Diaphragm ultrasound, as a convenient and non-invasive bedside visual monitoring technique, has gradually become a vital tool for assessing the morphology and function of the diaphragm in critically ill patients. By real-time monitoring of key indicators including diaphragmatic excursion, thickness, and thickening fraction, diaphragm ultrasound allows the early identification of diaphragmatic dysfunction, providing crucial evidence for respiratory monitoring and support for critically ill patients. In the formulation and implementation of mechanical ventilation management and weaning strategies, diaphragm ultrasound helps improve the weaning success rates and optimize the prognosis of critically ill patients. Currently, diaphragm ultrasound is in a critical stage of rapid popularization and continuous improvement, while standardized operational protocols and evaluation criteria for clinical practice remain lacking. To address this gap, the Critical Rehabilitation Branch of Guangzhou Rehabilitation Medicine Association and the Critical Care Medicine Branch of Guangdong Medical Association jointly organized a multidisciplinary consensus writing committee composed of domestic frontline clinical experts covering critical care medicine, ultrasound medicine, respiratory therapy and other related disciplines. In strict accordance with the principles of evidence-based medicine, the writing committee systematically retrieved and comprehensively evaluated the latest domestic and international guidelines, expert consensuses and high-quality clinical research evidence on diaphragm ultrasound. Combined with the characteristics of clinical practice in China and senior clinical experience of participating experts, the consensus was finalized through evidence-based demonstration and multiple rounds of seminars, namely the Expert consensus on the clinical application of diaphragm ultrasound in critically ill patients (2026 edition). A total of 21 recommendations have been formulated in this consensus, covering multiple aspects including the indications, technical specifications, examination procedures, clinical applications and multidisciplinary collaboration of diaphragm ultrasound, aiming to promote the standardized application of diaphragm ultrasound technology in the management of critically ill patients.
OBJECTIVE:To systematically map and synthesize the current evidence on the application of bedside ultrasound in the assessment of gastrointestinal function and the guidance of enteral nutrition in critically ill patients, and to explore its clinical value and future perspectives. METHODS:PubMed, Web of Science, Embase, Scopus, China National Knowledge Infrastructure (CNKI), Wanfang Database, VIP Database, Chinese Medical Journals Database, and Chinese Biomedical Literature Database were searched from inception to September 4, 2025 for studies on bedside gastrointestinal ultrasound. After removing duplicate literature using EndNote X9 software and the Rayyan online literature screening platform, the articles were independently screened and cross-checked by two researchers. The following data were independently extracted by two researchers: years, country, study type, study population and sample size, grouping criteria and inter-group comparison factors, assessment protocol, ultrasound scanning protocol and results, and outcome indicators. The Newcastle-Ottawa Scale (NOS) was used to evaluate the methodological quality of included case-control studies and cohort studies, and the Cochrane Risk of Bias tool (RoB 2) was used to evaluate the methodological quality of randomized controlled trials. Through comprehensive analysis of the included literature, the application characteristics and clinical significance of bedside ultrasound in gastrointestinal dysfunction assessment and enteral nutrition implementation in critically ill patients were analyzed. Descriptive grouping and visual methods were used to conduct a variability analysis of the included studies. The studies were categorized according to study design and ultrasound assessment methods. RESULTS:A total of 2 023 records were retrieved, and 36 studies were finally included after deduplication and screening. Included studies were published between 2019 and 2025, and comprised 19 randomized controlled trials, 15 case-control studies, and 2 cohort studies. The quality of case-control studies and cohort studies was evaluated as relatively high overall, while bias risks in randomization process and outcome reporting were found in some randomized controlled trials, with overall moderate quality and generally acceptable risk of bias. The main ultrasound assessment protocols were identified as gastric antral cross-sectional area (CSA), gastric antral motility index (MI), superior mesenteric artery (SMA) blood flow parameters, Acute Gastrointestinal Injury Ultrasound Score (AGIUS), Gastrointestinal and Urinary Tract Sonography (GUTS) score, and combined protocols. By comprehensive analysis of included studies, gastric antral CSA was found to accurately reflect gastric emptying and feeding tolerance, and high feasibility was demonstrated in predicting feeding intolerance and feeding achievement rate; gastric antral motility could be quantified by gastric antral MI, but its clinical application was limited by complex operation and fluid management. Intestinal structure and function could be objectively evaluated by AGIUS and GUTS scores, and high sensitivity and specificity in predicting 28-day mortality were demonstrated by AGIUS score≥2. Gastrointestinal structure, motility, and perfusion status could be comprehensively reflected by the gastric antral CSA combined with intestinal ultrasound protocol, and the diagnostic accuracy of acute gastrointestinal injury (AGI) and the success rate of enteral nutrition were improved. CONCLUSIONS:As a noninvasive and repeatable assessment tool, bedside ultrasound provides valuable support for gastrointestinal monitoring and nutritional management in critically ill patients. However, the current body of evidence still has issues such as inconsistency in parameter selection, lack of standardization in measurement methods, and variability in operational procedures. Future multicenter, large-scale studies are warranted to establish unified assessment frameworks and enable precise and dynamic gastrointestinal management.
OBJECTIVE:To explore the value of handheld simplified venous excess ultrasound (VExUS) grades in bedside venous congestion assessment in general intensive care unit (ICU) patients and to examine its associations with disease severity scores and fluid overload indicators. METHODS:This study was a secondary analysis based on data from a single-center prospective observational ICU cohort database. The data were derived from the existing ICU cohort database of the ICU of China-Japan Friendship Hospital. The original study included critically ill patients admitted to the ICU of China-Japan Friendship Hospital from June 14 to August 21 in 2024, all of whom underwent handheld ultrasound and conventional ultrasound VExUS-related examinations. Demographic data, severity of illness scores, laboratory indicators, fluid balance, and supportive treatment information were also collected simultaneously. The main ultrasound variables included the handheld simplified VExUS grading and its key component parameters (inferior vena cava short-to-long axis ratio, hepatic vein S/D ratio, and portal vein pulsatility fraction). Descriptive analysis was used to evaluate the overall distribution of handheld simplified VExUS indicators. Spearman rank correlation analysis was employed to evaluate the relationship between the handheld simplified VExUS grading and its key component parameters with the Acute Physiology And Chronic Health Evaluation II (APACHE II) score, Sequential Organ Failure Assessment (SOFA) score, N-terminal pro-brain natriuretic peptide (NT-proBNP), and fluid balance within 24 hours after ICU admission. The differences in clinical indicators among patients with different handheld simplified VExUS grading were compared, and the primary analysis of continuous ultrasound parameters employed the post-hoc mean values of independent measurements taken by two operators, and sensitivity analysis was conducted separately using the original measurements of the two operators. Multiple comparison correction for the primary correlation analysis was performed using the Benjamini-Hochberg false discovery rate (FDR). RESULTS:The original study included a total of 80 critically ill patients. After excluding 2 minor patients from this study, a total of 78 adult patients were finally included in the overall analysis. The overall disease severity of the 78 adult ICU patients was moderate, with an APACHE II score of 20.0 (15.3, 25.0) and a SOFA score of 7.0 (4.0, 11.0). The handheld simplified VExUS grading was mainly at grades 0 and 1, with 48 cases (62%) at grade 0, 26 cases (33%) at grade 1, and 4 cases (5%) at grade 2. The average values of the inferior vena cava short-to-long axis ratio, hepatic vein S/D ratio, and portal vein pulsatility fraction were 0.763 (0.668, 0.809), 1.358 (1.252, 1.571), and 0.243 (0.180, 0.303), respectively. In the primary correlation analyses, the mean inferior vena cava short-to-long axis ratio was positively correlated with APACHE II score and SOFA score (r values were 0.302 and 0.252, with unadjusted P values of 0.007 and 0.026, respectively), while portal vein pulsatility fraction was positively correlated with 24-hour fluid balance (r=0.290, unadjusted P value was 0.010). However, no significant correlation was observed between the handheld simplified VExUS grading and either the severity of illness scores or the volume overload indices. After Benjamini-Hochberg FDR correction, the correlation between the mean inferior vena cava short-to-long axis ratio and both the APACHE II score and the SOFA score did not reach statistical significance (FDR-corrected P values were 0.080 and 0.139, respectively). Similarly, the correlation between the mean portal vein pulsatility fraction and 24-hour fluid balance also failed to maintain statistical significance (FDR-corrected P value was 0.080). After stratification by the simplified handheld VExUS grading, there were no statistically significant differences in APACHE II score, SOFA score, NT-proBNP level, and 24-hour fluid balance among patients with different grades (all P>0.05). A sensitivity analysis was conducted using the original measurements from two operators on the core pairs with original correlation signals in the main analysis, and the results were largely consistent with the main analysis. However, the previously observed associations did not remain statistically significant after Benjamini-Hochberg FDR correction. CONCLUSIONS:In general ICU patients, the handheld simplified VExUS grade showed limited associations with disease severity scores and volume overload indicators. Some key component parameters showed exploratory signals related to disease severity or fluid balance in the original correlation analysis, but did not maintain statistical significance after FDR correction.
