D. Vitharana1, J. Dennis1, S. Trinh1, P. Deville1, F. Rais1, C. Ramos1, J. Robinson1, J. Duchesne2, P. Greiffenstein1, A. Smith1 2Tulane University School Of Medicine, New Orleans, LA, USA 1Louisiana State University Health Sciences Center, Surgery, New Orleans, LA, USA
Introduction:
Lactate is both a pro- and anti-inflammatory mediator in the inflammatory cascade. In trauma, lactic acidosis has been associated with a robust inflammatory response and poorer outcomes. However, its effect on cytokine production following trauma has not been elucidated. The aim of this study was to investigate how lactic acidosis affects cytokine production in peritoneal fluid of trauma patients. It was hypothesized that peritoneal fluid cytokine levels differ in patients with elevated lactate on admission.
Methods:
Peritoneal fluid was collected from adult patients undergoing damage control laparotomy at a Level 1 Trauma Center following blunt or penetrating trauma. Cytokine levels in the peritoneal fluid collected were measured using a 10 analyte multiplex assay. Patients were then stratified by lactate levels, with lactate above 2 mmol/L being defined as elevated. Univariate analyses were used to compare the two groups.
Results:
Of the 14 patients studied, 9 patients (64.3%) had a lactic acidosis on admission. No significant differences in baseline demographics between the groups (age, sex, race, BMI, and mechanism of injury) were observed (p > 0.05). IFN-γ was significantly higher in patients with lactic acidosis compared to those without (2.2 and 0.71 pg/mL respectively, p < 0.05). No significant differences in IL-4, IL-6, IL-1ß, IL-8, IL-10, IL-17A, MCP-1, and VEGF levels were observed (p > 0.05). Increased mortality (n = 2, p = 0.51) and prolonged admission (33 ± 30.3 days, p = 0.40) were observed in the lactic acidosis group, however neither were statistically significant.
Conclusion:
The results from this study suggest that lactic acidosis in trauma patients may alter cytokine levels, specifically IFN-γ, a potent pro-inflammatory mediator. IFN-γ activates macrophages to promote phagocytosis and killing of intracellular pathogens and plays an integral role in the pro-inflammatory cascade. Further investigation into the role of lactate as an inflammatory modulator in the setting of trauma may enable the development of treatments to counteract the profound inflammatory response in this population.