Search for other works by this author on: Hematopoietic SCT in Europe 2013: recent trends in the use of alternative donors showing more haploidentical donors but fewer cord blood transplants, Autoimmune cytopenia in chronic lymphocytic leukaemia: diagnosis and treatment, An evidence-based approach to the treatment of adults with sickle cell disease, How I treat autoimmune hemolytic anemias in adults, A review of transfusion practice before, during, and after hematopoietic progenitor cell transplantation, Clinical guide to ABO-incompatible allogeneic stem cell transplantation, Red blood cell-incompatible allogeneic hematopoietic progenitor cell transplantation, Allogeneic blood stem cell transplantation: peripheralization and yield of donor-derived primitive hematopoietic progenitor cells (CD34+ Thy-1dim) and lymphoid subsets, and possible predictors of engraftment and graft-versus-host disease, Bone marrow transplantation with major ABO blood group incompatibility using erythrocyte depletion of marrow prior to infusion, Outcomes after major or bidirectional ABO-mismatched allogeneic hematopoietic progenitor cell transplantation after pretransplant isoagglutinin reduction with donor-type secretor plasma with or without plasma exchange, Prevention of pure red cell aplasia after major or bidirectional ABO blood group incompatible hematopoietic stem cell transplantation by pretransplant reduction of host anti-donor isoagglutinins, Guidelines on the use of therapeutic apheresis in clinical practice-evidence-based approach from the Writing Committee of the American Society for Apheresis: the sixth special issue, Persistence of recipient plasma cells and anti-donor isohaemagglutinins in patients with delayed donor erythropoiesis after major ABO incompatible non-myeloablative haematopoietic cell transplantation, Prognostic impact of posttransplantation iron overload after allogeneic stem cell transplantation. Finally, disease relapse needs to be considered and ruled out. The reaction generally occurs in high-dose IVIG recipients [55]. They showed that the haemolytic reaction is induced by IgG anti-A/B antibodies present in immunoglobulin products. 7, 98. https://doi.org/10.1097/00000542-194601000 However, the propensity to form a new anti-RBC antibody may reflect an underlying pro-inflammatory comorbid state that itself may be influencing LOS. In contrast, the incidence for patients receiving a transfusion is estimated to be higher (about 1:5001:800 patients) because most recipients receive more than one blood unit. If a haemolytic transfusion reaction is suspected, medical personnel should immediately stop transfusing a blood component. In contrast, the presence of antigens from the Rh, Kell, Kidd and Duffy systems on the surface of red blood cells is determined in the range of 103104 per cell [12]. Delayed red cell engraftment due to host anti-donor isohemagglutinins may occur. It should be noted that an increase in body temperature and white blood cell count, typical for DHTR, can be interpreted as a sign of infection. Haemolytic post-transfusion reaction is caused by accelerated destruction of erythrocytes by immunological incompatibility between the donor and the recipient. Ness etal. In those with concurrent hemolysis, the red blood cell (RBC) breakdown may be severe enough to command supportive care. The patient's history, knowledge of the performed transplant procedure (type and intensity of conditioning, donor and recipient ABO blood group, graft source, and GVHD prophylaxis and therapy) and the patient's transfusion history are essential. Only in rare cases, platelet components have to be washed. 2020 The Author(s). << 38 0 obj<> endobj In addition, the widespread introduction of automation and computerisation to pre-transfusion studies, which significantly limits the possibility of errors in serology laboratories and blood banks. xb```f`` @1V h`f Contact our London head office or media team here. It is possible that technological progress enabling modification of red blood cells and the use of red blood cell substitutes will significantly change transfusion practice in the future and eliminate the occurrence of haemolytic transfusion reactions. WebFebrile non-hemolytic transfusion reaction (FNHTR): This is defined as an acute increase in body temperature >1C within 4 hours of the end of a transfusion and a temperature of >39C or 102.5F that cannot be explained by other Some symptoms of hemolytic anemia are the same as those for other forms of anemia. Haemolysis may also occur due to non-immunological reasons, such as thermal, osmotic or mechanical damage to the transfused blood; bacterial infection or extremely rare and blood transfusion from a donor with congenital haemolytic anaemia due to deficiency of glucose-6-phosphate dehydrogenase [2]. Impaired renal function is observed in both intravascular and extravascular haemolytic transfusion reactions, although definitely more frequently in the case of intravascular. The presence of fibrinogen degradation products from an absorbing haematoma can be interpreted as a DIC symptom. 