Invasive candidiasis is one of the common invasive fungal infections in the intensive care unit (ICU), characterized by high incidence, high mortality, and diagnostic difficulty. The clinical presentation of invasive candidiasis lacks specificity, and conventional diagnostic methods are time-consuming with low positivity rates, often leading to delayed treatment and increased death risk. Therefore, early and precise identification of high-risk patients, along with the development of sensitive and specific risk assessment tools to guide individualized antifungal strategies, remains a critical clinical challenge. In recent years, traditional prediction models based on clinical risk factors, Candida colonization status, and microbiological markers have been progressively refined and have played an important role in risk stratification and empirical antifungal therapy decisions. However, their positive predictive value and generalizability remain limited. With advances in precision medicine, biomarkers such as (1,3)-β-D-glucan (BDG), inflammatory and nutritional indicators, immune cell subsets, host response assays, and molecular diagnostic techniques are increasingly being incorporated into risk assessment frameworks, driving the evolution of predictive models from single clinical indicators to multidimensional integration. Meanwhile, artificial intelligence approaches, including machine learning, deep learning, and federated learning, can effectively mine complex information from electronic health records and have demonstrated considerable promise in improving predictive accuracy, enabling dynamic risk assessment, and supporting clinical decision-making. Nevertheless, most current models lack large-scale, multicenter prospective validation, and their interpretability, generalizability, and clinical utility require further clarification. This review summarizes the current state of research on invasive candidiasis prediction models in critically ill patients, covering traditional clinical predictive models, biomarker integration strategies, and artificial intelligence-based models, and discusses future research directions to facilitate early identification and precision diagnosis and treatment of invasive candidiasis in critically ill settings.
OBJECTIVE:To investigate the regulatory effects of cellular repressor of E1A-stimulated gene (CREG) on autophagy and polarization of alveolar macrophages in sepsis-induced acute respiratory distress syndrome (ARDS) and its clinical value. METHODS:1) Cell experiment: Mouse monocyte/macrophage cell line RAW264.7 was cultured in vitro. Cells in logarithmic growth phase were induced to differentiate into alveolar macrophages. The alveolar macrophages were divided into four groups: the blank control group was cultured with complete medium only; the lipopolysaccharide (LPS) group was stimulated with 5 mg/L LPS for 24 hours to establish the sepsis-induced ARDS model; the CREG overexpression group was transfected with 2 mg CREG overexpression plasmid pLNCX2-CREG for 6 hours, followed by 5 mg/L LPS stimulation for 24 hours; the CREG interference group was transfected with 2 μg CREG interference plasmid pSM2-siCREG for 6 hours, followed by 5 mg/L LPS stimulation for 24 hours. Western blotting was used to detect the expression of autophagy markers [autophagy initiation key protein Beclin1, microtubule-associated protein 1 light chain 3 (LC3), and autophagic substrate protein p62]. Flow cytometry was used to detect the expression of macrophage polarization markers [M1-type characteristic marker cluster of differentiation 86 (CD86) and M2-type characteristic marker CD206]. 2) Clinical trial: A prospective case-control study was conducted in patients with sepsis admitted to the respiratory intensive care unit of The First Affiliated Hospital of Hebei North University from January to December 2024. Patients were divided into sepsis with ARDS group and sepsis without ARDS group based on whether they developed ARDS within 72 hours after enrollment. In addition, healthy volunteers who underwent health check-ups at the hospital during the same period were selected as the controls. Demographic data including gender, age, Acute Physiology And Chronic Health Evaluation II (APACHE II) score, oxygenation index (PaO2/FiO2), and laboratory parameters were collected for each group, as well as the sites of infection for the septic patients. Serum levels of CREG and inflammatory markers [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), procalcitonin (PCT), and C-reactive protein (CRP)] were measured using enzyme-linked immunosorbent assay (ELISA). The differences in the above indicators were compared among groups. Multivariate Logistic regression analysis was used to identify independent influencing factors for sepsis complicated with ARDS. Receiver operator characteristic curve (ROC curve) was plotted to evaluate the predictive value of CREG for sepsis complicated with ARDS. RESULTS:1) Cell experiment results: Compared with the blank control group, the expressions of Beclin1, LC3-II/LC3-I ratio, and CD206 were decreased in each LPS group [Beclin1 protein (Beclin1/β-actin): 0.32±0.05 vs. 0.87±0.09, LC3-II/LC3-I ratio: 0.41±0.06 vs. 1.24±0.11, CD206: (27.14±3.52)% vs. (51.78±5.91)%, all P<0.05], while p62 and CD86 expressions were increased [p62 protein (p62/β-actin): 1.58±0.13 vs. 0.53±0.07, CD86: (38.35±4.67)% vs. (18.26±3.24)%, both P<0.05]. CREG overexpression significantly improved the above autophagy and polarization indicators, whereas CREG interference further exacerbated these indicators (all P<0.05). 2) Clinical trial results: Ultimately, 40 patients were included in the sepsis with ARDS group, 60 in the sepsis without ARDS group, and 20 in the healthy control group. There were no statistically significant differences in gender, age among the three groups, nor in the distribution of infection sites between the sepsis with ARDS and sepsis without ARDS groups (all P>0.05). Compared with the healthy control group, the patients with sepsis showed aggravated systemic inflammatory burden. Compared with the sepsis without ARDS group, the sepsis with ARDS group exhibited more severe disease, with lower PaO2/FiO2 and CREG levels, and higher levels of inflammatory markers (all P<0.05). As APACHE II score increased, serum CREG levels decreased progressively while inflammatory marker levels increased progressively. Multivariate Logistic regression analysis showed that elevated APACHE II score and inflammatory markers were independent risk factors for sepsis complicated with ARDS [all odds ratio (OR) >1, all P<0.05], while elevated CREG was a protective factor [OR=0.385, 95% confidence interval (95%CI) was 0.344-0.432, P=0.015]. ROC curve analysis showed that the area under the ROC curve (AUC) of CREG for predicting sepsis complicated with ARDS was 0.806 (95%CI was 0.713-0.899); at the optimal cut-off value of 7.85 μg/L, the sensitivity was 71.43% and the specificity was 78.57%. CONCLUSIONS:CREG exerts a protective role in sepsis-induced ARDS by positively regulating alveolar macrophage autophagy activity and correcting M1/M2 polarization imbalance. Elevated serum CREG is a protective factor for sepsis complicated with ARDS and has early predictive value for sepsis-induced ARDS.
