Suzanne H. Butch

Anti-A and anti-B titers in pooled group O platelets are comparable to apheresis platelets.

BACKGROUND: Although uncommon, acute hemolytic transfusion reactions (AHTRs) have been reported after transfusion of group O single‐donor apheresis platelets (SDPs) to group A, B, and AB recipients. Current methods for identifying “high‐titer” SDPs include tube and gel methods. The risk of a high‐titer unit is considered low with group O, poststorage, pooled platelet concentrates (PPLTs); however, data regarding anti‐A and anti‐B titers in PPLTs are lacking.

Electronic verification of donor-recipient compatibility : the computer crossmatch

Background: This article describes standard operating procedures (SOPs) for a computer crossmatch to replace the immediate‐spin crossmatch for ABO incompatibility between patient blood samples submitted for pretransfusion testing and the blood component selected for transfusion. These SOPs were developed following recent changes to the Standards for Blood Banks and Transfusion Services of the American Association of Blood Banks (AABB).

The evaluation of a positive direct antiglobulin test (autocontrol) in pretransfusion testing revisited.

Direct antiglobulin tests (DATs) using anti‐IgG were performed on 65,049 blood samples from prospective transfusion recipients; 3570 tests (5.49%) were positive. Using criteria published previously (primarily excluding patients not transfused within the preceding 14 days), 778 samples from other than neonatal patients were selected for further evaluation. Eluates that did not react were obtained on 518 (66.6%) of these samples. Warm‐reactive autoantibodies were apparent in 192 eluates, while 16 contained drug‐related antibodies, anti‐A or anti‐B from prior transfusion with ABO mismatched blood components, or anti‐D passively acquired from immune serum globulin. Fifty‐two eluates contained alloantibodies; however, in only six of these cases did the corresponding serum lack unexpected alloantibodies, as determined by routine pretransfusion studies. Three additional weakly reactive clinically significant alloantibodies were detected solely through additional serum tests performed on DAT‐positive samples.

Safety of leukoreduced, cytomegalovirus (CMV)-untested components in CMV-negative allogeneic human progenitor cell transplant recipients

Transfusion-transmitted cytomegalovirus (TT-CMV) infection can lead to significant morbidity and mortality in CMV-negative (CMV-N) hematopoietic progenitor cell (HPC) transplant patients. In 1995, Bowden and colleagues demonstrated the efficacy of leukoreduced components to reduce TT-CMV in most high-risk populations, although there remained safety concerns in CMV-N allogeneic HPC transplant recipients. As a result, several transplant programs recommended both leukoreduced and CMV-N components for CMV-N allogeneic HPC patients receiving transplants from CMV-N donors (CMV). A more recent study, however, has challenged the clinical benefit of requiring CMV-N, in addition to leukoreduction, in CMV HPC patients. In a 10-year study, Thiele and colleagues found no cases of TT-CMV in 23 CMV HPC patients transfused with 1847 CMVuntested (CMV-U), leukoreduced components. We would like to share our institution’s experience in 100 CMV allogeneic HPC patients transfused with 6465 CMV-N and CMV-U cellular components. Before July 2006, the University of Michigan provided, when available, CMV-N components to all CMV HPC transplant recipients. A preliminary 12-month retrospective review showed that 52% (14/27, 2004) had received leukoreduced, CMV-U blood components due to shortages in CMV-N products, with no cases of TT-CMV. As a result, the transfusion policy was changed in mid-2006 to provide leukoreduced, CMV-U products for all HPC patients, regardless of pretransplant CMV status. For quality assurance, we monitored the CMV conversion rate over a 36-month period (January 2005 to December 2007) covering an 18-month period before and after the change in transfusion policy (Table 1). Per institutional practice, CMV-N patients were screened for CMV IgG every 1 to 2 months pretransplant, followed by regular testing for CMV nucleic acid testing (NAT) after transplant. The minimum posttransplant follow-up was 12 months. All blood products were provided by Southeast Michigan American Red Cross (Detroit, MI) and were leukoreduced after storage (Leukotrap RC system, Pall Corp., Port Washington, CA). As shown in Table 1, 100 patients were available for analysis and included both adult and pediatric patients. All patients were CMV-N before transplant, received a CMV allogeneic HPC transplant, and underwent weekly posttransplant CMV NAT monitoring. Except for sex, there were no significant differences in patient demographics, transplant type, or transfusion support in the two study cohorts. In the CMV-N policy period, only 11% to 15% of cellular components were CMV-N, with most patients receiving a mix of CMV-N and CMV-U. Only five patients received 100% CMV-N products. All five patients had low transfusion needs, requiring 2 to 10 red blood cell (RBC) and two to three platelet (PLT) transfusions. Two adult male patients had a single positive test for CMV IgG at 3 and 5 weeks after transplant, respectively (Table 1). Both patients tested negative for CMV IgM and CMV NAT and had no evidence of clinical CMV infection. Each patient received between 42 and 45 CMV-U cellular components in the weeks before seroconversion: neither patient had received intravenous immune globulin before CMV IgG testing. There were no CMV seroconversions in the CMV-U period. The overall CMV IgG seroconversion rate was 2% per patient and 0.03% per unit, which is comparable to the findings by Bowden and coworkers (2.4% per patient, 0.023% per component). The rate of confirmed TT-CMV was 0%, consistent with the study by Thiele and coworkers and lower than that reported by Wu and coworkers (6.5% per patient, 0.23% per CMV-positive component). As discussed by Thiele and Wu, the CMV IgG detected in our patients likely represents passive antibody from recent transfusions. Our findings confirm those of Thiele and affirm the equivalent safety of CMV-U, leukoreduced components in CMV allogeneic HPC patients. The absence of clinical TT-CMV infection in our study and that by Thiele and coworkers, despite the combined transfusion of nearly 8000 CMV-U, leukoreduced components, contradicts sentiments from a past multivariate analysis, which advocated continued provision of CMV-N and leukoreduced components for CMV transplant patients. The improved safety of CMV-N over CMV-U, leukoreduced is also not supported by a recent large prospective study of 34,000 blood donors. Ziemann and colleagues found CMV viremia only among newly seroconverted donors and a few CMV-N donors, arguing that CMV-N components may present the higher risk of TT-CMV due to passive transfusion of free CMV DNA. In summary, policies stipulating leukoreduced, CMV-N components in CMV allogeneic HPC patients do not confer additional safety and are limited by product shortages and significant transfusion support required by many allogeneic HPC patients.

