TRALI is a life-threatening complication of transfusion which may have a very dramatic clinical presentation indistinguishable from adult respiratory distress syndrome. In most cases it begins within 2 hours of transfusion but may be up to 4 or 6 hours following administration of a blood component. Symptoms generally include fever, hypotension, chills, cyanosis, non-productive cough and dyspnea. Chest X-ray shows severe bilateral pulmonary edema or perihilar and lower lung field infiltration, without cardiac enlargement or involvement of the vessels. The X-ray findings may be much more severe than the auscultatory changes on examination. Severe hypoxia is usual, with very low arterial oxygen tensions, and the patient frequently requires mechanical ventilation. In contrast to patients with circulatory overload, those with TRALI have normal central venous pressure and normal or low pulmonary wedge pressure. It is possible that milder cases of TRALI may occur and not be recognized. Approximately 80% of patients with TRALI improve both clinically and physiologically within 2 or 3 days with adequate supportive care. Overall mortality appears to be in the region of 5-8%, in contrast to ARDS, which has a mortality rate of 40-50%. Differential diagnosis includes circulatory overload, anaphylactic transfusion reaction and bacterial contamination.
TRALI has been reported from all types of blood components including whole blood, red cells, aphaeresis platelets, whole blood platelets, fresh frozen plasma, cryoprecipitate, granulocytes, stem cell products and even IV immunoglobulin preparations.
TRALI is under- diagnosed and under- reported as many clinicians are not familiar with the syndrome. This is equally true for severe cases of TRALI where transfusion may not be considered as a possible cause and may be regarded as ARDS but also for mild case where mechanical ventilation is not required. TRALI can be misdiagnosed as TACO.
Two different etiologies have been proposed. The first is a single antibody-mediated event involving the transfusion of anti-HLA class I and class II or antigranulocyte antibodies into patients whose leukocytes express the cognate antigens. The second is a 2-event model: the first event is the clinical condition of the patient resulting in pulmonary endothelial activation and neutrophil sequestration, and the second event is the transfusion of a biologic response modifier (including lipids or antibodies) that activates these adherent PMNs, resulting in endothelial damage, capillary leak, and TRALI.
Supportive care is the mainstay of therapy in TRALI. Oxygen supplementation is employed and aggressive respiratory support is needed. Intravenous administrations of fluids, as well as vasopressors, are essential for blood pressure support. Use of diuretics, which are indicated in the management of TACO, should be avoided in TRALI. Corticosteroids can be beneficial.
Ventilation is indicated because of acute ventilatory failure, it could be speculated that a restrictive tidal volume ventilation should be applied to avoid worsening of lung injury (Ventilation with lower tidal volumes as compared with traditional Tidal volumes for acute lung injury and the acute respiratory distress syndrome).
It is unlikely that TRALI can ever be entirely prevented, but its frequency may be reduced by the judicious use of blood components only for indications that are justified based on sound medical evidence. Hospitals should have procedures in place (e.g. blood utilization guidelines, blood conservation programs) which minimize unnecessary transfusions. In addition, hospital medical staff must continue to have a high index of suspicion in order to diagnose TRALI.