Leading cause of transfusion<unk>  mortality in the US – 5-8% 
Occurs at a rate of 0.04-0.1%, or 1/5000, transfused blood components 
Higher in critically ill
Higher in critically ill
Two-hit mechanism 
Neutrophil sequestration and priming in<unk>  microvasculature
Recipient neutrophil activation by factor in the blood product (i.e. antibodies in blood component directed at recipient antigens, bioactive lipids, etc.)
Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
Leads to inflammatory pulmonary edema
Neutrophil sequestration and priming in<unk>  microvasculature
Recipient neutrophil activation by factor in the blood product (i.e. antibodies in blood component directed at recipient antigens, bioactive lipids, etc.)
Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
Leads to inflammatory pulmonary edema
Neutrophils release cytokines, reactive oxygen species, etc. that damage pulmonary capillary endothelium
Leads to inflammatory pulmonary edema
Leads to inflammatory pulmonary edema
Liver disease
Hematologic malignancy
Alcohol abuse
High peak airway pressures on mechanical ventilation
Current smoking
Positive fluid balance
Massive transfusion
Critical illness
Sepsis
Shock
Plasma or whole blood from female donor
Volume of HLA class II antibody reactive to recipient HLA antigen
Volume of transfused anti-human neutrophil antigen antibody
Highest risk components (though can occur with any, including pRBC)
Plasma
Apheresis platelet concentrates
Whole blood
Plasma
Apheresis platelet concentrates
Whole blood
Transfusion-related acute lung injury
Acute
Transfusion-associated circulatory overload
Intravascular hemolytic tranfusion reaction
Transfusion-associated graft-versus-host disease
Febrile nonhemolytic tranfusion reaction
Immune reconstitution inflammatory syndrome
Allergic tranfusion reaction