Critical Care最新文献

{"title":"Assessing fluid responsiveness with central venous oxygen saturation: the complex relationship between oxygenation and perfusion","authors":"Jaume Mesquida","doi":"10.1186/s13054-025-05294-x","DOIUrl":"https://doi.org/10.1186/s13054-025-05294-x","url":null,"abstract":"<p>In the process of hemodynamic resuscitation, the aim of volume expansion (VE) is to increase cardiac output (CO) and, consequently, oxygen delivery (DO<sub>2</sub>) to restore oxygen availability at the tissue level. Such intervention should ideally be performed only when tissue hypoxia is suspected. Otherwise, despite increasing CO, the intervention could potentially lead to harmful effects.</p><p>Since CO is not routinely monitored in daily practice, some authors have suggested that certain metabolic variables, such as central venous oxygen saturation (S<sub>cv</sub>O<sub>2</sub>), could serve as indirect markers for assessing fluid responsiveness [1]. Mallat and colleagues recently published an interesting study in <i>Critical Care</i>, further confirming the association between a positive CO response and S<sub>cv</sub>O<sub>2</sub> as a result of VE [2]. The authors propose that S<sub>cv</sub>O<sub>2</sub> can be used in the absence of CO measurements to define fluid responsiveness in critically ill patients. While there is extensive evidence supporting this association, the relationship between a flow variable (CO) and a metabolic variable (S<sub>cv</sub>O<sub>2</sub>) is more complex than it appears and warrants cautious consideration when integrated into bedside clinical decisions.</p><p>According to the proposed indirect approach to fluid responsiveness, a certain increase in S<sub>cv</sub>O<sub>2</sub> following VE would indicate a positive CO response, whereas an unchanged or marginally increased S<sub>cv</sub>O<sub>2</sub> would indicate a negative CO response. However, S<sub>cv</sub>O<sub>2</sub> changes are influenced not only by CO but also by the relationship between DO<sub>2</sub> and oxygen consumption (VO<sub>2</sub>). According to Fick's principle,</p><span>$${text{VO}}_{{2}} = {text{ CO }}cdot , left( {{text{C}}_{{text{a}}} {text{O}}_{{2}} - {text{ C}}_{{{text{mv}}}} {text{O}}_{{2}} } right) , cdot{ 1}0$$</span><p>where C<sub>a</sub>O<sub>2</sub> and C<sub>mv</sub>O<sub>2</sub> are the arterial and mixed venous oxygen contents, respectively. This can be further derived into:</p><span>$${text{CO }} = {text{ VO}}_{{2}} / , left( {{text{C}}_{{text{a}}} {text{O}}_{{2}} - {text{ C}}_{{{text{mv}}}} {text{O}}_{{2}} } right) , cdot{ 1}0$$</span><span>$${text{CO }} = {text{ VO}}_{{2}} / , left[ {{13}.{9 }cdot , } right[{text{Hb}}left] { , cdot , left( {{text{S}}_{{text{a}}} {text{O}}_{{2}} - {text{ S}}_{{{text{mv}}}} {text{O}}_{{2}} } right)} right]$$</span><span>$${text{S}}_{{{text{mv}}}} {text{O}}_{{2}} = {text{ S}}_{{text{a}}} {text{O}}_{{2}} - , left[ {{text{VO}}_{{2}} / , ({13}.{9 }cdot , } right[{text{Hb}}left] { , cdot{text{ CO}})} right]$$</span><p>Therefore, mixed venous oxygen saturation (S<sub>mv</sub>O<sub>2</sub>) depends on S<sub>a</sub>O<sub>2</sub>, VO<sub>2</sub>, hemoglobin concentration ([Hb]), and CO. Consequently, changes in S<sub>mv</sub>O<sub>2</sub> after VE depend on the fluids’ effects on each of these para","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"37 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470699","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":"Discarded intravenous medication in the ICU: the GAME-OVER multicenter prospective observational study","authors":"Erwan d’Aranda, Stéphanie Pons, Jonathan Chelly, Enora Atchade, Laure Bonnet, Claire Dahyot-Fizelier, Toufik Kamel, Fanny Giannoni, Olivier Collange, Emmanuel Besnier, Mathieu Schoeffler, Nicolas Mayeur, Pierre-Louis Quere, Ludivine Marecal, Cyril Pernod, Cyrille Geay, Pierre Esnault, Raphaël Cinotti, Magali Cesana, Pierre-Julien Cungi","doi":"10.1186/s13054-025-05299-6","DOIUrl":"https://doi.org/10.1186/s13054-025-05299-6","url":null,"abstract":"Medication waste is a contributor to the healthcare environmental footprint and impacts ecosystems. Data on medication waste in the intensive care unit (ICU) are scarce, and therefore are essential to develop new sustainable strategies. The GAME-OVER French multicenter prospective observational study was conducted from November 2022 to March 2023, over a 24-h period of choice, at the discretion of each participating center. Adult ICUs were enrolled in the study on a voluntary basis and hospitalized patients who did not express opposition were included in the analysis. The primary