ABO-incompatible Blood Transfusion Research Articles

An Analysis of Blood Grouping Discrepancies : Study From Tertiary Hospital based Blood Bank in Vadodara

Background:-ABO and Rhesus blood group system is considered as clinically significant blood groupsystems in transfusion practice . A feature of the ABO system is the regular occurrence of anti A and anti B inthe absence of the corresponding red cell antigen. A Discrepancy exists when results of forward testing doesnot match with reverse testing. Blood donors and patients must be correctly ABO and Rh grouped becausetransfusing ABO incompatible blood transfusions which may lead even death of patient.Aims and Objectives To assess the incidence and cause of blood grouping discrepancies in Blood Bankat Tertiary care teaching hospital during Jan 2019 to December 2019.Methods : Forward and reverse grouping were performed on blood samples from inpatients ,outpatientsand donors during the study period. ABO discrepancies were studied with their clinical details to group theirdiscrepancies and resolve them with suitable steps.Results: A total of 10,048 (patients and donors) who satisfied inclusion criteria were included and ABOtyped among which there were 55 discrepancies were observed (15 donors and 35 patients). The problemin patients was due to expression of weak antigens. The problem in patients were due to clinical conditions,the most common being autoimmune haemolytic anaemia.Conclusions: The ABO blood group discrepancy reported in present study is 0.49%. The study helped todetermine the incidence and causes of discrepancy encountered in tertiary care hospital. Discrepant resultsshould be recorded, and resolved by suitable measures and correct ABO & Rh Blood group should bereleased to avoid any mismatched transfusions.

Learning From ABO-incompatible Blood Transfusion: Looking Back on the past 10 Years and the Concern of Forgetting.

Learning From ABO-incompatible Blood Transfusion: Looking Back on the past 10 Years and the Concern of Forgetting.

Tissue Molecular Genotyping Improves Patient Blood Management in Syrian Injured Patients Treated in Israel

During the last two decades the importance of molecular biology in transfusion medicine has been growing. Reference centers for immunohematology commonly use molecular methods to clarify problems, discrepancies or unusual results in patient serology. Nowadays there are immunohematology reference laboratories that recommend using molecular genotyping for patient blood management. Our blood bank laboratory is not a reference center, but we routinely use molecular genotyping to solve serologic problems. Due to the proximity to the Syrian border, since the beginning of the Syrian civil war, our medical center has received hundreds of injured patients, some of them with unique features concerning the blood type testing. From our previous experience of such a case in Dec 2015, we realized that due to extreme war conditions and lack of medical amenities, severely injured patients are likely to receive unmatched blood transfusions in Syria, sometimes ABO-incompatible blood transfusions. The patients arriving to our medical center are usually in critical condition and without medical records. Serologic tests show double population (DP) blood type. Molecular genotype of blood samples is not helpful, because it can detect the blood type of the unmatched/incompatible donor. In these cases, we use molecular genotyping from a tissue specimen, usually skin. Until we receive the results, which take about 5 hours in our molecular lab, we give only type O blood and AB plasma. Since Dec 2015, 11 injured patients with DP on serologic typing were admitted to our medical center. Tissue genotyping was performed on 8 of these. We determined that seven of the eleven patients previously received ABO-incompatible blood in Syria. With one exception, all patients were transfused in Israel (detailed data not shown), three with incompatible blood upon admission, based on initial serotype (patients 1,3,4 in the table). Tissue genotyping allowed us to transfuse compatible ABO-matched blood components afterward. All patients survived and were released in good condition. Tissue molecular genotyping helps improve patient blood management in the population of injured causalities from Syria. DisclosuresNo relevant conflicts of interest to declare.

