroup (26.9%), followed by delayed eCPR and the lowest in the non-shockable rhythm group. Low-flow time and timing of eCPR initiation emerged as key determinants of survival, potentially outweighing traditionally emphasized prognostic factors such as initial rhythm. However, heterogeneity in eCPR initiation criteria across centres precluded detailed evaluation of these protocols.</p><p>As a relatively novel technology, evidence on eCPR efficacy continues to evolve. Kashiura et al. significantly contribute to this growing body of high-quality data. While ultimate judgments on eCPR’s benefit will depend on further studies, we emphasize the critical importance of looking beyond crude survival rates. Neurologically favourable survival must remain a central outcome of interest, as many survivors endure prolonged hospitalizations, chronic disability, or severe neurological impairment, with attendant reductions in quality of life [2, 3].</p><p>Severe cerebral disability and coma or vegetative state (CPC 3 or 4) occurred in 11.4%, meaning that alongside the 144 survivors with favourable outcome, another 175 patients suffered profound neurological impairment. Together, this account for more than half of all survivors [1]. These individuals often depend on others for daily care or long-term institutionalization, imposing substantial socioeconomic and emotional burdens on patients, families, healthcare providers, and society [4, 5]. Although follow-up was short and some patients may improve neurologically over time, this early picture remains sobering.</p><p>Ethical concerns in these cases permeate all pillars of medical ethics. Patient autonomy is particularly vulnerable, as eCPR is almost always initiated under “presumed consent”, precluding an informed evaluation of the patient’s preferences regarding potential outcomes. Even when eCPR restores organ function, the resulting long-term state, marked by profound disability, dependence on life-sustaining therapies, or permanent loss of independence, may not align with the patient’s wishes and values. This discordance becomes especially pressing given the invasive and high-risk nature of extracorporeal life support.</p><p>The cost of eCPR is not purely financial. For families of patients who do not survive or who experience severe neurological injury, eCPR may prolong the dying ","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"15 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899586","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}
Critical CarePub Date : 2025-08-21DOI: 10.1186/s13054-025-05614-1
Teodor Svedung Wettervik, Erta Beqiri, Anders Hånell, Stefan Yu Bögli, Ihsane Olakorede, Xuhang Chen, Adel Helmy, Andrea Lavinio, Peter J. Hutchinson, Peter Smielewski
{"title":"Correction: Revisiting the oxygen reactivity index in traumatic brain injury: the complementary value of combined focal and global autoregulation monitoring","authors":"Teodor Svedung Wettervik, Erta Beqiri, Anders Hånell, Stefan Yu Bögli, Ihsane Olakorede, Xuhang Chen, Adel Helmy, Andrea Lavinio, Peter J. Hutchinson, Peter Smielewski","doi":"10.1186/s13054-025-05614-1","DOIUrl":"https://doi.org/10.1186/s13054-025-05614-1","url":null,"abstract":"<p><b>Correction: Critical Care (2025) 29:20</b></p><p><b>https://doi.org/10.1186/s13054-025-05261-6</b></p><p>Following publication of the original article [1], the authors noticed that the 95% confidence interval of ORx was slightly wrong in Table 3, which was revised in the published article. However, the authors realized that they did not update this reference in the main text of the <b>Results</b> > <b>ORx in relation to outcome</b> section.</p><p>The last paragraph in the <b>Results</b> > <b>ORx in relation to outcome</b> section currently reads:</p><p>In a multivariable logistic outcome regression (Table 3), mean ORx (OR [95% CI] = 11.3 [25.87–12,271.11], <i>p</i> = 0.01) was independently associated with mortality, after adjustment for age, GCS, and PRx. However, ORx was not independently associated with favourable outcome.</p><p>The last paragraph in the <b>Results</b> > <b>ORx in relation to outcome</b> section should read:</p><p>In a multivariable logistic outcome regression (Table 3), mean ORx (OR [95% CI] = 11.3 [1.82–73.67], <i>p</i> = 0.01) was independently associated with mortality, after adjustment for age, GCS, and PRx. However, ORx was not independently associated with favourable outcome.