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Background The rationale of this study was to identify independent prognostic factors influencing the late-phase survival of polytraumatized patients defined according to the New Berlin Definition. Methods Retrospective data analysis on 173 consecutively polytraumatized patients treated at a level I trauma center between January 2012 and December 2015. Patients were classified into two groups: severely injured patients (ISS > 16) and polytraumatized patients (patients who met the diagnostic criteria for the New Berlin Definition). Results Polytraumatized patients showed significantly lower late-phase and overall survival rates. The presence of traumatic brain injury (TBI) and age > 55 years had a significant influence on the late-phase survival in polytraumatized patients but not in severely injured patients. Despite the percentage of severe TBI being nearly identical in both groups, severe TBI was identified as main cause of death in polytraumatized patients. Furthermore, severe TBI remains the main cause of death in polytraumatized patients > 55 years of age, whereas younger polytraumatized patients ( Conclusion Our results suggest that age beyond 55 years and concomitant (severe) TBI remain as most important influencing risk factor for the late-phase survival of polytraumatized patients but not in severely injured patients. Level of evidence Prognostic study, level III.

Acute respiratory distress syndrome (ARDS), which is associated with major morbidity and high mortality, is commonly developed by polytraumatized patients. Its pathogenesis is complex, and its development is difficult to anticipate, as candidate biomarkers for the prediction of ARDS were found not to be reliable for clinical use. In this prospective study, we assessed the serum antigen levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) of 28 survivors of blunt polytrauma (age ≥18 years; injury severity score ≥16) at admission and on days 1, 3, 5, 7, 10, 14, and 21 of hospitalization. Our results show that these patients presented high mean tPA and PAI-1 antigen levels at admission; despite their decline, these parameters remained elevated for 3 weeks. Over this period, the mean tPA antigen level was higher in polytrauma victims suffering from ARDS than in those without ARDS, whereas the mean PAI-1 level was higher in polytrauma victims sustaining pneumonia than in those without pneumonia. Moreover, in each individual developing ARDS, the polytrauma-related elevated tPA antigen level either continued to rise after admission or suffered a second increase up to the onset of ARDS, declining immediately thereafter. Therefore, our findings support the assessment of serum tPA antigen levels after the initial treatment of polytraumatized patients, as this parameter shows potential as a biomarker for the development of ARDS and for the consequent identification of high-risk individuals.

Background According to recently published findings, we hypothesized that serum interleukin-33 (IL-33) may qualify for predicting pulmonary complications in polytraumatized patients. Methods One hundred and thirty patients (age ≥ 18 years, ISS ≥ 16) were included in our prospective analysis after primary admission to our level I trauma center during the first post-traumatic hour. Serum samples immediately after admission and on day 2 after trauma were obtained and analyzed. Results Median initial IL-33 levels (in picograms per milliliter) were higher in polytrauma victims (1) with concomitant thoracic trauma [5.08 vs. 3.52; p = 0.036], (2) sustaining parenchymal lung injury (PLI) [5.37 vs. 3.71; p = 0.027], and (3) developing acute respiratory distress syndrome (ARDS) [6.19 vs. 4.48; p = 0.003], compared to the respective rest of the study group. The median initial IL-33 levels were higher in patients experiencing both PLI and ARDS compared to those sustaining PLI and not developing ARDS [6.99 vs. 4.69; p = 0.029]. ROC statistics provided an AUC of 0.666 (p = 0.003) and a cut-off value of 4.77 (sensitivity, 71.8%; specificity, 75.7%) for predicting ARDS. Moreover, a higher initial median IL-33 level was revealed in the deceased compared to the survivors [12.25 vs. 4.72; p = 0.021]. ROC statistics identified the initial level of IL-33 as a predictor of death with 11.19 as cut-off value (sensitivity, 80.0%; specificity, 80.0%; AUC = 0.805; p = 0.021). Conclusions Following tissue damage, IL-33 is abundantly released in the serum of polytraumatized patients immediately after their injuries occurred. As initial IL-33 levels were particularly high in individuals experiencing both PLI and ARDS, IL-33 release after trauma seems to be involved in the promotion of ARDS and might serve already at admission as a solid indicator of impending death in polytraumatized patients.