Therapeutic potential of staphylococcal superantigen-like protein 7 for acute complement activation mediated diseases

Abstract Previous studies have demonstrated that staphylococcal superantigen-like protein 7 (SSL7), a protein produced by the opportunistic bacterial pathogen Staphylococcus aureus, potently inhibits the formation of the complement membrane attack complex and release of C5a by binding to complement component 5 (C5). However, because of the predicted immunogenicity of SSL7 in humans, its potential as a new complement inhibitor for treating Complement-Mediated Diseases were uncertain. In this study, we found that administration of SSL7 efficiently protected red blood cells from complement-mediated lysis and reduced hemoglobinuria in a mouse model of paroxysmal nocturnal hemoglobinuria (PNH). Interestingly, at the dose required for effective complement inhibition in vivo, although repetitive administrations of SSL7 once every other week for six weeks elicited anti-SSL7 antibody production, SSL7 was still able to attenuate acute complement activation mediated Hemolysis and hemoglobinuria significantly in these mice. In addition, anterior chamber administration of SSL7 before repeatedly treating mice with SSL7 suppresses the production of SSL7-reactive antibodies and retain the treatment efficacy of SSL7. These results suggest that SSL7 could thus be developed as an economical alternative to the existing C5-targeted drug eculizumab, especially for controlling acute complement activation in catastrophic conditions such as drug-induced immune hemolytic anemia, ABO-incompatible red blood cell, transfusion, and cardiopulmonary bypass surgery.

Status of ABO Incompatible Blood Transfusion in Korea and Preventon

Status of ABO Incompatible Blood Transfusion in Korea and Preventon

Acute Hemolytic Transfusion Reaction due to ABO-Incompatible Blood Transfusion: A Fatal Case Report and Review of the Literature

Acute Hemolytic Transfusion Reaction due to ABO-Incompatible Blood Transfusion: A Fatal Case Report and Review of the Literature

A case of ABO-incompatible blood transfusion treated by plasma exchange therapy and continuous hemodiafiltration

ABO-incompatible blood transfusion is potentially a life-threatening event. A 74-year-old type O Rh-positive male was accidentally transfused with 280 mL type B Rh-positive red blood cells during open right hemicolectomy, causing ABO-incompatible blood transfusion. Immediately after the transfusion, the patient experienced a hypotension episode followed by acute hemolytic reaction, disseminated intravascular coagulation and acute kidney injury. Plasma exchange therapy was performed to remove anti-B antibody and free hemoglobin because they caused acute hemolytic reaction, disseminated intravascular coagulation, and acute kidney injury. Free hemoglobin levels decreased from 13 to 2 mg/dL for 2 h. Continuous hemodiafiltration was used to stabilize hemodynamics. The patient was successfully treated for acute hemolytic reaction, disseminated intravascular coagulation, and acute kidney injury. Plasma exchange therapy and continuous hemodiafiltration are likely to be effective treatments for ABO-incompatible blood transfusion, and further studies are required to assess this effectiveness in future.

Retrospective analysis of forward and reverse ABO typing discrepancies among patients and blood donors in a tertiary care hospital.

The aim of our study was to determine the incidence and causes of ABO typing discrepancies among patients and blood donors at our centre. An accurate interpretation of the ABO blood group of an individual is of utmost importance to ensure patient safety and good transfusion practices. A retrospective observational study was carried out in the Department of Transfusion Medicine in our hospital from March 2013 to December 2015. Records of all patient and blood donor samples were retrieved and analysed for ABO typing discrepancies. In total, 135 853 patient and 62 080 donor samples were analysed for ABO typing discrepancies. The incidence among patients and blood donors was found to be 0·1% (138/135853) and 0·02% (14/62080), respectively. The mean age for patients and blood donors was 48·4 and 29·2years, respectively. The most common cause of ABO typing discrepancies was due to cold autoantibodies among the patients (50·7%) and blood donors (57%) causing discrepant results in reverse typing. The various other causes of reverse typing discrepancies among patients were weak/missing antibody (25·4%), cold-reacting alloantibody (4·3%), warm autoantibody (2·2%), anti-A1 antibody (2·2%), Bombay phenotype (1·5%), transplantation (0·7%) and rouleaux (0·7%), whereas in blood donors, the causes were cold-reacting antibody (7%) and weak antibody (7%). The major cause of forward typing discrepancies among patients (12·3%) and blood donors (29%) was ABO subgroups. The resolution of ABO typing discrepancy is essential to minimise the chance of transfusion of ABO-incompatible blood.

