Transfusion related acute lung injury (TRALI) is a syndrome defined by acute pulmonary edema after transfusion of any blood component  Suspect TRALI is defined as fulfilmentof the definition of acute lung injury occuring within 6 hours of transfusion, in the absence of the other risk factors .
TRALI is considered one of the major causes of transfusion-related morbidity with ABO incompatibility and bacterial contamination, and the first cause of death in U.S. . Its incidence is similar in both sex and at any age and is about 1 in 5000 transfusions . The incidence is probably underestimated due to lack of application of diagnostic criteria.
The clinical pattern is dominated by acute respiratory distress syndrome (ARDS). TRALI can be differentiated from other forms of ARDS as invasive monitoring shows normal intracardiac pressures. Lung damage is generally transient and PO2 levels return to pre-transfusion levels within 48–96 hours. The symptoms may occur during 6 hours after transfusion, showing dyspnoea, tachypnea, hypotension and cyanosis . Clinical exam shows severe pulmonary distress but no signs of heart failure or volume overload, confirmed by CXR analysis.
Treatment of TRALI is supportive with oxygen therapy in the mild forms, and with mechanical ventilation in the severe forms. Further blood product transfusion is strongly discouraged. There is no evidence of benefit with diuretics of corticosteroids . Recovery is complete within 96 hours with no sequelae in the majority of the patients. A small percentage may present persistent pulmonary infiltrates up to seven days, and about 10% of cases have fatal outcome despite aggressive support .
The pathophysiology of TRALI is based on activation of neutrophil granulocytes at the onset of lung injury. These are trapped in the pulmonary microcirculation and oxygen free radicals and protheolitic enzymes are released. Pulmonary capillary leak syndrome develops with exudation of fluids and proteins. There are three main theories supported in literature: the first theory suggests the role of donor antibodies against recipient leukocytes causing complement and neutrophil activation with subsequent endothelial damage. This theory is supported by the presence of donorderived antibodies to HLA class I antigens and neutrophils in up to 89% of TRALI cases. The second theory is a “two hit hypothesis” where the first hit is an underlying condition of the patient with stimulation of adherence of neutrophils to the pulmonary epithelium. The second hit is associated with transfusion with reaction between antibody of the recipient and surface antigens on RBCs donor causing immediate degranulation of neutrophils . Cardiopulmonary Bypass used in cardiac surgery with its well-known systemic inflammatory response can be considered as part of the “first hit”. The third hypothesis justifies the presence of this syndrome also in neutropenic patients by suggesting direct lung damage with endothelial fenestration, caused by the presence of high levels of vascular endothelial growth factor (VEGF) or antibodies to class II HLA antigens in donor’s blood .
Prevention for this syndrome is difficult. The main procedures able to reduce the incidence of TRALI are the use of predominantly male plasma for preparation of high-volume plasma components and pooling of plasma products . Other strategies planned are to reduce the use of plasma from donors at high risk for HLA immunization (i.e. previously pregnant females) and not to transfuse patients at risk (i.e. those in severe clinical condition) with RBCs stored longer than 14 days or platelets stored longer than 2 days.