[Increasing overhead ressources of the trauma room]. / Steigender Vorhalteaufwand für den Schockraum.

BACKGROUND: Every year up to 35,000 people in Germany are severely injured in accidents in traffic, during work or leisure activities. The 24-h availability of the trauma room as well as surgical and intensive care unit capacities are essential to provide optimal acute care. This study analyzed the frequency of utilization of the resource trauma room in a level I trauma center in the past. METHODS: Data of a level I trauma center from 2005 to 2016 including trauma room alerts deployed by the rescue coordination center and the number of patients found to be severely injured (ISS ≥ 16) during trauma room diagnostics were analyzed retrospectively. Additionally, alerts due to trauma mechanism, accompanying by the emergency physician, ventilation and resuscitation were evaluated via a web-based interdisciplinary care capacity system (IVENA) from 2012 to 2016. Therefore, a comparison between the number of trauma room alerts and the number of severely injured patients was performed for the time after 2012. RESULTS: For the time from 2012 to 2016, data obtained by IVENA showed a continuous increase in the number of trauma room alerts (n = 367 to n = 623). At the same time, the number of patients admitted under resuscitation (n = 15 to n = 45) as well as ventilated patients (n = 78 to n = 139) increased significantly; however, there was also an increase in the number of trauma alerts due to trauma mechanisms (n = 84 to n = 194) as well as the number of patients admitted to the trauma room not accompanied by an emergency physician (n = 38 to n = 132). The ratio between the number of trauma room alerts and severely injured patients (ISS ≥ 16) increased from 3.1 in 2012 to 5.4 in 2015 and 4.6 in 2016. CONCLUSION: The data at hand showed a constant number of severely injured trauma patients admitted to a level I trauma center over the past few years. At the same time, there was a significant increase in utilization of the trauma room; however, in a considerable number of patients admitted to the trauma room the diagnostic process resulted in non-traumatic diagnostic findings. In the analyzed cohort, especially patients admitted to the trauma room due to trauma mechanism or without an accompanying emergency physician contributed to this development, necessitating an increased operational readiness of the trauma room team.

Decreased inflammatory responses of human lung epithelial cells after ethanol exposure are mimicked by ethyl pyruvate.

BACKGROUND AND PURPOSE: Leukocyte migration into alveolar space plays a critical role in pulmonary inflammation resulting in lung injury. Acute ethanol (EtOH) exposure exerts anti-inflammatory effects. The clinical use of EtOH is critical due to its side effects. Here, we compared effects of EtOH and ethyl pyruvate (EtP) on neutrophil adhesion and activation of cultured alveolar epithelial cells (A549). EXPERIMENTAL APPROACH: Time course and dose-dependent release of interleukin- (IL-) 6 and IL-8 from A549 were measured after pretreatment of A549 with EtP (2.5-10 mM), sodium pyruvate (NaP, 10 mM), or EtOH (85-170 mM), and subsequent lipopolysaccharide or IL-1beta stimulation. Neutrophil adhesion to pretreated and stimulated A549 monolayers and CD54 surface expression were determined. KEY RESULTS: Treating A549 with EtOH or EtP reduced substantially the cytokine-induced release of IL-8 and IL-6. EtOH and EtP (but not NaP) reduced the adhesion of neutrophils to monolayers in a dose- and time-dependent fashion. CD54 expression on A549 decreased after EtOH or EtP treatment before IL-1beta stimulation. CONCLUSIONS AND IMPLICATIONS: EtP reduces secretory and adhesive potential of lung epithelial cells under inflammatory conditions. These findings suggest EtP as a potential treatment alternative that mimics the anti-inflammatory effects of EtOH in early inflammatory response in lungs.

Discrimination and calibration of a prediction model for mortality is decreased in secondary transferred patients: a validation in the TraumaRegister DGU.