Sepsis-associated acute kidney injury (SA-AKI) is one of the most common complications of sepsis, characterized by high incidence and mortality. Currently, supportive treatment remains the main approach in clinical practice, lacking specific targeted drugs. Mitochondrial dysfunction and metabolic reprogramming play significant roles in the pathophysiological process of SA-AKI. The kidneys, with their high mitochondrial density and high energy demand, are particularly sensitive to mitochondrial dysfunction. Metabolic reprogramming is another important mechanism for the onset of SA-AKI. When sepsis occurs, the metabolic patterns of kidney cells undergo significant changes, initially shifting from oxidative phosphorylation (OXPHOS) to aerobic glycolysis metabolism, accompanied by inhibition of fatty acid oxidation (FAO). The initial intention is an adaptive protective response of the cells, but persistent metabolic imbalance leads to lipid accumulation and fibrosis, progressing to chronic kidney disease. The two mechanisms interact with each other, jointly causing the occurrence and progression of SA-AKI. This article focuses on these two core mechanisms, systematically reviews the research progress of targeted treatment strategies of SA-AKI, elaborates on the potential application value of mitochondrial protectants and metabolic regulators, deeply analyzes the mechanism of action, in vitro and in vivo experimental evidence, and clinical translation prospects of various drugs, summarizes the current research bottlenecks and looks forward to future development directions, aiming to provide theoretical basis and new research ideas for precise targeted treatment of SA-AKI.
OBJECTIVE:To compare extremely severe thermal burns with acid corrosive injury in terms of multidimensional clinical differences, and elucidate their distinct pathophysiological characteristics. METHODS:A retrospective cohort study was conducted to collect the clinical data of 23 patients with extremely severe thermal burns and 14 patients with acid corrosive injury admitted to Suzhou Municipal Hospital from January 2020 to December 2024. The patients were divided into thermal burn group and acid corrosive injury group based on the causative factors. The basic data (gender, age, and whether they had underlying diseases), and blood cell analysis indicators [white blood cell count (WBC), neutrophil count (NEUT), platelet count (PLT), platelet/lymphocyte ratio (PLR)], organ function indicators [albumin (Alb), alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum creatinine (SCr), blood urea nitrogen (BUN)], coagulation function indicators [D-dimer, fibrinogen (Fib), activated partial thromboplastin time (APTT)], and infection indicators [procalcitonin (PCT), C-reactive protein (CRP), heparin-binding protein (HBP), interleukin-6 (IL-6)] on the 1st, 2nd, 3rd, 7th, and 15th day after injury, as well as the severity of injury and wound healing time were compared between the two groups. RESULTS:There were no statistically significant differences in the basic data of patients between the thermal burn group and the acid corrosive injury group. The levels of WBC, NEUT, PLT and PLR in the thermal burn group were higher than those in the acid corrosive injury group, and there was a group effect (F values were 56.198, 50.133, 25.325 and 19.503, respectively, all P<0.05). The Alb level of patients in the acid corrosive injury group was higher on the first day, and there was an interaction effect between group and time point (F=7.893, P<0.05), but it decreased on the 7th and the 15th day after injury. The SCr level of patients in the thermal burn group increased, and there was a group effect (F=93.991, P<0.05). On the 15th day, the BUN level of patients in the acid corrosive injury group was higher, and there was an interaction effect between group and time point (F=5.033, P<0.05). In the early stage of burn (from the 2nd day to the 7th day), the D-dimer level of patients in the thermal burn group was higher, on the 15th day, the D-dimer, Fib and APTT levels of patients in the acid corrosive injury group were higher, and there was an interaction effect between group and time point (F values were 13.891, 10.170 and 8.530, respectively, all P<0.05). Compared with the acid corrosive injury group, the patients in the thermal burn group had elevated HBP, CRP, PCT, and IL-6 as early as the 2nd day and the 3rd day after injury, showing a group effect (F values were 139.123, 146.879, 31.831, and 24.506, respectively, all P<0.05). Although the absolute values of above infection indicators in the acid corrosive injury group were lower, they persisted for a longer time, indicating a time point effect (F values were 186.566, 55.375, 24.607, and 29.986, respectively, all P<0.05). The total burn area of patients in the thermal burn group was larger than that of the acid corrosive injury group [(74.4±10.7)% total body surface area (TBSA) vs. (62.3±9.8)% TBSA, P<0.05], while the wound healing time of patients in the acid corrosive injury group was longer than that in the thermal burn group (days: 57.6±10.3 vs. 48.4±8.1, P<0.05). CONCLUSIONS:Thermal burns are fundamentally characterized as "persistent high-inflammation-driven injuries," whereas acid corrosive injuries are primarily defined by "progressive metabolic and coagulation dysfunction injuries". The two types of injuries exhibit significant differences in the intensity of the inflammatory response, the pattern of organ damage, and the timing of coagulation dysfunction onset.
OBJECTIVE:To investigate the relationship between serum retinol-binding protein 4 (RBP4) and cystatin C (CysC) levels and cardiac function as well as ventricular remodeling in patients with myocardial infarction. METHODS:A case control study was conducted. A total of 185 patients with first diagnosed acute myocardial infarction (AMI) who were treated at Harrison International Peace Hospital between December 2022 and January 2025 were enrolled as the research subjects, and 150 healthy subjects who underwent physical examination at the same hospital during the same period were enrolled as the controls. Fasting peripheral venous blood samples were collected on the second day after admission for AMI patients and on the morning of physical examination for healthy controls. Serum levels of RBP4 and CysC were measured by an automatic biochemical analyzer. Cardiac function indexes [left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD)] and ventricular remodeling indexes [left ventricular end-systolic volume (LVESV), left ventricular end-systolic posterior wall thickness (PWS), left ventricular remodeling index (LVRI), left ventricular mass (LVM)] were detected by color Doppler ultrasound. Pearson correlation analysis was used to analyze the correlations of serum RBP4 and CysC levels with cardiac impairment and ventricular remodeling in AMI patients. Receiver operator characteristic curve (ROC curve) was plotted to evaluate the predictive value of serum RBP4, CysC alone and their combination for cardiac impairment and ventricular remodeling in AMI patients. RESULTS:No significant differences in gender and age were observed between the two groups (both P>0.05). Serum levels of RBP4 and CysC, as well as LVEDD, LVESV, PWS and LVM were significantly higher in the AMI group than those in the healthy control group [RBP4 (mg/L): 55.37±8.31 vs. 43.12±6.47, CysC (mg/L): 1.58±0.49 vs. 0.72±0.11, LVEDD (mm): 48.02±7.17 vs. 37.19±5.58, LVESV (mL): 67.42±10.11 vs. 48.61±7.29, PWS (mm): 13.52±1.03 vs. 9.36±1.10, LVM (g): 244.96±36.74 vs. 167.35±25.10, all P<0.05]. In contrast, LVEF and LVRI were significantly lower in the AMI group than those in the healthy control group [LVEF: 0.421±0.063 vs. 0.654±0.098, LVRI (g/mL): 0.85±0.13 vs. 1.24±0.19, both P<0.05]. Among 185 AMI patients, 64 were classified as Killip class I, 58 as class II, 44 as class III, and 19 as class IV. With the increase of Killip classification, serum RBP4 and CysC levels, LVEDD, LVESV, PWS and LVM were gradually elevated, while LVEF and LVRI were gradually decreased (all P<0.05). Pearson correlation analysis showed that serum RBP4 and CysC were negatively correlated with LVEF (r values were -0.453 and -0.424, respectively) and LVRI (r values were -0.479 and -0.443, respectively, all P<0.05), and positively correlated with LVEDD (r values werre 0.202 and 0.297, respectively), LVESV (r values were 0.248 and 0.267, respectively), PWS (r values were 0.285 and 0.272, respectively) and LVM (r values were 0.291 and 0.228, respectively, all P<0.05). ROC curve analysis indicated that serum RBP4 and CysC alone had moderate predictive value for cardiac impairment and ventricular remodeling in AMI patients, and the combined detection achieved higher predictive efficacy. The area under the ROC curve (AUC) with 95% confidence interval (95%CI) was 0.924 (0.863-0.984) and 0.913 (0.849-0.976), with sensitivity of 89.91% and 90.14%, and specificity of 88.92% and 88.68%, respectively. CONCLUSIONS:Serum RBP4 and CysC levels are significantly elevated in AMI patients and are closely related to the severity of cardiac impairment (Killip classification, LVEF, LVEDD) and ventricular remodeling (LVESV, PWS, LVM, LVRI). Combined detection of serum RBP4 and CysC shows high predictive value for cardiac impairment and ventricular remodeling in AMI patients.
