World journal of emergency medicine最新文献

Background: To investigate the prognostic value of the peripheral perfusion index (PPI) in patients with septic shock.

Methods: This prospective cohort study, conducted at the emergency intensive care unit of Peking University People's Hospital, recruited 200 patients with septic shock between January 2023 and August 2023. These patients were divided into survival (n=84) and death (n=116) groups based on 28-day outcomes. Clinical evaluations included laboratory tests and clinical scores, with lactate and PPI values assessed upon admission to the emergency room and at 6 h and 12 h after admission. Risk factors associated with mortality were analyzed using univariate and multivariate Cox regression analyses. Receiver operator characteristic (ROC) curve was used to assess predictive performance. Mortality rates were compared, and Kaplan-Meier survival plots were created.

Results: Compared to the survival group, patients in the death group were older and had more severe liver damage and coagulation dysfunction, necessitating higher norepinephrine doses and increased fluid replacement. Higher lactate levels and lower PPI levels at 0 h, 6 h, and 12 h were observed in the death group. Multivariate Cox regression identified prolonged prothrombin time (PT), decreased 6-h PPI and 12-h PPI as independent risk factors for death. The area under the curves for 6-h PPI and 12-h PPI were 0.802 (95% CI 0.742-0.863, P<0.001) and 0.945 (95% CI 0.915-0.974, P<0.001), respectively, which were superior to Glasgow Coma Scale (GCS), Sequential Organ Failure Assessment (SOFA) scores (0.864 and 0.928). Cumulative mortality in the low PPI groups at 6 h and 12 h was significantly higher than in the high PPI groups (6-h PPI: 77.52% vs. 22.54%; 12-h PPI: 92.04% vs. 13.79%, P<0.001).

Conclusion: PPI may have value in predicting 28-day mortality in patients with septic shock.

Background: A pathophysiological feature of septic organ failure is endothelial dysfunction in sepsis (EDS). The physiological and pathological mechanism of sepsis is considered to be vascular leakage caused by endothelial dysfunction. These pathological changes lead to systemic organ injury. However, an analysis using bibliometric methods has not yet been conducted in the field of EDS. This study was conducted to provide an overview of knowledge structure and research trends in the field of EDS.

Methods: Based on previous research, a literature search was performed in the Web of Science Core Collection (WoSCC) for publications associated with EDS published between the year 2003 and 2023. Various types of data from the publications, such as citation frequency, authorship, keywords and highly cited articles, were extracted. The "Create Citation Report" feature in the WoSCC was employed to calculate the Hirsch index (h-index) and average citations per item (ACI) of authors, institutions, and countries. To conduct bibliometric and visualization analyses, three bibliometric tools were used, including R-bibliometrix, CiteSpace (co-citation analysis of references), and VOSviewer (co-authorship analysis of institutions, co-authorship analysis of authors, co-occurrence analysis of keywords).

Results: After excluding invalid records, the study finaly included 4,536 publications with 135,386 citations. Most of these publications originated in the USA, China, Germany, Canada, and Japan. Harvard University emerged as the most prolific institution, while professor Jong-Sup Bae and his research team at Kyungpook National University emerged as authors with the greatest influence. The "protein C", "tissue factor", "thrombin", "glycocalyx", "acute kidney injury", "syndecan-1" and "biomarker" were identified as prominent areas of research. Future research may focus on molecular mechanisms (such as as vascular endothelial [VE]-cadherin regulation) and therapeutic interventions to enhance endothelial repair and function.

Conclusion: Our findings show a growing interest in EDS research. Key areas for future research include signaling pathways, molecular mechanisms, endothelial repair, and interactions between endothelial cells and other cell types in sepsis.

Background: Patients who present to the emergency department (ED) for suspected pulmonary embolism (PE) are often on active oral anticoagulation (AC). However, the diagnostic yield of computed tomography pulmonary angiography (CTPA) in screening for PE in patients who present on AC has not been well characterized. We aim to investigate the diagnostic yield of CTPA in diagnosing PE depending on AC status.

Methods: We reviewed and analyzed the electronic medical records of patients who underwent CTPA for PE at a university hospital ED from June 1, 2019, to March 25, 2022. Primary outcome was the incidence of PE on CTPA depending on baseline AC status and indication for AC.

