Everything posted by richmond
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Warm auto vs. High frequency Ab with positive DAT ?
Thank you ALL for your responses. The patient has continued to receive blds ( unfortunately " his symptoms are consistent with his diagonosis and receiving bld is only way he can extend his life ") and he is doing very well with those gel x/m compatible units. Maybe that one time transfusion rxn was due to "biochemical nasties" like Malcolm suggested. In addition, I have one more question. Suppose the patient is Dob negative with all the symptoms, rxns, current pt's conditions that I have provided. Would you send out the specimen to a reference lab to see if the patient has anti-Dob? Assuming that you already did some of testings that you would never get compensated for. And cost of testing for anti-Dob won't be compensated. (I remember reading something like cost of testing should be justified by clinical significance of testing.) Thank you in advance, Richmond.
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Warm auto vs. High frequency Ab with positive DAT ?
Thank you Malcolm. The patient is causasian and has chronic Gi bleeding issue (oh well.) Ab screen rxn and x/m reaction are 1+. Like I indicated before, some gel X/M ( about 15 %) are completely compatible looking. And so does one of screen cell. Completely negative. And yes, very recent rapid acid elution is all positive as it has been last three years. One day the patient was transfused with 2+ completely phenotype matched units, the patient had a transfusion rxn. Usually we give 1+ completely x/m unit, but I choose that unit because it was expiring. Then two weeks later I found out that there are some compatible units. But they were only Rh, K matched units. I gave the units (of course after informing a pathologist.) over completely phenotype matched yet incompatible units. The patient was fine. I have not been in transfusion service too long. How often do you see warm auto with completely negative x/m?
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Warm auto vs. High frequency Ab with positive DAT ?
I am puzzled with current patient with warm auto with transfusion need. May I ask for your expertise? Patient: Transfused biweekly for last three years. Gave molecular tested phenotypically matched units. (all significant ag) Rapid acid elution: all pos. alloadsorption: no alloantibody present. Autocontrol pos. DAT: Anti-IgG pos, Anti-C3 neg. I found out that there are quite of few units are actually completely gel XM compatible for this patient. I thought that you can't find compatible units for true warm auto. Or I am wrong. I think I did hear someone say sometime you get lucky to have compatible unit for "weak warm auto." Well I am happy that we have compatible units. But can someone please explain this "weak warm auto" to me and why there are compatible units? How do you know it is not high freq ab with DAT+ Thank you in advance, P.S. this patient once had transfusion reaction. (pulse, temp, bp, bilirubin) Richmond.
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Hello! I have a question.
Thank you so much Malcom. I was expecting more clear cut answer, but I guess such thing does not exist in BB. If I can bother you with more questions. 1. Where do you usually get A2 cell? I don't recall if we have one. 2. You indicated that anti-A1 is not considered significant unless it reactivity is observed at 37C. How do you test at 37C? 3. Suppose you get the same forward and reverse rxn and lectin result how far would you go in terms of testing.ex) Doing "confirming with Anti-A1 in A subgroup method" what you described. In other word when do you result as Anti-A1 and give A1 negative unit to patient.
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Hello! I have a question.
Hello. I am a rootie blood banker... shy...With lots of burning questions. I am from Richmond, VA. I did most of my blood bank work as a generalist. Since 2008 I have checked with site time to time, and I found this site very helpful and interesting. Thank you all! Can I please ask a question here? Forward is 4+,4+ Rh is 4+ . Reverse 1+, 0. Rh Control is negative. And patient's red cell is negative with lectin, Anti-A1 So the patient has A subgroup. Immediate xmatch is compatible. My question is... does patiet has anti-A1? I think he still has although it is weak, but my lab think it is cold. I ran short cold and everything is 1+ or weaker. To me it is simple text book question, but now I am very confused. Can someone explain to me? Thank you.