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Blood transfusion 

Blood transfusion

Blood transfusion

H.S. Alhumaiden

, P.L. Perrotta

, Y. Han

, and E.L. Snyder



New sections on processing blood components and pre-transfusion testing added with figures illustrating the processes; more processing steps that are performed in the blood bank added; new information on pathogen reduction technology; newly recognized transfusion reactions added; updated information on the molecular testing in the blood bank.

Updated on 30 May 2013. The previous version of this content can be found here.
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date: 27 March 2017

Transfusion of blood components is a life-saving treatment for patients with severe haemorrhage: it can also be used to replace coagulation factors and to ameliorate the effects of severe anaemia, thrombocytopenia, and impaired platelet function. However, blood transfusion has many hazards, hence its use should always be considered carefully and restricted to those who will gain benefit that outweighs the risks.

General considerations

Safe administration of blood components requires secure processes from vein to vein to prevent the wrong blood product from being given to the wrong patient. Reduction in transfusion risks is also achieved by (1) robust arrangements for the collection, storage, and delivery of appropriate supplies of blood products to their point of need; (2) better understanding of the antigenic structures on blood cells and the widespread introduction of advanced blood-group typing methods, screening for antibodies, and testing for compatibility before transfusion; (3) identification and screening for agents present in donors, as well as the use of sterile disposable materials.

Blood group systems—these include (1) ABO system—the codominantly expressed A and B genes code for glycosyl transferases that add either N-acetyl-d-galactosamine (A gene) or d-galactose (B gene) to the common precursor H antigen. Anti-A and Anti-B antibodies are ‘naturally occurring’ and responsible for most haemolytic transfusion reactions. (2) Rhesus system—the most clinically important Rh antigen is D because it is strongly immunogenic; anti-D is responsible for immune reactions including haemolytic disease of the newborn and immune-mediated transfusion reactions. (3) Other clinically significant blood group antigens—these include Kell (K), Duffy (Fy), Kidd (Jk) and the MNS systems; multiple antibodies can develop when the range of red-cell antigens in the donor population differ from that of patients who require repeated transfusion.

Clinical use of blood components

Cellular components—these include (1) red blood cells—symptomatic anaemia; (2) leucocyte-reduced components (red blood cells and platelets)—symptomatic anaemia, reduce febrile reactions from leucocyte antibodies, alternative to cytomegalovirus-negative components, prevent HLA alloimmunization; (3) washed components (red blood cells and platelets)—remove harmful plasma antibodies; (4) platelet components—thrombocytopenia with bleeding, prophylactic transfusion, platelet function abnormalities; (5) granulocytes (obtained by apheresis)—for neutropenic patients with infection unresponsive to antibiotics (rarely used, given increased use of haemopoietic growth factors in haematological practice); donor lymphocyte infusions can induce remission of disease and improve survival by exerting a graft-vs-leukaemia effect in some bone marrow transplant recipients.

Plasma, cryoprecipitate, and plasma derivatives—these include (1) fresh frozen plasma—replacement of plasma coagulation factors for which specific factor concentrates are not available, liver disease, disseminated intravascular coagulation, hypofibrinogenaemia, thrombotic thrombocytopenic purpura, dilutional coagulopathy, and reversal of vitamin K antagonists; (2) cryoprecipitate—fibrinogen and factor XIII replacement, factor VIII and von Willebrand factor replacement when recombinant and virus-inactivated concentrates are not available; (3) albumin—used principally in specialized surgical practice, replacement fluid in therapeutic plasma exchange, and in the treatment of liver disease; (4) intravenous immunoglobulin—used principally for immunodeficiency syndromes, autoimmune rheumatic/vasculitic diseases, Guillain–Barré syndrome and autoimmune haemolytic anaemias; specific Rh (D) immunoglobulin is used to prevent alloimmunization in D-negative mothers; specific immunoglobulin preparations are used as antivenoms and to treat viral infections e.g. hepatitis A and B.

Complications of transfusion therapy

Immune complications—these include (1) acute intravascular haemolytic reactions—usually caused by transfusions of ABO-incompatible blood resulting from patient identification or clerical errors; manifest with sudden onset of back pain, hypotension, tachycardia, fever, chills, diaphoresis, and dyspnoea; treatment consists of immediately stopping the transfusion and providing supportive care, but can be fatal despite best management; (2) delayed haemolytic reactions—usually caused by an antibody that is initially of a titre below the limits of detection on routine screening; (3) febrile nonhaemolytic reactions—usually attributed to the development of antibodies in the recipient directed against HLA and/or leucocyte-specific antigens on donor white blood cells and platelets; (4) allergic reactions—IgE mediated; IgA-deficient patients are particularly prone to anaphylactic reactions; (5) transfusion-related acute lung injury; (6) transfusion-associated graft-vs-host disease.

Nonimmune complications—these include (1) infection—organisms commonly implicated in septic reactions include Gram-positive (staphylococci) and Gram-negative (enterobacter, yersinia, pseudomonas) bacteria. Other infections that may be transmitted from the donor include malaria, babesiosis, syphilis, leishmania, toxoplasmosis, and viral infections such as hepatitis B and C, HIV1, HIV2, and West Nile virus. Immunocompromised recipients are also at risk from human cytomegalovirus and parvovirus B19. A few patients have been shown to have acquired variant Creutzfeld–Jacob disease, probably as a result of transfusion from latently affected donors. (2) Other complications—acute problems can include circulatory overload, dilutional coagulopathy, hypocalcaemia, and hypothermia; complications of multiple blood transfusions include iron overload.

Prevention of complications—risks of alloimmunization from donor leucocytes and transmission of viruses can be avoided or reduced by (1) autologous blood salvage during surgery or acute normovolaemic haemodilution immediately before surgery; (2) improved methods for leucocyte reduction and inactivation of infectious agents. Despite much research the introduction of blood substitutes has yet to be realized in clinical practice. Use of purified recombinant haematopoietic growth factors (e.g. erythropoietin, granulocyte colony stimulating factor) has reduced the need for transfusion of blood products in many patients.

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