PILOTING IN ED–EXTRA DIFFICULT OR EASILY DONE

Objectives & BackgroundPatient Identification is fundamental to the success of safe transfusion. ABO incompatible blood transfusion has been classed as a Never Event by the Department of Health.In 2014, 680...

Recommendations for the electronic pre-transfusion check at the bedside.

The current risk of acquiring viral transmission through blood components is very small1. Thus, serious non-infectious hazards of transfusion have emerged as the most common complications2. The risk of non-infectious complications, including risks related to hospital-based steps in transfusion care, is at least 100 times greater than the risk of acquiring human immunodeficiency virus or hepatitis C virus infection through blood components3. One of the most frequent causes of transfusion-associated morbidity or mortality is mistransfusion, when the wrong blood is transfused to the wrong patient. Mistransfusion is the final outcome of one or more procedural errors or technical failures in the transfusion process, starting with the decision to transfuse a patient and ending with the actual administration of blood components3. In particular, ABO-incompatible transfusions attributable to incorrect identification of the patient or the blood unit are among the most serious transfusion hazards3–5. The Japan Society of Transfusion Medicine and Cell Therapy (JSTMCT) conducted nationwide surveys in Japan regarding ABO-incompatible blood transfusions (1st survey: January 1995–December 1999; 2nd survey: January 2000–December 2004). They found that the main cause of ABO-incompatible transfusion was identification error between the patient and blood unit6. These two surveys reported 9 and 8 “preventable” fatalities, respectively. Mislabelled and wrongly collected patient samples (wrong blood in tube [WBIT]) can also initiate a chain of events leading to mistransfusion3. Thus, correct patient identification at the time of sample collection and administration of blood components is critical. The Serious Hazards of Transfusion (SHOT) scheme in England showed that approximately 70% of incorrect blood component transfused (IBCT) errors take place in clinical areas, with the most frequent error being failure of the final patient identification checking procedure at the bedside; the frequency of IBCT events was calculated as 7 per 100,000 components7. However, the true incidence of mistransfusion seems to be even higher due to a failure to recognise many of the errors, and because complete data on transfusion episodes are not available. Thus, the pre-transfusion checking procedure at the bedside is the most critical step to prevent mistransfusion, and represents the final opportunity to prevent blood component misuse. However, a large observational audit revealed a failure to perform the final bedside checking procedure8, in which the practice compliance of healthcare workers for identification and vital sign monitoring of patients receiving blood transfusions were substandard in many hospitals. Machine-readable identification technology, especially a bar code-based electronic identification system (EIS), is ideally suited for pre-transfusion checking procedures and has been reported to significantly improve transfusion practice9–15. The British Committee for Standards in Haematology (BCSH) Guidelines for the Use of Information Technology (IT) in blood transfusion laboratories were recently up-dated16, providing mainly guidance on the operational use of laboratory information management systems (LIMS). Thus, to our knowledge, there are no available recommendations addressing the issues regarding the pre-transfusion check procedures at the bedside employing an EIS. The JSTMCT Task Force proposed the original draft of recommendations for the electronic pre-transfusion check procedures at the bedside and raised public awareness regarding the draft of recommendations on the home page of the JSTMCT17. The draft of the current recommendations developed by the Task Force adopted the opinions were submitted without major changes to the description. The objective of this study was to establish recommendations for the electronic pre-transfusion checking procedures at the bedside, appropriate for clinical situations, where a bar code-based EIS is used.