endpoint was the percentage of discarded intravenous (IV) medication in the ICU, defined as the ratio of the discarded volume to the total volume of IV medication prepared. Secondary endpoints included identifying risk factors and main reasons for medication waste and estimating its related healthcare cost. Among the 81 ICUs and the 1076 enrolled patients, 408.9 L of 130 IV medications were prepared. The discarded volume was 43.8 L, resulting in a 10.7% discarded IV medication (95% Confidence Interval (CI), 9.9–11.5). Number of daily admissions/discharges in the ICU, as admission for elective surgery, Sequential Organ Failure Assessment score ≥ 7, endotracheal intubation, renal replacement therapy and body mass index were independently associated with increased discarded IV medication. Ninety percent of pharmaceutical waste was attributed to 25 key drugs, with an estimated national annual cost of 2,737,163€. Discarded intravenous medication in the ICU is considerable and results in significant costs for the health care system, without obvious patient-centered value. Risk factors associated with medication waste were largely nonmodifiable, emphasizing the need for sustainable practices in patient care and resource management. ClinicalTrials.gov: NCT05553054 . September 23, 2022. ","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"4 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470694","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":"Gaps in PLTP mechanism research in sepsis-associated acute kidney injury and improvement strategies based on new evidence","authors":"Dongrui Liang, Xiaodong Li","doi":"10.1186/s13054-025-05310-0","DOIUrl":"https://doi.org/10.1186/s13054-025-05310-0","url":null,"abstract":"<p>Dear editor,</p><p>We were highly intrigued by the study conducted by Jiang and colleagues, which illustrates the significant role of phospholipid transfer protein (PLTP) in sepsis-associated acute kidney injury (SA-AKI) [1]. The study on the role of PLTP in SA-AKI provides valuable insights into its potential as a therapeutic target. However, several critical gaps in the mechanistic understanding of PLTP's protective effects limit its translational potential. Here, we highlight these gaps and propose improvement strategies based on recent evidence.</p><p>The study suggests that PLTP exerts anti-inflammatory effects by neutralizing LPS and facilitating its clearance. However, the specific signaling pathways involved, such as TLR4/NF-κB, remain under-explored. Recent studies have shown that TLR4/NF-κB activation is a key driver of renal inflammation in sepsis [2]. Future research should investigate whether PLTP directly modulates this pathway by measuring downstream inflammatory markers and key proteins in renal tissues.</p><p>While the study observes improved mitochondrial structure in PLTP-treated mice, the molecular mechanisms underlying this protection are unclear. Mitochondrial dysfunction, characterized by impaired dynamics and increased oxidative stress, is a hallmark of SA-AKI. Recent work by Li et al. highlights the role of mitophagy in mitigating renal injury during sepsis [3]. Future studies should assess mitochondrial dynamics-related proteins and mitophagy markers to determine whether PLTP enhances mitochondrial quality control. Additionally, measuring reactive oxygen species (ROS) levels and antioxidant enzyme activity could clarify PLTP's role in reducing oxidative stress.</p><p>The study mentions PLTP's involvement in lipid transport but does not explore its impact on specific lipid mediators, such as sphingosine-1-phosphate (S1P). S1P, transported by HDL, has been shown to improve renal microcirculation and reduce inflammation through S1P1 receptor activation. Bajwa et al. reported that S1P1 receptor agonists attenuate ischemic kidney injury, suggesting a potential link between PLTP and S1P signaling [4]. Future research should measure S1P levels in plasma and renal tissues and evaluate S1P1 receptor expression to determine whether PLTP's protective effects are mediated through this pathway.</p><p>The study focuses on PLTP mRNA and protein expression but overlooks potential epigenetic and non-coding RNA regulation. Sepsis-induced epigenetic modifications, such as DNA methylation and histone acetylation, can significantly alter gene expression [5]. Additionally, miRNAs like miR-155 and miR-146a have been implicated in regulating inflammatory responses. Future studies should investigate whether PLTP expression is modulated by epigenetic changes or miRNAs, providing a more comprehensive understanding of its regulatory mechanisms.