The term transfusion-related acute lung injury (TRALI) was coined in 1985 to describe acute respiratory distress syndrome (ARDS) after transfusion, when another ARDS risk factor was absent; TRALI cases were mostly associated with donor leukocyte antibody. In 2001, plasma from multiparous donors was implicated in TRALI in a randomized controlled trial in Sweden.
In 2003 and in many years thereafter, the U.S. Food and Drug Administration reported that TRALI was the leading cause of death from transfusion in the United States. In 2003, the United Kingdom was the first among many countries to successfully reduce TRALI using male-predominant plasma. These successes are to be celebrated. Nevertheless, questions remain about the mechanisms of non-antibody TRALI, the role of blood products in the development of ARDS in patients receiving massive transfusion, the causes of unusual TRALI cases, and how to reduce inaccurate diagnoses of TRALI in clinical practice.
Regarding the latter, a study in 2013–2015 at 169 U.S. hospitals found that many TRALI diagnoses did not meet clinical definitions. In 2019, a consensus panel established a more precise terminology for clinical diagnosis: TRALI type I and TRALI type II are cases where transfusion is the likely cause, and ARDS are cases where transfusion is not the likely cause. For accurate diagnosis using these clinical definitions, critical care or pulmonary expertise is needed to distinguish between permeability versus hydrostatic pulmonary edema, to determine whether an ARDS risk factor is present, and, if so, to determine whether respiratory function was stable within the 12 hours before transfusion.
Pulmonologists, critical care specialists, translational researchers, and clinicians
At the conclusion of this activity, learners should be able to:
- Better diagnose transfusion-related acute lung injury (TRALI) type I
- Better diagnose TRALI type II
- Better diagnose acute respiratory distress syndrome (ARDS) in a transfused patient
1.00 AMA PRA Category 1 Credit
The American Thoracic Society is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
|Credit Type||Credit/Points||Credit Designation Statement|
|AMA PRA Category 1 Credit™||1.00||The American Thoracic Society designates this Journal for a maximum of 1.00 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.|
Article Authorship Disclosures (as submitted to the ATS prior to article publication date)
Pearl Toy, M.D. (University of California San Francisco, San Francisco, CA, USA) reported receiving consulting fees from British Society for Haematology, and serving on an advisory board for Anthos.
Mark R. Looney, M.D. (University of California San Francisco, San Francisco, CA, USA) reported no relevant financial relationships.
Mark Popovsky, M.D. (Velico Medical, Beverly, MA, USA) reported no relevant financial relationships.
Miodrag Palfi, M.D., Ph.D. (Linköpings Universitet, Linköping, östergötland, Sweden) reported no relevant financial relationships.
Gösta Berlin, M.D., Ph.D. (Linköpings Universitet, Linköping, östergötland, Sweden) reported no relevant financial relationships.
Catherine E. Chapman, M.D. (NHS Blood and Transplant, Newcastle-upon-Tyne, United Kingdom) reported no relevant financial relationships.
Paula Bolton-Maggs, M.D. (Manchester Blood Center, Manchester, United Kingdom) reported receiving consulting fees from British Society for Haematology.
Michael A. Matthay, M.D. (University of California San Francisco, San Francisco, CA, USA) reported receiving grants from Genentec-Roche, and consulting fees from Citius Pharmaceuticals, Novartis Pharmaceuticals, Johnson & Johnson Pharmaceuticals, and Gilead Pharmaceuticals.
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