Extracorporeal membrane oxygenation (ECMO) in patients following intracerebral hemorrhage (ICH) poses a critical dilemma between circuit thrombosis and catastrophic rebleeding. While nafamostat mesylate (NM) has been increasingly explored for ECMO anticoagulation in patients with ICH, it is conventionally administered as a systemic anticoagulant with high activated partial thromboplastin time (aPTT) targets, which still carries significant bleeding risks. Moreover, whether NM can achieve effective regional anticoagulation in venovenous (VV) ECMO remains highly controversial. Here, we present a post-ICH patient with severe ARDS who required VV-ECMO. Due to suspected rebleeding, anticoagulation was transitioned from heparin to an anticoagulant-free strategy, which subsequently led to significant oxygenator thrombosis. To navigate this crisis, NM was initiated with an ultra-low systemic target, but it initially failed to establish a regional anticoagulant effect when infused at the conventional pre-membrane, post-pump site. Crucially, relocating the NM infusion to the pre-pump position successfully established a significant circuit-to-systemic aPTT gradient. This technical optimization enabled effective circuit anticoagulation while minimizing systemic bleeding risk, allowing for successful ECMO weaning without bleeding complications. This dynamic intra-patient observation highlights the potential impact of infusion site on coagulation outcomes. We hypothesize that harnessing the centrifugal pump’s high-shear turbulence for homogenous drug mixing might serve as a crucial prerequisite for achieving regional anticoagulation in VV-ECMO. These findings bridge the gap between theoretical pharmacology and practical circuit engineering, offering a practical preliminary reference for the future anticoagulant management of similar high-bleeding-risk patients on ECMO.

ObjectiveTo explore a multidisciplinary cooperative nutrition management process for critically ill ICU patients in China for providing a standardized nutrition management process and improving the effect and safety of nutritional support.MethodsOur first draft of the “multidisciplinary nutrition management process for critical patients” and “enteral nutrition management process for critical patients”, which included five steps and 31 criteria, was prepared through literature review and analysis, referring to the domestic and foreign nutrition management guidelines for critical patients, and referring to the nutrition management process for critically ill patients abroad. We recruited consulting experts from Beijing, Zhejiang, Jilin, Guangdong, and Chongqing in China. Using the Delphi method, we conducted expert consultations to evaluate the initially prepared standardized process, subsequently refining and adjusting items based on their feedback.ResultsAfter two rounds of expert consultation, all 20 invited experts completed both rounds, 15 experts provided written opinions, and 43 expert opinions were collected. The nutrition management process was bifurcated into “multidisciplinary nutrition management process for critically ill patients” and “enteral nutrition management process for critically ill patients,” which collectively included five steps (within 24 h of admission, within 24–48 h of admission, after 48 h of admission and during hospitalization, during transfer to another department, and during discharge) and 31 standard processes. The 31 criteria were rated as desirable or necessary by 17–20 evaluators (85–100%).ConclusionThe multidisciplinary cooperative nutrition management process for critically ill patients established by us using the Delphi method is scientific and standardized and shows promise as a practical tool that may improve for nutritional management.Relevance to clinical practiceStructured multidisciplinary nutrition management operational processes can guide clinical practice. They has potential for implementation in similar settings in the clinical nutrition management of critically ill patients in the ICU or other departments.

BackgroundSepsis-induced coagulopathy (SIC) is a vascular endothelial cell injury and coagulation disorder caused by sepsis. The aim of this study was to construct a nomogram model of the risk of early onset of SIC in patients with sepsis by analyzing the risk factors for in-hospital development of SIC.MethodsPatients with sepsis admitted to the intensive care unit (ICU) of Hebei General Hospital and Handan Central Hospital (East District) from March 1, 2021 to March 1, 2024 were retrospectively included. Sepsis patients were divided into SIC and non-SIC groups according to whether SIC occurred during hospitalization. The patient data were randomly divided into training set and testing set in the ratio of 7:3. The data of sepsis patients admitted to the ICU of Hebei General Hospital between March 1, 2024 and October 31, 2024 were then retrospectively included as the validation set for external validation. All predictors were collected within 24 h of sepsis diagnosis to enable early risk prediction. Various clinical variables were collected, and independent risk factors for early onset of SIC were screened by one-way logistic regression, least absolute shrinkage and selection operator (LASSO) regression, and multifactorial logistic and a nomogram prediction model was constructed. The model was evaluated for accuracy, goodness of fit, and clinical utility value using testing set and validation set data. The accuracy of the predictive model was assessed by using the receiver operating characteristic curve (ROC) and calculating the area under the receiver (AUC), the fit was done by calibration curve, and the clinical utility of the predictive model was assessed by decision curve analysis (DCA).ResultsAmong 847 patients with sepsis, SIC occurred in 480 (56.7%) patients. A nomogram model was constructed containing eight variables: lactate, oxygenation index, total protein, total bilirubin, urea, calcitoninogen, activated partial thromboplastin time, and monocyte count. In the training set, the AUC value of the model was 0.783 [95% Confidence Interval (CI): 0.746, 0.820]; in the testing set, the AUC value was 0.768 (95% CI: 0.710, 0.826); and in the validation set, the AUC value was 0.782 (95% CI: 0.708, 0.856).ConclusionWe developed a nomogram model to predict the risk of SIC in patients with sepsis and validated its potential as a clinically reliable tool. The overall accuracy and clinical utility value of the model was high and the fit was good. The nomogram model can visualize the key variables associated with SIC in sepsis patients, supporting clinicians in individualized risk assessment and guiding timely interventions to improve patient outcomes.