OBJECTIVE:To analyze the incidence, etiological characteristics, and risk factors for death in patients with bloodstream infection in a medical intensive care unit (ICU). METHODS:A retrospective case-control study was conducted. Adult patients with bloodstream infection admitted to the medical ICU of The Third Xiangya Hospital of Central South University from January 2015 to December 2023 were enrolled. Data were collected from the hospital's electronic medical record system, including demographic characteristics [gender, age, body mass index (BMI)], clinical features (comorbidities, pathogen types, source of bloodstream infection, antibiotic use), laboratory parameters [routine blood test, liver and kidney function, results of bacterial culture and drug susceptibility test, C-reactive protein (CRP), procalcitonin (PCT), etc.], clinical management (red blood cell transfusion and usage of immunoglobulin, thymosin α1, glucocorticoid, empirical antibiotic therapy, mechanical ventilation, renal replacement therapy, etc.), and prognostic indicators (length of medical ICU stay and length of hospital stay after bloodstream infection). All patients were followed up for at least 3 months after the onset of bloodstream infection. Based on follow-up outcomes, patients were divided into survivor and non-survivor groups. Univariate analysis was used to identify variables associated with 3-month all-cause death in patients with bloodstream infection. Variables with P<0.05 in the univariate analysis were entered into multivariate Logistic regression analysis to identify independent risk factors for 3-month all-cause death. The Hosmer-Lemeshow test was used to assess the goodness-of-fit of the regression model. RESULTS:A total of 106 of the 4 820 medical ICU patients (2.2%) ultimately included in the study developed bloodstream infection during the 9 years. Among the 106 patients with bloodstream infection, the majority were male (71 cases, 67.0%), with an advanced age [(64.2±17.1) years]. The BMI was 23.0 (21.0, 23.0) kg/m2. The most common concomitant diagnosis was pulmonary infection (99 cases, 93.4%). Common comorbidities included type 2 diabetes mellitus (39 cases, 36.8%), gastrointestinal bleeding (26 cases, 24.5%), malignancy (23 cases, 21.7%), and chronic obstructive pulmonary disease (21 cases, 19.8%). The most common source of bloodstream infection was the lung (53 cases, 50.0%). At the time of bloodstream infection onset, patients presented with a clinical state characterized by immunosuppression, systemic inflammatory response, malnutrition and potential kidney injury. Septic shock was present at the time of bloodstream infection onset in 71 patients (67.0%). Forty patients (37.7%) received appropriate empirical antibiotic therapy after bloodstream infection onset. Mechanical ventilation was required in 83 patients (78.3%), and renal replacement therapy was required in 26 patients (24.5%). The median length of medical ICU stay and the median total hospital stay after bloodstream infection were 10.0 (4.0, 20.3) days and 16.0 (7.0, 28.3) days, respectively. A total of 113 bacterial or fungal strains were isolated from the blood of the 106 patients with bloodstream infection, among which Gram-negative bacteria were the predominant pathogens (73 strains, 64.6%). The most common pathogens were Enterobacteriaceae, predominantly Klebsiella pneumoniae (29 strains, 25.7%). Among the 106 patients, 68 patients (64.2%) died within 3 months after bloodstream infection onset, while 38 patients (35.8%) survived. Univariate analysis showed that, compared with the survivor group, the non-survivor group had significantly higher proportions of patients aged≥75 years, those with malignancy, those with carbapenem-resistant Gram-negative bacterial bloodstream infection, those with LYM≤0.5×109/L at bloodstream infection onset, those with septic shock at bloodstream infection onset, those requiring mechanical ventilation and renal replacement therapy. In contrast, the proportions of patients with BMI>23 kg/m2 and those receiving appropriate empirical antibiotic therapy after bloodstream infection onset were significantly lower in the non-survivor group (all P<0.05). Multivariate Logistic regression analysis showed that LYM≤0.5×109/L at bloodstream infection onset [odds ratio (OR)=3.268, 95% confidence interval (95%CI) was 1.196-8.927, P=0.021], septic shock at bloodstream infection onset (OR=3.637, 95%CI was 1.293-10.235, P=0.014), and the need for mechanical ventilation (OR=4.111, 95%CI was 1.242-13.610, P=0.021) were independent risk factors for 3-month all-cause death in patients with bloodstream infection, while receipt of appropriate empirical antibiotic therapy after bloodstream infection onset was a protective factor (OR=0.316, 95%CI was 0.118-0.844, P=0.022). The Hosmer-Lemeshow test yielded a χ 2 value of 5.082 with 6 degrees of freedom (P=0.533), indicating no evidence of overfitting. CONCLUSIONS:Bloodstream infection is a common complication among patients in the medical ICU, with Enterobacteriaceae being the most frequently isolated pathogens. The mortality of bloodstream infection is high. LYM≤0.5×109/L at bloodstream infection onset, septic shock at bloodstream infection onset, and the need for mechanical ventilation are independent risk factors for 3-month all-cause death in patients with bloodstream infection, while receipt of appropriate empirical antibiotic therapy after bloodstream infection onset is a protective factor.
