Anti-E alloimmunization from a platelet apheresis transfusion in a 22-month-old male with acute myeloid leukemia.

RhD alloimmunization from platelet transfusions have been documented in the literature. However, non-RhD platelet alloimmunization is much less frequent and the risk for non-RhD alloimmunization from platelets is thought to be extremely low and most associated with buffy coat pooled platelets. A 22-month-old male with acute myeloid leukemia received 99 mL apheresis platelets for thrombocytopenia. Three months later, an antibody screen, the direct antiglobulin test (DAT), and red blood cell (RBC) genotype were sent for laboratory evaluation. The antibody screen was positive, with anti-E identified. The DAT was negative and the RBC genotype of the patient was predicted to be negative for the E antigen whereas the platelet donor was predicted to be positive for E antigen. There is a risk of alloimmunization of non-RhD antigen from platelet pheresis transfusion even in a patient less than 2 years old.

Preventing transfusion-associated circulatory overload in acute care settings.

ABSTRACT: Transfusion-associated circulatory overload (TACO) is a potentially life-threatening complication that can occur with the transfusion of any blood component, and accounts for up to 24% of transfusion-associated patient fatalities. This article discusses how to develop evidence-based continuing education and guideline recommendations that will increase nursing staff awareness of TACO and guide nurses in prevention and prompt intervention.

The Viability of Hematopoietic Progenitor Cell Grafts after Cryopreservation Does Not Predict Delayed Engraftment in Allogeneic Hematopoietic Stem Cell Transplantation.

OBJECTIVE: Due to the COVID-19 pandemic, more peripheral blood stem cell (PBSC) allogeneic grafts are being frozen and infused thawed. Our objective was to study the influence of graft viability on engraftment outcome in patients treated with PBSCs. METHODS: Using trypan blue stain, we compared total nucleated cell (TNC) viability of both fresh and thawed grafts in allogeneic PBSCs. RESULTS: The viability of thawed PBSC grafts median was 74%, and fresh was 99.0%. The median number of CD34 + cells/kg infused thawed was 6.3 × 106/kg and median time to neutrophil and platelet engraftment was 17.5 and 20 days. Median number of CD34 + cells/kg infused fresh was 5.1 × 106/kg and median time to neutrophil and platelet engraftment was 18 and 19 days. There were no statistically significant differences in the time to engraftment between the 2 groups. CONCLUSION: A low TNC viability of thawed PBSC grafts does not have an effect on time to neutrophil and platelet engraftment when more than 2.85 × 106 CD34 + cells/kg are infused.

A comparison between liquid group A plasma and thawed group A plasma for massive transfusion activation in trauma patients.

BACKGROUND AND OBJECTIVES: The use of group A thawed 24-h plasma when resuscitating haemorrhagic shock patients has become more common; however, limited data exist on the clinical use of liquid plasma (LP). Our aim is to determine whether LP is of clinical benefit to patients requiring massive transfusion. MATERIALS AND METHODS: The objective of this retrospective study was to detect any difference in 24-h survival between patients receiving liquid or thawed plasma (TP) during their massive transfusion activation. Other objectives were to report any difference in hospital length of stay (LOS), intensive care unit (ICU) LOS and in-hospital survival. Data collected included gender, age, mechanism of injury, Injury Severity Score, Revised Trauma Score and Trauma Injury Severity Score. RESULTS: A total of 178 patients received 1283 units of LP, median 4 and range (1-56), whereas 270 patients received 2031 units of TP, median 5 and range (1-87). The two study groups were comparable in terms of gender, age, mechanism of injury, whole blood, red blood cells, platelets and cryoprecipitate transfused. The use of LP during the massive transfusion activation in traumatically injured patients was not associated with increased 24-h survival compared to when using TP, p = 0.553. CONCLUSION: Our study did not show a difference in 24-h or 30-day survival between the use of LP compared to TP in trauma patients. LP should be considered an alternative to TP in trauma patients requiring immediate plasma resuscitation.

Anti-S Antibody: A Rare Cause of Fetal Hydrops in a Previously Sensitized Mother.