INTRODUCTION: The Revised Injury Severity Classification II (RISC II) score represents a data-derived score that aims to predict mortality in severely injured patients. The aim of this study was to assess the discrimination and calibration of RISC II in secondary transferred polytrauma patients. METHODS: This study was performed on the multicentre database of the TraumaRegister DGU. Inclusion criteria included Injury Severity Score (ISS)≥9 points and complete demographic data. Exclusion criteria included patients with 'do not resuscitate' orders or late transfers (>24 hours after initial trauma). Patients were stratified based on way of admission into patients transferred to a European trauma centre after initial treatment in another hospital (group Tr) and primary admitted patients who were not transferred out (group P). The RISC II score was calculated within each group at admission after secondary transfer (group Tr) and at primary admission (group P) and compared with the observed mortality rate. The calibration and discrimination of prediction were analysed. RESULTS: Group P included 116 112 (91%) patients and group Tr included 11 604 (9%) patients. The study population was predominantly male (n=86 280, 70.1%), had a mean age of 53.2 years and a mean ISS of 20.7 points. Patients in group Tr were marginally older (54 years vs 52 years) and a had slightly higher ISS (21.5 points vs 20.1 points). Median time from accident site to hospital admission was 60 min in group P and 241 min (4 hours) in group Tr. Observed and predicted mortality based on RISC II were nearly identical in group P (10.9% and 11.0%, respectively) but predicted mortality was worse (13.4%) than observed mortality (11.1%) in group Tr. CONCLUSION: The way of admission alters the calibration of prediction models for mortality in polytrauma patients. Mortality prediction in secondary transferred polytrauma patients should be calculated separately from primary admitted polytrauma patients.

Cardiac Depression in Pigs after Multiple Trauma - Characterization of Posttraumatic Structural and Functional Alterations.

The purpose of this study was to define the relationship between cardiac depression and morphological and immunological alterations in cardiac tissue after multiple trauma. However, the mechanistic basis of depressed cardiac function after trauma is still elusive. In a porcine polytrauma model including blunt chest trauma, liver laceration, femur fracture and haemorrhage serial trans-thoracic echocardiography was performed and correlated with cellular cardiac injury as well as with the occurrence of extracellular histones in serum. Postmortem analysis of heart tissue was performed 72 h after trauma. Ejection fraction and shortening fraction of the left ventricle were significantly impaired between 4 and 27 h after trauma. H-FABP, troponin I and extracellular histones were elevated early after trauma and returned to baseline after 24 and 48 h, respectively. Furthermore, increased nitrotyrosine and Il-1ß generation and apoptosis were identified in cardiac tissue after trauma. Main structural findings revealed alteration of connexin 43 (Cx43) and co-translocation of Cx43 and zonula occludens 1 to the cytosol, reduction of α-actinin and increase of desmin in cardiomyocytes after trauma. The cellular and subcellular events demonstrated in this report may for the first time explain molecular mechanisms associated with cardiac dysfunction after multiple trauma.

Epidemiology and outcome of penetrating injuries in a Western European urban region.

PURPOSE: Severe life-threatening injuries in Western Europe are mostly caused by blunt trauma. However, penetrating trauma might be more common in urban regions, but their characteristics have not been fully elucidated. METHODS: Retrospective analysis of data from patients admitted to our urban university level I trauma center between 2008 and 2013 with suspicion of severe multiple injuries. Collection of data was performed prospectively using a PC-supported online documentation program including epidemiological, clinical and outcome parameters. RESULTS: Out of 2095 trauma room patients admitted over the 6-year time period 194 (9.3 %) suffered from penetrating trauma. The mean Injury Severity Score (ISS) was 12.3 ± 14.1 points. In 62.4 % (n = 121) the penetrating injuries were caused by interpersonal violence or attempted suicide, 98 of these by stabbing and 23 by firearms. We observed a widespread injury pattern where mainly head, thorax and abdomen were afflicted. Subgroup analysis for self-inflicted injuries showed higher ISS (19.8 ± 21.8 points) than for blunt trauma (15.5 ± 14.6 points). In 82.5 % of all penetrating trauma a surgical treatment was performed, 43.8 % of the patients received intensive care unit treatment with mean duration of 7.4 ± 9.3 days. Immediate emergency surgical treatment had to be performed in 8.0 vs. 2.3 % in blunt trauma (p < 0.001). Infectious complications of the penetrating wounds were observed in 7.8 %. CONCLUSIONS: Specific characteristics of penetrating trauma in urban regions can be identified. Compared to nationwide data, penetrating trauma was more frequent in our collective (9.3 vs. 5.0 %), which may be due to higher crime rates in urban areas. Especially, self-inflicted penetrating trauma often results in most severe injuries.

