Transfusion-related acute lung injury (TRALI) is defined clinically as the development of hypoxaemia and non-cardiogenic pulmonary oedema either during or within 6 h of blood transfusion . Despite supportive treatment, supplemental oxygen and mechanical ventilation, it has a mortality rate of 5–10% . Haemovigilance programs in the USA and the UK report TRALI to be the most frequent cause of transfusion-related morbidity [3,4].
Blood transfusion is not prescribed without clinical justification. Accumulating experimental evidence about the role of cellular priming resulting from the patient’s underlying clinical condition is receiving greater acceptance as being central to TRALI pathophysiology. Priming events are thought to activate endothelial cells (ECs), causing polymorphonuclear neutrophils (PMNs) to accumulate in the pulmonary microvasculature [5–8]. Subsequent activation of primed PMNs results in an augmented respiratory burst response whereby nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is assembled and reactive oxygen species (ROS) are generated. In the absence of a microbial target, this can instead result in collateral injury to the surrounding tissues. In vitro studies show that high concentrations of priming agents or exposure to sequential priming agents can activate PMNs . The ability of antibodies or non-antibody factors (NAFs) to prime the PMN respiratory burst in vitro has therefore been utilised to model their possible roles in the pathophysiology of TRALI. This paper examines current evidence behind the differing pathophysiologies of antibody mediated and non-antibody mediated TRALI.