The pathophysiology and organ-specific consequences of severe transfusion reactions

Abstract

Transfusion of blood components is usually required in the management of critically ill patients. However, pathologic interactions between blood products and organ function may result from transfusion reactions. Emerging understanding of the mediation and interruption of clinical inflammatory responses is applicable to severe transfusion reactions. The pathophysiology of four types of severe transfusion reactions are reviewed: a) acute hemolysis; b) bacterial contamination of blood components; c) transfusion-related acute lung injury (TRALI); and d) anaphylaxis. Acute hemolytic reactions are often caused by preventable errors in sample or patient identification. Renal toxicity, coagulopathy, and hypotension may result from circulating red cell stroma and immune-complex activation of complement and cytokine secretion. Bacterial contamination of blood components has caused patient sepsis in many cases; platelets stored at 20 degrees to 24 degrees C are of particular concern. Careful blood collection and handling is essential for prevention. TRALI is manifested by acute respiratory distress, which is usually caused by infusion of plasma containing antibodies against the patient's leukocytes. Complement activation and cytokine stimulation cause edema and neutrophil accumulation in the lungs. Anaphylactic reactions may result from patient immunoglobulin (Ig)E antibodies against donor plasma constituents. IgA-deficient patients are at risk for anaphylactic reactions if these patients develop anti-IgA antibodies. Vasoactive or complement-activating factors in a blood product may also cause anaphylactoid reactions in some patients.