ABO Rh (D) blood group distribution among whole blood donors at two different setups of tertiary care hospitals in North India

Background: The antigens for ABO blood group system are of paramount significance in transfusion medicine as they are the most immunogenic of all the blood group antigens known, followed closely by D antigen of rhesus blood group system. The ABO blood group system has been used in resolving many medico-legal issues related to paternity, by investigators in forensic science or in population studies by anthropologists. ABO-Rh D blood grouping is the commonest test done in blood banking and forms the mainstay of pretransfusion testing and any ABO-incompatible blood transfusion can be associated with acute intravascular hemolysis, renal failure, and even death. Methods: A retrospective study for ABO RhD blood group distribution was carried out on whole blood donors who successfully donated at two different blood centres, hospital I at New Delhi for a period of one year from July 1, 2011 to June 30, 2012 and hospital II at Dehradun from January 1, 2013 to 31 December, 2015. Results: It was observed that the frequencies (%) of blood group A, B, O and AB for hospital I and II were A =22.6, 23.4; B=37.8, 35.6; O=29.5, 29.5 and AB=10.1, 11.4 respectively. And at both the centers, Rh D positivity was observed as 94.5% and Rh D negativity as 5.5%. Conclusions: It is advisable to determine the distribution of ABO and Rh D phenotypes among blood donors in each blood centre so as to stock adequate number of respective blood group units and provide timely and adequate blood supply to the needy recipient even in the wee hours.

Thrombotic thrombocytopenic purpura secondary to ABO group incompatible blood transfusion

Sir, The recent report on thrombotic thrombocytopenic purpura (TTP) after transfusion of ABO incompatible blood is very interesting.[1] Solak et al. hypothesized that the TTP might be due to “transfusion of ABO incompatible blood” or “open cardiac surgery.”[1] Solak et al. also noted that “TTP secondary to ABO incompatible blood transfusion has never been reported in the literature until date.”[1] What the exact mechanism in the present case is still a myth and the data on confounding morbidity (such as occult cancer) in the present case is not well presented. In fact, it is no doubt that ABO incompatibility can induce TTP. The previous reports on TTP after ABO mismatched liver and renal transplantations are good example.[2,3] Hence, the cases of ABO blood transfusion should be no doubt for the pathogenesis of TTP.

Thrombotic thrombocytopenic purpura secondary to ABO group incompatible blood transfusion in a patient after cardiac surgery

The triggers of secondary thrombotic thrombopcytopenic purpura (TTP) include drug toxicity, radiation and high-dose chemotherapy, angioinvasive infections, surgery and acute graft versus host disease. TTP secondary to surgery have been reported in a number of cases. Most of the cases have been occurred after open heart surgery. Extensive endothelial damage is held responsible as the initiating mechanism in postoperative TTP cases. However, there is no report of secondary TTP describing development owing to ABO incompatible blood transfusion. Here, we describe a patient who developed TTP after transfusion of ABO incompatible blood during hospitalization for bypass surgery. We also propose a hypothesis which may account for the possible underlying mechanism.

Self-treatment of an ABO-incompatible blood transfusion

Unfortunately, transfusion errors continue to pose a major clinical problem. In practice there is a remarkable lack of understanding of the reasons behind transfusion medicine, a worrying disregard for protocol and an offhand attitude to bedside checking. Clearly transfusion medicine education, as often said, must be more extensively incorporated into the core curriculum of medical, nursing and laboratory staff. In this immunological case report, following accurate pre-transfusion procedures and routine laboratory testing, we highlight, once more, that it would be better for the patient to rely on proper bedside checking rather than on their own immune system in order to avoid serious side effects related to transfusions. Albeight this case we had “a happy ending”, we must always bear in mind that one cannot compromise on safety and the quality care of patients.