</p><p>In conclusion,while the study provides a foundational understanding of PLTP's role in SA-AKI, it","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"1 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443215","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":"Limitations of SpO2 / FiO2-ratio for classification and monitoring of acute respiratory distress syndrome—an observational cohort study","authors":"Rolf Erlebach, Una Pale, Tilman Beck, Sasa Markovic, Marko Seric, Sascha David, Emanuela Keller","doi":"10.1186/s13054-025-05317-7","DOIUrl":"https://doi.org/10.1186/s13054-025-05317-7","url":null,"abstract":"The ratio of pulse-oximetric peripheral oxygen saturation to fraction of inspired oxygen (SpO2/FiO2) has been proposed as additional hypoxemia criterion in a new global definition of acute respiratory distress syndrome (ARDS). This study aims to evaluate the clinical and theoretical limitations of the SpO2/FiO2-ratio when using it to classify patients with ARDS and to follow disease progression. Observational cohort study of ARDS patients from three high-resolution Intensive Care Unit databases, including our own database ICU Cockpit, MIMIC-IV (Version 3.0) and SICdb (Version 1.0.6). Patients with ARDS were identified based on the Berlin criteria or ICD 9/10-codes. Time-matched datapoints of SpO2, FiO2 and partial pressure of oxygen in arterial blood (PaO2) were created. Severity classification followed the thresholds for SpO2/FiO2 and PaO2/FiO2 of the newly proposed global definition. Overall, 708 ARDS patients were included in the analysis. ARDS severity was misclassified by SpO2/FiO2 in 33% of datapoints, out of which 84% were classified as more severe. This can be partially explained by imprecision of SpO2 measurement and equation used to transform SpO2/FiO2 to PaO2/FiO2. A high dependence of SpO2/FiO2-ratio on FiO2 settings was found, leading to major treatment effect and limited capability for tracking change in ARDS severity, which was achieved in less than 20% of events. The use of SpO2/FiO2 interchangeably with PaO2/FiO2 for severity classification and monitoring of ARDS is limited by its inadequate trending ability and high dependence on FiO2 settings, which may influence treatment decisions and patient selection in clinical trials.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"49 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443214","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":"The green ICU: how to interpret green? A multiple perspective approach","authors":"Elisabeth Smale, Heather Baid, Marko Balan, Forbes McGain, Scott McAlistar, Jan J. de Waele, Jan Carel Diehl, Erik van Raaij, Michel van Genderen, Dick Tibboel, Nicole Hunfeld","doi":"10.1186/s13054-025-05316-8","DOIUrl":"https://doi.org/10.1186/s13054-025-05316-8","url":null,"abstract":"Mitigating environmental impacts is an urgent challenge supported by (scientific) intensive care societies worldwide. However, making green choices without compromising high-quality care for critically ill patients may be challenging. The current paper describes a three-step approach towards green intensive care units. Starting with the measurement of environmental sustainability, intensive care units can identify hotspots, quantify the environmental impacts of products and procedures, and monitor sustainable progress. Subsequently, a multidisciplinary approach is proposed to improve environmental sustainability, including a collaboration of procurement specialists and healthcare professionals, using co-creation and green teams as efficient grassroots change agents. A context-specific approach for enhancing sustainable healthcare practices is key in order to fit local regulatory requirements and create support of professionals. A final step is to share results and create momentum, including publishing initiatives and participating in online (inter)national networks. Based on the core sustainability principles, this three-step approach towards green ICUs provides a valuable tool to professionals worldwide to facilitate change towards environmentally responsible intensive care units.