Anti-S is an IgG antibody and a rare cause of hemolytic disease of the fetus and newborn. A 38 year old woman with blood group O Rh-positive presented to the hospital at 30 weeks gestation. Her past medical history was significant for sickle cell disease and alloantibodies against the Fya, Jkb, and S antigens. Obstetric ultrasound showed the fetus to have developed scalp edema, cardiomegaly, small pericardial effusion, and large ascites. Periumbilical blood sampling results showed the fetus blood type as blood group O Rh-positive with anti-S and hemoglobin of 2 gm/dL. After multiple intrauterine transfusions of red blood cells, the fetal hemoglobin increased to 12.9 g/dL. Anti-S can cause fetal hydrops, although it is rare. All pregnant women with anti-S should be closely monitored and treated during pregnancy for the possibility of developing a severe hemolytic disease of the fetus and newborn.

Fatal sepsis associated with a storage container leak permitting platelet contamination with environmental bacteria after pathogen reduction.

BACKGROUND: Pathogen reduction technology and enhanced bacterial culture screening promise to significantly reduce the risk of transfusion-associated septic reactions due to contaminated platelets. Recent reports suggest that these interventions lack efficacy for post-collection and processing contamination with environmental organisms if the storage bag integrity is compromised. CASE REPORT: We report a fatal septic transfusion reaction in a 63-year-old patient with chronic kidney and liver disease who received a pathogen reduced platelet transfusion in anticipation of surgery. METHODS: The residual platelet concentrate was cultured, with the detected microorganisms undergoing 16S genotype sequencing. Separate pathogen reduction studies were performed on the recovered bacteria, including assessment for amotosalen photoproducts. The storage container was subjected to pressure testing and microscopic examination. Environmental culture screening was performed at the hospital. RESULTS: Gram negative rods were detected in the platelet unit and cultures of both platelet component and the patient's blood grew Acinetobacter baumannii complex, Leclercia adecarboxylata and Staphylococcus saprophyticus. These strains were effectively inactivated with >7.2, 7.7, and >7.1 log10 kill, respectively. The platelet storage container revealed a leak visible only on pressure testing. Hospital environmental cultures were negative and the contamination source is unknown. A. baumannii complex and S. saprophyticus 16S genotyping sequences were identical to those implicated in a previously reported septic reaction. CONCLUSION: Findings are compatible with post-processing environmental contamination of a pathogen reduced platelet concentrate via a non-visible, acquired storage container leak. Efforts are warranted to actively prevent damage to, and detect defects in, platelet storage containers, and to store and transport components in clean environments.

A comparison between leukocyte reduced low titer whole blood vs non-leukocyte reduced low titer whole blood for massive transfusion activation.

BACKGROUND: Hemorrhagic shock is the leading cause of survivable death in trauma patients and recent literature has focused on resuscitation strategies including transfusing low-titer group O whole blood (LTOWB). Debate remains regarding whether leukocyte reduced (LR) whole blood is of clinical benefit or detriment to patients requiring massive transfusion. This study compares survival outcomes between LR-LTOWB and non-LR LTOWB. STUDY DESIGN AND METHODS: The objective of this prospective, observational study was to detect any difference in 24-hour survival between patients receiving LR-LTOWB and non-LR LTOWB during their massive transfusion activation. Secondary objectives were to report any difference in ICU LOS, ventilation days, in-hospital survival, and hospital LOS. Data collected included patient sex, age, mechanism of injury, Injury Severity Score (ISS), Trauma Injury Severity Score (TRISS), cause of death, and number of LTOWB transfused. RESULTS: A total of 167 patients received 271 LTOWB transfusions. There were 97 patients that received 168 units of LR-LTOWB while 70 patients received 103 units of non-LR LTOWB. The two study groups were comparable in terms of age, sex, ISS, TRISS, and the number of LTOWB transfused. The use of LR LTOWB during the initial massive transfusion activation in traumatically injured patients was not associated with increased 24-hour survival compared to when using non-LR LTOWB. No transfusion associated adverse events were reported. CONCLUSIONS: The administration of either LR or non-LR LTOWB was not associated with >24 hours survival in patients presenting with massive hemorrhage. The high cost and the rapid decline in platelet count of LR whole blood may be a consideration.

