TRALI: Risk Factors

Basic, Organ-Based and Clinical Sciences

TRALI is thought to occur via a “two-hit” process, with the first hit being due to recipient factors, such as an underlying proinflammatory state, and the second hit being due to the transfusion itself. Risk factors can thus be divided into recipient (i.e. pre-transfusion) risk factors and blood component risk factors, respectively. Recipient risk factors include higher pre-transfusion plasma interleukin-8 levels (reflecting a proinflammatory state), current smoker, increased age, chronic alcohol abuse, end-stage liver disease, hematologic malignancy, thrombotic microangiopathy, cardiac surgery, liver transplant surgery, surgery requiring multiple transfusions, positive fluid balance, higher APACHE II score, postpartum hemorrhage, and mechanical ventilation with peak airway pressure > 30 cm H2O. Furthermore, sepsis and non-cardiogenic shock, which are also known risk factors for ARDS, put the patient at additional risk of TRALI [2,3]. Notably, most recipient factors associated with TRALI have not been consistently found across all studies, which may be explained by differences in study design, differing mixes of TRALI and pTRALI, prospective versus retrospective studies, and active versus passive reporting [2].

Risk mitigation strategies thus include both optimization of recipient status (such as judicious fluid use) as well as transfusion risk factors. This includes judicious blood product use, avoidance of donors implicated in a TRALI reaction, avoidance of donors more likely to be alloimmunized to leukocytes (such as multiparous females), testing of multiparous apheresis donors of plasma or platelets for anti-HLA antibodies, and use of a solvent/detergent-treated plasma product in place of FFP [4].


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Tyler Johnson, MD