Sepsis, a lethal organ dysfunction syndrome driven by aberrant host responses to infection, intertwines excessive inflammatory responses and dysregulated coagulation processes in its pathophysiology. Emerging research reveals the complement terminal membrane attack complex C5b-9 orchestrates ultralarge von Willebrand factor (ULVWF) release from vascular endothelial cells (ECs) through multifaceted mechanisms: C5b-9 compromises EC membrane integrity, activates calcium influx cascades, and provokes NLRP3 inflammasome signaling, triggering massive exocytosis of ULVWF stored within Weibel-Palade bodies (WPBs). When ADAMTS13 activity falters, undegraded ULVWF complexes with platelets to spawn microthrombi, precipitating microvascular occlusion and multiorgan collapse. Strikingly, elevated plasma von Willebrand factor (vWF) antigen levels in sepsis patients correlate robustly with endothelial injury, thrombocytopenia, and mortality-underscoring C5b-9-driven vWF release as a linchpin of septic coagulopathy. Current therapeutic strategies targeting these pathways, including recombinant ADAMTS13 (rhADAMTS13), N-acetylcysteine (NAC), and complement inhibitors like eculizumab, face limitations in clinical translation, necessitating further validation of their efficacy. Additionally, investigating complement regulatory molecules such as CD59 may unlock novel therapeutic avenues. Deciphering the intricate interplay within the C5b-9-vWF axis and advancing precision therapies hold transformative potential for ameliorating sepsis outcomes.

OBJECTIVES:This study aims to investigate the pathological mechanisms, clinical features, and prognostic differences between thrombotic thrombocytopenic purpura-like syndrome (TTP-like syndrome) and sepsis-induced coagulopathy (SIC) in patients experiencing septic shock. The findings will provide a basis for subtype-guided diagnosis and treatment of coagulation disorders. METHODS:In this single-center retrospective cohort, 250 septic shock patients were divided into TTP-like syndrome (n = 101), SIC (n = 113), and control (n = 36) groups. Platelet count, vWF, FM, Sequential Organ Failure Assessment (SOFA) scores, and 28-day mortality were analyzed to compare coagulation phenotypes and outcomes. RESULTS:The TTP-like syndrome group was characterized by thrombocytopenia, with a median platelet (PLT) decline rate of 49.10 %. This group also exhibited markedly elevated vWF antigen levels, averaging 334.66 ± 80.04 %. Additionally, all patients in this group presented with multiple organ dysfunction syndrome (MODS) at a rate of 100 %. In contrast, the SIC group demonstrated more severe platelet consumption, with a median PLT of 42 × 109/L, elevated fibrinogen degradation product (FM) levels (median 9.22 μg/mL), and a significantly higher 28-day mortality rate (35.40 % vs. 11.88 % in the TTP-like group). The patterns of organ injury varied between the two groups; the SIC group displayed more pronounced liver (SOFA 1.43 ± 1.08) and renal (SOFA 1.41 ± 1.47) involvement, while the TTP-like syndrome group predominantly exhibited circulatory (SOFA 2.46 ± 1.45) and respiratory (SOFA 2.53 ± 0.76) dysfunction. vWF and FM had some predictive value for 28-day mortality, with area under the curve values of 0.59 and 0.60, respectively. CONCLUSION:TTP-like syndrome and SIC represent heterogeneous coagulation phenotypes in septic shock, with differences in biomarkers, organ injury, and prognosis. A vWF- and FM-guided subtype classification may improve individualized treatment strategies and prognostic management.

The development of intensive care medicine is inseparable from the diversified monitoring data. Intensive care medicine has been closely integrated with data since its birth. Critical care research requires an integrative approach that embraces the complexity of critical illness and the computational technology and algorithms that can make it possible. Considering the need of standardization of application of big data in intensive care, Intensive Care Medicine Branch of China Health Information and Health Care Big Data Society, Standard Committee has convened expert group, secretary group and the external audit expert group to formulate Chinese Experts’ Consensus on the Application of Intensive Care Big Data (2022). This consensus makes 29 recommendations on the following five parts: Concept of intensive care big data, Important scientific issues, Standards and principles of database, Methodology in solving big data problems, Clinical application and safety consideration of intensive care big data. The consensus group believes this consensus is the starting step of application big data in the field of intensive care. More explorations and big data based retrospective research should be carried out in order to enhance safety and reliability of big data based models of critical care field.

