Type I hypersensitivity reaction in which preformed IgE antibodies on the surface of mast cells bind to donor plasma proteins (commonly donor IgA in recipients with IgA deficiency), leading to mast cell degranulation
Individuals with IgA deficiency should receive IgA-depleted blood products.
Clinical features: Sudden onset during or up to 3 hours after the transfusion
Occurs in patients who were previously sensitized to specific RBC antigens during transfusions, pregnancy, or transplantations
Particularly common in patients receiving repeated transfusions, such as patients with sickle cell disease or thalassemia.
Usually caused by alloantibodies that form following exposure to minor blood group antigens (e.g., Kidd or D (Rh) antigens)
Reexposure to the RBC antigens → anamnestic response resulting in an increase in anti-RBC alloantibody titers 24 hours to 28 days following transfusion → binding of alloantibodies to donor RBCs causing extravascular hemolysis
Clinical features
Onset days or weeks after transfusion (due to the delay in the anamnestic response)
Most commonly asymptomatic
May cause:
Mild fever
Jaundice
Anemia
Massive transfusion-related complications
Hypocalcemia
Resulting from the binding of ionized calcium by citrate (an anticoagulant added to RBC, platelet, FFP, and whole blood transfusion units)
Normally, following transfusion, citrate is rapidly metabolized to bicarbonate in the liver; however, when large volumes of blood are transfused rapidly, the excess citrate can chelate calcium in the plasma, leading to hypocalcemia due to decreased serum ionized calcium concentration.
This is most common with very high transfusion rates (eg, >9 units/hr), but it can also be seen at lower rates in patients with underlying hepatic insufficiency (eg, alcohol-associated liver disease).
Hyperkalemia
Resulting from the lysis of RBCs in stored blood units
