The pathogenesis of transfusion‐related acute lung injury (TRALI)

Abstract

SummaryIn recent years, transfusion-related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of transfusion-related major morbidities and fatalities. A clinical definition of TRALI was established in 2004, based on acute respiratory distress, noncardiogenic lung oedema temporal association with transfusion and hypoxaemia. Histological findings reveal lung oedema, capillary leucostasis and neutrophil extravasation. However, the pathogenesis of TRALI remains controversial. Leucocyte antibodies, present in fresh frozen plasma and platelet concentrates from multiparous donors, and neutrophil priming agents released in stored cellular blood components have been considered to be causative. As neutrophils and endothelial cells are pivotal in the pathogenesis of TRALI, a threshold model was established to try to unify the various reported findings on pathogenesis. This model comprises the priming of neutrophils and/or endothelium by the patient's co-morbidity, neutrophil and/or endothelial cell activation by the transfused blood component, and the severity of the TRALI reaction.

The incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of cardiac surgery patients: a prospective nested case-control study

“…24,25 We hypothesize that priming of the neutrophils may increase with the time on the bypass, thereby increasing the severity of the "first event" and the susceptibility to a TRALI reaction. A threshold model has been proposed, 19 in which the presence of a strong "first event" may require only a weak second event before TRALI occurs. [44][45][46] In accordance, in a mouse model of TRALI, the presence of an inflammatory reaction resulted in onset of TRALI after a lower dose of antibodies compared with healthy controls.…”

“…The "first event" is the presence of an inflammatory condition in the host, causing endothelial activation leading to neutrophil sequestration and priming in the lung. 19 The "second event" is transfusion of a blood product containing either antibodies or factors that accumulate during storage, providing additional signals for neutrophil activation resulting in the clinical syndrome of pulmonary edema. Two distinct mechanisms have been suggested for the "second event": the traditional theory proposes an antibody-mediated reaction between recipient neutrophils and antineutrophil antibodies from donors who were sensitized during pregnancy (multiparous women) or by previous transfusion.…”

Présentation de cas : lésion pulmonaire aiguë associée à la transfusion (TRALI) — Un danger net et présent

“…In fact these animal models suggest that pulmonary hypertension may only be a surrogate marker of TRALI with little pathophysiologic significance of its own. 13,15,16 The subsequent development of pulmonary hypotension in this case appears to have been secondary to the patient's generalized cardiovascular collapse, a not infrequently reported occurrence in TRALI that likely reflects the development of a systemic inflammatory response syndrome.…”

“…The onset of pulmonary hypertension was not consistent with either hypoxia-induced vasoconstriction or circulatory overload. It is possible that endothelial injury, thought to be a central component in the pathophysiology of TRALI, 13 resulted in either formation of occlusive platelet thrombi or induction of smooth muscle constriction. The development of acute pulmonary leukostasis is not a mechanism supported by animal data.…”

Prediction and prevention of pulmonary-pleural complications after heart valve surgery

“…Считается, что острое повреждение легочной ткани при переливании крови происходит за счет острой гипоксии с последующей клеточной инфильтрацией обоих легких во время гемо-трансфузии [11,23]. Описаны два механизма этого про-цесса: 1) при наличии хронического воспаления в легоч-ной ткани при гемотрансфузии происходит активация нейтрофилов и увеличение их тропности к эндотелию, в результате чего поражается легкое, имеющее большое число мелких сосудов [5]; 2) в переливаемой крови содер-жатся различные антитела и цитокины, которые накапли-ваются в процессе хранения, при взаимодействии их с нейтрофилами крови реципиента происходит активация последних, что клинически проявляется отеком легких Рис. 2.…”