Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

Abstract

Transfusion-related acute lung injury (TRALI) is a severe adverse event and a leading cause of transfusion-associated death. Its poor associated prognosis is due, in large part, to the current dearth of effective therapeutic strategies. Hence, an urgent need exists for effective management strategies for the prevention and treatment of associated lung edema. Recently, various preclinical and clinical studies have advanced the current knowledge regarding TRALI pathogenesis. In fact, the application of this knowledge to patient management has successfully decreased TRALI-associated morbidity. This article reviews the most relevant data and recent progress related to TRALI pathogenesis. Based on the existing two-hit theory, a novel three-step pathogenesis model composed of a priming step, pulmonary reaction, and effector phase is postulated to explain the process of TRALI. TRALI pathogenesis stage-specific management strategies based on clinical studies and preclinical models are summarized with an explication of their models of prevention and experimental drugs. The primary aim of this review is to provide useful insights regarding the underlying pathogenesis of TRALI to inform the development of preventive or therapeutic alternatives.

Identifying new safety risk of human serum albumin: a retrospective study of real-world data

“…The results of this study found that Transfusion-related acute lung injury (TRALI) had the strongest signal strength. TRALI is a clinical syndrome with clinical features including acute dyspnea, hypoxemia, fever, hypotension, tachycardia, and leukopenia ( Yu and Lian, 2023 )]. One of the major causes of transfusion-related death is the occurrence of hypoxia-associated acute noncardiogenic pulmonary oedema.…”

“…This can happen during or after a blood transfusion and is caused by damage to the pulmonary vasculature. Antibodies to human neutrophil antigens (HNAs) or human leukocyte antigens (HLAs) in the donor’s blood can bind to the recipient’s antigens and mediate this damage ( Yu and Lian, 2023 ).…”

Case report: Suspected transfusion-related acute lung injury type II in a child with refractory systemic juvenile idiopathic arthritis complicated by macrophage activation syndrome

“…Inadequate production of IL-10, a regulatory cytokine to counter-regulate interferon- γ , might be related to the development of MAS ( 24 ). Several of these cytokines (IL-6, IL-10) are also important in the pathophysiology of TRALI ( 21 ). Based on the several overlapping mechanisms involved in the pathophysiology of MAS in sJIA and those identified as triggers/risks for TRALI, our patient had significant recipient-related risk factors that could have contributed to the onset of TRALI.…”

“…In addition, monocyte and macrophage activation has also been implicated in the pathophysiology of TRALI. Several activation mechanisms of these cells have been described, such as those mediated by pathogen-associated and damage-associated molecular patterns and their receptors, antibodies, complement, as well as neutrophil extracellular traps (10,(19)(20)(21).…”