Transfusion-related acute lung injury is the leading cause of mortality following transfusion of blood components. Its characteristic feature is acute hypoxaemia during or 6 hours after transfusion. The syndrome should be differentiated from cardiogenic respiratory failure and transfusion-associated circulatory overload. This article presents: 1) The aetiology and pathomechanism of transfusion-related acute lung injury, which are still not fully understood despite numerous studies. The model currently accepted is the multi-event one which involves both factors related to the patient and to the transfused blood components. Transfusion-related acute lung injury may be either immunological, with anti-HLA/HNA antibodies in blood components, or non-immunological, with no antibodies. 2) The diagnosis of transfusion-related acute lung injury which is based on clinical signs, evidence of the relationship with blood component transfusion and detection of antibodies. 3) The treatment and prevention of transfusion-related acute lung injury. The most important element in the prevention of transfusion-related acute lung injury is a reduction in blood component transfusion, particularly of plasma and platelet concentrate. Yet, further studies on larger groups of patients are necessary to specify the limitations of blood component transfusion.

transfusion-related acute lung injury (TRALI), anti-HLA antibodies, anti-HNA antibodies, blood components, DAMPs