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Hi All, I was wondering if antibody titre is performed on a pregnant mother who previously had HDFN. According to the books, it mentions 'After the first affected pregnancy, the antibody titer is no longer useful'. Therefore does it mean that it doesn't matter what the antibody titre level is, and should be referred to fetal medicine specialist regardless? Or if there is more to this, I would be grateful for some enlightenment

Hi All, I am about to venture into performing my first ever validation of a test. I have been tasked to validate Rh+K phenotype testing on the BioRad IH-1000 (two of them). We have been, until now, performing the test manually, but as work is getting busier, performing it on the analyser might prove easier (or at least motivate people to perform phenotype). I have been given advise by my senior on how to go about it: Select 10 Donor Red Cell units which have Rh+K phenotype performed Perform the phenotype manually Perform the phenotype on the analyser compare the result pat myself on the back, provided I don't mess it up The issue I have is donor red cells doesn't indicate if they are K+, and I wanted some K+ as well as K-. I could always keep testing a lot of donor units until I come across a K+ unit, but I don't want to was a lot of cards (but that might be my last option). If I choose the NBS or BioRad Antibody Panel Cells, then the issue is the strength of the test cells, as they are, I think, 0.8%, and it does not fully represent the way we perform our phenotype manually, as it uses around 5%. I can always try and make the strength of the solution stronger, that is another option. So this is where I am at. If anyone has a suggestion, or better a complete plan, then I am happy to hear it. Also if there is any point I missed or need clarification, please feel free to ask, I'm fixed to this specific thread all night long. Cheers, Jermin

Hi, This is a very silly question, but I think I have confused myself. Why is it that when Rh phenotyping, we do not require incubation step, but when looking for antibodies, we need incubation to detect Rh antibodies?

Hi All, So I would like to present a scenario that happened to me and get your input. I received a specimen from the ED for ABO/Rh testing on a young female (she had a miscarriage, which at the time I was not aware). We use the BD Pink (EDTA) blood bank tubes for all of our blood bank testing, this particular sample was about a little more than 1/4 of the way full (yes not the best sample, learned my lesson with this case) - there were no visible clots in the tube or in the cell suspension I made for testing (testing was done fairly quickly since it was only an ABO/Rh and we use a STATSpin centrifuge so I had results out within 20mins of it being collected). These were my initial reactions at time of testing: Anti-A: 0 Anti-B: 4+ Anti-D: w1+ D Control: 0 A1 Cells: 4+ B Cells: 0 Du: 3+ Du Control: 0 CCC: 3+ So of course my interpretation was B Positive, which was reported. (We use the monoclonal Anti-D) All of our samples are retested by another technologist if we have no previous history on the patient. The samples sit at room temperature until they are tested and this was one was retested roughly 10 hours after my initial testing, these are the results: Anti-A: 0 Anti-B: 4+ Anti-D: 0 D Control: 0 A1 Cells: 4+ B Cells: 0 Du: 0 CCC: 3+ Du Control: 0 CCC: 3+ Interpretation: B Negative It was tested 2 more times by two other techs later that morning and the report corrected and the patient had to be called back to get Rhogam injection. So of course and event report was initiated at that point for root cause analysis. I was approached 3 days later after knowing nothing about what happened and told that I "miss-typed" a patient sample. After reviewing the work card I of course said No I didn't because I actually remember working on this particular sample due to the fact that the D got stronger at AHG phase. I was extremely puzzled by the results and pulled the sample at this point had been in the refrigerator for 3 days and found that the same had numerous large clots and lots of visible small clots in my cell suspension (however none of the previous techs noted or expressed this to my director). I performed (3 days later) a forward and reverse typing (B Neg), DAT, and IAT. The DAT (IgG and Poly) - Both negative (very sticky microscopically) and IAT in Gel was completely negative. So at this point it was very perplexing as to what happened with the Anti-D. Of course everyone my boss talked to said that this was impossible for the Anti-D to just disappear (I was not inferring that it disappeared to her) and I must have done something wrong, which really aggravates me to use the word "impossible" in medicine. She said it was more logical that I mixed the control tube and the Anti-D tube at the AHG phase when I read the tubes which makes absolutely no sense to me (if the results were reversed from the results I got at immediate spin, then yes that would make sense and I would have questioned the results and started over). OK, so here is my theory as to be the possible cause for this particular scenario has to do with a sub-optimal sample that was in the process of clotting at the time of initial testing - however I can only assume this theory and I know that it didn't interfere with the Anti-A or Control on the forward type, but these are all different antiseras with different blends of antibodies/proteins, etc.. I am thinking that since I didn't see or detect clots when I tested the EDTA sample the first time it is possible that something during the clotting process potentially interfered with the Anti-D causing it to be a false positive. Since the specimen wasn't tested again until 10 hours later when the clotting process was definitely complete there is no way to prove this, unless someone where to have retested it immediately after I performed the first test. We've seen cold autoantibodies disappear after sitting at room temperature due to autoadsorption, who is to say that since the clotting process was complete whatever was causing the interference may have been gone 10 hours later when the full clots formed. My boss refuses to even think this is remotely a possible and I had to have made an error, she said we use to use plain red clotted tubes all the time for blood bank and never had any problems (don't think she is getting that these tubes have no additive and normally the clotting process was a lot faster in plain red tubes with no additive. Then again she also couldn't understand how a clot would get stronger overtime (I wanted to bang my head on the desk with that remark). If I made an error or potentially made an error I would definitely own up to it, but in this instance her suggestion that I switched the test tubes around and reading the control as the patient makes no sense what so ever. Has anyone every encountered anything like this before and what is your thoughts on the potential reason for the various reactions between a 10 hour period? Thanks, -TxLabGuy82