A transfusion medicine physician in Michigan reports a case of a group AB Rh positive patient who received a group O Rh negative apheresis platelet unit. Toward the end of the platelet transfusion the patient complained of back pain, anxiety, and voided red urine. The transfusion was stopped. The patient's hemoglobin level dropped from 10 gm/dL pre-transfusion to 4.7 gm/dL post-transfusion. The Michigan physician did not comment that the patient was experiencing bleeding. The patient's transfusion reaction work up revealed a positive DAT (3+ with anti-IgG), and showed post-transfusion elevations of both LDH and indirect bilirubin levels. The patient required RBC transfusion, but eventually recovered with no apparent sequelae. Unfortunately, the implicated platelet unit was discarded before it could be examined for bacterial contamination or tested for ABO antibody titers. The Michigan physician suspects that this case represents a hemolytic reaction due to the transfusion of high titer ABO antibodies, and has asked the blood product supplier to explore this possibility; the blood supplier is in the process of recalling the donor of the implicated blood product to do the appropriate testing. The Michigan physician wonders about the frequency of hemolytic reactions associated with the transfusion of ABO incompatible plasma (such as occurred in this case report) when a unit of ABO-nonidentical plateletpheresis is transfused. The clinical team at the Michigan hospital had never seen this kind of reaction before, and the Michigan physician has seen only one other similar reaction in over 15 years of practice.

Editor's note: Previous e-Network Forum discussions below should be germane to the current discussion:

The following responses have been received.

ADDENDA Aug. 28, 2003

1. A physician in Australia reports that the attached file (PDF) may be of interest to this discussion. The Australian physician reports that he has been trying to get the blood supplier in Australia to adopt a similar approach to the NBS. Presently, in Australia he reports that they are now receiving buffy coat pooled platelets that are plasma depleted in 'T-Sol'. They are hopeful that eventually apheresis platelets will also be supplied in a similar manner so that the cross-group concern on the plasma side is effectively not an issue any more. He reports that they did have a similar case a few months back in a group B patient who was transfused with a unit of group O plateletpheresis. The Australian concludes that such a reaction is of more of a concern in pediatrics (according to the NBS position) but adults are still potentially at risk.

2. A colleague in the UK reports that this discussion is of interest at a hospital in Leeds, England, as they currently have a 3 month baby who is septic with DIC on ECMO following cardiac surgery, who has developed hemolysis following platelet transfusion. The baby girl is group A Rh negative, and has required substantial red cell and platelet transfusion support. The patient has been managed with group A Rh negative red cells, but on several occasions group O Rh negative platelets had to be used due to unavailability of group A Rh negative platelets and urgent requirement by the patient. All ABO mismatched platelet units were screened for high titer hemolysins and those lacking such high titer antibodies were labelled accordingly for use by this patient. In spite of this strategy, the child has developed measurable hemolysis including a strongly positive direct antiglobulin test (DAT) with anti-A eluting from the DAT positive red cells. However, because the child is also septic with DIC it is impossible to certain that the patient's hemolysis is caused primarily by the transfused ABO antibodies. However, in the opinion of the colleague from Leeds, because the hemolysis commenced immediately post transfusion of ABO incompatible platelets and the above described immunohematologic findings, they believe (without full proof) that the dominate causative factor in the hemolysis is the transfusion of ABO incompatible plasma and not sepsis with DIC. Furthermore, given the sick state of this infant it is very difficult to estimate the effect of hemolysis on her hemoglobin and bilirubin levels. The responding colleague reports that it is not uncommon for the group at Leeds hospital to use mismatched platelets in adults and they do not see problems of hemolysis. The colleague from Leeds comments that the NBS is looking into providing platelets suspended in additive solution (plasma removed) mainly because of thoughts to combat TRALI, however, such a strategy would also have the benefit of removing the consideration of hemolysis due to transfusion of ABO antibodies.

Editor's NOTE: This case demonstrates the importance of considering all likely causes of hemolysis in a patient receiving blood products. Had the above patient NOT received ABO incompatible plasma, yet developed hemolysis, the sepsis with DIC would be a reasonable mechanism for consideration as the cause of the hemolysis.

ADDENDA Sept. 5, 2003

3. A colleague in Lansing, Michigan reports that during the past two years, their transfusion service has incurred two cases that they believe to be ABO-mediated hemolysis following the transfusion of Group O apheresis platelets into Group A1 recipients. Both patients suffered brisk hemolysis following these transfusion, with the development of 3+ DATs and eluted anti-A. They further report that both group O donors were multiparous women who had recently delivered group A babies, and that both donors demonstrated high-titered anti-A (titers not stated). These cases were reported to their Transfusion Committee with followup with the treating physician. As their primary blood supplier is switching from distributing platelet concentrates to apheresis platelets, there is local concern about the potential increase in ABO-mediated hemolysis, following administration of group O platelet products to group A recipients, since it is believed that group O apheresis platelet transfusions are more likely to cause ABO-mediated hemolysis than do the transfusion of a pool of group O random platelet concentrates. They are now changing their donor screening policy to evaluate Group O donors who may have been pregnant. They will do ABO titer studies and assess their potential risk to a Group A recipient. Whenever possible, they transfuse ABO-Rh matched platelet products to their patients. With the current blood shortages in the U.S. and the high clinical demand for platelets, they are still forced to infuse group O apheresis platelets to Group A recipients.

4. A transfusion medicine physician in Alabama reports that at her academic medical center they always test for high-titer anti-A and anti-B prior to using ABO-mismatched platelets. They only use apheresis products. Furthermore, after seeing the development of a positive DAT and hemolysis in a group A bone marrow transplant patient who had received several "low-titer" group O platelets in the previous days, they now limit the number of group O platelets to 2 apheresis units per 3-day period. If they need to issue another ABO plasma-incompatible unit for lack of availability, they first perform a DAT and check for signs of hemolysis in the patient.

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Ira A. Shulman, MD
CBBS e-Network Forum Editor & Moderator