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. Splenectomy can be recommended to patients without contraindications. Renal failure and DIC are also more commonly associated with intravascular haemolysis. In addition, every HSCT candidate, as well as the corresponding donor, can have additional conditions leading to HA (eg, glucose-6-phosphate dehydrogenase deficiency). [55] analysed reports available in the literature describing cases of haemolysis in patients treated with intravenous immunoglobulins [55]. Low doses of dopamine (15g/kg/min) may be used to maintain renal circulation, but this may not be effective. Catheterisation of the pulmonary artery helps to monitor the situation. Delayed red cell engraftment due to host anti-donor isohemagglutinins may occur. However, clinicians should be aware that titer determination is not standardized and shows a wide intra-individual variability. Complement activation appears to be the most important determining factor in these cases. 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]. 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. Acute HA can occur during and immediately after graft infusion as a consequence of donor's RBC hemolysis. Post-reaction LOS was longer by a median of 5 or 7 days for NH-DSTR versus non-anti-RBC TRs and other anti-RBC TRs respectively. In some patient groups, it may be difficult to recognise a delayed haemolytic transfusion reaction. Copyright 2023 by American Society of Hematology, 401. In clinical practice, however, such antibodies can sometimes destroy donor blood cells. Positive reactions with allogeneic blood cells are accompanied by positive auto control of the patients red blood cells. They are mediated by the interaction of recipient antibodies to foreign antigens contained in any allogeneic blood products. Laboratory tests show anaemia, increased LDH and bilirubin, decreased haptoglobin and higher white blood cell counts in post-transfusion haemolytic reactions. Frequency of transfusion reactions from January 1, 2010 to December 31, 2015. Hemolysis in DHTR can be severe, because both the transfused and autologous red blood cells may be destroyed (so-called bystander hemolysis); DHTR WebFebrile nonhemolytic reaction: Headache, fever of38C/100.4F (or an increase of 1C/1.8F from baseline),chills, rigors, and generalized discomfort Allergic reaction: Generalized flushing, rash, hives, itching,angioedema, conjunctival edema, facial edema, hypotension,and/or asthmatic wheezing, and can progress to laryngealedema and *1 J "6DTpDQ2(C"QDqpIdy~kg} LX Xg` l pBF|l *? Y"1 P\8=W%O4M0J"Y2Vs,[|e92se'9`2&ctI@o|N6 (.sSdl-c(2-y H_/XZ.$&\SM07#1Yr fYym";8980m-m(]v^DW~ emi ]P`/ u}q|^R,g+\Kk)/C_|Rax8t1C^7nfzDpu$/EDL L[B@X! Various malignant and nonmalignant diseases are associated with immune-mediated or nonimmune hemolysis. The presence of O2 leads to oxidation of NO to NO3 and oxidation of Fe2+to Fe3+and the formation of methaemoglobin. This makes the subject more susceptible to haemolysis. However, transfusion requirement in acute AIHA can be a medical emergency and must not be delayed as RBC transfusions can be lifesaving. Transfusion support consists primarily in transfusion of RBC concentrates lacking the corresponding antigen. 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. FNHTR manifests as fever and/or chills without I think the LI part of TRALI refers to the fact that it sometimes presents like an ARDS type picture. Failure of central and/or peripheral tolerance is believed to be involved in the escape of auto-reactive lymphocytes, thus leading, if uncontrolled, to the development of ADs. How long does it take for a hemolytic transfusion to occur? To understand that hemolytic anemia (HA) is frequent after hematopoietic stem cell transplantation (HSCT), To discuss different etiologies of HA during and after allogeneic HSCT, To know how to approach and investigate HA in this situation for an accurate diagnosis, To know the prophylactic measures to reduce the extent of hemolysis in case of ABO-incompatible HSCT and to know currently available therapeutic options, To know the special transfusion requirements of patients before, during, and after HSCT, implying a close collaboration between clinicians, transplant physicians, and transfusion services. 