Transfusion-related acute lung injury (TRALI) is an acute lung injury (defined as PaO2/FiO2 ratio of less than 300 mm Hg in the setting of bilateral noncardiogenic pulmonary infiltrates on radiographic imaging) that occurs within 6 hours after a transfusion ends. It has been described with all products that contain plasma, but is most common after transfusion of fresh frozen plasma (FFP). There are currently two accepted models of TRALI pathophysiology: the "antibody-mediated" and the "two-hit" models. In the antibody-mediated model, anti-HLA (human leukocyte antigen) and anti-HNA (human neutrophil antigen) antibodies in donor plasma activate recipient macrophages and neutrophils, respectively. This triggers an inflammatory cascade that creates nonhydrostatic pulmonary edema and eventual respiratory failure. In the two-hit model, a first insult (e.g., sepsis, trauma, etc.) leads to lung injury and neutrophil sequestration within the lungs. The second hit is the transfusion itself, in which lipid degradation products from the transfused plasma activate the sequestered neutrophils. Again, nonhydrostatic pulmonary edema and respiratory failure ensues. A 2007 study identified FFP as most likely to lead to TRALI, followed by platelets, and then by PRBCs. TRALI has been infrequently described after transfusion of cryoprecipitate or IV immunoglobulin, though it can occur. Ultimately, the larger plasma volume associated with FFP and platelets leads to an increased risk of TRALI.