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Adverse Outcomes in Blood and Blood Component Therapy - page 2 / 19





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they occur. Transfusion reactions may be divided into immune mediated and non-immune mediated and may be categorized as immediate or delayed. The onset of a transfusion reaction may be misleading or delayed, and therefore, its detection requires astute assessment.2 The transfusionist who is often a nurse is responsible for recognizing when a transfusion reaction has occurred. The different types of transfusion reactions that may occur include: hemolytic transfusion reactions (HTRs), transfusion associated graft-versus-host disease (TA-GVHD), hemoglobinuria, post transfusion purpura (PTT), fever, circulatory overload, thrombophlebitis, urticaria, hyperkalemia, noncardiogenic pulmonary edema, and allergic and anaphylactic reactions. The transfusionist must become conversant with the signs and symptoms of a transfusion reaction and be prepared to react quickly.3 Each blood bank and transfusion service must have a system in place for detection, reporting and evaluating suspected complications of transfusion. In the event of a suspected transfusion reaction, the individual responsible for the transfusion must notify the ordering physician and the transfusion service immediately. Every transfusion reaction must be investigated promptly and the transfusion must not resume until the investigation is complete. Measures should be taken to to minimize harm to the patient.

The rate of fatal transfusion event is estimated to be about one per million units transfused but the rate of adverse reaction to transfusion of blood or blood component is estimated to be about 1 in every 200 transfusions.4 Causes of fatal transfusions reaction include misidentification of patient, mislabeling of blood sample, error in laboratory records, mistakes in blood typing, and incorrect antibody screening or crossmatching.4 Typical causes of transfusion associated deaths include acute hemolysis due to ABO incompatibility, acute pulmonary edema, bacterial contamination of product, delayed transfusion reactions, anaphylaxis, external hemolysis, and graft versus host disease (GVHD).2 In vivo hemolysis of red blood cell injured by immune processes may be intravascular or extravascular. ABO antibodies are very efficient in fixing complement following sensitization of incompatible cells and therefore may precipitate an intravascular hemolytic crisis. Other antibodies such as those of Kidd, Vel Tja and Lea are also very efficient at complement fixing and may likewise cause intravascular hemolysis. Activation of complement results in the release of complement components such as C3a and C5a which act on mast cells resulting in the production of vasoactive substances such as serotonin, and histamine which mediate clinical signs and symptoms of transfusion reactions.5 When the complement cascade proceed to completion, the membrane attack complex is formed which leads to the lysis of the red blood cells.

Antigen-antibody complexes can also activate factor XII, which acts on the kinin system.1 The resultant production of bradykinin increases capillary permeability, which causes the dilation of arterioles and leads to hypotension. Hypotension activates the sympathetic nervous system with the production of catecholamines, which result in vasoconstriction in the kidney. Factor XII and thromboplastic substances produced by lysed cells activate the intrinsic clotting system, which may precipitate disseminated intravascular coagulation (DIC). This may cause the formation of thrombi, which may lodge in the lungs, liver, and kidneys. This leads eventually to the consumption of coagulation factors, production of fibrin degradation products and uncontrolled hemorrhage and renal ischemia.1,5 Extravascular hemolysis results in red blood cell removal from the circulation and destruction by cells of the reticuloendothelial system in the liver and spleen. Antibodies commonly implicated in extravascular hemolysis include anti-Jka, anti-Fya and anti-K. Extravascular hemolysis is a less severe hemolytic crisis compared to intravascular hemolysis because complement activation is not complete and the sensitized cells are gradually removed from the circulation as they circulate through the liver and the spleen.

Immediate Hemolytic Transfusion Reactions Immediate hemolytic transfusion reactions (IHTR) occur soon after the transfusion of incompatible red blood cells. The transfused red cells are rapidly destroyed with the release of hemoglobin and stroma from the hemolyzed cells into the circulation. The cause of the hemolysis is usually due to the presence of preformed alloantibodies produced as a result of previous transfusion or pregnancy. More commonly, they are due to naturally occurring ABO antibodies. When incompatible red blood cells are transfused, antigen-antibody complexes are formed, which activate the complement, plasminogen, kinin and coagulation systems. Only a

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