Sepsis, a dysregulated host response to infection, is a leading cause of morbidity and mortality in critically ill patients, despite advancements in antimicrobial therapies. Recent innovations in extracorporeal blood purification therapies, such as the Selective Cytopheretic Device (SCD), Polymyxin B Hemoperfusion Cartridge (PMX-HP), and Seraph 100 Microbind Affinity Blood Filter (Seraph), have demonstrated promising potential as adjuncts to conventional therapies. The SCD targets activated white blood cells, while PMX-HP binds endotoxins in Gram-negative sepsis. The Seraph targets a broad range of pathogens, including viruses, bacteria and fungi. Evidence from several clinical trials and observational studies indicate that these therapies can improve organ function, and potentially improve survival in patients with sepsis. Despite the strong pathophysiological rationale for using these devices in sepsis, conclusive evidence of their effectiveness remains limited. Multicenter randomized controlled trials are currently underway with each of these devices to establish their role in improving patient outcomes. Further research is needed to establish optimal protocols for their initiation, duration, and integration into standard sepsis management.

The TyG index serves as a valuable tool for evaluating insulin resistance. An elevated TyG has shown a strong association with the occurrence of acute kidney injury (AKI). Nevertheless, existing literature does not address the relationship between the TyG index and acute kidney injury in patients with sepsis. Sepsis patients were identified from the MIMIC-IV database and categorized into four groups according to quadrilles of their TyG index values. The primary outcome of this study was the incidence of AKI. The relationship between the TyG index and the risk of AKI in septic patients was evaluated using Cox proportional hazards and restricted cubic spline models. Subgroup analyses were conducted to investigate the prognostic value of the TyG index in different subgroups. A total of 2,616 patients with sepsis (57% of whom were male) were included in this study. The incidence of AKI was found to be 78%. Cox proportional hazards analysis revealed a significant correlation between the TyG index and the occurrence of AKI in septic patients. Furthermore, a restricted cubic spline model revealed an approximately linear relationship between a higher TyG index and an elevated risk of AKI in septic patients. The trend of the hazard ratio (HR) remained consistent across various subgroups. These findings emphasize the reliability of the TyG index as an independent predictor for the occurrence of AKI and unfavorable renal outcomes in sepsis patients. Nevertheless, establishing a causal relationship between the two requires demonstration through larger prospective studies.

Acute kidney injury (AKI) is a common complication in heart failure (HF) patients. Patients with heart failure who experience renal injury tend to have a poor prognosis. The objective of this study is to examine the correlation between the occurrence of AKI in heart failure patients and different mean arterial pressure (MAP) trajectories, with the goal of improving early identification and intervention for AKI.

A retrospective study was conducted on patients with heart failure using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV). We utilized the group-based trajectory modeling (GBTM) method to classify the 24-hour MAP change trajectories in heart failure patients. The occurrence of AKI within the first 7 days of intensive care unit (ICU) admission was considered the outcome. The impact of MAP trajectories on AKI occurrence in heart failure patients was analyzed using Cox proportional hazards models, competing risk models, and doubly robust estimation methods.

A cohort of 8,502 HF patients was analyzed, with their 24-hour MAP trajectories categorized into five groups: Low MAP group (Class 1), Medium MAP group (Class 2), Low-medium MAP group (Class 3), High-to-low MAP group (Class 4), and High MAP group (Class 5). The results from the doubly robust analysis revealed that Class 4 exhibited a significantly increased AKI risk than Class 3 (HR 1.284, 95% CI 1.085-1.521, p = 0.003; HR 1.271, 95% CI 1.074-1.505, p = 0.005). Conversely, the risks of Class 2 were significantly lower than those of Class 3 (HR 0.846, 95% CI 0.745-0.960, p = 0.009; HR 0.879, 95% CI 0.774-0.998, p = 0.047).

The 24-hour MAP trajectory in HF patients influences the risk of AKI. A rapid decrease in MAP (Class 4) is associated with a higher AKI risk, while maintaining MAP at a moderate level (Class 2) significantly reduces this risk. Therefore, closely monitoring MAP changes is crucial for preventing AKI in HF.

Non-specificity and inadequate quantitative capability are the primary challenges faced by the surface-enhanced Raman scattering (SERS) technique, especially when it comes to detecting bacteria in real samples. Herein, a novel face-centered Au Convex Polyhedral Nanocrystal (Au CPNC) with high-index facets and its assembly Au CPNCs microarray chip were designed and fabricated to address these challenges, within the process where 4-mercaptophenylboronic acid (4-MPBA) was utilized as a multifunctional element. The as-prepared Au CPNC possesses anisotropic raised edges enjoying tunable localized surface plasmon resonance modes for SERS enhancement. Then we obtained long-region ordered Au CPNCs microarrays equipping even greater "hot spots" with a SERS enhancement factor (EF) up to 5.38 × 107. The constructed SERS probes excellently leveraged the outstanding SERS performance of Au CPNC and the superior functions of 4-MPBA, which enabled the differences among the bacterial "fingerprints" to be highlighted. Through partial least squares discriminant analysis (PLS-DA), we successfully identified Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa and Listeria monocytogenes with achieving limits of detection (LODs) in spiked whole blood samples of 3, 1, 2, and 2 cfu/mL, respectively. Notably, the LODs for all samples by SERS mapping visual readout mode were as low as 10 cfu/mL. In practical applications, our method demonstrated its efficacy by 100 % accurately classifying (20 cases) of real blood samples. Altogether, the theoretical significance and application value of this study reside in providing fundamental insights and approaches for the development of pathogenic bacteria detection field.

Among forensic and clinical cases, infections caused by the ingestion of foreign bodies are common. In general, timely removal of the foreign body and appropriate treatment prevent serious consequences. We herein report a rare case of death due to massive bleeding caused by splenic rupture following foreign body ingestion. To our knowledge, no similar cases have been reported in the Chinese or international literature, making this case particularly noteworthy. In this instance, the decedent was in a detention centre for a criminal offence and swallowed a wire unnoticed. The wire remained in his stomach for >50 days, leading to a severe suppurative infection in the gastric tissue. This resulted in suppurative inflammation affecting multiple organs, including the liver, pancreas, and spleen. The condition ultimately led to the rupture of splenic vessels and the formation of a rare, massive haematoma beneath the splenic capsule. Based on medical records and histopathological findings, we infer that the wire had remained in the stomach for ~50 days, triggering severe suppurative infections in multiple organs. The spleen eventually ruptured, and the victim died of massive haemorrhage.

