Transfusion–related acute lung injury (TRALI) is probably under-reported, particularly in the critically ill. The patho- genesis of TRALI is thought to be a “two hit”–entity. The first hit is a pro-inflammatory response of any origin, resulting in activa- tion of endothelium and priming of sequestrated neutrophils, thereby resembling acute lung injury. The second hit is provided by mediators in a transfused blood product. The critically ill are often exposed to clinical conditions which cause priming of pulmonary neutrophils such as pneumonia, aspiration and mechanical ventilation, and may therefore be at risk of developing a TRALI reac- tion. The aetiology and the course of TRALI may differ in the critically ill when compared with the general hospital population. The threshold model holds that patients with a pro-inflammatory response, in which pulmonary neutrophils are primed, require only a weak mediator in the transfused blood product to induce a TRALI reaction, whereas patients without acute lung injury need a strong mediator to overcome the threshold. However, as specific disease markers are lacking, distinguishing TRALI from pulmonary dys- function of other origin remains a challenge. Whether specific clinical conditions causing acute lung injury also predispose to TRALI remains to be established. Prospective studies are needed to fully assess attributable risk related to transfusion.
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