</p><p>The last paragraph in the Results > ORx in relation to outcome section has been updated in this correction article and the original article [1] has been corrected.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Svedung Wettervik T, Beqiri E, Hånell A, et al. Revisiting the oxygen reactivity index in traumatic brain injury: the complementary value of combined focal and global autoregulation monitoring. Crit Care. 2025;29:20. https://doi.org/10.1186/s13054-025-05261-6.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Department of Medical Sciences, Section of Neurosurgery, Uppsala University, 751 85, Uppsala, Sweden</p><p>Teodor Svedung Wettervik & Anders Hånell</p></li><li><p>Brain Physics Laboratory, Department of Clinical Neurosciences, Division of Neurosurgery, University of Cambridge, Cambridge, UK</p><p>Teodor Svedung Wettervik, Erta Beqiri, Stefan Yu Bögli, Ihsane Olakorede, Xuhang Chen & Peter Smielewski</p></li><li><p>Department of Clinical Neurosciences, Division of Neurosurgery, Addenbrooke’s Hospital, University of Cambridge, Cambridge, UK</p><p>Adel Helmy & Peter J. Hutchinson</p></li><li><p>Neurosciences and Trauma Critical Care Unit, Addenbrooke’s Hospital, Cambridge University Hospitals, Cambridge, UK</p><p>Andrea Lavinio</p></li></ol><span>Authors</span><ol><li><span>Teodor Svedung Wettervik</span>View author publications<p><span>Search author on:</span><span>PubMed<span> </","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"22 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899585","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}
Critical CarePub Date : 2025-08-21DOI: 10.1186/s13054-025-05587-1
Javier Hidalgo-Martín, María del Carmen Ruiz-Iniesta, María Dolores Pola-Gallego-de-Guzmán, Julia Manetsberger, María Belén Martínez-Lechuga, José Ángel Ramos-Cuadra, Carolina Castillo-Portellano, Juan Luis Manzano-Moreno, Crispín Colmenero-Aguilar, Manuel Castellanos-Hernández, Juan Carlos Fernández-Guerrero, Blanca Irene Ráfales-Perucha, María Leyre Lavilla-Lerma, Natacha Caballero-Gómez, Ricardo Rivera-Fernández, Manuel Ruiz-Bailén
{"title":"Detecting heart failure in severe asthma patients using speckle tracking echocardiography","authors":"Javier Hidalgo-Martín, María del Carmen Ruiz-Iniesta, María Dolores Pola-Gallego-de-Guzmán, Julia Manetsberger, María Belén Martínez-Lechuga, José Ángel Ramos-Cuadra, Carolina Castillo-Portellano, Juan Luis Manzano-Moreno, Crispín Colmenero-Aguilar, Manuel Castellanos-Hernández, Juan Carlos Fernández-Guerrero, Blanca Irene Ráfales-Perucha, María Leyre Lavilla-Lerma, Natacha Caballero-Gómez, Ricardo Rivera-Fernández, Manuel Ruiz-Bailén","doi":"10.1186/s13054-025-05587-1","DOIUrl":"https://doi.org/10.1186/s13054-025-05587-1","url":null,"abstract":"To determine the presence of acute myocardial dysfunction in status asthmaticus. From 2006 to 2025, we studied severe asthma patients, healthy controls, and weightlifters performing bench press. Group differences were evaluated using echocardiography with Speckle Tracking by velocity vector imaging (VVI). Asthma patients were followed for 6 months. Of 357 participants, 169 were controls. The median age of asthmatic patients (n = 188) was 58.11 ± 12.97 years, comparable to controls. Thirty-one patients died. All patients with severe asthma demonstrated reduced biventricular strain. After bench press, all echocardiographic values were higher compared to non-sportsmen and asthmatic patients. Acute asthma patients demonstrated lower strain in the four cavities, and more asynchrony versus controls. Right ventricular global longitudinal strain was ([− 27.56 ± 4.56] in the control group, [− 24.08 ± 1.23] in the basal weightlifters’ group, [− 30.88 ± 1.02] after bench press and [− 17.98 ± 2.57] in severe asthma, p value = 0.0001). Left ventricular global longitudinal strain (%) were (− 21.02 ± 3.28, − 19.34 ± 3.78, − 25.21 ± 9.32, − 14.88 ± 1.27, p value = 0.012) respectively. Multivariate analysis identified right atrial pump strain (OR 0.457 [0.189–0.746]) and as factors associated with mortality. Mechanical Ventilation was associated with RVGLS (OR 0.637, CI 95% [0.248–0.925]) and right atrial pump strain (OR 0.783, CI 95% [0.349–0.967]). At 6 months follow-up, asthmatic patients exhibited lower deformity parameters and decreased Speckle Tracking vectorial velocity analysis in all cardiac chambers compared to control groups. Patients with acute asthma exhibit decreased strain in all cardiac chambers, which remains reduced at the six-month follow-up. Asthma may contribute to latent heart failure.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"38 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899587","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}