Results: Of 2,846 patients, 242 were on AC for a history of venous thromboembolism (VTE), 210 were on AC for other indications, and 2,394 were not on AC. The incidence of PE on CTPA was significantly lower in patients on AC for other indications (5.7%) when compared to patients on AC for prior VTE (24.3%) and patients not on AC at presentation (9.8%) (P<0.001). In multivariable analysis among the whole cohort, AC was associated with a positive CTPA (odds ratio [OR] 0.26, 95% confidence interval [CI]: 0.15-0.45, P<0.001).

Conclusion: The incidence of PE among patients undergoing CTPA in the ED is lower in patients previously on AC for indications other than VTE when compared to those not on AC or those on AC for history of VTE. AC status and indication for AC may affect pre-test probability of a positive CTPA, and AC status therefore warrants consideration as part of future diagnostic algorithms among patients with suspected PE.

Background: The molecular mechanism of sepsis-associated acute kidney injury (SA-AKI) is unclear. We analyzed co-differentially expressed genes (co-DEGs) to elucidate the underlying mechanism and intervention targets of SA-AKI.

Methods: The microarray datasets GSE65682, GSE30718, and GSE174220 were downloaded from the Gene Expression Omnibus (GEO) database. We identified the co-DEGs and constructed a gene co-expression network to screen the hub genes. We analyzed immune correlations and disease correlations and performed functional annotation of the hub genes. We also performed single-cell and microenvironment analyses and investigated the enrichment pathways and the main transcription factors. Finally, we conducted a correlation analysis to evaluate the role of the hub genes.

Results: Interleukin 32 (IL32) was identified as the hub gene in SA-AKI, and the main enriched signaling pathways were associated with hemopoiesis, cellular response to cytokine stimulus, inflammatory response, and regulation of kidney development. Additionally, IL32 was significantly associated with mortality in SA-AKI patients. Monocytes, macrophages, T cells, and NK cells were closely related to IL32 and were involved in the immune microenvironment in SA-AKI patients. IL32 expression increased significantly in the kidney of septic mouse. Toll-like receptor 2 (TLR2) was significantly and negatively correlated with IL32.

Conclusion: IL32 is the key gene involved in SA-AKI and is significantly associated with prognosis. TLR2 and relevant immune cells are closely related to key genes.

Background: Ischemic stroke refers to a disorder in the blood supply to a local area of brain tissue for various reasons and is characterized by high morbidity, mortality, and disability. Early reperfusion of brain tissue at risk of injury is crucial for the treatment of acute ischemic stroke. The purpose of this study was to evaluate comfort levels in managing acute stroke patients with hypoxemia who required endotracheal intubation after multidisciplinary in situ simulation training and to shorten the door-to-image time.

Methods: This quality improvement project utilized a comprehensive multidisciplinary in situ simulation exercise. A total of 53 participants completed the two-day in situ simulation training. The main outcome was the self-reported comfort levels of participants in managing acute stroke patients with hypoxemia requiring endotracheal intubation before and after simulation training. A 5-point Likert scale was used to measure participant comfort. A paired-sample t-test was used to compare the mean self-reported comfort scores of participants, as well as the endotracheal intubation time and door-to-image time on the first and second days of in situ simulation training. The door-to-image time before and after the training was also recorded.

Results: The findings indicated that in situ simulation training could enhance participant comfort when managing acute stroke patients with hypoxemia who required endotracheal intubation and shorten door-to-image time. For the emergency management of hypoxemia or tracheal intubation, the mean post-training self-reported comfort score was significantly higher than the mean pre-training comfort score (hypoxemia: 4.53±0.64 vs. 3.62±0.69, t= -11.046, P<0.001; tracheal intubation: 3.98±0.72 vs. 3.43±0.72, t= -6.940, P<0.001). We also observed a decrease in the tracheal intubation and door-to-image time and a decreasing trend in the door-to-image time, which continued after the training.

Conclusion: Our study demonstrates that the implementation of in situ simulation training in a clinical environment with a multidisciplinary approach may improve the ability and confidence of stroke team members, optimize the first-aid process, and effectively shorten the door-to-image time of stroke patients with emergency complications.