0000002721 00000 n It was found that when red blood cells became the bystander of leukocyte reactions and antibodies directed to them, they underwent haemolysis. Due to the multitude of RBC antigens, it is impossible to match stem cell donors, blood donors, and recipients for all these antigens. MFk t,:.FW8c1L&9aX: rbl1 Table 2 presents the point algorithm for the diagnosis of acute disseminated intravascular coagulation. Udani etal. [60] compared the sensitivity of DAT performed by technique using monospecific IgG antiglobulin, flow cytometry and antibody elution. There is an association between TA-TMA and GVHD, although causality remains to be proven. A stepwise diagnostic workup with reasonable investigations is the basis for an accurate diagnosis and appropriate therapy. A characteristic feature of the cell membrane of these blood cells is the lack or weak expression of the CD55 (DAF) and CD 59 (MIRL) proteins, which are complement inhibitors. Heparin is recommended because it additionally acts as an inhibitor of the complement activity and limits haemolysis. CCL2 is mainly a chemotactic and activating factor for monocytes [1, 12]. 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. The specificity of the antibodies potentially responsible for intravascular and extravascular haemolysis is shown in Table 4. Factors that can affect the increase in the number of delayed haemolytic reactions include correctness in carrying out serological tests, longer survival of patients after transfusions and an increase in the number of transfused blood components. Additionally, transplantation-associated thrombotic microangiopathy (TA-TMA) may occur and is associated with significant morbidity and mortality. stream @~ (* {d+}G}WL$cGD2QZ4 E@@ A(q`1D `'u46ptc48.`R0) When acute reactions occur they are typically mild, with the most common reactions including fever and rash. In contrast to ABO incompatibility, donors and recipients lack naturally formed antibodies for non-ABO RBC antigens, occurring only after immunization. % Intravascular haemolysis is accompanied by haemoglobinaemia and usually also haemoglobinuria, whereas extravascular haemolysis can only be accompanied by anaemia. Haemolysis can be endogenous (usually acute) and exogenous with macrophages in the reticuloendothelial system of spleen or liver (delayed). Hemolytic disease of the fetus and newborn is an alloimmune hemolysis caused by maternal antibodies in the neonate's plasma, is most commonly anti-Rh, and One of them was the use of improved techniques for detecting clinically relevant alloantibodies, which reduce the number of haemolytic transfusion reactions observed in blood recipients. Interesting clinical point of view are antibodies from the Kidd system. In addition, acute and delayed transfusion reactions because of a transfusion error should always be excluded, according to the local policies. Their release causes an increase in the concentration of oxygen radicals, leukotrienes, nitric oxide and cytokines. Repeated transfusions of ABO incompatible platelet concentrate may lead to accumulation of anti-A antibodies in the recipients plasma, which may result in severe haemolytic reactions [52]. However, transfused blood is a foreign All other drugs have to be critically reviewed and withdrawn if appropriate. Concomitant hypotension and intravascular coagulation syndrome may increase renal impairment. Additionally, differential diagnosis is not always obvious and patients can present with several potential risk factors for TMA (Table 4). 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. Delayed immune This can be prevented through plasma volume reduction of the product.17, Passenger lymphocyte syndrome (PLS) is a significant and unpredictable complication after minor ABO-incompatible HSCT.18 It usually occurs 1-3 weeks after HSCT and is due to hemolysis of recipient's RBCs through isohemagglutinins produced by donor-derived immunocompetent lymphocytes. Consider HLA-alloimmunization. Is Whole Blood Poised for a Return in Civilian Trauma? The connection of NO with haeme Fe2+ impairs oxygen transport through Hb. /Filter /FlateDecode NH-DSTRs are associated with a longer LOS when compared with all other TRs. In approximately 11% of cases, more than one antibody specificity is detected. The severity of the reaction depends on the titre of anti-A and/or anti-B antibodies in the transfused plasma or in the blood component containing the plasma, and on its volume [47, 48, 49]. It enforces the introduction of procedures eliminating further errors. Asterisk with author names denotes non-ASH members. Further studies are needed to confirm this association. Importantly, alloantibodies can occur against antigens of donor, recipient, and third party-transfused RBCs. 