March 2023 Case

Transfusion-related acute lung injury (TRALI) is a serious complication that can develop either during or within 6 hours of blood transfusion. It is characterized by acute hypoxemia and noncardiogenic pulmonary edema and may progress to respiratory failure. The incidence of TRALI is estimated to occur with1 in 4500-5000 transfusions and has a fatality rate of 5–50%, however patients may recover with appropriate supportive care. There is a higher risk of TRALI from high volume plasma containing blood products due to the presence of antibodies against human leukocyte antigens (HLA) or human neutrophil antigens (HNA).

A female patient in her 60s with no significant past medical history was admitted to our institution for vertebral spine surgery. On post-operative day 2, she received 2 units of red blood cells and, within two hours, developed respiratory distress with diffuse interstitial infiltrates. Her pre-operative chest X-ray was normal. There was no evidence of left atrial hypertension, congestive heart failure or volume overload. Her condition worsened despite careful diuresis, and she was intubated and transferred to the intensive care unit (ICU). She remained intubated for 6 days, and following clinical improvement and successful extubation, transferred out of the ICU. The chest x-ray showed progressive clearing of the bilateral infiltrates, however, one day later she became acutely hypoxemic, was transferred back to ICU for worsening acute respiratory failure and was reintubated. There had been no additional blood transfusion or evidence of infection or cardiovascular dysfunction. Computerized tomography scan revealed findings consistent with acute respiratory distress syndrome (ARDS). Throughout her ICU stay there were multiple attempts to wean the patient from the ventilator that were ultimately unsuccessful in the setting of severe fibrotic lung disease and pulmonary hypertension. The patient was not a candidate for lung transplantation and the decision was made to transition to comfort care and she expired 6 weeks after the initial episode of acute respiratory distress in the absence of evidence for cardiac or infectious etiologies for the acute respiratory distress, the clinical impression was that this patient had suffered an episode of TRALI that initially showed signs of resolution with possible relapse and ultimate progression to ARDS and pulmonary fibrosis. Multiple studies including autoimmune and infectious workup were negative. Neither red cell donor was found to have anti-HLA or HNA antibodies nor testing of antibodies against HLA for the patient revealed multiple, high mean-fluorescent intensity class I and II anti-HLA antibodies.

This case report highlights rare but significant adverse effect of blood transfusion. Even though our patient initially recovered from TRALI and got extubated, the ARDS recurred and progressed into pulmonary fibrosis. Despite the intense workup to identify the recurrent ARDS, there was no explanation other than recurrent TRALI. In the literature there is not a single case of recurrent TRALI. This case may represent the first recurrent case of TRALI or TRALI exacerbation of an unknown lung pathology