Anti-M-Induced Delayed Hemolytic Transfusion Reaction.

BACKGROUND: Anti-M is most often assumed to be naturally occurring and can be comprised of a mixture of predominantly immunoglobulin(Ig)M with a lesser IgG component. Anti-M-antibodies usually do not react at 37°C and therefore are considered to be of little clinical significance. METHODS: A 28-year-old man presented with hemorrhagic shock from numerous injuries sustained in a motor vehicle collision. The patient received several units of red blood cells (RBCs). The antibody screen, the direct antiglobulin test (DAT), and the RBC genotype were sent for laboratory evaluation. RESULTS: A total of 12 days after the first antibody screening result was negative (7 days after transfusion), the lowest hemoglobin value was 5.5 g per dL, and we observed a positive antibody screening result and DAT with immunoglobulin (Ig)G anti-M identified. After transfusion of 4 units of M antigen-negative RBC, the post-transfusion hemoglobin level increased to 8.9 g per dL. CONCLUSION: Obtaining M antigen-negative compatible RBCs is necessary in patients demonstrating IgG anti-M in plasma.

Implementation of a new blood cooler insert and tracking technology with educational initiatives and its effect on reducing red blood cell wastage.

BACKGROUND: The objective was to report a successful implementation of a blood cooler insert and tracking technology with educational initiatives and its effect on reducing red blood cell (RBC) wastage. STUDY DESIGN AND METHODS: The blood bank database was used to quantify and categorize total RBC units issued in blood coolers from January 2010 to December 2015 with and without the new inserts throughout the hospital. Radiofrequency identification tags were used with special software to monitor blood cooler tracking. An educational policy on how to handle the coolers was initiated. Data were gathered from the software that provided a real-time location monitoring of the blood coolers with inserts throughout the institution. RESULTS: The implementation of the blood cooler with inserts and tracking device reduced mean yearly RBC wastage by fourfold from 0.64% to 0.17% between 2010 and 2015. The conserved RBCs corresponded to a total cost savings of $167,844 during the 3-year postimplementation period. CONCLUSIONS: The implementation of new blood cooler inserts, tracking system, and educational initiatives substantially reduced the mean annual total RBC wastage. The cost to implement this initiative may be small if there is an existing institutional infrastructure to monitor and track hospital equipment into which the blood bank intervention can be adapted when compared to the cost of blood wastage.

Successful ABO-Incompatible Renal Transplantation: Blood Group A1B Donor Into A2B Recipient With Anti-A1 Isoagglutinins.

OBJECTIVES: Transplantation of the blood group A2B in a recipient was successfully performed in the setting of receiving a deceased donor kidney from an "incompatible" A1B donor. METHODS: The donor and recipient were both typed for ABO blood group, including ABO genotyping. The donor and recipient were tested for ABO, non-ABO, and human leukocyte antigen (HLA) antibodies. The donor and recipient were typed for HLA antigens, including T- and B-flow cytometry crossmatch tests. RESULTS: The recipient's RBCs were negative with A1 lectin, and immunoglobulin G anti-A1 was demonstrated in the recipient's plasma. The donor-recipient pair was a four-antigen HLA mismatch, but final T- and B-flow cytometry crossmatch tests were compatible. The transplant procedure was uneventful; the patient experienced immediate graft function with no episodes of rejection or readmissions more than 2 years later. CONCLUSIONS: It may be safe to transplant across the A1/A2 blood group AB mismatch barrier in the setting of low titer anti-A1 isoagglutinins without the need for pretransplant desensitization even if the antibody produced reacts with anti-human globulin.

Discriminating complement-mediated acute transfusion reaction for type O+ red blood cells transfused into a B+ recipient with the complement hemolysis using human erythrocytes (CHUHE) assay.

