BackgroundOver the past, the severe thoracic trauma has had decisive influence on the outcome of multiple injured patients. Today, new therapies (e.g. extracorporeal membrane oxygenation (ECMO), protective ventilation methods and new forms of patient positioning) are available and applied regularly. What impact on the patient’s outcome does the thoracic trauma have today?MethodsProspective data collection of multiple injured patients in a level-I trauma center was performed between 2008 and 2014. Patients with an ISS ≥16 were included and divided into 2 groups: Severe thoracic trauma (STT: AISThorax ≥ 3) and mild thoracic trauma (MTT: AISThorax < 3). In addition to preclinical and trauma room care, detailed information about clinical course and outcome were assessed.ResultsIn total, 529 patients (STT: n = 317; MTT: n = 212) met the in- and exclusion criteria. The mean Injury Severity Score (ISS) was significantly higher in patients of the STT group (STT: 33.5 vs. MTT: 24.7; p < 0.001), while the RISC II Score showed no significant differences (STT: 20.0 vs. MTT: 17.1; p = 0.241). Preclinical data revealed a higher intubation rate, more chest tube insertions and a higher use of catecholamines in the STT group (p < 0.05). Clinically, we found significant differences in the duration of invasive ventilation (STT: 7.3d vs. MTT: 5.4d; p = 0.001) and ICU stay (STT: 12.3d vs. MTT: 9.4d; p < 0.001). While the complication rate was higher for the STT group (sepsis (STT: 11.4% vs. MTT: 5.7%; p = 0.017); lung failure (STT: 23.7% vs. MTT: 12.3%; p = 0,001)), neither the non-adjusted lethality rate (STT: 13.2% vs. MTT: 13.7%; p = 0.493) nor the Standardized Mortality Ratio (SMR) showed significant differences (STT: 0.66 vs. MTT: 0.80; p = 0.397). The multivariate regressive analysis confirmed that severe thoracic trauma is not an independent risk factor for lethality in our patient cohort.ConclusionDespite a higher injury severity, the extended need of emergency measures and a higher rate of complications in injured patients with severe blunt thoracic trauma, no influence on lethality can be proved. The reduction of the complication rate should be a goal for the next decades.

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Heterotopic ossification (HO) represents a common problem after tendon injury with no effective treatment yet being developed. Tenomodulin (Tnmd), the best-known mature marker for tendon lineage cells, has important effects in tendon tissue aging and function. We have reported that loss of Tnmd leads to inferior early tendon repair characterized by fibrovascular scaring and therefore hypothesized that its lack will persistently cause deficient repair during later stages. Tnmd knockout (Tnmd−/−) and wild-type (WT) animals were subjected to complete Achilles tendon surgical transection followed by end-to-end suture. Lineage tracing revealed a reduction in tendon-lineage cells marked by ScleraxisGFP, but an increase in alpha smooth muscle actin myofibroblasts in Tnmd−/− tendon scars. At the proliferative stage, more pro-inflammatory M1 macrophages and larger collagen II cartilaginous template were detected in this group. At the remodeling stage, histological scoring revealed lower repair quality in the injured Tnmd−/− tendons, which was coupled with higher HO quantified by micro-CT. Tendon biomechanical properties were compromised in both groups upon injury, however we identified an abnormal stiffening of non-injured Tnmd−/− tendons, which possessed higher static and dynamic E-moduli. Pathologically thicker and abnormally shaped collagen fibrils were observed by TEM in Tnmd−/− tendons and this, together with augmented HO, resulted in diminished running capacity of Tnmd−/− mice. These novel findings demonstrate that Tnmd plays a protecting role against trauma-induced endochondral HO and can inspire the generation of novel therapeutics to accelerate repair.

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