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. The most common reaction among the acute (approximately 30%) was haemolysis resulting from ABO incompatibility [5]. A contrasting example is the Lua antigen and anti-Lua antibodies. Open Access is an initiative that aims to make scientific research freely available to all. Special attention should thus be paid to the donor's ABO blood group and the stem cell source, because they differ in terms of the volume of RBC and plasma, and number of lymphocytes.9 RBC antigens are also expressed on other tissues, including endothelial cells (histo-blood groups). You can have an allergic reaction to a blood transfusion as well. This mechanism is called the classic pathway for complement activation and is shown in Figure 1. The C5B-C9 complex called membrane attack complex (MAC) creates pores in the cell membrane of a red blood cell that are 1/700 of its size. 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]. /Producer (Apache FOP Version 1.0) The decision to carry it out must be balanced and the course carefully monitored. The C1qrs complex is created and activates the C2 and C4 components and their distribution into C2a and C2b as well as C4a and C4b. If a haemolytic transfusion reaction is suspected, medical personnel should immediately stop transfusing a blood component. Hemolytic anemia (HA) is a condition in which the patient's red blood cells (RBCs) are prematurely destroyed. are uncommon. Although pretransfusion prophylactic paracetamol and diphenhydramine are often routinely administered, there is little evidence to support this practice. Proinflammatory cytokines affect blood coagulation and fibrinolysis, for example, TNF- and IL-1 increase TF expression and inhibit thrombomodulin (TM) expression on vascular endothelial cells [28]. WebA hemolytic transfusion reaction is a serious complication that can occur after a blood transfusion. 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]. How? Fibrin creates blood clots in the light of small vessels trapping the platelets. Brief introduction to this section that descibes Open Access especially from an IntechOpen perspective, Want to get in touch? Anti-erythroid antibodies are the classical marks of serologic and hemolytic transfusion reactions. The key pathogenetic phenomenon in DIC is excessive thrombin generation in the tissue factor (TF)-dependent pathway and activated factor VII (FVIIa-activated factor VII) [26]. Positive DAT indicates haemolysis of red blood cells of immunisation origin. Red blood cell (RBC) transfusion can be lifesaving for patients with severe anemia and/or bleeding and generally is safe. Identification is critical because of the high probability of a second patient receiving the wrong blood product at the same time. In contrast, prospective studies also contain errors due to reaction symptoms often remaining unrecognised or masked by associated diseases, for example, bleeding or liver disease [1]. This phenomenon is called delayed serologic transfusion reaction (DSTR) and should be differentiated from delayed haemolytic transfusion reaction [9]. Laboratory testsmainly serologicalare crucial for the diagnosis of an early haemolytic reaction. Autoimmune hemolytic anemia (AIHA). Suggested transfusion guidelines for patients undergoing ABO-incompatible HSCT6,8. By Osaro Erhabor, Tosan Erhabor, Teddy Charles Adias By Vivian Gonzaga, Bruna Policiquio, Cristiane Wences By Vernica Valdivieso-Gmez, Javier Garrancho-Prez, IntechOpen Limited The severity of this abnormality varies greatlyfrom asymptomatic increase in urea (BUN) and serum creatinine up to complete anuria. Hemolytic anemia (HA) is a condition in which the patient's red blood cells (RBCs) are prematurely destroyed. This has been tested for its use as a substitute for red blood cells. << Investigation may be difficult because the differential diagnosis is often broad. Data on the incidence of haemolytic transfusion reactions vary from country to country and change over time. In both methods, in addition to the reference blood cells, the patients autologous blood cells should be included. If positive results indicate alloantibodies are present, they should be identified. Please check for further notifications by email. Number of antigenic determinants on the cell surface of the red blood cell (according to [12, 13]). Diagnosis and treatment of transplantation-associated thrombotic microangiopathy: real progress or are we still waiting? 0000007661 00000 n Licensee IntechOpen. Attempts have been made to use high doses of intravenous immunoglobulins to prevent haemolytic reactions in patients who have been immunised for winter and for whom compatible red blood cells have not been selected [63]. Haemolytic transfusion reaction (HTR) is the result of accelerated destruction of red blood cells. 