In 2020, sepsis has been defined a worldwide health major issue (World Health Organization). Lung, urinary tract and abdominal cavity are the preferred sites of sepsis-linked infection. Research has highlighted that the advancement of sepsis is not only related to the presence of inflammation or microbial or host pattern recognition. Clinicians and researchers now recognized that a severe immunosuppression is also a common feature found in patients with sepsis, increasing the susceptibility to secondary infections. Lipopolysaccharides (LPS) are expressed on the cell surface of Gram-negative, whereas Gram-positive bacteria express peptidoglycan (PGN) and lipoteichoic acid (LTA). The main mechanism by which LPS trigger host innate immune responses is binding to TLR4-MD2 (toll-like receptor4-myeloid differentiation factor 2), whereas, PGN and LTA are exogenous ligands of TLR2. Nucleotide-binding oligomerization domain (NOD)-like receptors are the most well-characterized cytosolic pattern recognition receptors, which bind microbial molecules, endogenous by-products and environmental triggers. It has been demonstrated that high-density lipoproteins (HDL), besides their major role in promoting cholesterol efflux, possess diverse pleiotropic properties, ranging from a modulation of the immune system to anti-inflammatory, anti-apoptotic, and anti-oxidant functions. In addition, HDL are able at i) binding LPS, preventing the activating of TLR4, and ii) inducing the expression of ATF3 (Activating transcription factor 3), a negative regulator of the TLR signalling pathways, contributing at justifying their capacity to hamper infection-based illnesses. Therefore, reconstituted HDL (rHDL), constituted by apolipoprotein A-I/apolipoprotein A-IMilano complexed with phospholipids, may be considered as a new therapeutic tool for the management of sepsis.

Sepsis is a life-threatening condition characterized by systemic inflammation and microcirculatory dysfunction. Methylene blue (MB), a compound with known antioxidant and anti-inflammatory properties, has been proposed as a potential therapeutic agent. This study aimed to investigate the effects of MB on survival rates and the preservation of mesenteric microcirculation in a rat model of endotoxemia. A total of 36 rats underwent cecal ligation and puncture (CLP) surgery to induce varying degrees of sepsis: mild (4 perforations), moderate (10 perforations), and severe (20 perforations). Animals received intravenous treatment with either MB (4 mg/kg) or saline. Survival was monitored for ten days. Additionally, intravital microscopy was used to assess leukocyte rolling and adhesion in mesenteric vessels following lipopolysaccharide (LPS)-induced sepsis. The experimental groups included saline, LPS + saline, MB + saline, LPS + MB, and MB + LPS. MB treatment significantly improved survival in the severe sepsis group, with a 30 % survival rate at ten days (p = 0.02, 95 % CI: 0.12-0.48), whereas all animals in the severe sepsis + saline group died within nine days. No significant survival benefit was observed in the mild and moderate sepsis groups (mild sepsis: p = 0.45, 95 % CI: 0.08-0.34; moderate sepsis: p = 0.32, 95 % CI: 0.15-0.51). In the LPS-induced model, treatment with both LPS and MB significantly reduced leukocyte rolling and adhesion (p < 0.001, 95 % CI: 0.45-0.75 for rolling; p < 0.03, 95 % CI: 0.30-0.60 for adhesion), with values comparable to those of the control group. In contrast, MB alone had no effect on leukocyte rolling or adhesion.In summary, MB significantly improved survival in severe sepsis and inhibited leukocyte migration in mesenteric vessels. These findings suggest that MB may protect the microcirculation and enhance survival under severe septic conditions, representing a promising therapeutic approach for sepsis management.

Pneumonia-induced sepsis (PIS) is a life-threatening condition with high mortality rates, necessitating the identification of biomarkers and therapeutic targets. Sphingolipid, particularly ceramides, are pivotal in modulating immune responses and determining cell fate. In this study, we identified a novel gene signature related to sphingolipid metabolism, comprising ACER3, UGCG, and GBA, which are key enzymes involved in the synthesis and metabolism of ceramides. This signature, termed the "AUG model", demonstrated strong diagnostic performance and modest prognostic efficacy across both training (GSE65682) and validation (E-MTAB-1548 and E-MTAB-5273) datasets. A clinical cohort comprising 20 PIS patients, 31 pneumonia cases, and 11 healthy controls further validated the increased expression of AUG genes at both mRNA and protein levels in peripheral blood samples upon admission. Our comprehensive analysis of bulk and single-cell transcriptome datasets revealed that these genes are implicated in immune cell death pathways, including autophagy and apoptosis. Additionally, cell-communication analysis indicated that enhanced macrophage migration inhibitory factor (MIF) signaling may be associated with dysregulated sphingolipid metabolism, potentially driving the inflammatory cascade. This study identifies a novel predictive model for PIS, highlighting the role of sphingolipid metabolism-related genes in disease progression and suggesting potential therapeutic targets for sepsis management.

The Compendium of Materia Medica recorded that the traditional Chinese medicine Gastrodia elata Blume (G. elata) has applications in antibacterial and antiviral. GE05 was prepared from the rhizome of G. elata and its active ingredients have been proven to alleviate inflammatory response. However, the protective effect and the underlying mechanism of G. elata in sepsis remain unclear. Our study aims to uncover the efficacy and molecular mechanisms of GE05 in ameliorating sepsis-induced lung injury. Here, we have shown that GE05 could inhibit the expression of inflammatory cytokines in peritoneal macrophages. Bioinformatics analysis showed the activation of interleukin (IL)-17 signaling pathway in acute lung injury (ALI) mice. We established septicemia models and showed that GE05 improves survival rates and protects against sepsis-induced lung injury by downregulating the IL-23/IL-17 A axis. Quantitative real- time PCR (qPCR) analysis and immunohistochemistry have indicated that IL-17 A inhibition reduces the release of chemokine ligand (Cxcl) 1, Cxcl2, ‌granulocyte-macrophage colony stimulating factor (GM-CSF), and granulocyte colony-stimulating factor (G-CSF), mitigating neutrophil infiltration-induced lung tissue damage. Meanwhile, GE05 could inhibit the activation of the IL-17 A-related phosphatidylinositol 3-kinase/ c-Jun N-terminal kinase (PI3K/JNK) signaling pathway, suppressing the expression of tumor necrosis factor-alpha (TNF-α), IL-1β, and IL-6. These results demonstrated that GE05 is a promising agent that targets the IL-23/IL-17 A axis, providing new way for preventing and treating sepsis-induced lung injury.

As the most abundant protein in plasma, albumin (ALB) presents close association with prognosis of septic patients. Whereas, the benefit and the target level of ALB infusion remain controversial.

We conducted a retrospective investigation to assess whether on-treatment ALB levels could predict 28-day mortality and try to identify the optimal level for ALB infusion. All patients diagnosed as sepsis from January 2016 to December 2020 were recruited and re-evaluated using Sepsis-3 criteria.

