Abstract
The preeminent causes of blood transfusion-related morbidity and mortality are transfusion-associated circulatory overload (TACO) and transfusion-related acute lung injury (TRALI). These occur within hours of blood transfusion and lead to acute respiratory distress. The differentiation between TACO and TRALI has always been a great challenge in the context of underlying etiology, whether it is volume overload or lung injury, or both. This is a case report of a 64-year-old female with multiple comorbidities, who was brought to the emergency department with generalized weakness. She was hemodynamically unstable and encephalopathic. Her hemoglobin was 6.5 gm/dl with no active evidence of bleeding. She was started on a norepinephrine drip and one unit of packed red blood cells was transfused. A few hours post-transfusion, she became extremely tachypneic and hypoxic. A chest x-ray post-transfusion showed diffuse bilateral fluffy alveolar infiltrates and the N-terminal (NT)-pro hormone Brain Natriuretic Peptide (NT-proBNP) was significantly elevated. The transfusion reaction workup was negative. Due to worsening hypoxia, she required a rapid transition from non-invasive to invasive mechanical ventilation. The chronology of this case report depicts a unique presentation of acute respiratory distress and the course of hypoxemia.