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 Early haemolytic transfusion reactions should be differentiated with septic shock due to bacterial contamination of the blood component, as well as anaphylaxis and bleeding. Hemolytic transfusion reactions can be immune or non-immune mediated. There was no significant difference between groups when evaluating inpatient mortality. Tests on the ABO system titre in group O apheresis concentrates of platelets show that 26% of samples have an anti-A or anti-A, B antibody titre of 64 or higher. ABO-incompatible platelet transfusions can cause hemolysis, in particular, platelet concentrates from donors with high isohemagglutinin titers. Convertase breaks down molecules of C3 into C3a, C3b, C3c and C3d. Within the anti-RBC TRs, 159 (71.9%) were classified as NH-DSTRs. A case of acute hemolytic transfusion reaction due to anti-Dia antibody: A case report. 22-26% of A2B individuals can have anti A1 antibodies that react a temperature below 25 degrees and cause hemolytic transfusion reaction. (1,2) We present a rare case of an A2B positive blood group with postpartum hemorrhage, DIC in hypovolemic shock. Table 1 shows the number of antigenic determinants on the cell surface for selected red blood cell antigens. MM declares that she has no competing interests. Most data come from retrospective studies that do not include reactions not reported by clinicians. WebNon-immune hemolytic anemia (NIHA) is characterized by positive routine hemolytic tests but negative anti-human immunoglobulin (Coombs) test. xwTS7PkhRH H. In other cases, the C3b component activates C5 and C5a and C5b are formed. /Length 11 0 R [20] showed invitro that in the case of ABO incompatibility, monocytes are directly involved in the formation of acute haemolytic transfusion reaction [15]. However, it is important to avoid overloading the circulation with fluids, especially in patients with heart or kidney failure. To date our community has made over 100 million downloads. * Conditions that can occur alone or in combination in HSCT recipients. Differential diagnosis of delayed haemolytic transfusion reactions includes latent sources of infection, autoimmune haemolytic anaemia, cold agglutinin disease, nocturnal paroxysmal haemoglobinuria, bleeding, mechanical destruction of red blood cells, for example, artificial heart valves and TTP. Do you want to go to BMJ Best Practice for United Statesinstead? Therefore, if possible, blood without this antigen should be selected [41]. The mechanism of appearance of intravascular symptoms has not been fully explained, because although some of the antibodies bind complement components, their reactions end with C3 components. Finally, current therapeutic approaches for both TA-TMA and post-HSCT autoimmune HA, which are associated with high morbidity and mortality, are discussed. >> Again, evidence is too weak to support treatment with TPE.14,41, Autoimmune diseases (ADs) after both autologous and allogeneic (including cord blood) HSCT may occur regardless of the underlying disease.42-44 The exact mechanisms and the pathophysiology of post-transplant ADs are not yet fully understood. They are usually IgM molecules, are rarely active at 37C and usually do not bind complement. Such a blood cell, after being released from the macrophage, circulates in the blood as a spherocyte, whose survival is short. Copyright 2023 American Society of Anesthesiologists. HLA antigens found on leukocytes and plasma proteins), while red blood cells are only close to this immunological confusion [56]. Table 8 presents changes in laboratory indicators in transfusion haemolytic reactions [56]. Schonewille etal. In approximately 50% of cases, alloantibodies produced after transfusion or pregnancy cease to be detected after a few months, and this period of time depends on the specificity of the antibodies and the individual characteristics of the immune system. The blood unit should be checked at the patients bedside, whether it was properly administered. Hemolytic anemia conditions encountered before, during and after hematopoietic stem cell transplantation (HSCT). 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). %PDF-1.4 % {{{;}#tp8_\. The occurrence and severity of individual clinical symptoms can vary widely and are often non-specific [1, 8]. Spath etal. It was estimated that the frequency of reactions resulting from the ABO incompatibility was 1:27,318, acute haemolytic transfusion reactions 1:14,901 and delayed haemolytic transfusion reactions 1:9313 per unit of transfused red blood cell concentrate [5]. Other causes of HA should be excluded. In ABO incompatibility, in which anti-A, anti-B and anti-AB antibodies activate complement leading to intravascular haemolysis, a large amount of tumour necrosis factor- (TNF) and interleukins CXCL8 (IL-8) and CCL2 are released into the plasma (MCP-1) [19, 20, 21]. However, there is no accepted and clear definition for high-titer antibodies. They