A total of 199 eligible patients were enrolled in this study. Compared with the survival group, the non-survival group had more males (73.97 vs. 56.35%), older patients (62.78 ± 15.93 vs. 56.43 ± 18.46), and a higher proportion of Gram-positive bacterial infection (27.40 vs. 23.02%), higher Sequential Organ Failure Assessment (SOFA) score (7.00-13.00 vs. 6.00-12.00), higher APACHE II score (18.25-29.00 vs. 15.00-26.00), higher PCT (2.84-49.18 vs. 2.43-19.14), more patients with septic shock (65.75%vs. 43.65%), shorter ICU-stay days (11.04 ± 6.28 vs. 14.83 ± 8.58), longer mechanical ventilation days (7.23 ± 7.07 vs. 5.04 ± 8.52), with statistically significant differences (p < 0.050). Furthermore, we identified that the ALB level on day 7 (HR, 0.920; 95% CI, 0.847 to 0.999; p = 0.046) and the maximum ALB level within the first 14 days (HR, 0.900; 95% CI, 0.838 to 0.967; p = 0.004) were independent protective factor for the 28-day prognosis in septic patients. Moreover, ROC curve analysis indicated that optimal target level for first 14-day maximum and on day 7 were 33.45 g/L and 27.85 g/L, respectively. Correspondingly, a negative correlation between ALB level and mortality was defined with Kaplan-Meier survival curve analysis. Further subgroup analysis showed that the group with ALB above the cut-off value was associated with favorable outcomes in female patients under 60 years, with SOFA score less than 7, and APACHE II score less than 19.

ALB levels on day 7 and the maximum ALB level within first 14 days after ICU admission were closely associated with 28-day mortality. 27.85 g/L would work as the target level of ALB infusion on 7 day to improve the prognosis of sepsis patients.

Sepsis is a leading cause of death in intensive care units (ICU). Sepsis survivors are often left with significant morbidity, termed post-intensive care syndrome (PICS), impacting post-sepsis life. The aim was to present detailed data on the prognostic and functional long-term outcomes of ICU patients with sepsis in Japan, which is currently lacking and therefore prevents development of targeted solutions.

A multicenter prospective study, involving 21 ICUs in 20 tertiary hospitals in Japan, included all consecutive adult ICU patients between November 2020 and April 2022, and diagnosed with sepsis at ICU admission (Sepsis 3). Follow-ups were performed at 3, 6, and 12 months after hospital discharge by telephone and mail. Primary outcome was death or incidence of PICS, defined by any of physical dysfunction (Barthel Index ≤ 90), cognitive dysfunction (Short Memory Questionnaire < 40), or mental disorder (any subscales for anxiety or depression of Hospital Anxiety and Depression Scale ≥ 8, or Impact of Event Scale-Revised ≥ 25). Secondary outcomes included Quality of Life (QOL), employment, and use of hospital, emergency, rehabilitation, and psychiatric services. A multivariable analysis investigated independent factors associated with each dysfunction at each follow-up.

A total of 339 patients were included (median age 74 [67-82] years, 60% male, 77% septic shock, and a median SOFA of 9 [6-12]). Mortality was 23% at hospital discharge, increasing to 37% at 12 months. The rate of death for those who met PICS Criteria at hospital discharge was 89%, with a death or PICS incidence of 73%, 64%, and 65% at 3, 6, and 12 months, respectively. Limited improvements in QOL and return to work (44%), high rates of hospital readmissions (40%), frequent emergency service usage (31%), and low utilization of rehabilitation and psychiatric services (15% and 7%) were identified over the first year. The incidence of any PICS-related dysfunction was consistently an independent factor for the incidence of the same dysfunction at the following follow-ups.

This multicenter study identified the distinct realities of post-sepsis life in Japanese ICU patients, highlighting the unique challenges in improving their functions and returning to daily life. Trial Registration University Hospital Medical Information Network UMIN000041433.

The Sequential Organ Failure Assessment (SOFA) score originated as a tool for assessing organ dysfunction in critical illness but has expanded to become an outcome measure in clinical trials. We aimed to assess how the SOFA score was used as the primary or secondary endpoint of major randomized controlled trials (RCTs).

Independent reviewers searched MEDLINE/PubMed, Scopus, and Embase databases.

Articles were selected when they fulfilled: 1) RCT; 2) SOFA score was primary or secondary endpoint; and 3) published in the Lancet , New England Journal of Medicine , or Journal of the American Medical Association .

Data collection included study details, outcomes, statistical differences in SOFA score, choice of score statistics, timepoints of SOFA reporting, and how missing data and competing risks analysis were managed.

Twenty-three RCTs had SOFA score as outcome measure, eight used it as primary endpoint. Daily maximum SOFA was the key statistic in 11 RCTs, delta SOFA was used in eight, and mean SOFA in four. Mean SOFA was most frequently chosen as primary endpoint (4/8, 50%). There were 18 different outcome assessment timepoints, ranging from 1 to 28 days. Three RCTs reported statistically significant difference in SOFA between groups. Handling of missing SOFA scores was not described in ten of 23 RCTs. When described, it varied from study to study with variable imputation methods and variable accounting for the competing risk of mortality and ICU discharge.

There is major variability in the choice of summary statistic for SOFA score analysis and assessment timepoints, when using it as outcome measure in RCTs. There was either no information or great variability in the handling of missing values, use of imputation, and accounting for competing risk. The current use of SOFA scores in RCTs lacks sufficient reproducibility and statistical and methodological robustness.

The pathogenesis of sepsis is thought to be linked to a dysregulated immune response, particularly that involving neutrophils. We have developed a granulocyte adsorption column as a "decoy organ," which relocates the massive inflammation in organs in the body to a blood purification column. This study was conducted to assess the safety and experimental effectiveness of granulocyte monocyte adsorption apheresis-direct hemoperfusion (G1-DHP) in the treatment of patients with sepsis, using a prospective, multicenter design.

The study included patients diagnosed with sepsis and with an APACHE II score ranging from 17 to 34. A total of five G1-DHP were performed within 3 days of patient enrollment. The primary endpoint was the change in sequential organ failure assessment (SOFA) score from enrollment to 7 days, and the safety endpoints were adverse events and mortality at 28 days.

G1-DHP was performed on 82 patients. The median (interquartile range) SOFA score decreased from 10 (8-11) to 4 (3-7) after 7 days (n = 70; p < 0.01). Granulocytes, mainly neutrophils, were adsorbed, and the neutrophil-to-lymphocyte ratio significantly improved (p < 0.01). Notable improvements were observed in the SOFA scores for circulation and renal function. The acute physiology and chronic health evaluation II score of the 77 patients evaluated for mortality was 27, and the 28-day mortality rate was 7.8%.

