Risk factors, management and prevention of transfusion-related acute lung injury: a comprehensive update

ABSTRACT

Introduction: Despite mitigation strategies that include the exclusion of females from plasma donation or the exclusion of females with a history of pregnancy or known anti-leukocyte antibody, transfusion-related acute lung injury (TRALI) remains a leading cause of transfusion-related morbidity and mortality.

Areas covered: The definition of TRALI is discussed and re-aligned with the new Berlin Diagnostic Criteria for the acute respiratory distress syndrome (ARDS). The risk factors associated with TRALI are summarized as are the mitigation strategies to further reduce TRALI. The emerging basic research studies that may translate to clinical therapeutics for the prevention or treatment of TRALI are discussed.

Expert opinion: At risk patients, including the genetic factors that may predispose patients to TRALI are summarized and discussed. The re-definition of TRALI employing the Berlin Criteria for ARDS will allow for increased recognition and improved research into pathophysiology and mitigation to reduce this fatal complication of hemotherapy.

KEYWORDS:

• TRALI
• transfusion-related acute lung injury
• ALI
• acute lung injury
• acute respiratory distress syndrome
• ARDS
• risk factors
• mitigation
• prevention
• treatment
• management
• pathogenesis
• therapies

Article highlights

• Diagnostic criteria for TRALI, especially the nomenclatures possible TRALI (pTRALI) is an area of contention

• New nomenclature for TRALI will likely be reported soon

• Mitigation strategies including use of ‘low-risk’ plasma products have reduced TRALI incidence, but TRALI remains the leading cause of transfusion related mortality

• High risk patients may benefit from product modifications such as washing; clinical trials are currently underway to address this concept

• Additional clinical studies are needed to better understand pathogenesis of and identify clinical markers for TRALI

Declaration of interest

CC Silliman has acted on a Scientific Advisory Board for Hemanext Corporation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This work was supported in part by Vitalant Research Institute, grant P50 GM049222 from NIGMS, NIH, grant UM1-HL120877 from NHLBI, NIH, and Department of Defense Grant W81XWH-12-2-2008.