Background: Acute respiratory distress syndrome (ARDS) is a severe inflammatory pulmonary condition that leads to respiratory failure. The imbalance of Th17/Treg and M1/M2 is implicated in ARDS. A better understanding of the regulation of the balance of Th17/Treg and M1/M2 may provide novel therapeutic targets for ARDS. Methods: Plasma and BALF samples were collected from ARDS patients. Inflammatory cytokines were examined by ELISA. Th17, Treg, M1 and M2 were identified via immunofluorescence staining of ROR gamma t, Foxp3, iNOS and Arg-1. H&E and Masson's trichrome staining were applied for evaluating pulmonary damage and fibrosis. A mouse model of ARDS was established through LPS administration. HIF-1 alpha was immunoprecipitated and subjected to ubiquitination analysis via western blotting. The expression of SPP1, VHL and HIF-1 alpha was examined by RT-qPCR and western blotting.Results: ARDS patients showed elevated levels of inflammatory cytokines and ratios of Th17/Treg and M1/M2. SPP1 was upregulated in ARDS mice, and silencing of SPP1 alleviated lung injury and fibrosis. SPP1 inhibited VHL expression to reduce the ubiquitination and degradation of HIF-1 alpha in ARDS. Overexpression of SPP1 facilitated Th17, Treg and M1 polarization but inhibited M2 polarization through upregulation of HIF-1 alpha.Conclusion: SPP1 elevates Th17/Treg and M1/M2 ratio by suppressing VHL expression and ubiquitinationdependent HIF-1 alpha degradation, thus exacerbating ARDS. Our study provides novel mechanistic insights into ARDS pathogenesis and promising therapeutic targets.

Abstract Background: Since December 2019, the coronavirus disease (COVID-19) has spread worldwide, leading to a global health threat. This study aimed to investigate the effectiveness of tocilizumab in COVID-19 patients. Methods: We systematically searched PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, and World Health Organization International Clinical Trials Registry Platform to March 10, 2021 for randomized controlled trials in which patients were randomly assigned to receive tocilizumab plus usual care or usual care alone in hospitalized adults with COVID-19. A random-effects meta-analysis model was used to pool studies. All data analyses were performed using Review Manager version 5.4. Results: Eleven studies with 6579 patients were included in our meta-analysis, of which 3406 and 3173 were assigned to tocilizumab and control groups, respectively. Tocilizumab significantly reduced the 28 to 30-day mortality (relative risk [RR] = 0.89, 95% confidence interval [CI] 0.80-0.99, P = .04), incidence of mechanical ventilation (MV) (RR = 0.79, 95% CI 0.71-0.89, P < .001), composite outcome of MV or death (RR = 0.81, 95% CI 0.72-0.90, P < .001), time-to-hospital discharge (hazard ratio = 1.30, 95% CI 1.16-1.45, P < .001), intensive care unit admission (RR = 0.64, 95% CI 0.47-0.88, P = .006), serious infection (RR = 0.61, 95% CI 0.40-0.94, P = .02), and number of serious adverse events (RR = 0.64, 95% CI 0.47-0.86, P = .004). Conclusion: Tocilizumab reduced short-term mortality, incidence of MV, composite outcome of death or MV, intensive care unit admission, serious infection, serious adverse events, and time-to-hospital discharge in hospitalized COVID-19 patients. Further studies are required to determine the optimal dose.

Background: Sepsis affects millions of patients annually, resulting in substantial health and economic burdens globally. The role of esmolol potentially plays in the treatment of sepsis and septic shock in adult patients remains controversial. Methods: We undertook a systematic search of PubMed, EMBASE, and Cochrane Central Register of Controlled Trials databases from their inception to May 12, 2022, for randomized controlled trials that evaluated the efficacy of esmolol for sepsis and septic shock. A random-effects meta-analysis was performed. Two investigators independently screened articles, extracted data, and assessed the quality of included studies. Results: Eight studies from 7 randomized controlled trials were included in our meta-analysis of 503 patients with sepsis and/or septic shock. Compared with standard treatment, esmolol significantly decreased 28-day mortality (risk ratio 0.68, 95% confidence interval [CI] 0.52-0.88; P = .004), heart rate (standardized mean difference [SMD] -1.83, 95% CI -2.95 to -0.70, P = .001), tumor necrosis factor-a (SMD -0.48, 95% CI -0.94 to -0.02, P = .04), and the troponin I level (SMD -0.59, 95% CI -1.02 to -0.16, P = .008) 24 hours after treatment. No significant effect was found in terms of length of intensive care unit stay; mean arterial pressure, lactic acid, central venous pressure, or central venous oxygen saturation, interleukin 6, or white blood cell levels; stroke volume index; or the PaO2/FiO2 ratio. Conclusions: Esmolol treatment may be safe and effective in decreasing 28-day mortality, controlling heart rate, and providing cardioprotective function, but has no effect on lung injury in patients with sepsis or septic shock after early fluid resuscitation. Improvement in cardiac function may be related to changes in serum inflammatory mediators. No significant adverse effects on tissue perfusion and oxygen utilization were observed.