Critical CarePub Date : 2025-08-20DOI: 10.1186/s13054-025-05524-2
Till Hauffe, Bahar Nalbant, Lennart Wild, Mattia Müller, Aline Schöni, Rea Andermatt, Alix Buhlmann, Klaus Stahl, Christian Putensen, Christian Bode, Benjamin Seeliger, Sascha David
{"title":"Demographics and outcome of Legionella pneumonia in the intensive care unit: a retrospective multicenter cohort study","authors":"Till Hauffe, Bahar Nalbant, Lennart Wild, Mattia Müller, Aline Schöni, Rea Andermatt, Alix Buhlmann, Klaus Stahl, Christian Putensen, Christian Bode, Benjamin Seeliger, Sascha David","doi":"10.1186/s13054-025-05524-2","DOIUrl":"https://doi.org/10.1186/s13054-025-05524-2","url":null,"abstract":"Legionella pneumonia (LP) is a major cause of severe community-acquired pneumonia (CAP) that can lead to acute respiratory distress syndrome (ARDS) with high morbidity and mortality. ARDS may necessitate extracorporeal membrane oxygenation (ECMO) support, and evidence is limited about benefits of ECMO in LP. Therefore, we sought to analyze the clinical course, outcomes and predictive factors of ECMO patients with ARDS due to LP compared to non ECMO patients. This retrospective, multicenter cohort study analyzed ICU patients with LP across three tertiary university hospitals (Zurich, Switzerland; Hannover & Bonn, Germany) from 2013 to 2023. We examined demographics, clinical characteristics, and outcomes, with a focus on ECMO utilization and its impact on mortality. A total of 110 patients were included, with a median age of 60 years and 75% male. ECMO support was initiated in 40%. The overall 28-day mortality did not differ between groups, with 21% without ECMO vs. 25% with ECMO (OR 1.24 (0.49–3.05, p = 0.64), despite higher degree of organ failure in the ECMO group (SOFA score 24 h after ICU admission 9 vs. 12, p < 0.001). Only 57% of patients had adequate antibiotic LP coverage at ICU admission with no differences in outcome. Multivariable analysis found hospital acquired LP (OR 28.4 (3.44–614), p = 0.006) and lactate (OR 1.31 (1.05–1.75), p = 0.031) as independent risk factor for 28-day mortality. Patients suffering from LP requiring ECMO support had similar mortality rates compared to LP patients without ECMO support, despite higher SOFA scores. In addition, LP-induced respiratory failure requiring ECMO had a lower mortality rate compared to the published literature on the overall ARDS population. This indirect indication of a potential survival benefit may support bedside clinicians in their decision-making regarding ECMO initiation or withholding.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"15 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899453","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}
Critical CarePub Date : 2025-08-20DOI: 10.1186/s13054-025-05577-3
Chema Strik-Lips, Dirk van Lier, Antonius Eduard van Herwaarden, Tim Frenzel, Peter Pickkers
{"title":"Effects of angiotensin 2 infusion on the RAAS and alternative RAAS pathway","authors":"Chema Strik-Lips, Dirk van Lier, Antonius Eduard van Herwaarden, Tim Frenzel, Peter Pickkers","doi":"10.1186/s13054-025-05577-3","DOIUrl":"https://doi.org/10.1186/s13054-025-05577-3","url":null,"abstract":"<p>Dear editor,</p><p>With interest we read the article of Leisman et al. [1] describing the ‘AIMRITE’ blood pressure response to Angiotensin 2 infusion and its correlation with favorable outcome. In contrast to earlier data [2], baseline renin concentration did not predict the blood pressure response to Angiotensin II. To further forward our understanding of the physiological response to angiotensin II infusion in patients with septic shock we comprehensively assessed the Renin–Angiotensin–Aldosteron-System (RAAS) and the alternative RAAS [3]. The study was carried out in the Netherlands in accordance with the applicable rules concerning the review of research ethics committees and informed consent. All patients or legal representatives were informed about the study details and could decline to participate. Patients with a noradrenaline dose > 0.2 µg/kg/min were treated with angiotensin II between 6 and 48 h from the initiation of noradrenaline. A target mean arterial pressure (MAP) of ≥ 65 mmHg was maintained and patients were deemed a responder to angiotensin II if a reduction in noradrenalin infusion rate of > 25% was achieved. Blood samples were drawn at baseline, after 3 and 24 h. Renin, angiotensin I, angiotensin II, angiotensin 1–7 and angiotensin 1–5 were determined. We calculated angiotensin 1–7/1–5 ratio, as a proxy for Angiotensin-converting-enzyme (ACE) activity; and angiotensin II/1–7 ratio, as a proxy for ACE-2 activity. All data is presented as median [IQR].