0000000576 00000 n We have maintained this order throughout the review, the tables, and the graphical representation. The re-determination of the ABO and RhD blood group of the recipient before and after the transfusion and in the donors blood will exclude errors in the identification of the recipient or blood sample (wrong blood in tube (WBIT)). We follow the timeline of the transplantation process and discuss investigations, differential diagnosis, and prophylactic measures including graft processing to avoid hemolysis in case of ABO incompatibility. The blood unit should be checked at the patients bedside, whether it was properly administered. Additional fluid and diuretic therapy are usually not necessary. There is an association between TA-TMA and GVHD, although causality remains to be proven. Please check for further notifications by email. In different people, antibodies with a particular specificity most often occur in the same class of immunoglobulins and have a similar heat amplitude, for example, anti-A, anti-B and anti-AB from the ABO system often belong to both IgM and IgG classes, they bind complement and have an extended thermal amplitude of up to 37C. It had vasoconstrictive and, as a result, hypertensive effect. We can see youre on your way to BMJ Best Practice for, Do you want to go to BMJ Best Practice for, No, Id like to continue to BMJ Best Practice for, bleeding from mucous membranes, GI tract, or urinary tract, exfoliative dermatitis with mucocutaneous involvement, visual inspection of post-transfusion blood sample, repeat ABO testing on post-transfusion blood sample, Gram stain and culture of component and post-transfusion recipient samples. Antibodies destroying transfused blood cells are called clinically relevant antibodies that are active invitro at 37C. 0000001590 00000 n If blood transfusions are indicated, crossmatching can be unable to identify compatible RBC units, as the autoantibodies are directed against highly prevalent antigens. Most of the cells coated by the complement C3b component are destroyed by liver macrophages, that is, by Kupffer cells, while the cells coated with antibody molecules are mainly destroyed by spleen macrophages. Patients with antibodies found to be clinically insignificant may theoretically be given a blood transfusion from a donor with the antigen to which they are directed. Furthermore, transfusion of incompatible plasma is associated with increased transplant-related mortality due to an increased risk of infection, veno-occlusive disease, and multi-organ failure.22,23 Therefore, both donor- and recipient-compatible plasma should be transfused after HSCT to avoid hemolysis, due to the passive transfer of isohemagglutinins against recipient and/or donor RBC antigens (Table 3). Table 8 presents changes in laboratory indicators in transfusion haemolytic reactions [56]. EdwardB. Flink; The Distinction of Hemolytic and Nonhemolytic Transfusion Reactions. This can lead to hemolytic anemia, in which the body destroys the transfused 0 5 Princes Gate Court, NO can bind to thiol groups and haemoglobin haeme [35]. In those with concurrent hemolysis, the red blood cell (RBC) breakdown may be severe enough to command supportive care. Acute transfusion reactions range from bothersome yet clinically benign to life-threatening reactions. IVIG formulations with low isohemagglutinin titers and/or adjustment of dosage can prevent IVIG-induced HA, especially for patients with blood group A. TMA describes a syndrome characterized by microangiopathic HA, thrombocytopenia due to platelet consumption, and microvascular thrombosis (Table 4).25 The formation of platelet-rich thrombi induces mechanical RBC damage and thus intravascular hemolysis. ??accessibility.screen-reader.external-link_en_US?? This is called delayed haemolytic transfusion reaction (DHTR) in which current blood transfusion stimulates memory lymphocytes and stimulates the production of alloantibodies directed at incompatible antigen found on transfused blood cells [21, 42]. Treatment of early haemolytic transfusion reactions depends mainly on the patients condition, which must be closely monitored. >> Depending on the severity of the anaemia, transfusion of blood components should be avoided until the antibodies responsible for the reaction have been identified and the appropriate selection of blood cells has been made. microspherocytes? /N 3 The basic serological examination consists of direct antiglobulin testing (DAT); determination of blood group and RhD in donor and recipient; repetition of the serological compliance test. On blood cells with the Cromer mull phenotype, known as Inab, DAF inhibitor expression is absent [17, 18]. This means that after transfusion of red blood cells, the production of alloantibodies directed to the antigen found on the transfused blood cells occurs. Flow cytometry proved to be a similarly sensitive method. 