Diagnostic and pathogenetic considerations in transfusion‐related acute lung injury

TLDR

TRALI is an infrequent but life‑threatening complication of hemotherapy, a significant cause of transfusion‑associated morbidity that is often misdiagnosed. Blood banks need to identify donors whose plasma causes these reactions in order to prevent their recurrence. The study describes 36 cases and suggests that passive transfer of granulocyte or lymphocytotoxic antibodies can trigger complement activation, leading to pulmonary injury. TRALI presents with acute respiratory distress, hypoxemia, fulminant pulmonary edema, and hypotension within 4 hours of transfusion, yet most patients recover rapidly and completely; antibodies are detected in 89 % of cases, with HLA‑specific antibodies in 65 % of donors.

Abstract

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.