This study confirmed that G1-DHP can be safely used as an adjunct to standard sepsis treatment regimens. Although further investigations are required, G1-DHP is a promising supplemental therapy for sepsis.

jRCT1080225183 (Japan Registry of Clinical Trials identifier).

This review will explore the current knowledge, beginning with the physiologic underpinnings and delve into the evolving scientific literature, encompassing the inextricably intertwined diagnosis and management of sepsis and septic shock in human and small animal patients. Sepsis is a significant cause of morbidity and mortality in patients, mostly for failure to recognize or treat promptly and adequately. Diagnosis is based on the individual patient, clinical context, and clinical acumen. High quality supportive care in the intensive care unit setting is patient-centered with intensive nursing, focused on physiologic systems, goal-oriented, and multi-disciplinary with a team-based approach to patient care.

Sepsis is the most common acute insult in patients with acute-on-chronic liver failure (ACLF), and circulatory failure portends a poor prognosis in them.

This study aimed to compare terlipressin and noradrenaline as first-line vasopressors in patients with ACLF and septic shock.

This prospective, open-label, randomized controlled study was conducted from January 2021 to June 2022 at a tertiary care center. All patients presenting with ACLF as per the chronic liver failure consortium acute on chronic liver failure in cirrhosis study and septic shock were screened. Shock was defined as a mean arterial pressure (MAP) <65 mmHg/systolic blood pressure <90 mmHg. Patients with septic shock nonresponsive to crystalloids/colloids were randomized to receive terlipressin (group I) at 2.6 μg/kg/min and noradrenaline (group II) at 0.1 μg/kg/min. The primary outcome was an MAP >65 mmHg at 6 h. The secondary outcomes were 3-, 7-, 14-, and 28-day mortality, duration of hospital stay, cumulative dose of drug, and new events such as upper gastrointestinal bleed, acute kidney injury, jaundice, and hepatic encephalopathy within 28 days.

A total of 70 patients were randomized to group I (n = 35) and group II (n = 35). According to per-protocol analysis, a higher number of patients achieved an MAP > 65 mmHg at 6 h in group II (n = 23/31, 74%) than in group I (5/34, 14%) (P < 0.001). The 3-and 7-day mortality was significantly higher in group I than in group II, with no difference at 14 and 28 days. The 28-day mortality was highest in ACLF grade-3 in both group II (22/25, 88%) and group I (15/20, 75%).

Terlipressin did not prove to be noninferior to norepinephrine, and therefore, norepinephrine should be the first-line vasopressor in ACLF patients with septic shock. The mortality rate was highest in ACLF grade-3 patients in both the groups, irrespective of the initial response to vasopressors. This indicates that holistic management of these patients is most important.

Sepsis is a potentially life-threatening condition triggered by infection that is responsible for an estimated 48,000 deaths in the UK each year. Its pathophysiology is complex, its symptomology non-specific and its clinical presentations extremely varied. Despite numerous campaigns to raise awareness of sepsis, it still goes undetected. In 2024, the National Institute for Health and Clinical Excellence revised its guideline on sepsis and the UK Sepsis Trust published the seventh edition of its Sepsis Manual. This article discusses the pathophysiology of sepsis and how emergency nurses should assess and manage patients with suspected sepsis. It describes the tools available to them, including the National Early Warning Score 2 and the Sepsis 6, and emphasises the importance of early antibiotic administration, serial lactate measurements, source control and antimicrobial stewardship.

Septic surgical patients undergoing emergency general surgery represent a distinct population with unique challenges. This study aimed to identify predictors of cumulative 90-d mortality, including clinical and socioeconomic factors, and to analyze causes of death in this cohort.

A retrospective analysis was conducted on patients admitted to a surgical intensive care unit from 2011 to 2019 with sepsis (sequential organ failure assessment score ≥2) undergoing emergency intra-abdominal surgery (n = 498). Demographics, comorbidities, sepsis presentation, and socioeconomic metrics, including the area deprivation index (ADI), were analyzed. Independent predictors of mortality were identified using multiple logistic regression. The causes of death were categorized and analyzed.

Among 498 patients, 46% (n = 229) died within 90 d. Nonsurvivors were older (65 ± 13.7 versus 61.2 ± 13.5 y, P < 0.01), more often transferred from external facilities (59% versus 46%, P < 0.01), and had higher rates of liver disease, chronic kidney disease, metastatic cancer, obesity, and higher Charlson comorbidity index scores (P < 0.01 for all). Independent predictors of 90-d mortality included admission sequential organ failure assessment scores, serum lactate, obesity, ADI, Charlson comorbidity index, and transfer status. ADI remained a significant predictor, while the distressed communities index did not. Of the deaths, 76.9% were in-hospital deaths, with intra-abdominal catastrophes (35.4%), multisystem organ failure (25.2%), and pulmonary causes (16.4%) as the most common causes.

Intra-abdominal catastrophes, multiorgan failure, and pulmonary complications are leading causes of death in septic emergency general surgery patients. ADI is a robust socioeconomic predictor of mortality, underscoring the need for integrating social determinants into risk assessment and tailored care strategies. Developing comprehensive risk models may enhance prognostication and guide clinical decision-making in this critical population.

To delineate the clinical characteristics and investigate the determinants that may affect the prognosis of surgical patients with abdominal sepsis.

A case-control study was nested in a cohort of surgical patients with abdominal sepsis between 2008 and 2022. We extracted patient' medical records to execute descriptive statistical analyses. Multiple logistic regression models and subgroup analysis were employed to elucidate the risk factors of in-hospital mortality.

Two tertiary hospitals in China.

476 surgical patients diagnosed with abdominal sepsis between 2008 and 2022 were analysed.

None.

Descriptive statistics were used to examine pertinent patient information, including demographic details, laboratory findings, surgical interventions and anaesthetic records. Multivariate logistic regression was used to identify independent risk factors for in-hospital mortality. Subgroup analyses were conducted to explore the impact of specific clinical characteristics on outcomes.