OBJECTIVE:To investigate the relationship between the pathogen load kinetics detected by droplet digital polymerase chain reaction (ddPCR) and the prognosis of patients with suspected bloodstream infection (BSI). METHODS:A prospective observational study was conducted. Patients aged >18 years with suspected BSI admitted to intensive care unit department of Zhejiang Provincial People's Hospital from March 1, 2022 to October 31, 2023 were consecutively enrolled. Patients with blood ddPCR detection positive for pathogenic bacteria such as Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii, or Pseudomonas aeruginosa were included. Demographics, clinical profile, vital signs, and comorbidities data of patients upon admission were collected. Blood ddPCR testing, laboratory tests, and disease severity scoring were performed on days 0, 3, and 7. Based on whether the follow-up ddPCR test at day 7 showed a ≥50% decrease in all pathogen load compared to admission, patients were divided into the pathogen load decrease group and pathogen load non-decrease group. Baseline characteristics and the dynamic changes in perfusion indicators, inflammation indicators, and disease severity scores between two groups were compared. The correlation between ddPCR detection of pathogen load and perfusion indicators, inflammation indicators, and disease severity scores were analyzed using Spearman test. The 28-day cumulative survival rate of pathogen load decrease group and pathogen load non-decrease group was analyzed using Kaplan-Meier survival curve. Patients were divided into the survival group and death group according to the 28-day prognosis, and the clinical data were compared between the two groups. Independent risk factors for 28-day mortality in patients with suspected BSI were identified using multivariate Cox proportional hazards regression models. RESULTS:A total of 189 suspected BSI patients with ddPCR positive for Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii, or Pseudomonas aeruginosa infection were enrolled, of whom 121 underwent dynamic monitoring. Among these 121 patients, 82 showed a decrease in ddPCR pathogen load at day 7, while 39 did not. During the 28-day follow-up, 76 survived and 45 died, and the 28-day mortality was 37.2%. Compared to the pathogen load decrease group, the pathogen load non-decrease group had a higher proportion of patients receiving vasoactive drug support and mechanical ventilation, and a higher 28-day mortality (all P<0.05). In patients with suspected BSI, the ddPCR pathogen load on day 0 showed significant positive correlations with high-sensitivity C-reactive protein (hs-CRP), procalcitonin (PCT), blood lactate (Lac), Acute Physiology and Chronic Health Evaluation II (APACHE II), and Sequential Organ Failure Assessment (SOFA; r values were 0.150, 0.273, 0.370, 0.334, 0.311, respectively; all P<0.05). The Lac, hs-CRP, PCT and APACHE II in pathogen load decrease group decreased with time. However, hs-CRP and PCT did not decrease in pathogen load non-decrease group, and APACHE II and SOFA scores further increased. At day 7, compared to the pathogen load non-decrease group, the pathogen load decrease group showed significant reductions in hs-CRP, PCT, APACHE II and SOFA scores (all P<0.05); however, there was still no statistically significant difference in Lac between the two groups. Kaplan-Meier survival curve analysis showed that the 28-day cumulative survival rate of the pathogen load decrease group was significantly higher than that of the pathogen load non-decrease group (Log-rank test: χ 2=5.969, P=0.015). Compared to the survival group, the death group was older, had higher SOFA score, lower platelet count (PLT) and higher total pathogen load detected by ddPCR at day 7, and had a higher proportion receiving continuous renal replacement therapy (CRRT) and a higher proportion belonging to the non-decreased pathogen load. Multivariate Cox regression analysis showed that increasing age [hazard ratio (HR)=1.048, 95% confidence interval (95%CI) was 1.020-1.078, P<0.001], higher SOFA score (HR=1.127, 95%CI was 1.027-1.235, P=0.007), and pathogen load non-decrease (HR=2.165, 95%CI was 1.148-4.091, P=0.017) were independent risk factors for 28-day mortality in patients with suspected BSI. CONCLUSIONS:Dynamic monitoring of pathogen load changes by ddPCR can reflect the prognosis of patients with suspected BSI, suggesting the role of ddPCR detection in therapeutic monitoring for patients with BSI.
Cardiac arrest is a prevalent clinical emergency characterized by its high incidence, sudden onset, challenges in resuscitation, and low success rates. Timely and effective cardiopulmonary resuscitation (CPR) is the key to improving the success rate of patient rescue. Currently, manual CPR serves as the primary clinical approach. Due to the high intensity of physical exertion, the depth and frequency of external chest compression decrease with the extension of CPR time, resulting in a lower success rate of CPR. Although existing mechanical resuscitation devices address issues such as compression frequency, amplitude, and reduce the physical burden on medical staff, they are associated with complications for patients (e.g., sternum and rib fractures). Additionally, these devices are often expensive, bulky, and reliant on external power sources, limiting their clinical utility. To address these issues, the medical staff of the department of critical care medicine of the Second Affiliated Hospital of Zunyi Medical University designed a cardiac resuscitation device specifically for critical care and obtained a National Utility Model Patent of China (patent number: ZL 2019 2 2003762.8). The device is 25 cm long, 20 cm wide, 25 cm high, and weighs approximately 2.5 kg. On one side of the main body, there are longitudinally arranged adjustment knobs, a power switch, a power jack, and a heat dissipation window. The left side of the device features a touchscreen display, which shows parameters including screen contrast, alarm volume, defibrillation energy, time, battery level, heart rate, and electrocardiogram waveforms. Below the touchscreen, a physical control interface—comprising up/down keys, left/right keys, and function buttons—allows adjustment of all parameters displayed on the screen. To the right of the control interface, there is a shock current device that can be directly removed and placed closely to the patient for defibrillation treatment. There is a 48 V lithium battery inside the device, and a solar panel on the other side wall of the main body, which can automatically charge via sunlight. There is a strap on the other side wall of the main body, which contains a flexible sponge layer for comfortable wearing. The upper wall of the main body is equipped with a handle for easy carrying. The heartbeat restorer for critical care medicine has a simple structure, small size, light weight, low cost, easy operation, and strong mobility. It can meet the needs of cardiac arrest patients in different places, especially those in disaster areas who cannot be sent to the hospital for rescue in a timely manner. It is worthy of clinical promotion and application.
Reports of Hafnia infections in humans are infrequent, and the triad of Hafnia infection complicated by lung abscess and pneumothorax remains rarely documented. On January 25, 2025, a patient with a critical case of invasive Hafnia alvei pneumonia complicated by lung abscess and pneumothorax was admitted to Guangde Traditional Chinese Medicine Hospital. The patient had underlying comorbidities including diabetes mellitus and hepatitis B liver cirrhosis. The medical team identified severe pneumonia and its causative pathogen, Hafnia alvei through detailed examinations. An individualized treatment plan was formulated based on the results of drug susceptibility tests. However, the patient's condition progressed rapidly, and he experienced endotracheal intubation, mechanical ventilation, complicated by shock. Re-examination of imaging after treatment revealed progression of pulmonary cavities, along with the complication of lung abscess and tension pneumothorax. The neurological prognosis was poor after cardiopulmonary resuscitation (CPR), and the patient was discharged voluntarily. The triad of pneumonia, lung abscess, and pneumothorax caused by Hafnia alvei in this case has unique clinical manifestations, suggesting that clinicians should be alert to infections caused by rare pathogens such as Hafnia alvei when facing infected patients with multiple underlying diseases. Early identification of the invasive characteristics of the pathogen (rapidly progressive cavity plus secondary abscess/pneumothorax) is crucial. This case provides diagnostic and therapeutic insights for clinicians encountering similar infections, improving their understanding and management of Hafnia alvei infections.
Sepsis-associated encephalopathy (SAE) refers to diffuse brain dysfunction caused by a systemic inflammatory response, in the absence of direct central nervous system infection, structural brain abnormalities, or clinical/laboratory evidence of other types of encephalopathy. It is a common complication in sepsis, and its pathogenesis has not yet been fully elucidated. Recent studies have revealed that dysregulated cerebral glucose metabolism plays an important role in the development of SAE, in which glucose transporters (GLUTs) are critically involved. This article reviews the research progress on the involvement of brain glucose metabolism mediated by GLUTs in the regulation of SAE. The study focuses on: 1) The expression and function of GLUT1, GLUT3 and GLUT4 in brain tissue. 2) The function and expression of GLUTs in brain tissue are regulated by multiple factors: estrogen, cytokines, metabolic state and mitochondrial status. 3) The mechanisms of GLUTs in SAE and related brain disorders (such as neurodegenerative diseases associated with aging, cerebral hemorrhage, meningitis, encephalopathy caused by human immunodeficiency virus infection and encephalopathy caused by burns or burns combined with infection). 4) Potential therapeutic strategies for SAE based on glucose metabolism regulation: improving the expression of GLUTs associated with blood-brain barrier function; modulating the function of GLUTs involved in neuroinflammation; enhancing mitochondrial function, reducing oxidative stress, and increasing adenosine triphosphate production to indirectly boost GLUTs expression and activity; metabolic reprogramming-adjusting key metabolic enzymes or pathways to alter cellular metabolic characteristics and adapt to the energy demands during sepsis. The aim is to provide a theoretical basis for a deeper understanding of the pathophysiological mechanisms of SAE and the development of new therapeutic targets.
