Transfusion-related acute lung injury (TRALI) is an infrequent but life-threatening complication of hemotherapy. The findings in 36 cases are described. The typical clinical presentation includes acute respiratory distress characterized by hypoxemia and fulminant pulmonary edema. The onset is usually within 4 hours of transfusion and is accompanied by hypotension. In most patients (81%), recovery is rapid and complete. In 89 percent of cases, granulocyte or lymphocytotoxic antibodies are found in the serum of the implicated blood product which contained plasma. HLA-specific antibodies were identified in donor serums in 65 percent of cases evaluated. The passive transfer of these antibodies may promote complement activation and subsequent pulmonary injury. TRALI is an important cause of transfusion-associated morbidity and is probably often misdiagnosed. Blood banks need to identify donors whose plasma causes these reactions in order to prevent their recurrence.

Using the definition in this report, clinicians can diagnose and report TRALI cases to the blood bank; importantly, researchers can use this definition to determine incidence, pathophysiology, and strategies to prevent this leading cause of transfusion-associated mortality.

TRALI is the result of two clinical events, the first being a predisposing clinical condition and the second being the transfusion of biologically active lipids in stored blood.

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Donation-related vasovagal syncopal reactions are a multifactorial process determined largely by age, weight, and first-time donor status.

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BACKGROUND: Transfusion‐related acute lung injury (TRALI) is a serious, sometimes fatal, complication of transfusion. Granulocyte and HLA class I antibodies present in blood donors have been associated with TRALI. HLA class II antibodies have recently been described in a few cases of TRALI. STUDY DESIGN AND METHODS: Donors involved in TRALI reactions reported to a blood center over an 18‐month period were tested for HLA class I and II antibodies as well as granulocyte antibodies, if HLA antibodies were not identified. RESULTS: HLA class II antibodies were identified, in at least one donor, in 7 (64%) of 11 cases of TRALI. HLA class I antibodies were identified in combination with HLA class II antibodies in 5 of these 7 cases. HLA class I antibodies were exclusively identified in 2 cases. Granuloctye antibodies were identified in 1 case, and no antibodies were identified in another. CONCLUSION: In addition to HLA class I antibodies, HLA class II antibodies are associated with TRALI. Testing of donors for HLA class II antibodies as well as HLA class I and granulocyte antibodies is recommended as part of the investigation of suspected cases of TRALI.

In most cases of TRALI, a correlation between antigen and antibody can be identified. Activation of monocytes and their subsequent release of cytokines may play a role in the pathogenesis of TRALI.