TRALI is a severe transfusion reaction associated with antibodies to leukocyte antigens present in transfused plasma. It was first described by Brittigham in 1957 (Vox Sang 1957;2:242-248). It is estimated to occur in about 1:5000 blood component transfusions and is associated with a mortality as high as 15%.
TRALI is an acute lung injury associated with anti-leukocyte antibodies transfused with the blood component in question. However, the mere presence of these antibodies in the transfused product is not sufficient to cause TRALI. Thirty-six patients received plasma from a donor who had neutrophil antibodies. There was one fatal pulmonary reaction and 8 had severe pulmonary reaction and 7 had mild to moderate pulmonary reaction (JAMA2002;287:1968-1971). It is believed that two events are needed for the TRALI. The transfusion of leukocyte antibodies is believed to be just one of the events. This explains why not all patients who are transfused antibodies develop TRALI. The first event is the modification/activation of pulmonary vascular endothelium by biological response modifiers resulting in trapping of leucocytes. The second event activated these leukocytes resulting in capillary leak and pulmonary edema. This is where the antibodies play a role.
Patients with TRALI present with sudden deterioration in lung function between 2 and 6 hours after a blood transfusion. Conscious patients complain of tightness of the chest, shortness of breath, dry cough, rigors, nausea dizziness. Examination reveals evidence of hypoxia, hypotension and tachycardia with widespread crepitations over the chest. There is a copious white frothy exudate in the trachea.
There is no test for TRALI. TRALI is diagnosed by documenting evidence of acute lung injury within 6 hours of a transfusion in the absence of other causes to explain pulmonary edema. In 2004 consensus criteria for diagnosis were proposed. These include acute onset of hypoxia during or within 6 hours of transfusion of blood products accompanied by bilateral nodular lung infiltrates on a frontal chest radiograph. Other causes for pulmonary oedema should be absent. Hypoxia is defined as oxygen saturations <90% by pulse oxymeter on room air or PaO2/FiO2 ≤300mm of Hg. The presence of leucopenia and/or monocytopenia and a B-type natriuretic peptide less than 250pg/mL favours the diagnosis of TRALI over other causes of pulmonary edema.
The treatment of TRALI is supportive. Patients should be administered oxygen with positive airway pressure if needed. This may be done with a mask or mechanical ventilation as the needs be. Fluid replacement should be guided by the central venous pressure. Diuretics are indicated only in case of concomitant fluid overload or cardiac failure. They can be harmful in other patients by causing hypovoluaemia. Steroids are of uncertain value. They are likely to be helpful is therapy is initiated early. Further transfusions from of plasma rich products from female donors should be avoided.
Improvement in symptoms may be seen as early as 6 hour. Most patients show an improvement by 24 hours. The chest x-ray clears by 2-4 days. Long-term damage to the lungs is unusual.
One must avoid unnecessary transfusions of plasma containing blood products. The value of eliminating plasma from donors that pose high risk of TRALI is being assessed. Blood collected from parous women and previously transfused individuals is more likely to cause TRALI. Eliminating plasma from parous female donors for production all plasma rich products has been shown to be effective in reducing TRALI. One product that is associated with a low incidence of TRALI is solvent treated pooled plasma. This may be used where the risk of TRALI is high.