OBJECTIVE:To evaluate the predictive value of ten commonly used clinical scoring systems for 28-day mortality in adult sepsis patients in the intensive care unit (ICU), and to identify the optimal scoring system for assessing short-term outcomes in adult sepsis patients. METHODS:Clinical data were extracted from the Medical Information Mart for Intensive Care-IV (MIMIC-IV, 3.0 database) for sepsis patients aged 18-90 years on their first ICU admission, including demographic information, vital signs, comorbidities, laboratory indicators, assessment scales, and prognostic outcomes. Patients were divided into survival and death groups based on 28-day outcome after ICU admission, and clinical data were compared between the two groups. Lasso regression analysis was used for preliminary screening for variables associated with the prognosis of sepsis patients, and factors affecting the prognosis of sepsis patients were analyzed through univariate and multivariate Logistic regression analysis. The predictive value of ten scoring systems for 28-day mortality in sepsis patients was assessed using receiver operator characteristic curve (ROC curve). RESULTS:A total of 7 631 adults with sepsis were included in the MIMIC-IV database, of which 5 575 survived for 28 days and 2 056 died. Compared with the survival group, patients in the death group were older, had higher proportions of type 2 diabetes and heart failure, exhibited worse respiratory, circulatory, and metabolic conditions, carried a higher infection risk, and had significantly higher scores on the Sequential Organ Failure Assessment (SOFA), Acute Physiology Score III (APS III), Acute Physiology and Chronic Health Evaluation II (APACHE II), Simplified Acute Physiology Score II (SAPS II), Oxford Acute Severity of Illness Score (OASIS), Charlson comorbidity index (CCI; all P<0.05). Lasso regression analysis was initially applied to screen 49 characteristic variables, identifying 32 that were preliminarily associated with sepsis prognosis. These 32 variables were subsequently included in univariate and multivariate Logistic regression analyses. The results revealed that 18 variables were associated with 28-day mortality in sepsis patients (all P<0.05). Among these, an increase in APS III score [odds ratio (OR)=1.089, 95% confidence interval (95%CI) was 1.081-1.096, P<0.001], SAPS II score (OR=1.052, 95%CI was 1.048-1.056, P<0.001), Glasgow Coma Scale (GCS; OR=0.976, 95%CI was 0.962-0.991, P<0.001), and CCI score (OR=1.195, 95%CI was 1.175-1.215, P<0.001) were identified as independent risk factors for 28-day mortality in sepsis patients. ROC curve analysis demonstrated that among the ten scoring systems evaluated, the APS III and SAPS II scores showed superior predictive performance compared to the others. Their areas under the curve (AUC) with 95%CI were 0.721 (0.708-0.734) and 0.701 (0.687-0.714), respectively. CONCLUSIONS:Among the ten commonly used clinical scoring systems, the APS III score demonstrates a relatively favorable performance in predicting the risk of 28-day mortality in adult sepsis patients. It can provide a reliable basis for timely clinical intervention, thereby reducing patient mortality risk.
OBJECTIVE:To investigate the role and underlying mechanism of the protein kinase B (Akt)/sirtuin 3 (SIRT3) signaling pathway in hyperoxia-induced acute lung injury (HALI). METHODS:1) In vivo experiments: C57BL/6J mice were randomly assigned to a control group (normoxia) or a HALI group (≥95% oxygen), with six mice in each group. After 24 hours of exposure, lung histopathological changes were evaluated by hematoxylin-eosin (HE) staining, and the lung wet/dry weight (W/D) ratio was calculated. Apoptosis-related proteins in total lung lysates (cleaved caspase-3, Bax, and Bcl-2) and mitophagy-related proteins in mitochondrial fractions [p62, Beclin-1, and microtubule-associated protein light chain 3-II/I (LC3-II/I)] were measured by Western blotting. 2) In vitro experiments: Mouse type II alveolar epithelial cells (AEC II) MLE-12 in the logarithmic growth phase were used. Cells were divided into control group, H2O2 group (500 μmol/L H2O2 to mimic the HALI), and H2O2+3-methyladenine (3-MA) group. After 24 hours, cell viability was assessed by cell counting kit-8 (CCK-8), apoptosis was quantified by flow cytometry, and related proteins were detected by Western blotting. To explore the role of mitophagy in H2O2-induced apoptosis, cells were pretreated 2 hours before modeling with 10 μmol/L 3-MA, a mitophagy inhibitor. In additional experiments, cells were divided into control, H2O2, H2O2+Ly294002, and H2O2+SC-79 groups; 10 μmol/L Ly294002 (Akt inhibitor) or SC-79 (Akt activator) was added 2 hours before modeling to investigate the involvement of Akt signaling in mitophagy-mediated protection against H2O2-induced apoptosis. SIRT3 was further knocked down to determine whether it functions downstream of Akt in this protective pathway. RESULTS:1) In vivo results: Under light microscopy, the control group exhibited clear and regularly arranged alveolar structures, whereas the HALI group showed marked inflammatory cell infiltration, edema, and thickened alveolar walls. The lung W/D ratio was higher in the HALI group than that in the control group (11.5±1.1 vs. 5.4±0.8, P < 0.05). Compared with the control group, the HALI group showed increased expression of pro-apoptotic proteins Bax, cleaved caspase-3 [Bax (Bax/GAPDH): 0.49±0.06 vs. 0.18±0.05, cleaved caspase-3 (cleaved caspase-3/GAPDH): 1.71±0.07 vs. 0.63±0.06, both P<0.05], and decreased expression of anti-apoptotic protein Bcl-2 (Bcl-2/GAPDH: 0.39±0.05 vs. 1.03±0.08, P<0.05). Mitophagy-related markers were also altered, with increased LC3-II/I ratio and Beclin-1 [LC3-II/I ratio: 2.16±0.06 vs. 1.10±0.10, Beclin-1 (Beclin-1/GAPDH): 1.04±0.08 vs. 0.42±0.04, both P<0.05], and decreased p62 (p62/GAPDH: 0.41±0.04 vs. 0.99±0.08, P<0.05), suggesting that apoptosis and mitophagy may be involved in HALI progression. 2) In vitro results: Compared with the control group, H2O2 treatment reduced cell viability, Bcl-2, and p62 [cell viability: (48.45±6.48)% vs. (96.80±2.27)%, Bcl-2 (Bcl-2/GAPDH): 0.57±0.07 vs. 0.82±0.05, p62 (p62/GAPDH): 0.39±0.06 vs. 1.03±0.07, all P<0.05], while increasing apoptosis rate, LC3-II/I ratio, Beclin-1, Bax, and cleaved caspase-3 [apoptosis rate: (16.12±1.76)% vs. (6.54±0.75)%, LC3-II/I ratio: 2.05±0.12 vs. 0.97±0.07, Beclin-1 (Beclin-1/GAPDH): 0.69±0.05 vs. 0.18±0.03, Bax (Bax/GAPDH): 0.53±0.07 vs. 0.29±0.04, cleaved caspase-3 (cleaved caspase-3/GAPDH): 0.63±0.04 vs. 0.19±0.04, all P<0.05]. Compared with the H2O2 group, 3-MA pretreatment further aggravated apoptosis [cell viability: (34.00±5.05)% vs. (48.45±6.48)%, apoptosis rate: (22.21±3.05)% vs. (16.12±1.76)%, cleaved caspase-3 (cleaved caspase-3/GAPDH): 1.03±0.09 vs. 0.63±0.04, Bax (Bax/GAPDH): 0.69±0.07 vs. 0.53±0.07, Bcl-2 (Bcl-2/GAPDH): 0.30±0.04 vs. 0.57±0.07, p62 (p62/GAPDH): 0.64±0.05 vs. 0.39±0.06, Beclin-1 (Beclin-1/GAPDH): 0.34±0.04 vs. 0.69±0.05, LC3-II/I ratio: 1.64±0.05 vs. 2.05±0.12, all P<0.05], indicating that inhibition of mitophagy promotes MLE-12 apoptosis. Similar changes were observed after adding the Akt inhibitor Ly294002, whereas the Akt activator SC-79 produced effects opposite to those of 3-MA, suggesting that Akt activation promotes mitophagy and thereby suppresses apoptosis. Compared with the H2O2+SC-79 group, SIRT3 knockdown (H2O2+SC-79+siSIRT3) increased apoptosis rate, cleaved caspase-3, Bax, and p62 [apoptosis rate: (10.30±0.96)% vs. (8.82±0.95)%, cleaved caspase-3 (cleaved caspase-3/GAPDH): 0.69±0.05 vs. 0.44±0.05, Bax (Bax/GAPDH): 0.99±0.06 vs. 0.49±0.04, p62 (p62/GAPDH): 0.59±0.06 vs. 0.38±0.04, all P<0.05], and decreased SIRT3, Bcl-2, and Beclin-1 [SIRT3 (SIRT3/GAPDH): 0.48±0.05 vs. 0.68±0.04, Bcl-2 (Bcl-2/GAPDH): 0.64±0.05 vs. 0.78±0.05, Beclin-1 (Beclin-1/GAPDH): 0.68±0.04 vs. 0.79±0.04, all P<0.05]. These findings indicate that SIRT3 knockdown attenuates SC-79-induced mitophagy and enhances apoptosis, supporting SIRT3 as an important downstream effector of the Akt pathway. CONCLUSIONS:Activation of the Akt/SIRT3 signaling pathway promotes mitophagy to inhibit alveolar epithelial cell apoptosis, thereby attenuating HALI.
