[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.

Sera from severe trauma patients with pneumonia and without infectious complications have differential effects on neutrophil biology.

BACKGROUND: Major trauma patients (TP) developing imbalanced immune response are at high risk for infectious post-injury complications including pneumonia. Neutrophils play a central role in the host defense against bacteria and thereby pathogenesis of infections. While there are numerous studies about neutrophil function after trauma, data about their biology in patients who suffer from pneumonia following trauma are sparse. Here, we studied the effect of serum isolated from patients who do and do not develop infection (inf.) on the biology of neutrophils from healthy volunteers. METHODS: Sera samples from eighteen TP with an injury severity score above 16 were obtained. Nine patients were grouped to no inf. group (TP without pneumonia), and nine to inf. group (TP with pneumonia). Samples were obtained at admission to emergency department (ED), a day prior pneumonia diagnosis (1 d prior inf) or at the day of diagnosis (1 d prior inf). Samples from the equal post-injury days in the corresponding no inf. group were used. Neutrophils from nine healthy volunteers were isolated. Effects for sera isolated from infected and non-infected patients on neutrophil biology were analyzed. Migratory capacity of neutrophils towards TP's serum, their CD11b and CD62L membrane receptor expression and oxidative burst activity after stimulation with TP's serum were determined and compared between groups. RESULTS: Migratory capacity of neutrophils was significantly increased after trauma and persisted during the study period. CD11b expression in all groups was significantly increased. CD62L expression decreased generally in samples from ED and recovered later to baseline. Stratifying no inf. and inf. groups showed significantly decreased migratory capacity, increased CD11b and significantly decreased CD62L expression in the no inf. group. These differences persisted during the complete observational period. ROS production was strongly reduced in the no inf. group compared to the inf. group at later experimental time points. CONCLUSIONS: This data indicate that patients at risk for pneumonia development have differentially and early activated neutrophils following trauma compared to patients who are not at risk for post-injury complication. Studies about the differential biology of neutrophils and their immediately after trauma modified activity depending on the post-injury clinical course are warranted, and may deliver predictive or even therapeutic strategies to control inflammation.

Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells.

Increases in pro-inflammatory cytokine levels and tissue-infiltrating leukocytes have been closely linked to increased systemic and local inflammation, which result in organ injury. Previously, we demonstrated the beneficial and hepatoprotective anti-inflammatory effects of acute ethanol (EtOH) ingestion in an in vivo model of acute inflammation. Due to its undesirable side-effects, however, EtOH does not represent a therapeutic option for treatment of acute inflammation. Therefore, in this study, we compared the effects of acute EtOH exposure with ethyl pyruvate (EtP) as an alternative anti-inflammatory drug in an in vitro model of hepatic and pulmonary inflammation. Human hepatocellular carcinoma cells Huh7 and alveolar epithelial cells A549 were stimulated with either interleukin (IL) IL-1ß (1 ng/ml, 24 h) or tumor necrosis factor (TNF) (10 ng/ml, 4 h), and then treated with EtP (2.5-10 mM), sodium pyruvate (NaP, 10 mM) or EtOH (85-170 mM) for 1 h. IL-6 or IL-8 release from Huh7 or A549 cells, respectively, was measured by an enzyme­linked immunosorbent assay. Neutrophil adhesion to cell monolayers and CD54 expression were also analyzed. Bcl-2 and Bax gene expression was determined by RT-qPCR, and western blot analysis was performed to determine the mechanisms involved. Treating A549 cells with either EtOH or EtP significantly reduced the IL-1ß- or TNF­induced IL-8 release, whereas treating Huh7 cells did not significantly alter IL-6 release. Similarly, neutrophil adhesion to stimulated A549 cells was significantly reduced by EtOH or EtP, whereas for Huh7 cells the tendency for reduced neutrophil adhesion rates by EtOH or EtP was not significant. CD54 expression was noticeably reduced in A549 cells, but this was not the case in Huh7 cells after treatment. The Bax/Bcl-2 ratio was dose­dependently decreased by EtOH and by high-dose EtP in A549 cells, indicating a reduction in apoptosis, whereas this effect was not observed in Huh7 cells. The underlying mechanisms involve reduced phosphorylation of Akt and nuclear factor-κB (NF-κB) p65. We noted that as with EtP, EtOH reduced the inflammatory response in lung epithelial cells under acute inflammatory conditions. However, due to the low impact which EtP and EtOH had on the hepatocellular cells, our data suggest that both substances exerted different effects depending on the cellular entity. The possible underlying mechanisms involved the downregulation of Akt and the transcription factor NF-κB, but further research on this subject is required.