</p><p>Ten patients were included (Table 1), six patients responded to angiotensin II with a reduction of noradrenaline infusion rate of 72% [48–89%]. Kinetics of the RAAS pathway are shown in Fig. 1. Angiotensin II infusion rate was lower in responders than in non-responders at 3 h (23.8 [15.1–28.0] versus 35.0 [29.7–40.0] ng/kg/min) and 24 h (18.8 [4.7–19.8] versus 40.0 [40.0–40.0] ng/kg/min). Accordingly, the measured angiotensin II plasma concentrations were lower (612 [313–886] versus 1021 [593–1069] µU/ml) in the MAP-responders compared to non-responders. Plasma renin concentration decreased from 282 [95–368] to 71 [46–121] (3 h) and 34 [23–40] µU/ml (24 h) in patients responding to angiotensin II, while the decline in renin was much less pronounced in non-responders, from 446 [274–691] at baseline to 310 [272–581] and 300 [230–321] µU/ml, respectively. Angiotensin 1–7 plasma concentration was similar at baseline, but higher at 3 and 24 h in patients not responding to angiotensin II infusion. Also, baseline angiotensin 1–7/1–5 ratio was similar between responders and non-responders, and increased in patients not responding to angiotensin II infusion, illustrating attenuation of ACE activity. While ACE activity decreased, Angiotensin II infusion resulted in an increase in ACE-2 activity in non-responders, illustrated by a decrease in Angiotensin II/1–7 ratio.</p><figure><figcaption><b data-test=\"table-caption\">Table 1 Baseline characteristics, numbers are absolute va","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"27 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899455","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}
Critical CarePub Date : 2025-08-20DOI: 10.1186/s13054-025-05611-4
Je Min Suh, Nattaya Raykateeraroj, Boris Waldman, Nuanprae Kitisin, Cilla Haywood, Rinaldo Bellomo, Anoop N. Koshy, David Pilcher, Dong-Kyu Lee, Laurence Weinberg
{"title":"Correction: Characteristics, outcomes, and complications among nonagenarian and centenarian patients admitted to the intensive care unit: a scoping review","authors":"Je Min Suh, Nattaya Raykateeraroj, Boris Waldman, Nuanprae Kitisin, Cilla Haywood, Rinaldo Bellomo, Anoop N. Koshy, David Pilcher, Dong-Kyu Lee, Laurence Weinberg","doi":"10.1186/s13054-025-05611-4","DOIUrl":"https://doi.org/10.1186/s13054-025-05611-4","url":null,"abstract":"<p><b>Correction: Critical Care (2025) 29:112</b> <b>https://doi.org/10.1186/s13054-025-05349-z</b></p><p>Following the publication of the original article [1], the authors identified an error in the author name of Nattaya Raykateeraroj.</p><p>The incorrect author name is:</p><p>Nattaya Raykageeraroj.</p><p>The correct author name is:</p><p>Nattaya Raykateeraroj.</p><p>The author group has been updated in this correction article and the original article [1] has been corrected.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Suh JM, Raykateeraroj N, Waldman B, et al. Characteristics, outcomes, and complications among nonagenarian and centenarian patients admitted to the intensive care unit: a scoping review. Crit Care. 2025;29:112. https://doi.org/10.1186/s13054-025-05349-z.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Je Min Suh and Nattaya Raykateeraroj are first coauthors</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Anaesthesia, Austin Health, 154 Studley Road, Heidelberg, VIC, 3084, Australia</p><p>Je Min Suh, Boris Waldman & Laurence Weinberg</p></li><li><p>Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand</p><p>Nattaya Raykateeraroj & Nuanprae Kitisin</p></li><li><p>Department of Geriatric Medicine, Austin Health, Heidelberg, Australia</p><p>Cilla Haywood</p></li><li><p>Department of Intensive Care, Austin Health, Heidelberg, Australia</p><p>Cilla Haywood & Rinaldo Bellomo</p></li><li><p>Department of Critical Care, The University of Melbourne, Melbourne, VIC, Australia</p><p>Rinaldo Bellomo & Laurence Weinberg</p></li><li><p>Department of Cardiology, Austin Health, Heidelberg, Australia</p><p>Anoop N. Koshy</p></li><li><p>Department of Intensive Care, Alfred Health, Prahran, Australia</p><p>David Pilcher</p></li><li><p>Department of