38 14 WebHemolytic disease of the newborn (also known as HDN or erythroblastosis fetalis) Rh D hemolytic disease of the newborn (also known as Rh disease) ABO hemolytic disease of the newborn (the direct Coombs test may only be weakly positive) Anti-Kell hemolytic disease of the newborn Rh c hemolytic disease of the newborn Patients have clinical and laboratory evidence of HA, a positive DAT (usually positive for IgG C3d in warm-type and positive for C3d in cold-type AIHA), and a positive, panreactive indirect antiglobulin test. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. It is worth noting that the estimation of the frequency of haemolytic reactions depends on the number of transfusions in a given centre. CCL2 is mainly a chemotactic and activating factor for monocytes [1, 12]. As a consequence of antibody-dependent cell-mediated cytotoxicity (ADCC) haemoglobinemia and haemoglobinuria may occur similarly to intravascular haemolysis, although the antibodies that caused it do not bind complement components. Within the anti-RBC TRs, 159 (71.9%) were classified as NH-DSTRs. For example, for 70kg recipient, about 18ml of transfused red blood cells are destroyed per hour. found that, using current laboratory methods, 25% of red blood cell antibodies become indeterminate on average after about 10months from production [43]. In both methods, in addition to the reference blood cells, the patients autologous blood cells should be included. Prospects through stem cell manipulation and graft processing have to be followed in the future. These include, among others, errors in collecting blood samples from patients and blood transfusions to a wrong patient. {{{;}#tp8_\. [62]. Performing DAT in the red blood cell eluate, its sensitivity was 1%. Therefore, prior to conducting laboratory tests of donor blood, bacteriological examination of the component remaining after the transfusion cessation should be conducted. In approximately 11% of cases, more than one antibody specificity is detected. Human Blood Group Systems and Haemoglobinopathies, Submitted: June 11th, 2019 Reviewed: January 6th, 2020 Published: March 3rd, 2020, Edited by Osaro Erhabor and Anjana Munshi, Total Chapter Downloads on intechopen.com. Data on the incidence of haemolytic transfusion reactions vary from country to country and change over time. No cases of acute haemolytic reaction caused by anti-Lua antibodies have been reported, delayed transfusion haemolytic reaction is rare and occurs only in mild form. Early haemolytic transfusion reactions should be differentiated with septic shock due to bacterial contamination of the blood component, as well as anaphylaxis and bleeding. Antibodies capable of destroying transfused blood cells are called clinically relevant antibodies, and the transfusion reaction in the event of immunological incompatibility depends on: (1) specificity of antibodies; (2) thermal amplitude of the antibodies; (3) IgG classes and IgG subclasses; (4) number, density and spatial configuration of antigenic sites on red blood cells; (5) the ability of antibodies to activate the complement system; (6) plasma concentrations of antibodies and (7) volumes of transfused red blood cells. Antibodies stimulated for synthesis may cause symptoms of haemolysis after 310days, usually very mild and their presence can be detected after 1021days. The quoted breakdown of reactions is somewhat artificial, because the symptoms associated with haemolytic reactions sometimes overlap [1]. Approximately one-third of patients who were examined 25days after the onset of the reaction presented a positive DAT due to autoantibodies with broad specificity [9]. In incompatibility, in which non-complement IgG antibodies cause extravascular haemolysis, cytokines belonging to two categories differing in response rates are produced: (1) synthesised at a concentration higher than 1g/ml within 24h and (2) synthesised at a concentration of about 100pg/ml. WebFebrile