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"40 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443243","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":"An index of the initial blood pressure response to angiotensin II treatment and its association with clinical outcomes in vasodilatory shock","authors":"Daniel E. Leisman, Patrick M. Wieruszewski, Laurence W. Busse, Lakhmir S. Chawla, Kathryn A. Hibbert, Damian R. Handisides, Ashish K. Khanna, Marlies Ostermann, Michael T. McCurdy, Christopher D. Adams, Tony N. Hodges, Rinaldo Bellomo","doi":"10.1186/s13054-025-05311-z","DOIUrl":"https://doi.org/10.1186/s13054-025-05311-z","url":null,"abstract":"No standardized index exists to assess cardiovascular responsiveness to angiotensin-II. We hypothesized that a standardized index of initial blood pressure response to angiotensin-II treatment would be associated with clinical outcomes. Using data from the Angiotensin Therapy for High Output Shock (ATHOS-3) trial, we developed an Angiotensin-II Initial MAP Response Index of Treatment Effect (AIMRITE) defined as (MAP at hr1 – MAP at baseline)/study drug dose. We assessed AIMRITE continuously and, based on observed distributions, we additionally categorized patients as “responsive” or “resistant”, with responsiveness defined by an AIMRITE ≥ 0.90 mmHg/ng/kg/min. The primary clinical outcome was 28-day mortality. Secondary outcomes included days alive and vasopressor- or ventilator- or renal replacement therapy-free at day-7. Biological outcomes included baseline renin, angiotensin-II, and renin/angiotensin-II ratio, and their change at hr3. Of 158 placebo patients, as expected, 157 (99%) had AIMRITE < 0.90 mmHg/ng/kg/min (median AIMRITE 0.02; IQR − 0.03–0.10). In contrast, 163 patients assigned to angiotensin-II had a median AIMRITE of 1.43 mmHg/ng/kg/min (IQR 0.35–2.83). Of these, 97 (60%) were responsive (median AIMRITE 2.55; IQR 1.66–4.12) and 66 (40%) were resistant (median AIMRITE 0.24; IQR 0.10–0.52). Each 1.0-unit increase in AIMRITE was associated with a 16% lower hazard of death (HR: 0.84 per-mmHg/ng/kg/min [95% CI 0.74–0.95], p = 0.0062). Responsive patients had half the mortality hazard than resistant patients (HR: 0.50 [95% CI 0.32–0.78], p = 0.0026) and placebo patients (HR 0.58 [95% CI 0.40–0.86], p = 0.0064). Resistant patients had a similar mortality hazard to placebo (HR 1.17 [95% CI 0.80–1.72], p = 0.41). Compared to resistant patients, responsive patients had lower baseline renin and renin/angiotensin-II ratio, but a greater decrease in both at hr3. When stratified by baseline renin level, mortality was highest in placebo patients with high renin (69%) and angiotensin-II resistant patients with low renin (61%). Among patients with catecholamine-refractory vasodilatory shock treated with angiotensin-II, the AIMRITE was associated with mortality at day-28. Responsive angiotensin-II patients had higher survival versus both angiotensin-II resistant patients and those treated with placebo plus standard vasopressors. This index may serve as a prognostic indicator and early identifier of patients most likely to benefit from angiotensin-II.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"64 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443248","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":"Individual mHLA-DR trajectories in the ICU as predictors of early infections following liver transplantation: a prospective observational study","authors":"M. C. Delignette, A. Riff, T. Antonini, T. Soustre, M. Bodinier, E. Peronnet, F. Venet, M. Gossez, S. Pantel, J. Y. Mabrut, X. Muller, K. Mohkam, F. Villeret, D. Erard, J. Dumortier, F. Zoulim, L. Heyer, C. Guichon, A. Blet, F. Aubrun, G. Monneret, F. Lebossé","doi":"10.1186/s13054-025-05305-x","DOIUrl":"https://doi.org/10.1186/s13054-025-05305-x","url":null,"abstract":"Infections are a leading cause of early mortality after liver transplantation (LT). Prior to transplantation, cirrhosis-associated immune dysfunction significantly increases the risk of infection. This study investigated the potential of immune monitoring, with a focus on monocytic HLA-DR (mHLA-DR) expression, as a predictor of post-LT complications. We conducted a prospective study on 130 patients awaiting LT at Lyon University Hospital to assess mHLA-DR expression, lymphocyte subsets, and T-cell function before and after LT. Multivariate analysis and K-means longitudinal clustering were performed to explore the relationships between immune trajectories and clinical outcomes. Among the 99 patients who underwent LT, 35.4% experienced infections early post-LT. No difference in outcome was found regarding lymphocyte count or function. Delayed mHLA-DR recovery (Day 7 < 11,000 AB/C) and pre-LT MELD scores > 30 emerged as independent infection risk factors, with ORs of 12.1 [4.4–38.2], p < 0.0001 and 4.9 [1.4–18.4], p = 0.01, respectively. Patients with delayed mHLA-DR restoration also had reduced one-year survival (77.8% versus 98.3%, p = 0.003). K-means clustering revealed three distinct mHLA-DR recovery profiles, with the slowest recovery group showing the poorest outcomes. Our findings highlight mHLA-DR as an early predictor of post-LT infections. Monitoring post-LT immune function through mHLA-DR expression could guide individualized management strategies to improve outcomes. Trial registration The study was registered in the ClinicalTrials.gov registry: NCT03995537, date: June 20, 2019.