TRANSFUSION REACTION

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TRANSFUSION REACTIONS :

TRANSFUSION REACTIONS BY: Mansoor Alimardani MD, MPH Infectious disease specialist Abhar – Iran 2010

TRANSFUSION REACTIONS :

TRANSFUSION REACTIONS

Blood Group Antigens & Antibodies :

Blood Group Antigens & Antibodies ABO Antigens and Antibodies Rh System Other Blood Group Systems and Alloantibodies

Other Blood Group Systems and Alloantibodies :

Other Blood Group Systems and Alloantibodies More than 100 blood group systems are recognized, composed of more than 500 antigens. Antibodies to Lewis system carbohydrate antigens are the most common cause of incompatibility during pretransfusion screening. Lewis antigens may be adsorbed onto tumor cells and may be targets of therapy. Some patients with cold agglutinin disease or lymphomas can produce anti-I autoantibodies that cause RBC destruction. Most adults lack i expression; thus, finding a donor for patients with anti-i is not difficult. Even though most adults express I antigen, binding is generally low at body temperature. Thus, administration of warm blood prevents isoagglutination.

Other Blood Group Systems and Alloantibodies :

Other Blood Group Systems and Alloantibodies P system: Its clinical significance is in rare cases of syphilis and viral infection that lead to paroxysmal cold hemoglobinuria. The MNSsU system: Anti-S and anti-s IgG antibodies may develop after pregnancy or transfusion and lead to hemolysis. Anti-U antibodies are rare but problematic; virtually every donor is incompatible because nearly all persons express U. The Kell protein is very large (720 amino acids), The absence of the Kell precursor protein (controlled by a gene on X) is associated with acanthocytosis, shortened RBC survival, and a progressive form of muscular dystrophy that includes cardiac defects and CGD. This rare condition is called the McLeod phenotype. The Duffy antigens are codominant alleles, Fya and Fyb, that also serve as receptors for Plasmodium vivax. More than 70% of persons in malaria-endemic areas lack these antigens, probably from selective influences of the infection on the population. The Kidd antigens, Jka and Jkb, may elicit antibodies transiently. A delayed hemolytic transfusion reaction that occurs with blood tested as compatible is often related to delayed appearance of anti-Jka.

Pretransfusion Testing :

Pretransfusion Testing "type and screen.“ Is done with 2 methods 1-"forward type“ 2- "reverse type" The alloantibody screen identifies antibodies directed against other RBC antigens. The alloantibody screen is performed by mixing patient serum with type O RBCs that contain the major antigens of most blood group systems and whose extended phenotype is known. The specificity of the alloantibody is identified by correlating the presence or absence of antigen with the results of the agglutination. Cross-matching is ordered when there is a high probability that the patient will require a packed RBC (PRBC) transfusion. Blood selected for cross-matching must be ABO compatible and lack antigens for which the patient has alloantibodies. Nonreactive cross-matching confirms the absence of any major incompatibility and reserves that unit for the patient. In the case of Rh-negative patients, every attempt must be made to provide Rh-negative blood components to prevent alloimmunization to the D antigen.

Blood Components :

Blood Components

Whole Blood :

Whole Blood Whole blood provides both oxygen-carrying capacity and volume expansion. It is the ideal component for patients who have sustained acute hemorrhage of 25% total blood volume loss. Whole blood is stored at 4°C to maintain erythrocyte viability, but platelet dysfunction and degradation of some coagulation factors occurs. In addition, 2,3-bisphosphoglycerate levels fall over time, leading to an increase in the oxygen affinity of the hemoglobin and a decreased capacity to deliver oxygen to the tissues, a problem with all red cell storage. Whole blood is not readily available since it is routinely processed into components.

Packed Red Blood Cells :

Packed Red Blood Cells This product increases oxygen-carrying capacity in the anemic patient. Adequate oxygenation can be maintained with a hemoglobin content of 70 g/L in the normovolemic patient without cardiac disease; however, comorbid factors often necessitate transfusion at a higher threshold. The decision to transfuse should be guided by the clinical situation and not by an arbitrary laboratory value. In the critical care setting, liberal use of transfusions to maintain near-normal levels of hemoglobin may have unexpected negative effects on survival. In most patients requiring transfusion, levels of hemoglobin of 100 g/L are sufficient to keep oxygen supply from being critically low. PRBCs may be modified to prevent certain adverse reactions. Leukocyte reduction of cellular blood products is increasingly common, and universal prestorage leukocyte reduction has been recommended. Prestorage filtration appears superior to bedside filtration as smaller amounts of cytokines are generated in the stored product. These PRBC units contain <5 x 106 donor white blood cells (WBCs), and their use lowers the incidence of posttransfusion fever, cytomegalovirus (CMV) infections, and alloimmunization. Other theoretical benefits include less immunosuppression in the recipient and lower risk of infections. Plasma, which may cause allergic reactions, can be removed from cellular blood components by washing.