Objective:To investigate the factors influencing the apnea test (AT) and its clinical effects in brain death determination under updated criteria, and to provide evidence for optimizing and reducing the risk of false-negative results and complications.Methods:Based on the data from the Anhui Provincial Brain Injury Evaluation Quality Control Center, the data of brain-dead patients who completed AT with an off ventilator duration of 5-11 minutes were analyzed retrospectively. Data from January 2018 to March 2025 were used as the model development cohort, and the data from June to December 2025 were used as the external validation cohort. Demographic characteristics, clinical data, evaluation and examination indicators, AT operation details, etc. were extracted using standardized case report form. Temporal trends of AT positive rate and the incidences of severe hypercapnia, acidosis, hypoxemia and other complications when offline for 5-11 minutes were evaluated using the Cochran-Armitage trend test, and the key factors affecting the change of arterial partial pressure of carbon dioxide (PaCO 2) and pH were analyzed by multiple linear regression model. Results:The model development cohort included 384 patients with brain death, and the external validation cohort included 47 patients with brain death. There was no significant difference in baseline characteristics between the two cohorts (all P>0.05). With the extension of offline time, the positive rate of AT was gradually increased (Cochran-Armitage trend test: Z=3.52, P<0.001), rising from 76.5% (13/17) at 5 minutes to 91.7% (11/12) at 7 minutes, and plateaued after 7 minutes. The trend analysis of complications in the same period showed that the incidence of severe hypercapnia (PaCO 2>80 mmHg, 1 mmHg=0.133 kPa) showed a significant increasing trend ( Z=4.09, P<0.001), and was higher at 10 minutes than at 9 minutes [44.7% (59/132) vs. 21.6% (8/37), P<0.05]. Severe acidosis (pH<7.20) became more frequent over time ( Z=-4.69, P<0.001), and was higher at 10 minutes than at 7 minutes [73.5% (97/132) vs. 58.3% (7/12), P<0.05]. The incidence of hypoxemia [arterial partial pressure of oxygen (PaO 2)<60 mmHg] showed a decreasing trend ( Z=-5.21, P<0.001), with no statistically significant difference in incidence between 7-11 minutes ( F=0.859, P=0.525). The prediction model was established by multiple regression, indicated that offline time, pre-AT PaCO 2, pre-AT pH, heart rate, and body weight collectively influenced post-AT PaCO 2 ( R2=0.284, P<0.001). Offline time, pre-AT pH, heart rate, and hemoglobin were associated with post-AT pH ( R2=0.455, P<0.001). External validation indicated good performance for the pH model (mean absolute error was 0.038, R2=0.69) and acceptable performance for the PaCO 2 model (mean absolute error was 6.21 mmHg, R2=0.62). Conclusions:When implementing the dual-criteria standard (PaCO 2 and pH), an offline time window of 7 to 9 minutes can balance diagnostic efficacy for brain death with patient safety. Pre-intervention strategies, such as lowering pH or raising PaCO 2 before disconnection, may shorten the time needed to reach AT targets. However, should be guided by a comprehensive assessment of individualized patient factors, including baseline pH, PaCO 2, heart rate, hemoglobin, and body weight.
OBJECTIVE:To evaluate the predictive value of the Comorbidity Index combined with Identification of Seniors at Risk (ISAR) score for 30-day unplanned emergency department revisits among older emergency patients. METHODS:A retrospective study was conducted including patients aged 65 years and older who presented to the emergency department of Wuhan Central Hospital from January to August 2024. Gender and age, vital signs at emergency department presentation, the Comorbidity Index (constructed based on the 14-item Cumulative Illness Rating Scale, with each item scored as 1 if rated≥3 and summed to generate the index), and ISAR score were collected. Patients were divided into revisit group and non-revisit group based on the occurrence of an unplanned emergency department revisit within 30 days of the index visit, and the differences in various indicators between the two groups were compared. Multivariable Logistic regression analysis was performed to identify factors associated with 30-day emergency department revisits, and a nomogram prediction model was subsequently constructed. The predictive performance of the Comorbidity Index, ISAR score, and their combination were assessed using receiver operator characteristic curve (ROC curve), calibration curve, and decision curve analysis (DCA). RESULTS:A total of 435 older emergency department patients were included, of whom 359 did not revisit the emergency department and 76 experienced an unplanned emergency department revisit within 30 days. Compared with the non-revisit group, patients in the revisit group were significantly older and had higher heart rate and lower pulse oxygen saturation (all P<0.05), both the Comorbidity Index and ISAR score were significantly higher in the revisit group (Comorbidity Index: 3.07±1.69 vs. 1.87±1.07, ISAR score: 2.93±1.19 vs. 1.52±1.18, both P<0.05). Multivariate Logistic regression analysis showed that, after adjustment for age, gender, emergency triage level, and patient disposition, the Comorbidity Index [odds ratio (OR)=1.976, 95% confidence interval (95%CI) was 1.549-2.567, P<0.001] and ISAR score (OR=2.351, 95%CI was 1.831-3.080, P<0.001) remained independent predictors of 30-day emergency department revisits. The combined model showed an area under the curve (AUC) of 0.839 (95%CI 0.793-0.884) for predicting 30-day emergency department revisits, which outperformed the Comorbidity Index alone (AUC=0.725) or the ISAR score alone (AUC=0.797). Calibration curve showed good agreement between predicted and observed outcomes, and DCA indicated that the combined model provided greater net clinical benefit across a range of threshold probabilities. CONCLUSIONS:The combination of the Comorbidity Index and ISAR score effectively identifies older emergency department patients at high risk of unplanned 30-day emergency department revisits, demonstrating good predictive performance and potential clinical utility.