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"6 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434986","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":"Impact of age and mean intracranial pressure on the morphology of intracranial pressure waveform and its association with mortality in traumatic brain injury","authors":"Magdalena Kasprowicz, Cyprian Mataczyński, Agnieszka Uryga, Adam I. Pelah, Eric Schmidt, Marek Czosnyka, Agnieszka Kazimierska","doi":"10.1186/s13054-025-05295-w","DOIUrl":"https://doi.org/10.1186/s13054-025-05295-w","url":null,"abstract":"Morphological analysis of intracranial pressure (ICP) pulse waveforms provides indirect information on cerebrospinal compliance, which might be reduced by space-occupying lesions but also by intracranial hypertension and aging. This study investigates the impact of age and mean ICP on the shape and amplitude of ICP pulse waveform in traumatic brain injury (TBI). Additionally, it explores the association between morphological parameters and mortality after TBI. ICP recordings from 183 TBI patients (median age: 50 (30, 61) years) from the CENTER-TBI database were retrospectively analyzed. ICP morphology was assessed using the artificial intelligence-based pulse shape index (PSI) and peak-to-peak amplitude of ICP pulse waveform (AmpICP). The impact of mean ICP, age, and their interaction on PSI and AmpICP were estimated using factorial ANOVA. To account for influence of disturbance in the intracranial volume on AmpICP and PSI, a multiple regression analysis was performed using age, mean ICP, and the Rotterdam CT score as explanatory variables. The associations of AmpICP and PSI with six-month mortality were assessed using the area under the ROC curve (AUC). Age had a predominant influence on PSI (p < 0.01), accounting for 33.1% of its variance, while mean ICP explained 6.6% (p < 0.01). Conversely, mean ICP primarily affected AmpICP (p < 0.01), explaining 22.8% of its variance, with age contributing 8.0% (p < 0.01). A combined effect of age and mean ICP on AmpICP (p = 0.01) explained 11.7% of its variance but did not influence PSI. After accounting for Rotterdam CT score, the results remained consistent, indicating that advanced age has the strongest impact on PSI (β = 0.342, p < 0.01) while elevated mean ICP has dominant influence on AmpICP (β = 0.522, p < 0.01). Both AmpICP and PSI were moderately associated with mortality (AUC: 0.76 and 0.71, respectively). AmpICP and PSI capture distinct aspects of cerebrospinal compliance. PSI appears to reflect age-related stiffening of the cerebrovascular system, while AmpICP, influenced by mean ICP, indicates acute volume compensatory changes. Combined, they provide a more comprehensive assessment of cerebrospinal volume–pressure compensation. Both morphological metrics are associated with mortality after TBI. As cerebrospinal compliance declines with age, older TBI patients become more susceptible to uncontrolled rises in ICP, which can worsen their outcome.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"180 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434987","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":"Urinary proteomics in sepsis-associated AKI","authors":"Jill Moser, Tamar J. van der Aart, Hjalmar R. Bouma","doi":"10.1186/s13054-025-05306-w","DOIUrl":"https://doi.org/10.1186/s13054-025-05306-w","url":null,"abstract":"&lt;p&gt;To the Editor,&lt;/p&gt;&lt;p&gt;We read with interest the recent article by Stanaway et al. titled &lt;i&gt;“Urinary proteomics identifies distinct immunological profiles of sepsis-associated AKI sub-phenotypes”&lt;/i&gt; [1]. The study represents a significant advancement in understanding acute kidney injury (AKI) in sepsis through urinary proteomics, offering promising insights to improve early recognition, predict responses to therapy, and implement or develop targeted treatment strategies. However, some aspects of the study warrant further discussion.