476 patients diagnosed with abdominal sepsis were analysed, exhibiting an in-hospital mortality rate of 7.56%. Advanced age (OR 6.77, 95% CI 2.46 to 18.66, p<0.001), the presence of diabetes (OR 2.61, 95% CI 1.04 to 6.56, p=0.041) and higher preoperative Sequential Organ Failure Assessment (SOFA) score (OR 3.48, 95% CI 1.16 to 10.43, p=0.026) were identified as significant predictors of increased in-hospital mortality risk through a multinomial logistic regression model. Conversely, individuals afflicted with biliary diseases (OR 0.15, 95% CI 0.04 to 0.64, p=0.010) demonstrated a reduced risk of in-hospital mortality. Subgroup analysis revealed that low serum albumin levels emerged as a risk factor for in-hospital mortality in the patients with gastrointestinal diseases (OR 20.23, 95% CI 2.21 to 184.84, p=0.008) or advanced age (OR 10.52, 95% CI 2.29 to 48.31, p=0.002) through multinomial logistic regression analysis.

In this retrospective analysis, we delineated the clinical characteristics of surgical patients with abdominal sepsis and pinpointed risk factors associated with in-hospital mortality. These findings underscore the necessity for more tailored perioperative management strategies for patients with sepsis characterised by advanced age, diabetes, higher preoperative SOFA score and reduced preoperative albumin levels. Clinicians should prioritise early recognition and aggressive management of these high-risk individuals, including timely surgical intervention, optimisation of nutritional status and vigilant monitoring of organ function. These insights underscore the critical role of individualised care in enhancing the prognosis of surgical patients with abdominal sepsis.

ChiCTR2400081823.

Background: Takotsubo Syndrome (TTS) is a transient left ventricular systolic dysfunction typically characterized by anteroseptal-apical dyskinetic ballooning of the left ventricle with a hyperkinetic base, without significant obstructive coronary artery disease. The interplay between systemic inflammation and hemodynamic stress in sepsis exacerbates susceptibility to TTS. We aim to investigate the characteristics and factors associated with TTS in critically ill patients with sepsis admitted to the intensive care unit. Methods: A retrospective cohort study was conducted on 361 patients admitted to the medical ICU at a tertiary care hospital in New York City. All patients underwent transthoracic echocardiography (TTE) within 72 h of sepsis diagnosis. Patients were divided into TTS and non-TTS groups. Clinical data, comorbidities, and hemodynamic parameters were extracted from electronic medical records and analysed using multivariate logistic regression to determine independent predictors of TTS. Results: Among 361 patients, 24 (6.65%) were diagnosed with TTS. Female sex (OR 3.145, 95% CI 1.099-9.003, p = 0.033) and higher shock index (OR 4.454, 95% CI 1.426-13.910, p = 0.010) were significant predictors of TTS. Individuals with ≥ 25 kg/m2 had a lower odds of developing TTS as compared to their obese counterparts (OR 0.889, 95% CI 0.815-0.969, p = 0.007). Conclusions: The findings highlight that Female sex, higher shock index and a BMI < 25 kg/m2 emerge as possible predictors for development of TTS in patients with sepsis. Further research is needed to unravel the mechanisms behind the "obesity paradox" in TTS and optimize clinical strategies for high-risk patients.

Sepsis is a life-threatening condition often associated with metabolic and acid-base imbalances. Alactic base excess (ABE) has emerged as a novel biomarker to assess metabolic disturbances in critically ill sepsis patients, but its prognostic value remains underexplored. We aimed to investigate the relationship between ABE and 30-day/90-day ICU all-cause mortality in a large sepsis cohort in the intensive care unit (ICU) setting.

This study utilised data from a large US ICU sepsis cohort. ABE was calculated as the sum of lactate and base excess (BE) values from the first day of ICU admission. Patients were divided into quartiles based on ABE values. Kaplan-Meier survival analysis, Cox proportional hazards models, and restricted cubic spline analyses were used to examine the associations between ABE and mortality outcomes. The predictive performance of ABE combined with the SOFA score was assessed using the area under the curve, Net Reclassification Improvement, and Integrated Discrimination Improvement.

17,099 patients with sepsis were included in this analysis, with median (IQR) age of 67.82 (56.80, 78.04) years and 59.7% males. Our analysis revealed a U-shaped association between ABE and 30-day and 90-day ICU all-cause mortality. Both the lowest (Q1) and highest (Q4) quartiles of ABE were linked to increased mortality risks, with 30-day mortality showing HRs of 1.27 (95% CI 1.13-1.44) for Q1 and 1.17 (95% CI 1.06-1.31) for Q4, while 90-day mortality showed HRs of 1.28 (95% CI 1.16-1.44) for Q1, 1.12 (95% CI 1.02-1.23) for Q2, and 1.22 (95% CI 1.11-1.34) for Q4. ABE demonstrated superior predictive performance for mortality compared to BE and lactate. Incorporating ABE into the SOFA score improved predictive performance, emphasizing ABE's value in better risk stratification. The identified thresholds (2.5 mmol/L for 30-day mortality and 2.2 mmol/L for 90-day mortality) indicate optimal ABE levels that may be associated with improved survival outcomes.

ABE demonstrated a U-shaped association with 30-day and 90-day ICU all-cause mortality in critically ill sepsis patients, suggesting its superiority over BE and lactate as a predictive biomarker. Incorporating ABE with the SOFA score may further enhance prognostic predictions. Further studies are needed to determine whether ABE should serve solely as a biomarker for monitoring the clinical course or could also be considered a potential therapeutic target.

Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to infection, remains the third leading cause of maternal mortality globally. Pregnancy-associated physiological adaptations predispose pregnant individuals to infection, impair maternal response to infection, affect antibiotic pharmacokinetics and metabolism, and complicate diagnosing infections and sepsis. Therefore, it is tantamount that clinicians readily recognize maternal sepsis and understand antibiotic regimens and treatment principles to avoid adverse maternal outcomes. In this article, we present an overview of the diagnosis and management of maternal sepsis and the physiological changes in pregnancy that alter antibiotic pharmacokinetics. Common microorganisms implicated in maternal sepsis are discussed with an emphasis on E. coli and Group A Streptococcus due to their prevalence and morbidity in the pregnant population. Lastly, we provide an overview of commonly used antibiotics and dosage recommendations in the treatment of maternal infection and sepsis.

Elevated central blood pressure (BP) and arterial stiffness are risk factors for cardiovascular mortality. However, their prognostic value in patients with hemodynamic shock has not been studied broadly. Evolved BP monitoring devices enable the noninvasive assessment of central BP and arterial stiffness. The objective of this study was to evaluate the prognostic value of central BP and arterial stiffness measurements, delivered by 2 noninvasive devices, in patients with septic or cardiogenic shock admitted to the intensive care unit.

This is a monocenter, prospective, cohort study.

This study was conducted in a tertiary university hospital.

We enrolled 57 patients who were admitted to the intensive care unit with septic or cardiogenic shock.

None.

