This is the first study to assess the association of ΔPrs with outcomes in a specific population of chest trauma patients. The main finding is that the ΔPrs value at the onset of ARDS was not associated with the duration of mechanical ventilation, mortality risk or ICU length of stay either in survival analysis or multivariate analysis. Our analysis demonstrates therefore that ΔPrs is an unreliable predictor of outcomes in this specific population.
Nowadays, ΔPrs, usually called the driving pressure, is used universally in clinical practice to reflect the mechanical stress generated by VT on the ventilated lung . ΔPrs also means respiratory system compliance for a given VT. Thus, a high ΔPrs may indicate impairment of respiratory system compliance by a decrease in the functional size of the lung. This phenomenon, called baby lung within context of ARDS, is related to alveolar collapse.
Many studies have demonstrated that ΔPrs is associated with mortality in patients with ARDS [9, 10, 18]. However, these previous studies focused on ARDS in medical settings. The morbid association between ΔPrs and mortality may nevertheless be altered in different clinical situations. Thus, De Jong et al  have reported that in obese patients with ARDS, ΔPrs was not associated with mortality. Similarly, our data suggest the absence of a relationship between ΔPrs and outcomes in the case of patients with ARDS related to trauma. One of the main physiopathological explanations for this difference observed between the medical and trauma contexts could be significant modifications of chest wall compliance related to traumatic injuries. Traumatic parietal dehiscence increases chest wall compliance, which may lead to an increase in ΔPrs . Thus, ΔPrs is a reflection of both chest wall and lung compliance and it may be directly modified by strong variation in chest wall compliance in cases of severe chest trauma. ΔPrs = chest wall driving pressure, ΔPcw + transpulmonary driving pressure, ΔPl; consequently, ΔPl would offer a better reflection of actual lung compliance and alveolar collapse . Similarly to obese patients, in chest trauma patients, much of the pressure provided by the ventilator will be used to distend the chest wall rather than the lung. Hence, there may not be an increase in transpulmonary pressure with accompanying lung overdistension. The only way to monitor the ΔPl of real interest from bench to bedside is to measure oesophageal pressure, which is a surrogate for ΔPcw. Thus, physicians may quickly differentiate a high ΔPrs due to an increase in ΔPcw, without a real lung injury, or inversely a high ΔPrs with a normal ΔPcw, a sign of lung pathology.
ARDS related to chest trauma represents a low percentage of case of ARDS and has its own specific properties . Its incidence is estimated to be between 10% and 30% of critically ill trauma patients, mainly depending on the severity of the trauma in severely injured patients. Surprisingly, trauma-related ARDS is known to be to twice less likely to lead to death than medical ARDS . Our cohort presents similar results with a low mortality rate in the ARDS group (7%). Traumatic ARDS is characterized by a typical immunological profile different from ARDS in a medical setting. The early phase following trauma is thus characterized by an important and uncontrolled inflammatory response in the lung tissues. The importance of this inflammatory response depends on the intensity of the initial trauma but also on the genetic profile of the patient. A previous work by Xiao et al.  in a severe trauma population showed that the early leukocyte genomic response was simultaneously associated with increased expression of genes involved in the systemic inflammatory, innate immune, and compensatory anti-inflammatory responses, as well as in the suppression of genes involved in adaptive immunity. All these modifications induce a massive release of damage-associated molecular pattern molecules from injured tissues . Massive release of epithelial biomarkers such as sRAGE, for example, is responsible for dysfunction of the capillary-alveolar barrier, increase in inflammation, and oxidative stress favouring fibrosis in cases of ARDS [25, 26]. These specific characteristics explain the specificities of ARDS after chest trauma, its lower lethality rate, and maybe the absence of association between ΔPrs and outcomes in the trauma context.
The present study has some limitations. First, its design was monocentric with a retrospective analysis, which limits extrapolation of the results. However, the data were collected prospectively with the ICU software, and the management of patients with ARDS was standardized according to international recommendations. Only a few data are missing regarding the driving pressure (28 of 329; 8%) in trauma patients under mechanical ventilation. Second, no threshold analysis was performed according to the ΔPrs. Patients who died from traumatic brain injury or from haemorrhagic shock in first 48 h after admission were excluded from our study. Consequently, only 15 non-survivors are present in our final analysis. This may lead to a lack of power and threshold analysis is impossible. However, previous work also used a threshold of 14 cm H2O for ΔPrs [9, 18]. Third, patients in our cohort were severely injured with a mean ISS of 32, and about 25% of the cohort also had abdominal injuries. Increase in abdominal pressure may also be involved in the change in chest wall compliance and create an analysis bias. It is therefore impossible to exclusively attribute our results only to chest injuries. However, multiple trauma is a frequent situation, which makes our study close to real life.