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The objective of this review is to present the two-event model of transfusion-related acute lung injury (TRALI), a life-threatening complication of transfusions that has been the most common cause of transfusion-related death over the past 2 yrs in the United States. The two-event model of TRALI, which is identical to the pathogenesis of the acute respiratory distress syndrome (ARDS), is reviewed and contrasted to antibody-mediated TRALI. Laboratory studies, both in vitro and in vivo, are discussed as well as human studies of TRALI. Methods to avoid patient exposure to blood components that may cause TRALI are also discussed. [ABSTRACT FROM AUTHOR]

Objective: To determine whether prehospital antiplatelet therapy was associated with reduced incidence of acute lung dysfunction, multiple organ failure, and mortality in blunt trauma patients., Design: Secondary analysis of a cohort enrolled in the National Institute of General Medical Sciences Trauma Glue Grant database., Setting: Multicenter study including nine U.S. level-1 trauma centers., Patients: A total of 839 severely injured blunt trauma patients at risk for multiple organ failure (age > 45 yr, base deficit > 6 mEq/L or systolic blood pressure < 90 mm Hg, who received a blood transfusion). Severe/isolated head injuries were excluded., Measurements and Main Results: Primary outcomes were lung dysfunction (defined as grades 2-3 by the Denver multiple organ failure score), multiple organ failure (Denver multiple organ failure score >3), and mortality. Patients were documented as on antiplatelet therapy if taking acetylsalicylic acid, clopidogrel, and/or ticlopidine. Fifteen percent were taking antiplatelet therapy prior to injury. Median injury severity score was 30 (interquartile range 22-51), mean age 61 + 0.4 yr and median RBCs volume transfused was 1700 mL (interquartile range 800-3150 mL). Overall, 63% developed lung dysfunction, 19% had multiple organ failure, and 21% died. After adjustment for age, gender, comorbidities, blood products, crystalloid/12 hrs, presence of any head injury, injury severity score, and 12 hrs base deficit > 8 mEq/L, 12 hrs RBC transfusion was associated with a significantly smaller risk of lung dysfunction and multiple organ failure among the group receiving antiplatelet therapy compared with those not receiving it (lung dysfunction p = 0.0116, multiple organ failure p = 0.0291). In addition, antiplatelet therapy had a smaller risk (albeit not significant, p = 0.06) of death for patients receiving RBC compared to those not on antiplatelet therapy after adjustment for confounders,, Conclusions: Pre-injury antiplatelet therapy is associated with a decreased risk of lung dysfunction, multiple organ failure, and possibly mortality in high-risk blunt trauma patients who received blood transfusions. These findings suggest platelets have a role in organ dysfunction development and have potential therapeutic implications.

Objective: We hypothesized that aerosolized inhaled hypertonic saline given at the onset of resuscitation will decrease acute lung injury following hemorrhagic shock, by inhibiting the release of epithelial derived proinflammatory mediators., Design: Animal study., Setting: Animal-care facility procedure room in a medical center., Subjects: Adult male Sprague-Dawley rats., Interventions: Rats underwent hemorrhagic shock followed by 2 hrs of resuscitation and 1 hr of observation. In the study group, nebulized hypertonic saline was delivered at the end of the shock period and after 1 hr and 2 hrs of resuscitation., Measurements and Main Results: Shock provoked acute lung injury, which was attenuated with inhaled hypertonic saline (1.56 ± 0.2 mg protein/mL vs. 0.95 ± 0.3 mg protein/mL bronchoalveolar lavage fluid, shock vs. shock + hypertonic saline, p < .01). Nebulized hypertonic saline reduced inflammation (cytokine-induced neutrophil chemoattractant-1 accumulation in bronchoalveolar lavage fluid 5999 ± 1267 pg/mL vs. 3342 ± 859 pg/mL, shock vs. shock + hypertonic saline, p = .006). Additionally, nebulized hypertonic saline inhibited matrix -metalloproteinase-13 accumulation in the bronchoalveolar lavage fluid (1513 ± 337 pg/mL bronchoalveolar lavage fluid vs. 230 ± 19 pg/mL, shock vs. shock + hypertonic saline, p = .009) and pretreatment with a matrix metalloproteinase-13 inhibitor was sufficient to attenuate postshock acute lung injury (1.42 ± 0.09 mg/mL vs. 0.77 ± 0.23 mg/mL bronchoalveolar lavage protein, shock vs. shock + matrix metalloproteinase-13 inhibitor CL-82198, p = .002)., Conclusion: Inhaled hypertonic saline attenuates postshock acute lung injury by exerting an anti-inflammatory effect on the pulmonary epithelium, suggesting a new clinical strategy to treat acute lung injury/acute respiratory distress syndrome.

Unlabelled: Postinjury multiple organ failure (MOF) may result from overwhelming systemic hyperinflammation. Secretory phospholipase A2 (sPLA2) produces many inflammatory lipid mediators, and levels have been correlated with both the severity of patient injury and postinjury mortality. The objective of this study was to characterize the plasma activity of sPLA2 type IIa in severely injured patients and to determine whether the activity of this enzyme correlates with the subsequent development of MOF., Patients: Seventeen severely injured patients at known risk for MOF had blood sampled on postinjury days 0, 1, 2, 3, and 5., Design: sPLA2 activity was sequentially measured and correlated with MOF scores., Results: Six patients (35%) developed MOF. In comparison with non-MOF patients, MOF patients had elevated sPLA2 activity beginning 36 hrs postinjury (MOF sPLA2, 2.4 +/- 0.97, vs. non-MOF sPLA2, 0.86 +/- 0.16 active units (AU); p < .05) and continuing over the ensuing 5 days. To rule out the possibility that stored blood components required for patient resuscitation was the source of sPLA2, the sPLA2 was measured in packed red blood cells, platelet concentrates, and fresh frozen plasma over the routine storage time. None of the products tested had elevated levels of sPLA2 compared with fresh plasma from healthy adult volunteers., Conclusions: We conclude that increased sPLA2 activity is associated with the development of postinjury MOF.