Platelets :

Platelets The threshold for prophylactic platelet transfusion is 10,000/L. In patients without fever or infections, a threshold of 5000/L may be sufficient to prevent spontaneous hemorrhage. For invasive procedures, 50,000/L platelets is the usual target level. In an unsensitized patient without increased platelet consumption [splenomegaly, fever, disseminated intravascular coagulation (DIC)], six to eight units of RD platelets (about 1 unit per 10 kg body weight) are transfused, Patients who may require multiple transfusions are best served by receiving SDAP and leukocyte-reduced components to lower the risk of alloimmunization. Refractoriness to platelet transfusion may be evaluated using the corrected count increment The platelet count performed 1 h after the transfusion is acceptable if the CCI is 10 x 109/mL, and after 18–24 h an increment of 7.5 x 109/mL is expected. Patients who have suboptimal responses are likely to have received multiple transfusions and have antibodies directed against class I HLA antigens. Refractoriness can be investigated by detecting anti-HLA antibodies in the recipient's serum. Additional clinical causes for a low platelet CCI include fever, bleeding, splenomegaly, DIC, or medications in the recipient.

Fresh-Frozen Plasma :

Fresh-Frozen Plasma FFP contains stable coagulation factors and plasma proteins: fibrinogen, antithrombin, albumin, as well as proteins C and S. Indications for FFP include correction of coagulopathies, including the rapid reversal of warfarin; supplying deficient plasma proteins; and treatment of thrombotic thrombocytopenic purpura. FFP should not be routinely used to expand blood volume. FFP is an acellular component and does not transmit intracellular infections, e.g., CMV. Patients who are IgA-deficient and require plasma support should receive FFP from IgA-deficient donors to prevent anaphylaxis .

Cryoprecipitate :

Cryoprecipitate Cryoprecipitate is a source of fibrinogen, factor VIII, and von Willebrand factor (vWF). It is ideal for supplying fibrinogen to the volume-sensitive patient. When factor VIII concentrates are not available, cryoprecipitate may be used since each unit contains approximately 80 units of factor VIII. Cryoprecipitate may also supply vWF to patients with dysfunctional (type II) or absent (type III) von Willebrand disease.

Plasma Derivatives :

Plasma Derivatives Plasma from thousands of donors may be pooled to derive specific protein concentrates, including albumin, intravenous immunoglobulin (IVIG), antithrombin, and coagulation factors. In addition, donors who have high-titer antibodies to specific agents or antigens provide hyperimmune globulins, such as anti-D (RhoGam, WinRho), and antisera to hepatitis B virus (HBV), varicella-zoster virus, CMV, and other infectious agents.

Immune-Mediated Reactions :

Immune-Mediated Reactions Acute Hemolytic Transfusion Reactions Delayed Hemolytic and Serologic Transfusion Reactions Febrile Nonhemolytic Transfusion Reaction Allergic Reactions Anaphylactic Reaction Graft-versus-Host Disease Transfusion-Related Acute Lung Injury Posttransfusion Purpura Alloimmunization

Acute Hemolytic Transfusion Reactions :

Acute Hemolytic Transfusion Reactions recipient has preformed antibodies that lyse donor erythrocytes. The ABO isoagglutinins are responsible for the majority of these reactions, Rh, Kell, and Duffy, may result in hemolysis. may present with hypotension, tachypnea, tachycardia, fever, chills, hemoglobinemia, hemoglobinuria, chest and/or flank pain, and discomfort at the infusion site. The immune complexes that result in RBC lysis can cause renal dysfunction and failure. Diuresis should be induced with intravenous fluids and furosemide or mannitol. Tissue factor released from the lysed erythrocytes may initiate DIC. Coagulation studies including prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, and platelet count should be monitored in patients with hemolytic reactions.

Immune-Mediated Reactions :

Delayed Hemolytic and Serologic Transfusion Reactions :

Delayed Hemolytic and Serologic Transfusion Reactions DHTRs are not completely preventable. The alloantibody is detectable 1–2 weeks following the transfusion, and the posttransfusion direct antiglobulin test (DAT) may become positive due to circulating donor RBCs coated with antibody or complement. No specific therapy is usually required, although additional RBC transfusions may be necessary. Delayed serologic transfusion reactions are similar to DHTR, as the DAT is positive and alloantibody is detected; however, RBC clearance is not increased.

Immune-Mediated Reactions :

Febrile Nonhemolytic Transfusion Reaction :

Febrile Nonhemolytic Transfusion Reaction The most frequent reaction associated with the transfusion of cellular blood components is a febrile nonhemolytic transfusion reaction (FNHTR). These reactions are characterized by chills and rigors and a 1°C rise in temperature. FNHTR is diagnosed when other causes of fever in the transfused patient are ruled out. Antibodies directed against donor leukocyte and HLA antigens may mediate these reactions; thus, multiply transfused patients and multiparous women are felt to be at increased risk. leukoreduction before storage may prevent these reactions. The incidence and severity of these reactions can be decreased in patients with recurrent reactions by premedicating with acetaminophen or other antipyretic agents.

