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IS Crossmatch


Geriann

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Our current policy and procedure is to use IS crossmatch when the Antibody Screen is negative. We recently have had 2 cases of hemolytic transfusion reaction involving antibodies to low incident antigens. The first case was late spring 2005 an anemic male with no transfusion historical record. The patient was found to have antibody to Wright A. The most recent was a multiparus Asian female. Our reference lab was unable to identify the antibody at this time but ruled out antibodies to common low incident antigens. In both cases the unit transfused was incompatible 2+ in the AHG testing phase for both pre and post transfusion specimens. Has anyone out there encountered transfusion reactions related to antibodies to low incident antigens not detectable using routine antibody screening techniques? Does anyone have different guidelines for using IS crosmatch for patients previously transfused and or pregnant? Any comments? Are there any statistics on patient's having transfusion complications related to antibodies to low incident antigens?

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I needed a good laugh....I hope our quota is out of the way. The first case was by far the most severe...it was presented by our reference lab at a seminar last summer. The second case just occured and the patient appears to be ok thus far. Both cases in such a short time has made our pathologists want to reconsider IS crossmatch policy. In both cases our nursing staff was right on top of the symptoms and my transfusion CLS took immediate action.

In the most recent case the patient presented with severe chills and abdominal pain just a little more than an hour into the transfusion. The plasma from the post transfusion specimen was very icteric (not red or pink). The pre and post DATs and ABSCs were negative. The pre and post crossmatches were both 2+ in the AHG phase.

The earlier case the patient required dialysis...it was more severe reaction but may also have been related to his physical condition at the time of transfusion.

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It's tough to make decisions based on the odds when you have seen the rare consequence occur. Tell your paths to think about all the other things in health care that no one tests the patients in advance for: drug reactions, unexpected bleeding in surgery, pre-existing infections or anemia, etc. etc. (especially nowdays when much less routine labwork is done). Diagnoses almost always play the odds, but they aren't always right the first time. I never hear that any other health care providers feel guilty for these problems.

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"Mabel, we transfuse around 50 RBC a day, and I cannot think of any transfusion reactions I have seen due to antibodies to low incidence antigens in over 17 years. We pick up 1 or 2 antibodies a year (usually Kpa or Jsa) in our patient who have other antibodies. We do see incompatible units at crossmatch in sickle cell patients who have built a lot of antibodies. Higher incidence of V+ units comes to mind.

Over the past 11 years, we have dispensed 60,000+ red cell units using an electronic crossmatch and a 2-cell antibody screen (gel) without a single adverse reaction due to an antibody directed against a low-frequency antigen. I do recall years ago (after the emergence of the type and screen and release of units by immediate-spin crossmatch with a negative antibody screen, reports of patients in two different hospitals who experienced hemolytic transfusion reactions (I believe non-fatal) due to anti-Wra. One hospital decided to return to routine antiglobulin crossmatch and the other did not. Years later, an SBB student at the Los Angeles-Orange Counties Regional Blood Center did a study on litigation involving blood transfusion in the state of California. The results: what little he/she did find regarding serological pretransfusion testing was about ABO incompatibility."

Here are 2 answers from my query on the AABB discussion board regarding the frequency of your problem. Hope this helps.

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We have been doing electronic crossmatch since 1996. We transfuse about 13,000 units a year. I can not recall an incident of a reaction due to an antibody against a low frequency antigen. The odds are that we have, indeed, transfused an antigen positive unit to a patioent with such an antibody. Either the reaction was so mild that it was not detected clinically or the transfusion was one of many during a massive transfusion episode.

Several years back, we had a severe case of hemolysis in the absence of detectable antibody by gel and PeG. The patient never had a positive DAT. We sent the sample to a reference lab and they could not find an antibody. Nursing denied using a pressure infusor, using a solution other than normal saline, or doing anything else that could cause mechanical hemolysis. A few days later we gave the patient a second unit of blood, using an in-vivo crossmatch. Hemolysis began after about 100 cc. We phenotyped the patient and the two units to look for an antigen that was absent in the patient but positive on both units. What we found was big C. We sent the sample to George Garratty's lab for polybrene testing and low and behold they detected anti-C. So, there are rare instances where our methods "miss" clinically significant antibodies.

I agree with Mabel...no need to feel guilty. No method will detect everything. In my opinion, going back to full AHG crossmatching would have more of a negative impact on overall patient care by delaying the availability of blood to all your patients. You have to look at the big picture and do what is best for the vast majority of patients rather than dwell on the rare events.

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