non-hemolytic transfusion reaction (FNHTR) is the most common type of transfusion reaction. During the haemolytic reaction, C3a, C4a, C5a and C5a-des-arg anaphylatoxins are released. Disturbances deemed unrelated to transfusion were excluded. Membrane inhibitor of reactive lysis (MIRL) (CD59) and decay accelerating factor (DAF) (CD55) are essential to protect red blood cells from haemolysis. To which extent the above-mentioned immunosuppressants are directly responsible for or sustain TA-TMA remains speculative. The incidence of autoantibodies after DHTR may be even higher because autoantibodies may mimic the specificity of alloantibodies. Another group are patients with absorbing haematomas. Hematology Am Soc Hematol Educ Program 2015; 2015 (1): 378384. TMA is a well-recognized complication after HSCT (TA-TMA). Books > endstream endobj 39 0 obj<> endobj 41 0 obj<> endobj 42 0 obj<>/Font<>/ProcSet[/PDF/Text]/ExtGState<>>> endobj 43 0 obj<> endobj 44 0 obj<> endobj 45 0 obj[/ICCBased 50 0 R] endobj 46 0 obj<> endobj 47 0 obj<> endobj 48 0 obj<> endobj 49 0 obj<>stream WebIf the recipient's immune system attacks the red blood cells of the donor, it is called a hemolytic reaction. Frequency varies according to reports and may be seen in up to 35% of patients, depending on the diagnostic criteria and definitions.26-28 In contrast to thrombotic thrombocytopenic purpura (TTP), where an inborn or acquired deficiency of the von Willebrand factor multimer cleaving protease ADAMTS13 is the cause, the exact etiology and pathophysiology of TA-TMA remain unclear.25,28-30 Clinical presentation is heterogeneous and it is likely that TA-TMA represents a clinical syndrome that is a common end product of different pathophysiologic processes involving also the coagulation system. DAF regulates C3a-converting activity. In oxyHb, cysteine is exposed at position 93 of the haemoglobin amino acid chain (Cys 93). Initial symptoms of haemolytic transfusion reactions. D indicates donor ABO blood group; PLT, platelet; R, recipient ABO blood group; and RBC, red blood cell. HA can also occur after high doses of intravenous immunoglobulins (IVIGs), as these products are manufactured from human plasma and some of them may contain isohemagglutinins if the manufacturing process does not include a removal step.24 IVIGs are often administered to patients after HSCT to prevent or treat infectious complications. Andreas Holbro, Jakob R. Passweg; Management of hemolytic anemia following allogeneic stem cell transplantation. Acute reactions occur within 24 hours of transfusion and include acute haemolytic, febrile non-haemolytic, allergic, and transfusion-related acute lung injury (TRALI). In addition, their degradation products (fibrinogen/fibrin degradation products (FDP)) resulting from the breakdown of fibrinogen and fibrin exhibit anticoagulant properties, inhibit platelet function, act as cytotoxic vascular endothelium and increase capillary permeability, further disrupting haemostasis mechanisms [26]. In summary, awareness of possible complications after ABO-incompatible HSCT and early recognition and institution of appropriate measures are essential. Blood 2016; 128 (22): 2633. doi: https://doi.org/10.1182/blood.V128.22.2633.2633. Receptors for complement activation products C3a and C5a are found on many cells: monocytes, macrophages, neutrophils, platelets, endothelium and smooth muscle. The condition for complement activation is the binding of the C1q molecule by two Fc fragments of adjacent IgG antibodies or by one IgM molecule. @~ (* {d+}G}WL$cGD2QZ4 E@@ A(q`1D `'u46ptc48.`R0) In the annual report Serious Hazards of Transfusion (SHOT), published in England, in 2017, 42 haemolytic transfusion reactions were reported in reference to 3230 of all reactions observed following transfusion of blood components, of which 13 cases of acute haemolytic transfusion reaction and 29 cases of delayed haemolytic reaction (including 6 cases of hyperhemolysis) were reported. Massive immune haemolysis after allogeneic peripheral blood stem cell transplantation with minor ABO incompatibility, Transfusion policy in ABO-incompatible allogeneic stem cell transplantation, Immune hemolysis involving non-ABO/RhD alloantibodies following hematopoietic stem cell transplantation, Non-ABO red blood cell alloantibodies following allogeneic hematopoietic stem cell transplantation, ABO incompatibility as an adverse risk factor for survival after allogeneic bone marrow transplantation, ABO-incompatible bone marrow transplantation: the transfusion of incompatible plasma may exacerbate regimen-related toxicity, Adverse effects of immunoglobulin G therapy: thromboembolism and haemolysis, Blood and marrow transplant clinical trials network toxicity committee consensus summary: thrombotic microangiopathy after hematopoietic stem cell transplantation, Validation of recently proposed consensus criteria for thrombotic microangiopathy after allogeneic hematopoietic stem-cell transplantation, Small vessels, big trouble in the kidneys and beyond: hematopoietic stem cell transplantation-associated thrombotic microangiopathy. Febrile non-hemolytic transfusion reaction (FNHTR) Febrile non-hemolytic transfusion reactions are the most common reaction reported after a transfusion. FNHTR is characterized by fever or chills in the absence of hemolysis (breakdown of red blood cells) occurring in the patient during or up to 4 hours after a transfusion. Autoimmune hemolytic anemia. Copyright 2023 American Society of Anesthesiologists. In addition, due to immunosuppression, patients are at a risk of various infections, which in turn can cause HA or result in the development of post-transplant lymphoproliferative diseases; the latter, in rare cases, can manifest as AIHA.48. Some patients may experience organ failure such as the pancreas, heart and even multiple organ failure that threatens the patients life. This has been tested for its use as a substitute for red blood cells. Other etiologies of TMA should be excluded, although the discrimination between drug-induced TMA and TA-TMA in transplanted patients is difficult. Data Collection In general, switching to another calcineurin inhibitor or sirolimus is not recommended. Alvarez etal. Features of late hemolytic transfusion reaction and time of their occurrence [21]. The course is acute, dynamic, with thrombocytopenia, increased concentration of fibrin degradation products, prolonged prothrombin time (PT), extended partial thromboplastin time after activation (activated partial thromboplastin time (APTT)) and hypofibrinogenaemia. Hemolytic conditions in allogeneic hematopoietic stem cell transplant recipients. Finally, current therapeutic approaches for both TA-TMA and post-HSCT autoimmune HA, which are associated with high morbidity and mortality, are discussed. IL-1ra (receptor antagonist) is produced in extravascular haemolysis, which is an IL-1 receptor antagonist. Clinically, this is manifested by unexpected bleeding and/or a decrease in blood pressure. doi: https://doi.org/10.1182/asheducation-2015.1.378. Optimal management of HA after allogeneic HSCT implies an interdisciplinary approach and a close collaboration between clinicians, transfusion service and blood bank and the stem cell laboratory. Haemolysis can be endogenous (usually acute) and exogenous with macrophages in the reticuloendothelial system of spleen or liver (delayed). Licensee IntechOpen. In the case of haemolysis of red blood cells, the free haemoglobin released from them reacts with NO much faster and more strongly than Hb inside cells [35]. @Rt CXCP%CBH@Rf[(t CQhz#0 Zl`O828.p|OX Patients with liver failure are a special problem. They activate the complement system to the stage of binding of the C3b component, causing extravascular haemolysis. Further studies are needed to confirm this association. Laboratory testsmainly serologicalare crucial for the diagnosis of an early haemolytic reaction. They are destroyed by the complement system, although they did not participate directly in the antigen-antibody reaction. If negative results are obtained, additional tests should be performed, for example, PTA PEG, polybrene test and PTA NaCl test. They are mediated by the interaction of recipient antibodies to foreign antigens contained in any allogeneic blood products. The evaluation of haptoglobin and free hemoglobin in serum and urine can be helpful. 0000002797 00000 n Hemoglobin monitoring (sometimes repetitively in 1 day in case of severe hemolysis), a full blood count including reticulocytes, blood smear (schistocytes? Delayed haemolytic transfusion reactions are well tolerated by most patients. Therefore, one may speculate that ABO incompatibility could have an association with the pathogenesis of GVHD. Acute HA can occur during and immediately after graft infusion as a consequence of donor's RBC hemolysis. CXCL8 primarily activates neutrophils, which leads to the accumulation of leukocytes in the lung vessels of small diameter and damage to the endothelium of blood vessels and their higher permeability [1, 12]. This varies depending on the graft source, as bone marrow contains more RBCs compared with peripheral blood progenitor cells (PBSCs) collected by apheresis and cord blood (CB).

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