may be similar to delayed haemolytic reactions. In all these cases, haemolysis takes place via the classical pathway of complement activation. Andreas Holbro, Division of Hematology, Department of Internal Medicine, University Hospital, Petersgraben 4, 4031 Basel, Switzerland; Phone: 0041-61-265-25-25; Fax: 0041-61-265-44-50; e-mail: andreas.holbro@usb.ch. Laboratory tests that help to differentiate haemolysis include determination of free haemoglobin in the blood and urine, haptoglobin and lactate dehydrogenase (LDH) and bilirubin. IL-1ra (receptor antagonist) is produced in extravascular haemolysis, which is an IL-1 receptor antagonist. Lack of these particles may increase the susceptibility of red blood cells to intravascular haemolysis due to complement activation [19]. Acute hemolysis may also rarely occur after minor ABO-incompatible HSCT through transfer of high-titer donor isohemagglutinins contained in the graft or in recipients with small blood volume (pediatric patients). In addition, immune haemolysis of nocturnal paroxysmal haemoglobinuria or autoimmune anaemia should also be considered. The safety of body cells is enabled by factors that regulate complement activity present in plasma and on cells of various tissues, including red blood cells. The nature of the reaction may not be immediately apparent, Other etiologies of TMA should be excluded, although the discrimination between drug-induced TMA and TA-TMA in transplanted patients is difficult. Hemolysis can be severe, even fatal, and persists until all the recipient RBCs are replaced by transfused or donor-derived RBCs. Therapeutic options in haemolytic transfusion reactions [1]. Anesthesiology 1946; 7:98 doi: https://doi.org/10.1097/00000542-194601000-00029. The distribution of TRs (Figure 1) included 562 (71.8%) non-anti-RBC TRs and 221 (28.2%) anti-RBC TRs. In those with concurrent hemolysis, the red blood cell (RBC) breakdown may be severe enough to command supportive care. D indicates donor ABO blood group; PLT, platelet; R, recipient ABO blood group; and RBC, red blood cell. Prompt recognition of an immune-mediated transfusion reaction is fundamental to improving patient outcome. These errors are the most common cause of ABO incompatible transfusions, threatening the patients life. 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. WebTransfusion Reactions Also known as AHTR (acute hemolytic transfusion reaction) DHTR (delayed hemolytic transfusion reaction) FNHTR (febrile non-hemolytic In the case of minor incompatibility both immediate and delayed hemolysis can occur.21 In this case, management is similar to ABO-incompatibility. Alloantibody testing should be performed in the intermediate antiglobulin test (IAT) and enzyme test. 2015 by The American Society of Hematology. HWr6}WiL i A2$Tfk+'Ly8#J&E,U[.5O}@JYjE"t,VbptZ[1z/I8~:{;y2F"@i"DGA,?Th)BZ(E. Treatment depends upon the type of transfusion reaction. PLS is more common in patients with blood group A, with a donor of group O, and cyclosporine A (CYA) alone as GVHD prophylaxis. Another group are patients with absorbing haematomas. This topic will mainly address immune-mediated transfusion reactions, which comprise an array of distinct adverse clinical responses to transfusion. How do I approach ABO-incompatible hematopoietic progenitor cell transplantation? Primarily, calcineurin inhibitors and/or sirolimus should be reduced in dose or discontinued if alternative drugs for the prevention or treatment of GVHD can be administered (eg, steroids, mycophenolate mofetil). Only in rare cases, platelet components have to be washed. On the other hand, the formation of a large amount of blood clots will consume blood coagulation factors and platelets, which will manifest as a haemorrhagic diathesis. Antibodies of the IgM and IgG class (outside the IgG4 subclass) bind the C1q protein in the initial stage of activation. They include acute haemolytic, febrile non-haemolytic, allergic (with or without anaphylaxis), and transfusion-related acute lung injury (TRALI). Red blood cell transfusion can also stimulate the production of alloantibodies without the occurrence of haemolysis. Another cause for haemolytic transfusion reaction may be a secondary immune response in patients who have developed alloantibodies during previous transfusions of blood components or pregnancy. This icon denotes a clinically relevant abstract. Bilirubin concentration depends on the severity of haemolysis and liver function. Steroids should be administered at a dosage of 1-2 mg/kg. Blood clots that form in the renal arterioles cause cortical kidney attacks. 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].
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