BACKGROUND: A patient with B+ sickle cell disease received 3 units of red blood cells (RBCs) from two O+ donors and developed fever and hypotension after the first unit, consistent with an acute transfusion reaction (ATR). Anti-B titers in plasma from each O+ donor were markedly elevated and nondiscriminatory. In order to evaluate the potential for the transfused units to produce complement-mediated hemolysis of B+ RBCs, hemolytic complement testing was performed. STUDY DESIGN AND METHODS: Plasma from each donor was diluted in veronal buffer and incubated with B+ RBCs, and free hemoglobin was measured by spectrophotometer in the complement hemolysis using human erythrocytes (CHUHE) assay. Peptide inhibitor of complement C1 (PIC1) was used to confirm antibody-initiated complement pathway activation. RESULTS: A 96-fold difference (p = 0.014) in hemolysis was measured between plasma samples from the two O+ donors using the CHUHE assay. The extremely high degree of hemolysis produced by the one plasma was inhibited by PIC1 in a dose-dependent manner. CONCLUSION: These results indicate that hemolytic complement testing with the CHUHE assay can be used to assess the risk of antibody-initiated, complement-mediated hemolysis from a transfusion beyond what can be achieved with antibody titers alone.

Fatal autoimmune hemolytic anemia due to immunoglobulin g autoantibody exacerbated by epstein-barr virus.

Most cases of autoimmune hemolytic anemia (AIHA) are caused by the production of an autoantibody that targets determinants on red blood cells (RBCs). This autoantibody can be immunoglobulin (Ig) G, IgM, or IgA. Some autoantibodies react optimally at 0° to 4°C (ie, cold agglutinin) and usually are clinically insignificant. High-titer cold agglutinins are associated with IgM autoantibody and complement fixation induced by infectious agents, including the Epstein-Barr virus (EBV). This case report describes a 31-year-old man who had jaundice, a hemoglobin of 6.0 gdL, and was diagnosed with a hemolytic crisis of AIHA. He received a total of 11 RBC transfusions during a 15-hour period without sustained response and later died. The direct antiglobulin test results for this patient were positive, whereas the cold-agglutinin-testing results were negative. We detected EBV DNA in blood via polymerase chain reaction (PCR). We report a rare case of AIHA associated with an IgG autoantibody and exacerbated by EBV infection, causing a fatal hemolytic anemia.

Successful unintentional ABO-incompatible renal transplantation: Blood group A1B donor into an A2B recipient.

OBJECTIVES: To report a successful unintentional transplantation of a deceased donor kidney from an "incompatible" A1B donor into a recipient who was blood group A2B with unsuspected preformed anti-A1 antibodies. METHODS: The donor and recipient were both typed for ABO antigens. The recipient was tested for ABO and non-ABO antibodies. The recipient was typed for HLA class I and class II antigens, including HLA antibody screen. The T-and B-flow cytometry crossmatch test was performed using standard protocol. RESULTS: The donor-recipient pair was a complete six-antigen human leukocyte antigen mismatch, but final T- and B-flow cytometry cross-match tests were compatible. The recipient was a 65-year-old woman with a medical history of end-stage renal disease secondary to diabetic nephropathy who underwent kidney transplantation from a 46-year-old brain-dead standard criteria donor. The recipient's RBCs were negative with A1 lectin, and the recipient was thus typed as an A2 subgroup. Anti-A1 could be demonstrated in the recipient's plasma. The donor's RBCs were positive with A1 lectin, thereby conferring an A1 blood type. CONCLUSIONS: It is safe to transplant across the A1/A2 blood group barrier provided that the preformed antibodies are not reactive at 37°C and with anti-human globulin.

Analysis of a high-throughput HLA antibody screening assay for use with platelet donors.

