Objectives: Uncontrolled hemorrhagic shock is the leading cause of potentially preventable death in major trauma patients. Damage control resuscitation (DCR), a strategy combining the techniques of permissive hypotension, hemostatic resuscitation, and damage control surgery, has been highly recommended for trauma patients. This study investigated whether emergency department (ED) crowding was associated with poor performance of the DCR strategies in treating hemorrhagic shock trauma patients.Methods: This was a retrospective cohort study in an urban tertiary hospital conducted from January 2010 to December 2013. Major trauma patients who presented to the ED with hemorrhagic shock were included. ED crowding, measured by ED occupancy rate, was categorized into three groups (low, medium, and high). The performance of DCR and inpatient outcomes were analyzed using multivariate logistic analysis.Results: Of the 3,037 major trauma patients assessed, 852 met the inclusion criteria and were enrolled in the study. Patients in the high-crowding group had delayed initiation of transfusion (high vs. medium and low, 2.5 hours vs. 2.1 hours and 1.0 hours, respectively, p = 0.01), received less blood products in the ED (both comparisons p < 0.01), and experienced delays in procedures (4.5 hours vs. 3.3 hours and 2.4 hours, p < 0.01). However, the amount of crystalloid solution was similar among patients in all three groups (p = 0.17). In multivariate analysis, more patients from the high-crowding group developed traumatic coagulopathy in the intensive care unit (29.7% vs. 24.1% and 16.3%, p < 0.01), while no clear relationship was found between ED crowding and 30-day mortality or early lactate clearance rate (p > 0.05).

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BackgroundIncreased production of matrix metalloproteinases (MMPs) is closely related to the progression of osteoarthritis (OA). The present study was performed to investigate the potential value of biochanin A in inhibition of MMP expression in both rabbit chondrocytes and an animal model of OA.MethodsMTT assay was performed to assess chondrocyte survival in monolayers. The mRNA and protein expression of MMPs (including MMP-1, MMP-3, and MMP-13) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in interleukin-1 < beta > (IL-1β)-induced rabbit chondrocytes were determined by quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. The involvement of the NF-kappaB (NF-κB) pathway activated by IL-1β was determined by western blotting. The in vivo effects of biochanin A were evaluated by intra-articular injection in an experimental OA rabbit model induced by anterior cruciate ligament transection (ACLT).ResultsBiochanin A downregulated the expression of MMPs and upregulated TIMP-1 at both the mRNA and protein levels in IL-1β-induced chondrocytes in a dose-dependent manner. In addition, IL-1β-induced activation of NF-κB was attenuated by biochanin A, as determined by western blotting. Moreover, biochanin A decreased cartilage degradation as determined by both morphological and histological analyses in vivo.ConclusionsTaken together, these findings suggest that biochanin A may be a useful agent in the treatment and prevention of OA.

Sepsis may result in lung injury through a complex cascade of events including interstitium infiltration of inflammatory cells. Quercetin, the most abundant dietary flavonoid found in various plants and food products, possesses potent anti-inflammatory and antioxidative properties. The purpose of this study was to investigate whether preventive administration of quercetin could exert beneficial effects on experimental septic acute lung injury induced by lipopolysaccharide (LPS). C57/BL6 mice were challenged with LPS and survival time was monitored from 0-96 h after LPS treatment. Quercetin markedly rescued lethality, improved survival time, and inhibited serum necrosis factor α, interleukin 1β, and interleukin 6, and nitric oxide (NO), and increased IL-10 secretion. Moreover, quercetin decreased lung pathological changes, myeloperoxidase activity, and malondialdehyde levels. Quercetin also reduced the lung permeability changes and neutrophil and macrophage recruitment to the bronchoalveolar lavage fluid compared to the vehicle. Additionally, quercetin significantly reduced COX-2, HMGB1, iNOS expression, and NF-κB p65 phosphorylation. These results suggest that treatment with quercetin in septic mice improved survival time and lung injury. Quercetin may be a promising potential therapeutic reagent for LPS-induced acute lung injury.