In silico analysis of antibody–carbohydrate interactions and its application to xenoreactive antibodies

Antibody–carbohydrate interactions play central roles in stimulating adverse immune reactions. The most familiar example of such a process is the reaction observed in ABO-incompatible blood transfusion and organ transplantation. The ABO blood groups are defined by the presence of specific carbohydrates expressed on the surface of red blood cells. Preformed antibodies in the incompatible recipient (i.e., different blood groups) recognize cells exhibiting host-incompatible ABO system antigens and proceed to initiate lysis of the incompatible cells. Pig-to-human xenotransplantation presents a similar immunological barrier. Antibodies present in humans recognize carbohydrate antigens on the surface of pig organs as foreign and proceed to initiate hyperacute xenograft rejection. The major carbohydrate xenoantigens all bear terminal Galα(1,3)Gal epitopes (or αGal). In this study, we have developed and validated a site mapping technique to investigate protein–ligand recognition and applied it to antibody–carbohydrate systems. This site mapping technique involves the use of molecular docking to generate a series of antibody–carbohydrate complexes, followed by analysis of the hydrogen bonding and van der Waals interactions occurring in each complex. The technique was validated by application to a series of antibody–carbohydrate crystal structures. In each case, the majority of interactions made in the crystal structure complex were able to be reproduced. The technique was then applied to investigate xenoantigen recognition by a panel of monoclonal anti-αGal antibodies. The results indicate that there is a significant overlap of the antibody regions engaging the xenoantigens across the panel. Likewise, similar regions of the xenoantigens interact with the antibodies.

Consecutive national surveys of ABO‐incompatible blood transfusion in Japan

Morbidity and mortality from ABO-incompatible transfusion persist as consequences of human error. Even so, insufficient attention has been given to improving transfusion safety within the hospital. National surveys of ABO-incompatible blood transfusions were conducted by the Japanese Society of Blood Transfusion, with support from the Ministry of Health, Labor and Welfare. Surveys concluded in 2000 and 2005 analysed ABO-incompatible transfusion data from the previous 5 years (January 1995 to December 1999 and January 2000 to December 2004, respectively). The first survey targeted 777 hospitals and the second, 1355 hospitals. Data were collected through anonymous questionnaires. The first survey achieved a 77.4% response rate (578 of 777 hospitals). The second survey collected data from 251 more hospitals, but with a lower response rate (61.2%, or 829 of 1355 hospitals). The first survey analysed 166 incidents from 578 hospitals, vs. 60 incidents from 829 hospitals in the second survey. The main cause of ABO-incompatible transfusion was identification error between patient and blood product: 55% (91 of 166) in the first survey and 45% (27 of 60) in the second. Patient outcomes included nine preventable deaths from 1995 to 1999, and eight preventable deaths from 2000 to 2004. Misidentification at the bedside persists as the main cause of ABO-incompatible transfusion.

Blood group serology

Blood group serology

ABO-Incompatible Blood Transfusion and Invasive Therapeutic Approaches During Pediatric Cardiopulmonary Bypass

Human error has been identified as a major source of ABO-incompatible blood transfusion which most often results from blood being given to the wrong patient. We present a case of inadvertent administration of ABO-incompatible blood to a 6-mo-old child who underwent congenital heart surgery and discuss the use of invasive therapeutic approaches. Invasive techniques included total circulatory arrest and large-volume exchange transfusion, along with conventional ultrafiltration and plasmapheresis, which could all be performed rapidly and effectively. The combination of standard pharmacologic therapies and alternative invasive techniques after a massive ABO-incompatible blood transfusion led to a favorable outcome in our patient.

