The Role of Leukocyte Depletion In Prevention of Transfusion-Related Acute Lung Injury

Summary

Transfusion related acute lung inquiry (TRALI) is a pulmonary com-plication attributed to blood transfusion which clinically resembles adult respiratory distress syndrome. The frequency of occurrence of TRALI is unknown, as it is likely that many cases go undiagnosed. TRALI is thought to be due to an interaction between granulocytes (most often of host, but possibly of donor origin) and anti-granulocyte antibodies (most often of donor but, sometimes of recipient origin) in which activated complement components participate in alveolar damage. Prognosis is generally good, although prompt and aggressive respiratory support is required.

The vast majority of cases are related to the presence of antileukocyte antibodies in donor plasma. Some cases (approximately 10%) may be mediated by intact donor granuloyctes or substances generated during in vitro storage of leukocytes. The impact of leukodepletion (preferably prestorage) in reducing the frequency of TRALI is considered to be only slight.

The paucity of attention given by standard textbooks of medicine and surgery to pulmonary complications of transfusion might suggest that the respiratory system is a rare target of injury from hemotherapy. When pulmonary problems are noted at all, it is usually in the context of circulatory overload from hypertransfusion or anaphylactic transfusionreactions. Pulmonary edema from hyper-transfusion may occur as frequently as 1:3000 transfusion episodes¹ while anaphylactic transfusion reactions are extremely rare, estimated at 1:20,000 transfusions.² It is only in the last decade that another complication, acute lung injury, has been recognized as an important complication of transfusion. One of the reasons for the lack of earlier recognition of this transfusion reaction was that there were so few case reports and these utilized several terms to describe the same entity. The transfusion-related acute lung injury (TRALI) syndrome has previously been referred to as “pulmonary leukoagglutinin reaction,”³ allergic pulmonary edema,”⁴ and “hypersensitivity reaction,”⁵ but these terms obscure the clinical picture and underlying mechanism.