Book review

Article Outline

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THIS IS AN up-to-date text on transfusion-related acute lung injury (TRALI) by 2 individuals well versed in the field, Dr Steven Kleinman and Dr Mark Popovsky. They have assembled a number of transfusion medicine specialists to author most of the chapters and provide a comprehensive overview of TRALI. The chapters tend to be well referenced and are nicely illustrated; however, there is some duplication between chapters. Especially useful is a table, in chapter 2, on the differential diagnosis of pulmonary transfusion reactions.

Although the 2 proposed mechanisms for TRALI are carefully evaluated, the evidence for leukocyte antibodies as the main cause of TRALI is most compelling. Thus, various studies cited that 61% to 90% of blood components implicated in TRALI events have detectable leukocyte antibodies. When not found in the donors, they are sometimes detected in patients reacting with the leukocytes present in a nonleukoreduced transfused component. Further, TRALI has been elicited in healthy volunteers infused with leukocyte antibody–containing components, showing that this is sufficient to cause a TRALI event without invoking some underlying disease or associated clinical condition. Bioactive lipids in a “2-hit” model of TRALI may explain some cases of TRALI where red blood cell (RBC) concentrates near their outdate are implicated and no leukocyte antibodies can be identified in the blood component associated with that TRALI event. This mechanism however does not explain cases wherein plasma-only or plasma-rich components alone appear to cause a TRALI event. This occurs even if leukocyte antibodies are not found; assuming a thorough search had been made for the latter.

There are some flaws and missing items in this otherwise authoritative work. These include (a) a critical assessment as to why TRALI does not result when leukocyte antibodies are transfused to a blood component recipient whose leukocytes bear the cognate antigen; (b) a discussion of the relevance of the brain natriuretic peptide, which is now referred to as B or beta natriuretic peptide and other similar or related peptides that have been described; (c) the reason why only the lungs appear to be affected during TRALI-related events; (d) why only the transplanted lung was affected in the case reported by Dykes et al (Br J Haematol 2000;109:674-676) is not explained; (e) possible approaches to reducing the risk of TRALI should have been more thoroughly covered, especially for platelets and RBC transfusions; (f) the use of platelet additive solutions, RBC additive solutions, leukoreduction, pathogen reduction processes, and pooling plasma before viral inactivation processes should also have been mentioned; and most importantly, (g) communication with implicated donors, for example, sample letters and a discussion of their impact on donors, should have been presented.

Overall, TRALI: Mechanisms, Management, and Prevention is a good review and summary of this important topic. With the publication of this book, much current information on TRALI is now available in a single volume.