A computer‐assisted transfusion management system and changed transfusion practices contribute to appropriate management of blood components

ABO-incompatible blood transfusions attributable to inadequate identification (ID) of the patient or the blood unit are among the most serious of transfusion hazards. It has been unclear whether a computer-assisted transfusion management system connected to a bar code ID system could contribute to the appropriate management of blood components, as well as to the prevention of mistransfusions. A transfusion management system has been developed that links the hospital information system, a bar code patient-blood unit ID system, and an automated device for pretransfusion testing. The guidelines for issuing blood components from the transfusion service were also changed. The appropriateness of blood management was evaluated by monitoring the time to initiate transfusion after issuing a blood unit from the transfusion service (time after issuing [TAI]) and by calculating the number of units issued and subsequently returned, as well as the rate of date-expired red cell (RBC) components. From July 2002 to December 2006, a total of 49,974 blood components were transfused without a single mistransfusion. The monitoring of TAI and the notice to use the issued blood immediately had the effect of shortening TAI in the inpatient ward. The number of issued and subsequently returned RBC components, as well as the rate of date-expired RBC components, decreased significantly after the introduction of the system. A computer-assisted transfusion management system and changing transfusion practices appear useful in preventing mistransfusions and in contributing to the appropriate management of blood components.

Red Blood Cell Exchange Transfusion (RBCET) in the Management of Acute Hemolytic Transfusion Reaction (AHTR).

Acute hemolytic transfusion reaction (AHTR) is a potentially serious complication associated with the transfusion of ABO incompatible blood. It results in disseminated intravascular coagulation (DIC), shock, renal failure and death. Patient misidentification, sample mislabeling are some of the causes of an AHTR. To-date there is no data available on the use of RBCET in the management of an AHTR. We report the clinical course and successful management of an AHTR following massive ABO incompatible blood transfusion. The patient is a 68-year-old female with known coronary artery disease and type O Rh negative blood, who presented to the emergency room with unstable angina. She was taken emergently to the operating room for a quadruple coronary artery bypass graft. Due to sample mislabeling, she received 7 units of incompatible type A Rh negative packed red blood cells (PRBC) intra-operatively. During the immediate post-operative period, she was noted to have increased drainage from the surgical site, decreased urine output, hematuria and a precipitous drop in hemoglobin to 6.5 g/dL. She underwent re-exploration and received an additional 2 units of incompatible type A Rh negative PRBC and other blood products including fresh frozen plasma (FFP), platelets and cryoprecipitate that were ABO incompatible. In the recovery room, family members confirmed her blood type as type O Rh negative. Immediate re-typing utilizing pre-transfusion blood samples collected for CBC and chemistry, and obtaining blood bank records from her previous admission from another hospital a diagnosis of ABO incompatible AHTR was established. Further work-up revealed a strong positive DAT (3+ IgG) with a positive eluate (patient's anti-A antibodies coating the transfused type A RBC's). Hemolysis parameters showed elevated LDH 753 IU, bilirubin 2.1 mg/dL, and decreased haptoglobin 29.4 mg/dL. Her urine output continued to decrease with increase in serum creatinine to 2.4mg/dL. A continuous veno-venous hemodialysis (CVVHD) was started along with fluid resuscitation and urine alkalinization. A RBCET was performed within 11 hours after the transfusion of the last incompatible unit, which was followed by a second RBCET 24 hours later. Each RBCET consisted of 8 units of type O Rh negative blood. Following the two RBCET her blood type became type O Rh negative. Hemolysis parameters improved over the next several days and became normal. Serum creatinine progressively improved with increasing urine output. Dialysis was discontinued on day 13. Patient continued to do well and was discharged home in good condition with a normal renal function three weeks after her initial admission. The severity and course of an AHTR is dictated by the load of incompatible blood cells in the circulation. The high mortality rate associated with an AHTR warrants an aggressive approach in addition to supportive care. RBCET is used in the management of severe hemolytic disease of the new born, complications of sickle cell disease, and to lower the parasite load in malaria and babesiosis. The role of RBCET in AHTR is not established. There are two case reports in the Japanese literature where a RBCET was performed in the management of an AHTR with successful outcome. The course of this patient suggests that aggressive management including supportive care, timely RBCET, and renal replacement treatment may prevent DIC, organ damage and alter the grave prognosis associated with AHTR following incompatible blood transfusion.