Anaesthesiology and Pain Medicine, Dongguk University Ilsan Hospital, Goyang, Republic of Korea</p><p>Dong-Kyu Lee</p></li><li><p>Australian and New Zealand Intensive Care Research Centre, Monash University, Prahran, Republic of Korea</p><p>David Pilcher</p></li></ol><span>Authors</span><ol><li><span>Je Min Suh</span>View author publications<p><span>Search author on:</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Nattaya Raykateeraroj</span>View author publications<p><span>Search author on:</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Boris Waldman</span>View author publications<p><span>Search author on:</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Nuanprae Kitisin</span>View author publications<p><span>Search author on","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"70 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899454","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}
Critical CarePub Date : 2025-08-20DOI: 10.1186/s13054-025-05449-w
Ori J. Lieberman, Virginia Yao, Gerardo Velasquez, Matheus Otero, Kevin Bao, Katherine Peterson, Firas H. Kobeissy, Jonathan Z. Pan, Zhonghui Guan, H. E. Hinson, Sergio E. Baranzini, J. Claude Hemphill, Neel S. Singhal, Edilberto Amorim
{"title":"Higher circulating short-chain fatty acids are associated with good neurologic outcome after cardiac arrest","authors":"Ori J. Lieberman, Virginia Yao, Gerardo Velasquez, Matheus Otero, Kevin Bao, Katherine Peterson, Firas H. Kobeissy, Jonathan Z. Pan, Zhonghui Guan, H. E. Hinson, Sergio E. Baranzini, J. Claude Hemphill, Neel S. Singhal, Edilberto Amorim","doi":"10.1186/s13054-025-05449-w","DOIUrl":"https://doi.org/10.1186/s13054-025-05449-w","url":null,"abstract":"<p>Nearly 6 million people suffer cardiac arrest (CA) annually. Many die or are severely impaired by systemic and neurologic injury. Predicting functional recovery remains challenging. Current electrophysiologic, radiographic, and blood-based biomarkers of neurologic outcome after CA focus on brain-specific injury. Whether the discovery of novel, mechanism-informed biomarkers that reveal the interplay between brain and systemic injury after CA may aid prognostication remains unclear. </p><p>Gut injury from ischemia during CA is associated with poor neurologic outcome [1]. Emerging evidence suggests that the gut microbiome, whose composition changes during gut ischemia, impacts a variety of neurologic diseases. Impaired production of short-chain fatty acids (SCFAs) mediates this connection. SCFAs are produced from dietary fiber by gut bacteria and enter the systemic circulation where they act distally by modulating cytokine release, blood–brain barrier permeability and brain-resident immune cells [2]. In this study, we hypothesized that higher circulating levels of SCFAs are associated with good neurologic outcome after CA.</p><p>We performed a single-center, prospective cohort study of comatose adult patients that were resuscitated from out-of-hospital CA (n = 25) at an urban safety-net hospital as a convenience sample. Prisoners, pregnant women and patients with pre-admission antibiotic administration were excluded from the study. Baseline and resuscitation characteristics were extracted from the electronic health record. The Sequential Organ Failure Assessment (SOFA) and MIRACLE<sub>2</sub> scores [3] were used to estimate illness severity and predict neurologic outcome based on the resuscitation characteristics, respectively. Plasma samples were collected approximately 24 (range: 18–30) hours after CA. This time point was chosen as results would not only be relevant for neuroprognostication but also allow critical care interventions and gut injury during CA to impact SCFA levels. Gas chromatography-electron ionization-mass spectrometry (GC-EI-MS) was used to measure SCFAs [4]<i>.</i> The gray matter cortex score, a qualitative measurement of hypoxic ischemic brain injury after CA that is associated with neurologic outcome, was determined from the apparent diffusion coefficient sequence of magnetic resonance imaging (MRI) of the brain obtained 3–5 days after CA [5]. Additional details regarding the GC-EI-MS method and brain MRI are available in the supplemental material. Cerebral Performance Category (CPC; good defined as CPC 1–2 and poor defined as CPC 3–5) was determined at hospital discharge (censored at 12 months after CA). The Institutional Review Board at the University of California, San Francisco approved this study.</p><p>Cohort characteristics are detailed in supplemental Table S1.</p><p>In subjects with a good neurologic outcome at discharge, plasma levels of SCFAs were significantly higher than in subjects with a poor neurologic out","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"27 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899589","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}
