Abstract
(1) Background: Current findings emphasize the potential contribution of platelets to the immunological response after severe trauma. As clinical relevance remains unclear, this study aims to analyze the correlation between platelets and lung dysfunction in severely injured patients. (2) Methods: We retrospectively enrolled all multiple trauma patients presenting to our level 1 trauma center from 2015 to 2016 with an Injury-Severity Score (ISS) ≥ 16. Apart from demographic data, platelet counts and PaO2/FiO2 as an approximate indicator for lung physiology were analyzed and correlated on subsequent days after admission. (3) Results: 83 patients with a median ISS of 22 (IQR 18–36) were included. Compared to day 1, platelet counts were decreased on day 3 (p ≤ 0.001). Platelet counts were significantly lower on day 3 in patients with an ISS ≥ 35 (p = 0.011). There were no differences regarding PaO2/FiO2 index. Correlation analysis revealed a positive link between increased platelet counts and PaO2/FiO2 index on day 1 only in severely injured patients (p = 0.007). (4) Conclusions: This work supports the concept of platelets modulating the posttraumatic immune response by affecting lung dysfunction in the early phase after multiple trauma in dependence of injury severity. Our findings contribute to the understanding of the impact of platelets on systemic processes in multiple trauma patients.
Highlights
Trauma-induced injury is the leading cause of death among people until 44 years of age in the United States as well as one of the leading global causes of death and disability [1,2]
With an Injury-Severity Score (ISS) higher than 16 and full datasets for the measurement of PaO2/FiO2 index and platelet count on subsequent days, 83 individuals were found to be appropriate for inclusion in this research
The present retrospective clinical study is the first to investigate the clinical relevance of posttraumatic platelet count, highlighting the correlation between platelets and injury-induced respiratory organ failure
Summary
Trauma-induced injury is the leading cause of death among people until 44 years of age in the United States as well as one of the leading global causes of death and disability [1,2]. Late posttraumatic mortality is caused by systemic hyperinflammation, leading to multiple organ failure (MOF) with high lethality rates up to 50% [3–6]. High intensity and disbalance of these conflicting trauma-induced inflammatory responses trigger the progress of inflammation and development of organ dysfunction and MOF [7–12]. Lung injury is frequently observed after multiple trauma and is either caused directly (e.g., thoracic trauma) or indirectly in the context of posttraumatic hyperinflammation or sepsis [13–15]. Complex intercellular pathways and various cytokines lead to increased endothelial permeability with consecutive alveolar edema and impaired gas exchange. This is followed by a local inflammation, which further contributes to cytokine release and promotes systemic inflammation leading to MOF [16–18]. Lung injury clinically manifests as acute respiratory distress syndrome (ARDS), which, according to the latest definition, consists of acute hypoxemia, conspicuous radiological investigations, and exclusion of hydrostatic edema due to cardiac failure [19]
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