Central BP and arterial stiffness indices like pulse wave velocity (PWV) and Aix were recorded with a Mobil-o-Graph 24h PWA and SphygmoCor XCEL. Age, catecholamine dosage, resuscitation incidence before inclusion, C-reactive protein, leukocytes, and creatinine were recorded as possible confounders. With regard to the confounders, central systolic BP measured in the first 24 hours, was predictive of 6-month mortality (odds ratio, 0.9; p < 0.05). Aix, recorded by Mobil-o-Graph 24h PWA, was associated with death in the first 14 days (odds ratio, 1.11; p = 0.03). An increased PWV was not associated with adverse outcomes.

Low central BP and increased Aix were linked to a higher mortality in shock patients. PWV had no prognostic value.

Sepsis-induced thrombocytopenia (SIT) is a widely accepted predictor of poor prognosis during sepsis, while the mechanism of SIT remains elusive. In this study, we revealed that SIT patients and septic mice exhibited higher levels of pro-inflammatory macrophages and phosphorylated Bruton's tyrosine kinase (p-BTK) expression in macrophages, which were closely correlated with platelet counts. Treatment with the BTK inhibitor BGB-3111 in SIT mice resulted in enhanced production of megakaryocytes and platelets. Depletion of macrophages in SIT mice and coculture experiments further confirmed the critical role of macrophages in the improvement of platelet count induced by BGB-3111. By performing single-cell RNA sequencing on bone marrow-derived cells from SIT mice, we not only confirmed the connection between macrophages and megakaryocytes influenced by BTK but also identified a potential mediation through the Rap1 signaling pathway in macrophages. Subsequent experiments in macrophages demonstrated that inhibition of BTK signaling impeded the pro-inflammatory polarization of macrophages by targeting the Rap1/NF-κB signaling pathway. In conclusion, our study highlights the crucial role of macrophages in SIT, and inhibiting phosphorylation of BTK in macrophages may alleviate SIT through the Rap1/NF-κB signaling pathway.

Sepsis is a common condition associated with significant morbidity and mortality. Emergency physicians play a key role in the diagnosis and management of this condition.

This paper evaluates key evidence-based updates concerning the management of sepsis and septic shock for the emergency clinician.

Sepsis is a life-threatening syndrome, and rapid diagnosis and management are essential. Antimicrobials should be administered as soon as possible, as delays are associated with increased mortality. Resuscitation targets include mean arterial pressure ≥ 65 mmHg, mental status, capillary refill time, lactate, and urine output. Intravenous fluid resuscitation plays an integral role in those who are fluid responsive. Balanced crystalloids and normal saline are both reasonable options for resuscitation. Early vasopressors should be initiated in those who are not fluid-responsive. Norepinephrine is the recommended first-line vasopressor, and if hypotension persists, vasopressin should be considered, followed by epinephrine. Administration of vasopressors through a peripheral 20-gauge or larger intravenous line is safe and effective. Steroids such as hydrocortisone and fludrocortisone should be considered in those with refractory septic shock.

An understanding of the recent updates in the literature concerning sepsis and septic shock can assist emergency clinicians and improve the care of these patients.

Background: Sepsis is a critical medical condition characterized by a dysregulated host response to infection. Platelet abnormalities frequently manifest in sepsis patients, but the causal role of platelets in sepsis remains unclear. This study employed a bidirectional two-sample Mendelian randomization (MR) approach to investigate the causal direction between platelets and sepsis. Methods: MR analysis was used to investigate the causal effect of four platelet traits-platelet count (PLT), platelet crit (PCT), mean platelet volume (MPV), and platelet distribution width (PDW)-on sepsis risk and prognosis. Additionally, the study explored the reverse causality, assessing the impact of sepsis on these platelet traits. Genetic variants from large-scale genome-wide association studies served as instrumental variables to infer causality. Sensitivity analyses and heterogeneity tests were conducted to ensure the validity and robustness of the results. Results: Genetically predicted decreased PCT (OR = 0.938, P = 0.044) and MPV (OR = 0.410, P = 0.006) were associated with an increased risk of sepsis. In the reverse direction, 28-day sepsis mortality was significantly associated with decreased PLT (OR = 0.986, P = 0.034). No significant causal relationships were observed between sepsis and other platelet traits. Conclusions: This study suggests a causal association between low PCT and MPV levels and increased risk of sepsis. Additionally, sepsis with a poor prognosis was causally linked to decreased PLT. These findings provide novel evidence for the causal relationship between platelet traits and sepsis.

Blood cultures are critical in diagnosing bloodstream infections and guiding the treatment of sepsis, which carries a significant mortality risk. Traditional blood culture protocols often recommend a five-day incubation period to ensure the recovery of clinically significant pathogens. However, recent evidence suggests that a shorter incubation period may be sufficient, potentially reducing laboratory workload and the recovery of contaminants.

This quality improvement project was conducted to evaluate the performance of a four-day incubation protocol using the BD BACTEC automated blood culture system in a large academic center with over 1,000 beds, processing more than 70,000 blood culture requests annually. A retrospective analysis was performed on 71,862 blood cultures processed in 2022.

Results indicated that 99.2% of all positive cultures, including those in pediatric cases, were detected within four days, with a mean time to positivity of 23.97 h. Only 0.8% of blood cultures flagged positive after the four-day mark, and these were predominantly cases with previous positive cultures or repeat cultures that did not alter patient management.

We conclude that a four-day incubation period is sufficient for the detection of clinically significant pathogens using the BD BACTEC system. This change not only optimizes laboratory operations by increasing capacity and reducing waste but also supports timely clinical decision-making.

Sepsis is an underappreciated yet severe threat to human life, marked by organ dysfunction and high mortality resulting from disordered inflammatory responses to blood infection. Unfortunately, no specific drugs are available for effective sepsis treatment. As a pivotal biomarker for sepsis, lactate levels are closely related to vascular permeability and sepsis-associated mortality. Herein, a dual-pipeline lactate removal strategy is reported from circulating blood to ameliorate vascular permeability and lipopolysaccharide (LPS)-induced sepsis. This is achieved by formulating lactate oxidase (LOX)-encapsulated hollow manganese dioxide (HMnO2) nanohybrids (LOX@HMnO2-P[5]A) bearing pillar[5]arene (P[5]A) macrocycle with excellent host-guest properties. The highly biocompatible nanohybrids enable direct lactate consumption through LOX catalytic degradation and block lactate production by P[5]A-mediated LPS trapping, allowing for dual-pipeline lactate removal to maximize the reversal of lactate-mediated vascular hyperpermeability. Besides, HMnO2 cores decompose hydrogen peroxide produced from lactate oxidation into oxygen, further contributing to lactate consumption and mitigating the hypoxic inflammatory environment. In vivo investigations demonstrate that intravenous administration of LOX@HMnO2-P[5]A nanohybrids with extended blood circulation can effectively ameliorate endothelial barrier dysfunction, inflammatory responses, and multiple organ injury, ultimately improving survival outcomes in LPS-induced sepsis. Taken together, this dual-pipeline lactate removal strategy offers a promising approach for efficient sepsis treatment.