Critical CarePub Date : 2025-08-20DOI: 10.1186/s13054-025-05595-1
Isabelle Arctaedius, Johan Wassélius, Margareta Lang, Mattias Drake, Mikael Johnsson, Hans Friberg, Christoph Leithner, Martin Kenda, Anna Lybeck, Marion Moseby-Knappe
{"title":"The semi-quantitative cardiac arrest brain ischemia (CABI) score for magnetic resonance imaging predicts functional outcome after cardiac arrest","authors":"Isabelle Arctaedius, Johan Wassélius, Margareta Lang, Mattias Drake, Mikael Johnsson, Hans Friberg, Christoph Leithner, Martin Kenda, Anna Lybeck, Marion Moseby-Knappe","doi":"10.1186/s13054-025-05595-1","DOIUrl":"https://doi.org/10.1186/s13054-025-05595-1","url":null,"abstract":"Magnetic resonance imaging (MRI) is recommended by guidelines to evaluate the severity of brain ischemia after cardiac arrest for functional outcome prediction. However, standardized assessment criteria are lacking. We have developed a semi-quantitative Cardiac Arrest Brain Ischemia (CABI) score to assess the extension of brain ischemia on MRI. To evaluate the prognostic performance of a novel semi-quantitative CABI score in comparison to qualitative routine radiological MRI assessment after cardiac arrest. A retrospective, multicenter observational study of adults (≥ 18 years-old) admitted to intensive care after cardiac arrest at four Swedish hospitals from 2014 to 2018. Four radiologists, blinded to clinical information except patient age, assessed the MRI as per guideline recommendations and according to the CABI score. The CABI score evaluates extension of ischemia in 12 predefined territories (3 cortical and 2 deep grey nuclei territories bilaterally based on vascular supply; the cerebellum; and the brainstem) from 0–3 (0 = No acute ischemic lesion; 3 ≥ 50% of the territory). The CABI score ranges from 0–36. Poor functional outcome was defined as Cerebral Performance Category 3–5 assessed at 2–6 months post-arrest. Prognostic ability was evaluated with sensitivity and specificity and with the area under the receiver operating characteristics curve (AUC). Inter-rater reliability was calculated by Fleiss´ Kappa or intraclass correlation coefficient. Ninety (n = 90) patients examined with MRI at median 5 days (IQR: 3.7−6.3) were included Median age was 63.7 years (IQR: 58.3−70.5), 74.4% (n = 67) were men and 85.6% (n = 77) had a poor functional outcome. Among four blinded raters, routine qualitative assessment according to guidelines showed 84.6–100% specificity and 61–76.6% sensitivity for poor outcome. Inter-rater reliability for the qualitative assessment was moderate (Fleiss κ = 0.64, 95% CI: 0.53−0.75). The CABI score achieved an AUC of 0.87–0.92 (p< 0.05 vs. routine assessment) and a sensitivity of 59.7−85.7% while maintaining high specificity (76.9–100%) at cut-off ≥ 8 points. The intraclass correlation coefficient (ICC) for the CABI score was 0.67 (95% CI: 0.58–0.75), reflecting moderate agreement among raters. A semi-quantitative approach to MRI evaluations after cardiac arrest may increase the prognostic accuracy compared to non-standardized routine assessment. SweCrit biobank, retrospectively registered at ClinicalTrials.gov no. NCT04974775 18th of June 2021.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"31 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899452","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}
Critical CarePub Date : 2025-08-19DOI: 10.1186/s13054-025-05621-2
Luke Churchill, Lawrence Caruana, Nicole White, John F Fraser, Allison Mandrusiak, Jennifer Paratz, Anna-Liisa Sutt, Peter J Thomas, Stacey Verner-Wren, Oystein Tronstad
{"title":"Exercise in patients with a tracheostomy and speaking valve: a randomised crossover-controlled trial.","authors":"Luke Churchill, Lawrence Caruana, Nicole White, John F Fraser, Allison Mandrusiak, Jennifer Paratz, Anna-Liisa Sutt, Peter J Thomas, Stacey Verner-Wren, Oystein Tronstad","doi":"10.1186/s13054-025-05621-2","DOIUrl":"10.1186/s13054-025-05621-2","url":null,"abstract":"","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"29 1","pages":"368"},"PeriodicalIF":9.3,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}