OBJECTIVE:To investigate the structural and functional alterations of intestinal goblet cells and the mucus barrier in rats with hypertriglyceridemia acute pancreatitis (HTG-AP), and to evaluate the potential mechanism involved in the progression to severe HTG-AP. METHODS:Twenty-four specific pathogen-free male Sprague-Dawley rats were divided into control group, biliary acute pancreatitis (BAP) group, hypertriglyceridemia (HTG) group, and HTG-AP group using a random number table method, with six rats in each group. In the BAP group, the BAP model was established by retrograde injection of 3.5% sodium taurocholate (0.3 mL/min) at 2 mL/kg through the pancreaticobiliary duct. In the HTG group, a polyethylene glycol-polypropylene glycol block copolymer was administered intraperitoneally at 0.50 g/kg once daily for 7 days to establish the HTG model. In the HTG-AP group, after the HTG model had been established, caerulein was administered intraperitoneally at 50 μg/kg once every one hour on day eight, and injections were continued for 7 days to induce HTG-AP. The control group received an equal volume of normal saline (2 mL/kg). All rats were sacrificed at 24 hours after modeling. Hematoxylin-eosin (HE) staining was performed to assess histopathological changes in the pancreas, ileum, and colon, and pathological scores were calculated. Western blotting was performed to determine the expressions of CD4, CD8, ZO-1, and Occludin. Enzyme linked immunosorbent assay (ELISA) was performed to measure secretory immunoglobulin A (sIgA) level in intestinal mucosa. Alcian blue/periodic acid-Schiff (AB/PAS) staining was performed to evaluate mucus layer structure and to measure mucus layer thickness and goblet cell number. Double immunofluorescence staining was performed to detect NOD-like receptor protein 6 (NLRP6) and mucin 2 (MUC2) expression and their colocalization. RESULTS:1) Compared with the control group, the BAP, HTG, and HTG-AP groups showed intestinal inflammatory changes of varying degrees. The HTG-AP group exhibited the most severe intestinal inflammation, accompanied by extensive acinar necrosis, hemorrhage, and marked edema; the pancreatic histopathological score was higher in the HTG-AP group than that in the BAP group (12.95±1.31 vs. 7.30±1.59, P<0.05). In addition, inflammatory cell infiltration in the ileum and colon extended through the full thickness of the intestinal wall, with massive loss of crypt goblet cells. 2) Intestinal immune function and barrier function were impaired in the BAP, HTG, and HTG-AP groups, and the impairment was most pronounced in the HTG-AP group. Compared with the BAP group, the HTG-AP group showed higher CD4 and CD8 expressions in the ileum (CD4/β-actin: 6.664±0.034 vs. 3.524±0.042, CD8/β-actin: 3.135±0.034 vs. 1.118±0.028, both P<0.05), a lower sIgA level in ileal mucosal supernatant (ng/L: 150.00±44.72 vs. 410.00±54.89, P<0.05), and decreased ZO-1 and Occludin expressions in the colon (ZO-1/β-actin: 0.46±0.13 vs. 0.59±0.20, Occludin/β-actin: 0.33±0.12 vs. 0.60±0.07, both P<0.05). 3) AB/PAS staining showed that the mucus layer of the colonic mucosal epithelium was altered in the BAP, HTG, and HTG-AP groups; the HTG-AP group exhibited severe mucus layer injury with more evident mucus depletion in goblet cells. Compared with the BAP group, the HTG-AP group had a thinner colonic mucus layer (μm: 10.20±4.69 vs. 16.80±4.38, P<0.05) and fewer mucus-containing goblet cells (cells/crypt: 4.30±1.34 vs. 7.52±1.93, P<0.05). 4) Double immunofluorescence staining showed that, compared with the control group, colonic NLRP6 and MUC2 expression and their colocalization signals were decreased in the BAP, HTG, and HTG-AP groups, and the decrease was most evident in the HTG-AP group. CONCLUSIONS:Disruption of the intestinal mucus barrier may be an important mechanism contributing to the progression to severe HTG-AP, and the NLRP6/MUC2 axis may serve as a potential therapeutic target.
Extracorporeal membrane oxygenation (ECMO) is a vital cardiopulmonary life support technology and one of the key therapeutic measures for extracorporeal life support in critically ill patients. To secure the cannula and prevent catheter-related bloodstream infections, the current clinical practice involves covering the catheter puncture site locally with a sterile transparent dressing. However, due to the large diameter of ECMO cannulas, inadequate shaping during dressing application can compromise the seal of the dressing, increasing the risk of infection. Simultaneously, direct contact of the cannula with the patient's skin can easily lead to local device-related pressure injuries. Furthermore, the large surface area of ECMO dressings and varying levels of skill among healthcare professionals in shaping the dressings further compromise the effectiveness of fixation. To address the aforementioned issues, the department of critical care medicine at Zhongda Hospital affiliated with Southeast University has invented a moldable applicator for securing ECMO cannulas, which has been granted a National Utility Model Patent of China (patent number: ZL 2022 2 1954859.2). The device is shaped like scissors and primarily consists of two symmetrically crossing clamping bodies, a connecting part, and a handle. The cross-section of each clamping body is semi-circular. Its hard outer shell is adhesively bonded to an internal soft cushion, ensuring airtight adaptation to catheters of different sizes, thus forming an "Ω"-shaped lifting platform to effectively prevent potential infection and pressure injury risks. The connecting part is equipped with a recoil component—when catheter shaping is complete, releasing the handle causes the clamps to automatically open, facilitating the next step in the procedure for nurses. The handle is designed with anti-slip finger rings, enhancing grip stability and ensuring effective anti-slip performance. With its practical design and user-friendly operation, the product helps prevent infection risks, reduce pressure injuries, and improve nursing efficiency, demonstrating significant value for clinical promotion.
Objective:Predict the occurrence of pressure injury in critically ill patients by using machine learning models and conducting internal validation.Methods:A prospective cohort study was conducted. Critically ill patients admitted to the intensive care unit (ICU) of the North District of Hangzhou First People's Hospital from January 2023 to March 2024 were enrolled using convenience sampling. Patients were divided into two groups based on the occurrence of pressure injury during their ICU stay, and the differences in pressure injury related indicators were compared between the groups. The dataset was randomly divided into a training set (75%) and a validation set (25%). Feature selection was performed using the Lasso regression. Independent risk factors were then identified via multivariate Logistic regression analysis. An extreme gradient boosting (XG-Boost) machine learning model was developed to predict pressure injury risk. The model's performance was comprehensively evaluated using receiver operator characteristic curve (ROC curve), calibration curve, and clinical decision curve analysis (DCA). The Shapley Additive exPlanations (SHAP) method was used to rank feature importance.Results:A total of 350 critically ill patients were included, of whom 102 (29.1%) developed pressure injuries. There were statistically significant differences in consciousness status, mechanical ventilation, sedative use, length of ICU stay, Braden score, use of warm blankets, white blood cell count, neutrophil count, blood glucose, and lactate level between the pressure injury and non-pressure injury groups (all P<0.05). Lasso regression analysis identified six predictive variables: consciousness status, mechanical ventilation, use of warm blankets, length of ICU stay, neutrophil count, and blood glucose. Multivariate Logistic regression analysis subsequently revealed that mechanical ventilation, use of warm blankets, prolonged ICU stay, elevated neutrophil count, and elevated blood glucose were independent risk factors for pressure injuries [mechanical ventilation: odds ratio ( OR)=2.338, 95% confidence interval (95% CI) was 1.768-3.089, P=0.002; use of warm blankets: OR=1.772, 95% CI was 1.341-2.338, P=0.039; prolonged ICU stay: OR=1.081, 95% CI was 1.067-1.097, P<0.001; elevated neutrophil count: OR=1.044, 95% CI was 1.022-1.067, P=0.036; elevated blood glucose: OR=1.062, 95% CI was 1.031-1.094, P=0.027]. Based on these six risk factors, a predictive model was constructed using the XG-Boost method. The ROC curve analysis demonstrated the model has high predictive performance, with an area under the curve (AUC) of 0.896 (95% CI was 0.863-0.929) in the training set and 0.835 (95% CI was 0.761-0.908) in the validation set. The calibration curve indicated good agreement between predicted probabilities and actual outcomes. DCA further suggested that the model had clinical utility across a wide range of threshold probabilities. SHAP analysis ranked feature importance in descending order as follows: length of ICU stay, mechanical ventilation, neutrophil count, consciousness status, blood glucose, and use of warm blankets. Conclusions:The constructed XG-Boost machine learning model has high performance in predicting the occurrence of pressure injury in critically ill patients. Identify key predictive factors can aid clinical risk assessment and intervention.
