A blood transfusion is a common, life-saving medical procedure that requires the precise matching of blood types. Receiving incompatible blood immediately triggers a catastrophic immune reaction known as an acute hemolytic transfusion reaction. Introducing Type A donor blood into a Type B recipient is a textbook example of this incompatibility. This mismatch initiates a rapid, systemic immune attack that can lead to severe organ damage and be fatal if not immediately addressed.
How Type A and Type B Blood Differ
Blood typing is governed by the ABO system, which classifies blood based on the presence or absence of specific antigens on the surface of red blood cells. These antigens are carbohydrates or proteins that determine a person’s blood group. A person’s plasma naturally contains antibodies designed to target and destroy any antigens they do not possess themselves.
Type A blood has the A antigen coating its red blood cells. The plasma of a Type A individual contains pre-formed anti-B antibodies. Conversely, a person with Type B blood has B antigens on their red blood cells. This individual’s plasma contains naturally occurring anti-A antibodies, which recognize and attack any cells carrying the A antigen.
The anti-A antibodies in the Type B recipient’s plasma are the immediate threat when Type A blood is introduced. These antibodies are naturally present from early childhood and do not require prior exposure to the foreign antigen to cause a reaction.
The Immune Response to Incompatible Blood
The moment Type A red blood cells enter the Type B bloodstream, circulating anti-A antibodies immediately bind to the A antigens on the donor cells. This binding initiates an acute immune response. The primary antibodies involved in this reaction are typically Immunoglobulin M (IgM) antibodies.
The binding of IgM antibodies to the A antigens activates the complement cascade, a powerful part of the innate immune system. This cascade culminates in the formation of a membrane attack complex, which punctures the membrane of the transfused red blood cells. This rapid destruction within the blood vessels is known as intravascular hemolysis. Before rupture, the antibodies cause the donor cells to clump together, a process called agglutination.
The massive destruction of red blood cells releases large quantities of free hemoglobin into the plasma. This free hemoglobin is toxic and overwhelms the body’s natural clearing systems, such as the binding protein haptoglobin. The activated complement cascade also releases inflammatory mediators, which trigger systemic symptoms and lead to the activation of the coagulation (clotting) system.
Clinical Outcome and Medical Intervention
The consequences of this immune assault manifest almost immediately, often within minutes of the incompatible transfusion beginning. Early signs include fever, chills, back pain, flank pain, and a feeling of impending doom. As the reaction progresses, systemic damage becomes evident through severe symptoms like shortness of breath and a dangerous drop in blood pressure, leading to hypovolemic shock.
The free hemoglobin released from the ruptured red blood cells is particularly damaging to the kidneys. This excess hemoglobin can obstruct the renal tubules, causing acute tubular necrosis, which quickly leads to acute kidney injury (AKI). Furthermore, activation of the clotting cascade results in disseminated intravascular coagulation (DIC), a severe condition where widespread clotting consumes clotting factors and platelets, paradoxically leading to uncontrolled bleeding.
The immediate medical intervention upon suspecting an incompatible transfusion is to stop the blood flow immediately. The intravenous line is kept open with a compatible solution, typically normal saline, to maintain circulation. Treatment is primarily supportive, focusing on managing complications. This includes aggressive fluid resuscitation and the use of vasopressors to manage low blood pressure and combat shock.
Diuretics, such as furosemide, are often administered to maintain urine output and prevent kidney failure. These help flush the toxic free hemoglobin through the renal system.