Immune-Mediated Reactions :

Allergic Reactions :

Allergic Reactions Urticarial reactions are related to plasma proteins found in transfused components. Mild reactions may be treated symptomatically by temporarily stopping the transfusion and administering antihistamines (diphenhydramine, 50 mg orally or intramuscularly). The transfusion may be completed after the signs and/or symptoms resolve. Patients with a history of allergic transfusion reaction should be premedicated with an antihistamine. Cellular components can be washed to remove residual plasma for the extremely sensitized patient.

Immune-Mediated Reactions :

Anaphylactic Reaction :

Anaphylactic Reaction This severe reaction presents after transfusion of only a few milliliters of the blood component. Symptoms and signs include difficulty breathing, coughing, nausea and vomiting, hypotension, bronchospasm, loss of consciousness, respiratory arrest, and shock. Treatment includes stopping the transfusion, maintaining vascular access, and administering epinephrine (0.5–1.0 mL of 1:1000 dilution subcutaneously). Glucocorticoids may be required in severe cases. Patients who are IgA-deficient, <1% of the population, may be sensitized to this Ig class and are at risk for anaphylactic reactions associated with plasma transfusion.

Immune-Mediated Reactions :

Graft-versus-Host Disease :

Graft-versus-Host Disease (GVHD) is a frequent complication of allogeneic stem cell transplantation, in which lymphocytes from the donor attack and cannot be eliminated by an immunodeficient host. Transfusion-related GVHD is mediated by donor T lymphocytes that recognize host HLA antigens as foreign and mount an immune response, which is manifested clinically by the development of fever, a characteristic cutaneous eruption, diarrhea, and liver function abnormalities. GVHD can also occur when blood components that contain viable T lymphocytes are transfused to immunodeficient recipients or to immunocompetent recipients who share HLA antigens with the donor (e.g., a family donor). In addition to the aforementioned clinical features of GVHD, transfusion-associated GVHD (TA-GVHD) is characterized by marrow aplasia and pancytopenia. TA-GVHD is highly resistant to treatment with immunosuppressive therapies, including glucocorticoids, cyclosporine, antithymocyte globulin, and ablative therapy followed by allogeneic bone marrow transplantation. Clinical manifestations appear at 8–10 days, and death occurs at 3–4 weeks posttransfusion. TA-GVHD can be prevented by irradiation of cellular components (minimum of 2500 cGy) before transfusion to patients at risk. Patients at risk for TA-GVHD include fetuses receiving intrauterine transfusions, selected immunocompetent (e.g., lymphoma patients) or immunocompromised recipients.

Immune-Mediated Reactions :

Transfusion-Related Acute Lung Injury :

Transfusion-Related Acute Lung Injury This uncommon reaction results from the transfusion of donor plasma that contains high-titer anti-HLA antibodies that bind recipient leukocytes. The leukocytes aggregate in the pulmonary vasculature and release mediators that increase capillary permeability. The recipient develops symptoms of respiratory compromise and signs of noncardiogenic pulmonary edema, including bilateral interstitial infiltrates on chest x-ray. Treatment is supportive, and patients usually recover without sequelae. Testing the donor's plasma for anti-HLA antibodies can support this diagnosis. The implicated donors are frequently multiparous women, and transfusion of their plasma component should be avoided.

Immune-Mediated Reactions :

Posttransfusion Purpura :

Posttransfusion Purpura This reaction presents as thrombocytopenia 7–10 days after platelet transfusion and occurs predominantly in women. Additional platelet transfusions can worsen the thrombocytopenia and should be avoided. Treatment with intravenous immunoglobulin may neutralize the effector antibodies, or plasmapheresis can be used to remove the antibodies.

Immune-Mediated Reactions :

Alloimmunization :

Alloimmunization A recipient may become alloimmunized to a number of antigens on cellular blood elements and plasma proteins. Alloantibodies to RBC antigens are detected during pretransfusion testing, and their presence may delay finding antigen-negative cross-match-compatible products for transfusion. Women of childbearing age who are sensitized to certain RBC antigens (i.e., D, c, E, Kell, or Duffy) are at risk for bearing a fetus with hemolytic disease of the newborn. Matching for D antigen is the only pretransfusion selection test to prevent RBC alloimmunization. Alloimmunization to antigens on leukocytes and platelets can result in refractoriness to platelet transfusions. Once alloimmunization has developed, HLA-compatible platelets from donors who share similar antigens with the recipient may be difficult to find. Hence, prudent transfusion practice is directed at preventing sensitization through the use of leukocyte-reduced cellular components, as well as limiting antigenic exposure by the judicious use of transfusions and use of SDAPs.