BACKGROUND: Passive infusion of HLA antibodies has been implicated in transfusion reactions. A rapid, inexpensive method of screening blood donors for HLA antibodies might reduce the incidence of reactions. A high-throughput microbead-flow analyzer HLA antibody detection technique was compared with an enzyme-linked immunosorbent assay (ELISA) method. STUDY DESIGN AND METHODS: Ninety-six apheresis platelet (PLT) donors were tested for antibodies to Class I and II HLA antigens with mixed-antigen microbead-flow analyzer and ELISAs. For both assays, samples reactive in the mixed-antigen assay were tested with a panel-reactive antibody (PRA) assay. Samples reactive in both the mixed-antigen and the PRA assays were considered positive. RESULTS: In the mixed-antigen microbead assay, 46 (48%) samples were reactive to Class I antigens and 20 (21%) to Class II. Further testing in the microbead PRA assay revealed that 34 (35%) had antibodies to Class I antigens, 18 (19%) to Class II, and 42 (44%) to either Class I or Class II. Class I antibodies were present in 56 percent of females and 36 percent of males. In the mixed-antigen ELISA, 4 samples were reactive with Class I antigens, 4 with Class II antigens, and 5 with Class I or Class II. All 5 reactive samples were also reactive in the ELISA PRA assay and were from females. CONCLUSION: The microbead assay was more sensitive than the ELISA and detected antibodies in a large proportion of donors. Samples reactive in the mixed-antigen microbead assay should be confirmed by a second assay before concluding that antibodies are present.

Leukocyte antigen and antibody detection assays: tools for assessing and preventing pulmonary transfusion reactions.

Antibodies to neutrophil and HLA antigens can cause pulmonary transfusion reactions, and in some cases acute lung injury. When evaluating cases of pulmonary transfusion reactions, it is often necessary to test donors for neutrophil and HLA antibodies and also type the recipient for neutrophil and HLA antigens. A variety of enzyme-linked immunosorbent assay (ELISA) and flow cytometry-based solid phase assays are available to test for HLA class I and class II antibodies, but not neutrophil antibodies. Screening for neutrophil antibodies requires the preparation of panels of fresh neutrophils and testing in agglutination, immunofluorescence, or flow cytometry assays. Genotyping of HLA class I and II antigens is performed with a variety of sequence-specific primers, sequenced-specific oligonucleotide probe, and sequence-based typing assays. Neutrophil-specific antigens HNA-1a, -1b, -1c, -4a, and -5a can be genotyped, but not HNA-2a or -3a. Phenotyping of HNA-2a can be performed with CD177 monoclonal antibodies, but the gene encoding HNA-3a has not been identified, and the genomic basis for the HNA-2a-negative phenotype is not known. In conclusion, patients and donors involved with pulmonary transfusion reactions can be quickly typed for HLA antigens and tested for HLA antibodies, but testing for neutrophil antibodies and antigens requires the use of a reference laboratory.

The transfusion of neutrophil-specific antibodies causes leukopenia and a broad spectrum of pulmonary reactions.

BACKGROUND: Antibodies to neutrophil-specific antigens are the best characterized cause of transfusion-related acute lung injury (TRALI). CASE REPORT: A double-apheresis platelet (PLT) component was divided and transfused into two patients. One experienced chills, rigors, and dyspnea and the other experienced chills and headache. Transient leukopenia developed in both patients. RESULTS: Evaluation of donor plasma revealed an anti-HNA-2a and no HLA Class I antibodies. The donor had donated 26 previous apheresis PLT components. The 27 donations resulted in 39 separate transfusions and 12 transfusion reactions in 9 patients. Five reactions occurred immediately after the transfusion, 10 within 1 hour, and all within 2.5 hours. Nine of the reactions involved symptoms or signs of pulmonary dysfunction. The symptoms were mild to moderate in nature. None of the inpatients required intensive care transfer nor did any outpatients require hospital admission. Recipient white blood cell (WBC) counts were measured within 8 hours after 38 of 39 transfusions. Leukopenia occurred in 9 of 12 (75%) transfusions with reactions and in 9 of 26 (35%) transfusions without. The reactions did not correlate with pretransfusion WBC count. CONCLUSIONS: Neutrophil antibodies cause a wide variety of transfusion reactions that do not necessarily meet the definition of TRALI. Donors of blood products causing even mild pulmonary reactions or leukopenia should be tested for neutrophil-specific antibodies.