The lung appears to be the main site for leukocyte activation and bears the majority of tissue damage in TRALI. Possible explanations for this include that the pulmonary microcirculation is the first to encounter transfusion-associated antibodies or immune complexes and that it also contains pulmonary macrophages that can become activated.
The pathogenesis of TRALI depends on the blood product transfused, the underlying mechanism, and “threshold effects” that (may) allow more than 1 mechanism to participate in the lung injury. Nearly all plasma-containing blood products and a variety of blood components have been implicated in TRALI pathogenesis, including whole blood, packed RBC, FFP, platelet concentrates or apheresis, granulocytes, cryoprecipitate, intravenous immunoglobulin, and bone marrow stem cells. Generally, TRALI reactions have not been attributed to washed red cells, albumin, and clotting factor concentrates.
The EHN (European Haemovigilance Network) subtypes TRALI based on underlying mechanism into immune (antibody mediated) or nonimmune TRALI (non-antibody mediated). Others, however, favor a “Two hit” model of TRALI pathogenesis that can apply to both antibody mediated and non-antibody mediated TRALI cases.
Ref: Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008
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