Effects of leukoreduced blood on acute lung injury after trauma: A randomized controlled trial*

Publisher Website
Google Scholar
Abstract
The requirement for a blood transfusion after trauma is associated with an increased risk of acute lung injury. Residual leukocytes contaminating red cells are potential mediators of this syndrome. The goal of this trial was to test our hypothesis that prestorage leukoreduction of blood would reduce rates of posttraumatic lung injury. Double blind, randomized, controlled clinical trial. University-affiliated level I trauma center in King County, Seattle, WA. Two hundred sixty-eight injured patients requiring red blood cell transfusion within 24 hrs of injury. Prestorage leukoreduced vs. standard allogeneic blood transfusions. We compared the incidence of acute lung injury and acute respiratory distress syndrome at early (≤72 hrs) and late (>72 hrs) time points after injury. In a subset, we compared plasma levels of surfactant protein-D and von Willebrand factor antigen between intervention arms. Rates of acute lung injury (relative risk [RR] 1.06, 95% confidence interval [CI] .69–1.640) and acute respiratory distress syndrome (RR .96, 95% CI 0.48–1.91) were not statistically different between intervention arms early after injury. Similarly, no statistically significant effect of leukoreduced transfusion on rates of acute lung injury (RR .88, 95% CI .54–1.44) or acute respiratory distress syndrome (RR .95, 95% CI .58–1.57) was observed to occur late after injury. There was no significant difference in the number of ventilator-free days or in other ventilator parameters between intervention arms. No statistically significant effect of leukoreduced blood on plasma levels of surfactant protein-D or von Willebrand factor antigen was identified. Prestorage leukoreduction had no effect on the incidence or timing of lung injury or on plasma measures of systemic alveolar and endothelial inflammation in a population of trauma patients requiring transfusion. The relationship between transfusion and lung injury is not obviously explained by mechanistic pathways involving the presence of transfused leukocytes.