Hemolytic reactions occur when the recipient's serum contains antibodies directed against the corresponding antigen found on donor red blood cells. This can be an ABO incompatibility or an incompatibility related to a different blood group antigen.
Disseminated intravascular coagulation (DIC), renal failure, and death are not uncommon following this type of reaction.
The most common cause for a major hemolytic transfusion reaction is a clerical error, such as a mislabelled specimen sent to the blood bank, or not properly identifying the patient to whom you are giving the blood. DO NOT ASSUME IT IS SOMEONE ELSE'S RESPONSIBILITY TO CHECK!
Allergic reactions to plasma proteins can range from complaints of hives and itching to anaphylaxis. Such reactions may occur in up to 1 in 200 transfusions of RBCs and 1 in 30 transfusions of platelets.
White blood cell reactions (febrile reactions) are caused by patient antibodies directed against antigens present on transfused lymphocytes or granulocytes. The risk for febrile reaction is 1 in 1,000 to 10,000.
Symptoms usually consist of chills and a temperature rise > 1 degree C.
Transfusion related acute lung injury (TRALI)
TRALI is now the leading cause for transfusion-related mortality. It is caused most often when donor plasma contains HLA or leukocyte (usually granulocyte) specific antibodies. Recipient leukocytes may be 'primed' by underlying illness to become more adherent to pulmonary alveolar epithelium. Introduction of the donor antibodies into the recipient causes granulocyte enzymes to be released, increasing capillary permeability and resulting in sudden respiratory distress from pulmonary edema, typically within 6 hours of tranfusion. Leukopenia may transiently occur. Most cases improve within 2 days.
TRALI most often occurs with administration of blood products with plasma, such as FFP. Use of plasma from men reduces the incidence of TRALI, since women who have been pregnant are more likely to have higher titer HLA antibodies.
Circulatory overload can occur with administration of blood or any intravenous fluid, particularly in patients with diminished cardiac function.
Massive Blood Loss
massive blood loss, which s defined as the loss of one blood volume within a 24 hour period, a 50% loss in less than 3 hours for acute scenarios, or a rate of loss of 150 ml/min.
Massive transfusion is the lifesaving treatment of hemorrhagic shock that requires the transfusion of one blood volume. Major complications that may arise in patients who require massive transfusion include hypothermia, coagulopathy, and/or citrate toxicity with electrolyte abnormalities and metabolic derangements, such as acidosis and alkalosis.
RBC transfusions can expose the patient to RBC antigens not recognized as self. If an antibody is produced, future transfusions can be delayed because extended donor blood typing will be required to identify compatible units.
O negative blood released uncrossmatched in emergencies could result in a hemolytic transfusion reaction if the patient has an alloantibody produced after a previous transfusion.
Alloantibody production in a female can result in hemolytic disease of the newborn.
Hemolytic Disease of the Newborn
Previous pregnancies expose the mother to novel (paternally derived) antigens. The most common alloimmunization associated with pregnancy is the exposure of maternal Rh D negative blood to fetal Rh D positive blood. This results in the production of maternal IgG against the "D" antigen that can cross the placenta and attack fetal red blood cells, resulting in hemolytic disease of the newborn, also called erythroblastosis fetalis.
This can be prevented by the use of Rho(D) immune globulin, commonly known as RhoGAM. RhoGAM consists of IgG anti-D antibodies that will help neutralize the antigen and prevent the mother's immune system from sensitization to the antigen, and preventing the immune response that generates the alloantibodies. The use of RhoGAM and greatly reduced the incidence of Rh anti-D erythroblastosis fetalis, and so other blood group antigens, such as Kell, may be implicated.
Platelets contain HLA and A & B antigens. Prior exposure to non-self HLA antigens (from WBC contamination of red cell products) can result in antibodies that will render future platelet transfusions useless.
Obtaining Compatible Blood Products
If an alloantibody is detected, then RBC units may be crossmatched randomly, assuming that the alloantibody is against a "low incidence" antigen which most units will lack. Chances are, enough compatible units will be identified.
If an alloantibody is directed at a "high incidence" antigen, then there will be few, if any, units available that match. In that case, "rare" blood units lacking the antigen may be requested from a facility that stores such blood. Cryopreservation of RBCs is done to store special, rare RBCs for up to 10 years in a glycerol solution. The thawed units are washed of the glycerol, and by doing so are also depleted of plasma and leukocytes.
For platelets, HLA (MHC) typing may be necessary to identify compatible donors with the same HLA type. HLA unmatched platlets (random donor platelets) are likely to be destroyed readily.
The process of identifying alloantibodies and finding compatible blood products is time consuming.
Graft Versus Host Disease (GVHD)
GVHD is a situation where transfused lymphocytes engraft and multiply in immunocompromised patients (e.g., bone marrow transplant patients). The newly engrafted lymphocytes attack the host. This is the opposite of a host rejecting a transplanted organ (e.g., a heart).
Transfusion-associated graft versus host disease (TAGVHD) is a different disease from GVHD in allogeneic bone marrow transplant recipients. TAGVHD is uniformly fatal and untreatable. It occurs when the blood products contain T-lymphocytes and attack many host tissues. It occurs when the recipient is immunocompromised
TAGHVD is prevented by gamma-irradiating the blood products to be transfused.