The evaluation of a positive direct antiglobulin test in pretransfusion testing.

The results of serologic studies on 879 blood samples with a positive direct antiglobulin test (DAT) are presented. All blood samples were from patients who were either anemic, for reasons other than blood loss, recently transfused, or had serum antibodies detected during routine pretransfusion tests. Blood samples from only 81 of the patients included in this study had serologically reactive eluates (64 autoantibodies, three antibodies to penicillin and cephalothin treated red blood cells, three passively acquired anti‐A antibodies, and 11 transfusion‐induced alloantibodies). The eluted antibodies were also detected in the serum by routine pretransfusion tests in 13 of the patients whose red blood cells eluted autoantibodies, and in five of the patients whose red blood cells eluted transfusion‐induced alloantibodies. All but one of the 11 transfusion‐induced alloantibodies were detected within 14 days posttransfusion. Based on these findings, a cost‐effective and safe approach to the management of blood samples with a positive DAT would be to restrict the preparation and testing of eluates to those samples from recently transfused patients. It is the contention of the authors that the incorporation of the DAT in pretransfusion testing should primarily serve to detect alloantibody formation before such antibodies are evident in the serum, and should not be used to screen patients for unsuspected autoimmune hemolytic anemia. Furthermore, the authors question the necessity for blood banks to routinely perform an autocontrol on all blood samples from prospective transfusion recipients.

Is a room-temperature crossmatch necessary for the detection of ABO errors?

The detection of anti‐A and anti‐B isohemagglutinins by low‐ionic‐strength saline tests at 37°C and by the indirect antiglobulin technique, without an “immediatespin” or room‐temperature phase, has been studied. Using such a procedure, all but one of 2746 patient blood samples reacted in accordance with ABO type when tested against A2 and B red cells. However, the discrepant sample also was nonreactive when tested by “immediate‐spin” technique against saline‐suspended A2 red cells. Our findings indicate that compatibility tests performed at 37°C in low‐ionic‐strength saline are as sensitive as “immediate‐spin” tests with saline‐suspended red cells for the detection of ABO errors. Performing serologic tests for unexpected alloantibodies and donor‐recipient compatibility without an “immediate‐spin” or room‐temperature phase abbreviates pretransfusion testing and reduces the detection of clinically insignificant alloantibodies solely reactive at room temperature.

Urgent Need for Blood: Administrative Issues

Providing blood components when there is an urgent need for transfusion depends on competent staff following standard operating procedures. These procedures should allow staff to efficiently issue uncrossmatched blood and perform pretransfusion testing. Accurate and timely communication between the transfusion service and the patient’s physician is critical in determining if blood components should be issued and transfused before the problem resolution is complete.