World journal of emergency medicine最新文献

Background: The lack of a stable, easy-to-operate animal model for severe trauma has hindered the research progress. The aim of this study is to develop a mouse model that replicates the pathophysiological conditions of severe trauma, providing a reliable research tool.

Methods: Male C57BL/6J mice (aged 8-10 weeks and weighting approximately 20 g) were used to establish the severe trauma model. Under anesthesia, a midshaft femoral fracture was created and packed with sterile cotton. A midline incision was made from the inguinal region to the sternum, exposing the abdominal organs for 30 min. The right femoral artery was cannulated to induce controlled blood loss at 30%, 35%, 40%, and 50% of the total blood volume. Survival rates were monitored for 24 h post-induction. In the mice that experienced 30% blood loss, the mean arterial pressure, body temperature, blood gas parameters, peripheral blood inflammatory markers, and major organ pathological changes were assessed.

Results: Mice with femoral fractures, soft tissue injuries, abdominal organ exposure, and 30% blood loss exhibited stable survival rates. Increased blood loss significantly reduced survival rates. Mean arterial pressure decreased initially, recovering within 0-15 min and returning to baseline by 50 min. Similarly, the body temperature decreased initially and gradually recovered to baseline within 50 min. Levels of peripheral blood inflammatory markers remained elevated for 12 h post-injury. Distant organs, including intestines, lungs, liver, spleen and kidneys, displayed varying degrees of injury.

Conclusion: The established mouse model replicates the pathophysiological responses to severe trauma, indicating stability and reproducibility, which could be an useful tool for further trauma research.

Background: Electrolyte imbalance is common following traumatic brain injury (TBI) and can significantly impact patient outcomes. We aimed to explore the occurrence, patterns, and consequences of electrolyte imbalance in adult patients with TBI.

Methods: A retrospective study was conducted from 2016 to 2021 at a level 1 trauma center among hospitalized TBI patients. On admission, the levels of serum electrolytes, including sodium, potassium, calcium, magnesium, and phosphate, were analyzed. Demographics, injury characteristics, and interventions were assessed. The primary outcome was the in-hospital mortality. Multivariate logistic regression analysis was performed to identify independent predictors of mortality in TBI patients.

Results: A total of 922 TBI patients were included in the analysis, of whom 902 (98%) had electrolyte imbalance. The mean age of patients with electrolyte imbalance was 32.0±15.0 years. Most patients were males (94%). The most common electrolyte abnormalities were hypocalcemia, hypophosphatemia, and hypokalemia. The overall in-hospital mortality rate was 22% in the entire cohort. In multivariate logistic analysis, the predictors of mortality included age (odds ratio [OR]=1.029, 95% confidence intervals [CI]: 1.013-1.046, P<0.001), low GCS (OR=0.883, 95%CI: 0.816-0.956, P=0.002), high Injury Severity Score (ISS) scale (OR=1.051, 95%CI: 1.026-1.078, P<0.001), hypernatremia (OR=2.175, 95%CI: 1.196-3.955, P=0.011), hyperkalemia (OR=4.862, 95%CI: 1.222-19.347; P=0.025), low serum bicarbonate levels (OR=0.926, 95%CI: 0.868-0.988, P=0.020), high serum lactate levels (OR=1.128, 95%CI: 1.022-1.244, P=0.017), high glucose levels (OR=1.072, 95%CI: 1.014-1.133, P=0.015), a longer activated partial thromboplastin time (OR=1.054, 95%CI: 1.024-1.084, P<0.001) and higer international normalized ratio (INR) (OR=3.825, 95%CI: 1.592-9.188, P=0.003).

Conclusion: Electrolyte imbalance is common in TBI patients, with the significant prevalence of hypocalcemia, hypophosphatemia, and hypokalemia. However, hypernatremia and hyperkalemia were associated with the risk of mortality, emphasizing the need for further research to comprehend electrolyte dynamics in TBI patients.

Background: Whether lipid-modifying drugs directly impact the outcome of sepsis remains uncertain. Therefore, systematic investigations are needed to explore the potential impact of lipid-related therapies on sepsis outcomes and to elucidate the underlying mechanisms involving circulating inflammatory cytokines, which may play critical roles in the pathogenesis of sepsis. This study aimed to utilize drug-target Mendelian randomization to assess the direct causal effects of genetically proxied lipid-modifying therapies on sepsis outcomes.

Methods: First, a two-sample Mendelian randomization study was conducted to validate the causal associations among high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and sepsis. A subsequent drug-target Mendelian randomization study assessed the direct causal effects of genetically proxied lipid-modifying therapies on the risk of sepsis, sepsis-related critical care admission, and sepsis-related death. The identified lipid-modifying drug targets were subsequently explored for direct causal relationships with 36 circulating inflammatory cytokines. Finally, enrichment analyses of the identified cytokines were conducted to explore the potential relationships of lipid-modifying drugs with the inflammatory response.

Results: Genetically proxied cholesteryl ester transfer protein (CETP) inhibitors were significantly associated with sepsis-related critical care admission (OR=0.84, 95% CI [0.74, 0.95], P=0.008,) and sepsis-related death (OR=0.68, 95% CI [0.52, 0.88], P=0.004). The genetically proxied CETP inhibitors were strongly associated with the levels of 15 circulating inflammatory cytokines. Enrichment analyses indicated that CETP inhibitors may modulate inflammatory cytokines and influence the inflammatory response pathway.

Conclusion: This study supports a causal effect of genetically proxied CETP inhibitors in reducing the risk of sepsis-related critical care admission and death. These findings suggest that the underlying mechanism may involve the modulation of some circulating inflammatory cytokines, influencing the inflammatory response pathway.