Definition: Noncardiogenic pulmonary edema (acute lung injury or ARDS) resulting from transfusion of blood products; also known as pulmonary leukoagglutinin reaction.

Epidemiology: ~2 cases per 10000 units of blood administered and 16 per 10000 patients transfused at one institution.

Pathophysiology: Probably results from anti-granulocyte antibodies, usually originating from the blood donor. Antibodies are believed to bind primarily to granulocytes in the pulmonary microvasculature, initiating a series of immune reactions (complement- and enzyme-mediated, etc.) that may increase further recruitment of leukocytes to the lung and cause microvascular endothelial injury in the lung, resulting in capillary leak and pulmonary edema. Preceding trauma or stress or cytokine treatment may be a predisposing factor.

Clinical Presentation: Onset of acute SOB 1-6 hours after transfusion (average 2 hours). Concomitant fever, tachycardia, and hypotension may be present. Hypoxemia requiring mechanical ventilation may occur in as many as 70%! CXR shows bilateral patchy airspace opacities consistent with ARDS.

Resolution is generally rapid, regardless of severity of hypoxemia. Most patients can be extubated within 48 hours and CXR will return to normal within 4-5 days.
Mortality is ~5%.

Diagnosis: Usually made clinically: dyspnea, hypoxemia, and pulmonary infiltrates occurring during or within a few hours of initiation of transfusion.

Other findings may include granulocyte, leukoagglutinating, or lymphocytotoxic antibodies in serum from either donor or recipient; decline in C3 or C5a levels 12-36 hours after symptom onset followed by a rise in levels 4-7 days later; and transient leukopenia/eosinophilia.

Treatment: Supportive, including O₂ and/or mechanical ventilation/ECMO if needed. Diuretics should be used with caution. IV corticosteroids are controversial in TRALI (anecdotal data only) and are generally not recommended since TRALI usually resolves quickly with supportive care only.

D. Suh 3/26/01