Sepsis and septic shock are common conditions evaluated and managed in the emergency department (ED), and these conditions are associated with significant morbidity and mortality. There have been several recent updates in the literature, including guidelines, on the evaluation and diagnosis of sepsis and septic shock.

This is the first paper in a two-part series that provides emergency clinicians with evidence-based updates concerning sepsis and septic shock. This first paper focuses on evaluation and diagnosis of sepsis and septic shock.

The evaluation, diagnosis, and management of sepsis have evolved since the first definition in 1991. Current guidelines emphasize rapid diagnosis to improve patient outcomes. However, scoring systems have conflicting data for diagnosis, and sepsis should be considered in any patient with infection and abnormal vital signs, evidence of systemic inflammation (e.g., elevated white blood cell count or C-reactive protein), or evidence of end-organ dysfunction. The clinician should consider septic shock in any patient with infection and hypotension despite volume resuscitation or who require vasopressors to maintain a mean arterial pressure ≥ 65 mmHg. There are a variety of sources of sepsis but the most common include pulmonary, urinary tract, abdomen, and skin/soft tissue. Examples of other less common etiologies include the central nervous system (e.g., meningitis, encephalitis), spine (e.g., spinal epidural abscess, osteomyelitis), cardiac (e.g., endocarditis), and joints (e.g., septic arthritis). Evaluation may include biomarkers such as procalcitonin, C-reactive protein, and lactate, but these should not be used in isolation to exclude sepsis. Imaging is a key component of evaluation and should be based on the suspected source.

There have been several recent updates in the literature including guidelines concerning sepsis and septic shock; an understanding of these updates can assist emergency clinicians and improve the care of these patients.

Sepsis is a syndrome of life-threatening acute organ dysfunction caused by a dysregulated host response to infection. Sepsis-associated encephalopathy (SAE) refers to the diffuse brain dysfunction observed in sepsis cases, clinically characterized by a spectrum of neuropsychiatric manifestations ranging from delirium to coma. SAE is independently associated with increased short-term mortality and long-term neurological abnormalities, with currently no effective preventive or treatment strategies. The pathogenesis is intricate, involving disruptions in neurotransmitters, blood-brain barrier (BBB) breakdown, abnormal brain signal transmission, and oxidative stress, among others. These mechanisms interact or act in conjunction, contributing to the complexity of SAE. Scholars worldwide have made significant strides in understanding the pathogenesis of SAE, offering new perspectives for diagnosis and treatment. This review synthesizes recent mechanistic breakthroughs and clinical evidence to guide future research directions, particularly in targeting BBB restoration and oxidative stress.

Sepsis-associated acute kidney injury (SA-AKI) is a prevalent and severe complication in critically ill patients. However, diagnostic and therapeutic advancements have been hindered by the biological heterogeneity underlying the disease. Both transcriptomic endotyping and biomarker profiling have been proposed individually to identify molecular subtypes of sepsis and may enhance risk stratification. This study aimed to evaluate the utility of combining transcriptomic endotyping with protein-based biomarkers for improving risk stratification in SA-AKI.

This secondary analysis of the PredARRT-Sep-Trial included 167 critically ill patients who met Sepsis-3 criteria. Patients were stratified into three transcriptomic endotypes-inflammopathic (IE), adaptive (AE), and coagulopathic (CE)-using a validated whole-blood gene expression classifier. Eight protein-based biomarkers encompassing kidney function, vascular integrity, and immune response were measured. Predictive performance for the primary endpoint kidney replacement therapy or death was assessed using receiver operating characteristic curve analysis and logistic regression models.

Stratification into transcriptomic endotypes assigned 33% of patients to IE, 42% to AE, and 24% to CE. Patients classified as IE exhibited the highest disease severity and were most likely to meet the primary endpoint (30%), compared to AE and CE (17% and 10%, respectively). Kidney function biomarkers showed stepwise increases with AKI severity across all endotypes, whereas non-functional biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], soluble urokinase plasminogen activator receptor [suPAR], and bioactive adrenomedullin [bio-ADM]) exhibited endotype-specific differences independent of AKI severity. NGAL and suPAR levels were disproportionately elevated in the IE group, suggesting a dominant role of innate immune dysregulation in this endotype. In contrast, bio-ADM, a marker of endothelial dysfunction, was the strongest risk-predictor of outcomes in CE. The combination of transcriptomic endotyping with protein-based biomarkers enhanced predictive accuracy for the primary endpoint and 7-day mortality, with the highest area under the receiver operating characteristic curve of 0.80 (95% CI 0.72-0.88) for endotyping + bio-ADM and 0.85 (95% CI 0.78-0.93) for endotyping and suPAR, respectively. Combinations of endotyping with functional and non-functional biomarkers particularly improved mortality-related risk stratification.

Combining transcriptomic endotyping with protein-based biomarker profiling enhances risk-stratification in SA-AKI, offering a promising strategy for personalized treatment and trial enrichment in the future. Further research should validate these findings and explore therapeutic applications.

This study aims to predict and diagnose pediatric septic shock through the screening of immune infiltration-related biomarkers. Three gene expression datasets were accessible from the Gene Expression Omnibus repository. The differentially expressed genes were identified using the R 4.3.2 ( https://www.r-project.org/ ), followed by gene set enrichment analysis. Thereafter, the genes were identified utilizing machine-learning algorithms. The receiver operating characteristic curve was employed to assess the discrimination and effectiveness of the hub genes. The inflammatory and immune status of pediatric septic shock was evaluated through cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT). The correlation between diagnostic markers and infiltrating immune cells was further examined. Overall, we detected 12 differentially expressed genes. CD177, MCEMP1, MMP8, and OLAH were examined as diagnostic indicators for pediatric septic shock, revealing statistically significant differences (P < 0.01) and diagnostic efficacy in the validation cohort. The immune cell infiltration analysis suggests that various immune cells may contribute to the onset of pediatric septic shock. Furthermore, all diagnostic characteristics may exhibit varying degrees of correlation with immune cells. This study identifies four potential biomarkers-CD177, MCEMP1, MMP8, and OLAH-that provide diagnostic value and novel insights into immune dysregulation in pediatric septic shock. Through the integration of bioinformatics and machine learning methodologies, we offer a novel perspective on the immune mechanisms involved in pediatric septic shock, potentially facilitating more targeted and personalized therapies for individual patients.

