Etiology and Risk Factors
The etiology of TRALI is currently not fully understood. TRALI is thought to be immune mediated. Antibodies directed toward Human Leukocyte Antigens (HLA) or Human Neutrophil Antigens (HNA) have been implicated. Women who are multiparous (have had more than one child) develop these antibodies through exposure to fetal blood; transfusion of blood components obtained from these donors is thought to carry a higher risk of inducing immune-mediated TRALI. Previous transfusion or transplantation can also lead to donor sensitization. To be at risk of TRALI via this mechanism, the blood recipient must express the specific HLA or neutrophil receptors to which the implicated donor has formed antibodies. A two-hit hypothesis has been suggested wherein pre-existing pulmonary pathology (i.e. the first-hit) leads to localization of neutrophils to the pulmonary microvasculature. The second hit occurs when the aforementioned antibodies are transfused and attach to and activate neutrophils, leading to release of cytokines and vasoactive substances that induce non-cardiac pulmonary edema.
A non-immune mechanism has been studied and proposed by Silliman, involving the accumulation of bioactive lipids in stored blood components (red cells, platelets, plasma) that possess neutrophil priming capabilities.
TRALI is typically associated with plasma products such as FFP, but can also occur in recipients of packed red blood cells due to the residual plasma present in the unit. The AABB (formerly the American Association of Blood Banks) recommended on 11/03/2006 in association bulletin 06-07 that blood banks use high plasma volume components from female donors for further manufacturing instead of transfusion due to the higher risk of TRALI.
Read more about this topic: Transfusion Related Acute Lung Injury
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