The effect of brain injury on the inflammatory response following severe trauma.

INTRODUCTION: The inflammatory response is an important part of the pathophysiology of severe injury and, in particular, of severe traumatic brain injury (TBI). This study evaluates the inflammatory course following major trauma and focuses on the effect of severe TBI on inflammatory markers. MATERIAL AND METHODS: This was a retrospective analysis of prospectively collected data in 123 severely injured (ISS ≥16) trauma patients. The study cohort was divided into patients with isolated TBI (Head AIS ≥3, all other AIS <3), polytraumatized patients with severe TBI (Head AIS ≥3; AIS of other body area ≥3; Polytrauma+TBI) and polytraumatized patients without TBI (Head AIS <3; Polytrauma). Levels of inflammatory markers (Interleukin-6 [IL-6], C-reactive Protein [CRP], leukocytes) measured upon arrival and through hospital days 1-3 were compared between the groups. RESULTS: On admission and through hospital day 3, IL-6 levels were significantly different between the 3 groups (admission: isolated TBI vs. Polytrauma+TBI vs. Polytrauma; 94±16 vs. 149±20 vs. 245±50pg/mL; p<0.05). Interleukin-6 levels peaked on hospital day 1 and declined thereafter. C-reactive protein and leukocyte counts were not significantly different between the cohorts on arrival and peaked on hospital day 2 and 1, respectively. In patients with severe TBI, admission IL-6 levels significantly predicted the development of septic complications (ROC analysis, AUC: 0.88, p=0.001, 95% CI: 0.79-0.97) and multiple organ dysfunction (ROC analysis, AUC: 0.83, p=0.001, 95% CI: 0.69-0.96). CONCLUSION: Severe TBI reduced the inflammatory response following trauma. Significant correlations between admission IL-6 values and the development of MOF, sepsis and the neurological outcome were found in patients with TBI.

Characterization of blunt chest trauma in a long-term porcine model of severe multiple trauma.

Chest trauma has a significant relevance on outcome after severe trauma. Clinically, impaired lung function typically occurs within 72 hours after trauma. However, the underlying pathophysiological mechanisms are still not fully elucidated. Therefore, we aimed to establish an experimental long-term model to investigate physiological, morphologic and inflammatory changes, after severe trauma. Male pigs (sus scrofa) sustained severe trauma (including unilateral chest trauma, femur fracture, liver laceration and hemorrhagic shock). Additionally, non-injured animals served as sham controls. Chest trauma resulted in severe lung damage on both CT and histological analyses. Furthermore, severe inflammation with a systemic increase of IL-6 (p = 0.0305) and a local increase of IL-8 in BAL (p = 0.0009) was observed. The pO2/FiO2 ratio in trauma animals decreased over the observation period (p < 0.0001) but not in the sham group (p = 0.2967). Electrical Impedance Tomography (EIT) revealed differences between the traumatized and healthy lung (p < 0.0001). In conclusion, a clinically relevant, long-term model of blunt chest trauma with concomitant injuries has been developed. This reproducible model allows to examine local and systemic consequences of trauma and is valid for investigation of potential diagnostic or therapeutic options. In this context, EIT might represent a radiation-free method for bedside diagnostics.