Abstract:Objective: The aim of the present study was to examine dynamic changes in serum cholinesterase (ChE) activity during early-stage severe trauma and the clinical significance of these changes. Methods: This prospective, observational study included 81 patients with severe trauma who were treated between October 2011 and April 2013 in the emergency intensive care unit (EICU) of a university-affiliated, tertiary-care, grade A general hospital in China. Serum ChE activity was measured on Days 1, 3, and 7 post-injury. The correlation of dynamic changes in serum ChE activity with trauma severity and prognosis was assessed. Correlations between changes in serum ChE activity after injury and albumin (ALB), prealbumin (PAB), transferrin (TRF), and C-reactive protein (CRP) levels were also analyzed. Results: Serum ChE activity in trauma patients was 42.3%-50.2% lower on Days 1, 3, and 7 compared with the control (P<0.001 for all time points), and it continued to decrease after Day 7 in both the survival and death subgroups. In the subgroup with an injury severity score (ISS) of ≤25, serum ChE activity initially decreased, but eventually increased. However, activity decreased continuously in the ISS>25 subgroup. ChE activity was significantly lower in both the death and the ISS>25 subgroups than in the survival and ISS≤25 subgroups on Days 1, 3, and 7 after injury. Activity was negatively correlated with ISS and acute physiology and chronic health evaluation III (APACHE III) at all time points. When comparing the receiver operating characteristic (ROC) curves for predicting prognosis, the area under the curve (AUC) in the plot of serum ChE was similar to the AUCs in plots of ISS and APACHE III, but significantly smaller than the AUC in the plot of the trauma and injury severity score (TRISS). Serum ChE activity was positively correlated with ALB, PAB, and TRF at all time points post-injury. Activity was not significantly correlated with CRP on Day 1, but was significantly and negatively correlated with CRP on Days 3 and 7. Conclusions: There is a significant decrease in serum ChE activity after severe trauma. Serum ChE may be regarded as a negative acute phase protein (APP) and the dynamic changes in serum ChE may be useful as an auxiliary indicator for evaluating trauma severity and predicting prognosis.

BackgroundThe aim of this study was to investigate the effects of zinc finger protein A20 on lipopolysaccharide (LPS)-induced pulmonary inflammation/anti-inflammatory mediators in an acute lung injury/acute respiratory distress syndrome (ALI/ARDS) rat model.Material/MethodsForty-eight ALI/ARDS rats were selected and assigned into normal saline (NS) (injected with NS), LPS (injected with LPS), LPS-C1 (injected with pEGFP-C1, NS and LPS), and A20 groups (injected with pEGFP-C1-A20, NS, and LPS). The wet/dry (W/D) ratio of rat lung tissues and total protein concentration and the number of neutrophils in bronchoalveolar lavage fluid (BALF) were detected. Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR were applied to detect the protein and mRNA expressions of A20, IL-10, and TNF-α, respectively. Western blotting was employed to detect the protein expressions of A20, nuclear factor-kappa B (NF-κB) p65 and NF-κB p-P65 in rat lung tissues.ResultsCompared with the NS group, the W/D ratio of rat lung tissues and total protein concentration and the number of neutrophils in BALF in the other 3 groups increased significantly. The protein and mRNA expressions of A20, IL-10, and TNF-α were significantly higher in the LPS group than in the NS group. The protein and mRNA expressions of A20 and IL-10 were significantly up-regulated and the expression of TNF-α, NF-κB p65, and NF-κB p-P65 was significantly down-regulated in rats injected with A20 compared to those in the LPS group.ConclusionsThe study provided evidence that zinc finger protein A20 can alleviate pulmonary inflammation by inhibiting TNF-α, NF-κB p65, and NF-κB p-P65 expressions and promoting IL-10 expression.

Posttraumatic fistula between the internal pudendal artery and urethra is rarely reported in the literature. We report a case of bilateral internal pudendal artery-urethral fistula formation by pseudoaneurysm, following a blunt pelvic trauma in which superselective angiography revealed the site of bleeding. The fistula was treated with superselective arterial embolization.

Rationale:There have been occasional reports of respiratory dysfunction associated with acute chlorine gas inhalation. However, management of acute chlorine-related inhalation injury is largely empirical, supportive, and sometimes challenging.Patient concerns:A 43-year-old man was transferred to the emergency department because of accidental chlorine inhalation and rapidly progressive dyspnea.Diagnoses:The patient was diagnosed with acute respiratory distress syndrome due to chlorine gas exposure.Interventions:Because this patient had failed on conventional treatments including mechanical ventilation and high-dose intravenous corticosteroid therapy, we applied high-volume hemofiltration (HVHF).Outcomes:The patient recovered quickly after four sessions of HVHF and was discharged uneventfully on day 28.Lessons:HVHF is a potential method for improvement of chlorine-induced acute respiratory failure and worsening hypoxemia.