&lt;/p&gt;&lt;p&gt;The observation that bacterial infections were more common in AKI-SP2, whereas COVID-19 predominated in AKI-SP1, supports the phenotype of endothelial dysfunction and inflammation. However, this raises the question of whether AKI-SP2 represents a distinct AKI sub-phenotype or reflects endothelial dysfunction typically associated with bacterial sepsis. Additionally, the observed overlap of proteins associated with AKI-SP2 and those linked to the risk of renal replacement therapy (RRT) raises the question of whether AKI-SP2 represents a distinct sub-phenotype or reflects a continuum of severe AKI. Clarification of this overlap could enhance our biological understanding of these processes. Moreover, the finding that urinary proteomic profiles of AKI-SP1 were largely similar to those of non-AKI patients suggests the need to refine diagnostic thresholds or explore alternative biomarker panels to improve classification accuracy. Addressing this issue may require the use of more specific biomarkers directly associated with the pathophysiological mechanisms of AKI to improve patient phenotyping. Given the study’s emphasis on urinary proteomics, defining sub-phenotypes directly from urinary proteomic data seems feasible, potentially yielding kidney-specific classifications that more accurately reflect local injury processes, which could enable tailored therapeutic strategies.&lt;/p&gt;&lt;p&gt;The timing of sample collection from patients with sepsis remains a significant challenge as the onset and progression of critical symptoms can vary widely between individuals. This variability is influenced by patient-related factors, type of pathogen involved, and specific organs affected. Given the dynamic progression of sepsis, aligning sample collection more precisely with the timing of sepsis onset could reduce variability and improve data consistency; however, this remains an extremely challenging, if not impossible, task. Alternatively, patients could be aligned based on the onset of AKI as defined by the KDIGO guidelines [2] or using predictive or functional AKI biomarkers such as Cystatin C rather than ICU admission, which may provide a more clinically relevant timeline for analysis, reduce inter-patient variability, and provide a clearer picture of AKI-related changes in urinary proteomic profiles as AKI evolves. Longitudinal analysis with repeated sampling could enable the identification of temporal proteomic changes associated ","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"67 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143417251","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":"Early high-sensitivity troponin elevation and short-term mortality in sepsis: a systematic review with meta-analysis","authors":"Abraham I. J. Gajardo, Santiago Ferrière-Steinert, Joaquín Valenzuela Jiménez, Sebastián Heskia Araya, Thomas Kouyoumdjian Carvajal, José Ramos-Rojas, Juan Nicolás Medel","doi":"10.1186/s13054-025-05249-2","DOIUrl":"https://doi.org/10.1186/s13054-025-05249-2","url":null,"abstract":"Serum cardiac troponin (cTn) elevation is a well-established phenomenon in sepsis. However, the clinical significance of this phenomenon with high-sensitivity (hs) assays and the current sepsis definition needs to be settled. What is the association between early serum cTn levels measured by hs-assays and the risk of short-term mortality in septic patients? We conducted a systematic review using a comprehensive PubMed, Scopus, and Embase search. Studies were eligible if they reported association data on early hs-cTn and mortality in an adult sample with sepsis that met the Sepsis-3 definition. For the synthesis of the effect of hs-cTn on mortality, we applied random effect models on the pooled unadjusted and adjusted odds ratio (OR and aOR, respectively) of elevated vs. normal hs-cTn serum values, and on the crude standardized mean difference (SMD) of hs-cTn between survivors and non-survivors. In total, 6242 patients from 17 studies were included, with short-term mortality rates ranging from 16.9% to 53.8%. Using a crude analysis, non-survivor patients showed higher hs-cTn than survivors (SMD of 0.87, 95%CI: 0.41–1.33). Elevated hs-cTn was associated with increased mortality (OR = 1.78, 95% CI: 1.41–2.25). However, this prognostic effect was absent in studies that adjusted for different confounders (aOR = 1.06, 95% CI: 0.99–1.14). Non-survivors of sepsis exhibited significantly elevated hs-cTn levels. While elevated hs-cTn levels are associated with an increased risk of mortality, they are not independently associated with this outcome in sepsis.","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":"64 1","pages":""},"PeriodicalIF":15.1,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143418360","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}