What is the pathophysiology of transfusion related acute lung injury (TRALI)?

Updated: Jan 12, 2021
  • Author: S Gerald Sandler, MD, FCAP, FACP; Chief Editor: Emmanuel C Besa, MD  more...
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TRALI has two proposed pathophysiologic mechanisms: the antibody hypothesis and the neutrophil priming hypothesis. [8, 9] Both mechanisms lead to pulmonary edema in the absence of circulatory overload.

The antibody hypothesis states that a human leukocyte antigen (HLA class I, HLA class II) or human neutrophil antigen (HNA) antibody in the transfused component reacts with neutrophil antigens in the recipient (ie, when antileukocyte antibodies are transfused passively in a plasma-containing blood component). [10] The recipient's neutrophils lodge in the pulmonary capillaries and release mediators that cause pulmonary capillary leakage. As a consequence, many patients with TRALI will develop transient leukopenia. [11] However, transfusions of blood components containing neutrophil antibodies may cause a wide range of reactions, including leukopenia, that do not meet the definition of TRALI. [12]

The neutrophil priming hypothesis does not require antigen-antibody interactions and occurs in patients with clinical conditions that predispose to neutrophil priming and endothelial activation such as infection, surgery, or inflammation. Bioactive substances in the transfused component activate the primed, sequestered neutrophils, and pulmonary endothelial damage occurs.

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