Acute hemolytic transfusion reaction
An acute hemolytic transfusion reaction, also called immediate hemolytic transfusion reaction, is a life-threatening reaction to receiving a blood transfusion. AHTRs occur within 24 hours of the transfusion and can be triggered by a few milliliters of blood. The reaction is triggered by host antibodies destroying donor red blood cells. AHTR typically occurs when there is an ABO blood group incompatibility, and is most severe when type A donor blood is given to a type O recipient.
Signs and symptoms
Early acute hemolytic transfusion reactions are typically characterized by fever, which may be accompanied by rigors. Mild cases are also typically characterized by abdominal, back, flank, or chest pain. More severe cases may be characterized by shortness of breath, low blood pressure, hemoglobinuria, and may progress to shock and disseminated intravascular coagulation. In anesthetized or unconscious patients, hematuria may be the first sign of AHTR. Other symptoms include nausea, vomiting, and wheezing.Causes
The most common cause of acute hemolytic transfusion reaction is ABO incompatibility, which is typically due to human error that results in a recipient receiving the incorrect blood product. Rarely, other blood type incompatibilities can cause AHTR, the most common of which is Kidd antigen incompatibility. Rh, Kell, and Duffy antigen incompatibility have also been implicated in AHTR.Mechanism
Acute hemolytic transfusion reactions result when antibodies against A and/or B antigens present in the recipient's blood destroy the respective donor red blood cells. This is mediated through the antibodies IgM which cause activation of the complement cascade, with complement C5-C9 forming the membrane attack complex which leads to pore formation and red blood cell lysis. The lysed red blood cells release free hemoglobin into the bloodstream, overwhelming hemoglobin binding proteins such as albumin, haptoglobin, and hemopexin, with the excess free hemoglobin leading to renal vasoconstriction, which then leads to acute tubular necrosis and acute kidney injury.The antibodies also activate the coagulation cascade via factor XII, which can lead to disseminated intravascular coagulation and kidney damage. Isohemagglutinins also activate the complement cascade via C3a and C5a, which then promote inflammatory cytokine release from white blood cells. C3a and C5a also activate mast cells which release serotonin and histamine, which along with fragments of red blood cells that were destroyed, further stimulate the release of inflammatory cytokines. These inflammatory cytokines include IL-1, IL-6, IL-8, and TNF-alpha, which cause increased capillary permeability and vasodilation leading to symptoms of low blood pressure, fever, chest pain, nausea, vomiting, and wheezing.