Septic shock is commonly associated with reduction in vasomotor tone, mainly due to vascular hyporesponsiveness to norepinephrine (NE). Although the diastolic arterial pressure (DAP)/heart rate (HR) ratio reflects vasomotor tone, it cannot be a reliable index of vascular responsiveness to NE (VNERi). We hypothesized that adjusting DAP/HR for the NE dose could yield a VNERi value (VNERi = DAP/(NE dose x HR)), knowledge of which can help guiding therapeutic strategies in cases of persistent hypotension despite NE (e.g., increasing NE doses vs. introducing additional vasopressors). For our hypothesis be valid, at least VNERi should demonstrate a stronger association with patient outcome than DAP, DAP/HR or mean arterial pressure (MAP)/NE dose, a global marker of NE responsiveness.

We conducted a post-hoc analysis of the ANDROMEDA-SHOCK database. Hemodynamic variables and initial NE doses were recorded at the randomization time-point, within 4 h of septic shock diagnosis. NE doses were expressed in µg/kg/min (using the bitartrate NE formulation). A multivariate model was employed to compare the associations between these variables and key clinical outcomes, including in-hospital mortality, numbers of vasopressor-free days and of renal replacement therapy (RRT)-free days up to day 28.

The ANDROMEDA-SHOCK database included 424 patients with septic shock receiving NE. The median DAP was 52 mmHg [IQR: 45-50] and the median NE dose at inclusion was 0.2 µg/kg/min [IQR: 01-0.4]. In-hospital mortality was 43%. VNERi demonstrated the strongest association with in-hospital mortality compared to DAP, DAP/HR, and MAP/NE dose, emerging as the most significant covariate in the multivariate model. Similar findings were found for the associations with numbers of vasopressor-free days and RRT-free days up to day 28. The model revealed an inverted J-shaped relationship between in-hospital mortality and VNERi, with a nadir point at 6.7, below which mortality increased.

In patients receiving NE during early septic shock, VNERi demonstrated the strongest association with outcome compared to DAP, DAP/HR, and MAP/NE dose. Due to its physiological basis and robust association with outcomes, VNERi may serve as a valuable bedside marker of the vascular responsiveness to NE. This index could potentially be integrated into decision-making of early septic shock.

Fluid replacement is the primary treatment for life-threatening shock but is challenging in harsh environments. This study explores low-intensity pulsed ultrasound (LIPUS) as a resuscitation strategy. Cervical LIPUS stimulation effectively elevated blood pressure in shocked rats. It also improved cerebral and multiorgan perfusion. Mechanistically, LIPUS activated pathways related to sympathetic nerve excitation and vascular smooth muscle contraction, increasing plasma catecholamines and stimulating blood pressure-regulating neural nuclei. Partial sympathetic nerve transection reduced LIPUS efficacy, while complete inhibition of these nuclei abolished the response. Preliminary clinical trials demonstrated LIPUS's ability to raise blood pressure in shock patients. The findings suggest that LIPUS enhances sympathetic nerve activity and activates blood pressure-regulating nuclei, offering a noninvasive, neuromodulation-based approach to shock treatment. This method holds potential for improving blood pressure and organ perfusion in shock patients, especially in resource-limited environments.

The aim of this study was to develop a valuable clinical prediction model for pneumonia-associated bloodstream infections (PABSIs).

The study retrospectively collected clinical data of pneumonia patients at the First Medical Centre of the Chinese People's Liberation Army General Hospital from 2019 to 2024. Patients who met the definition of pneumonia-associated bloodstream infections (PABSIs) were selected as the main research subjects. A prediction model for the probability of bloodstream infections (BSIs) in pneumonia patients was constructed using a combination of LASSO regression and logistic regression. The performance of the model was verified using several indicators, including receiver operating characteristic (ROC) curve, calibration curve, decision curve analysis (DCA) and cross validation.

A total of 423 patients with confirmed pneumonia were included in the study, in accordance with the Inclusion Criteria and Exclusion Criteria. Of the patients included in the study, 73 developed a related bloodstream infection (BSI). A prediction model was constructed based on six predictors: long-term antibiotic use, invasive mechanical ventilation, glucocorticoids, urinary catheterization, vasoactive drugs, and central venous catheter placement. The areas under the curve (AUC) of the training set and validation set were 0.83 and 0.80, respectively, and the calibration curve demonstrated satisfactory agreement between the two.

This study has successfully constructed a prediction model for bloodstream infections associated with pneumonia cases, which has good stability and predictability and can help guide clinical work.

Polymethyl methacrylate (PMMA) membranes are increasingly recognized for their effectiveness in treating acute kidney injury (AKI) due to their strong adsorption capabilities, particularly for inflammatory mediators like β2-microglobulin and IL-6. These membranes ensure mechanical stability and chemical inertness, minimizing adverse reactions during blood filtration.

In acute conditions such as sepsis and acute respiratory distress syndrome (ARDS), PMMA membranes show promising findings. In sepsis, they may help reduce multiorgan failure by modulating immune responses, although further research is needed to confirm their routine use. For ARDS, PMMA membranes could mitigate "cytokine storms" by adsorbing key cytokines, improving oxygenation and hemodynamic stability, which may reduce ICU stays and reliance on mechanical ventilation. Monitoring biomarkers like IL-6, TNF-α is critical for tracking efficacy and tailoring therapy to individual needs. In chronic conditions, such as hemodialysis for chronic kidney disease, PMMA membranes help lower oxidative stress and β2-microglobulin levels, reducing complications such as amyloidosis. By decreasing oxidative damage, they provide long-term protective benefits for dialysis patients.

While these advantages are notable, large-scale studies are needed to establish PMMA's efficacy, refine treatment protocols, and confirm its broader role in acute and chronic disease management. The potential of PMMA membranes highlights their value, but standardized clinical evidence is necessary for widespread adoption.

Ischemia-reperfusion injury (IRI) is a critical condition that poses a significant threat to patient safety. The production of lactate increases during the process of IRI, and lactate serves as a crucial indicator for assessing the severity of such injury. Lactylation, a newly discovered post-translational modification in 2019, is induced by lactic acid and predominantly occurs on lysine residues of histone or nonhistone proteins. Extensive studies have demonstrated the pivotal role of lactylation in the pathogenesis and progression of various diseases, including melanoma, myocardial infarction, hepatocellular carcinoma, Alzheimer's disease, and nonalcoholic fatty liver disease. Additionally, a marked correlation between lactylation and inflammation has been observed. This article provides a comprehensive review of the mechanism underlying lactylation in IRI to establish a theoretical foundation for better understanding the interplay between lactylation and IRI.