Transfusion-related acute lung injury is seen following the transfusion of
blood components. The reported incidence is approximately 1 in 2000 transfu
sions. Clinically, it is similar to adult respiratory distress syndrome. Th
e pathophysiology is unclear but has been attributed to HLA antibodies, gra
nulocyte antibodies, and more recently to biologically active mediators in
stored blood components. We report a case with laboratory evidence that sup
ports the role of biologically active mediators in the pathogenesis of tran
sfusion-related acute lung injury. To our knowledge, the case reported here
is the first to use lipid extractions of patient samples to determine that
lipid-priming activity was present at the time transfusion-related acute l
ung injury was identified clinically.