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This is well known and there are indeed other threads concerning this. Transfused cells may have different densities to the patient's own cells and therefore when you spin the tubes in the centrifuge you may find that the transfused cells and the patient's cells separate. Then, depending on where you sample from in the tube, you will either get only transfused cells, only patients cells or a mixture, giving a mixed field. Typically instruments will select cells from the bottom of the tube, whereas pipetting by hand, one normally samples from the top, giving a discrepancy between the two methods.

To much make refractoriness a non-problem, one needs to administer leukoreduced and ABO identical blood components. In our hands, that pretty much abrogates the problem entirely. Almost all of our 3-5 refractory patients per year (out of hundreds) are treated elsewhere first with non-ABO identical components which randomized trial data show increases the rate of HLA alloimmunization. One cannot control what other people do, obviously. So when a patient is clinically refractory, we will HLA type them, try to characterize the antibodies (PRA) and either give HLA matched, or avoid specificities when that is feasible. Either works about as well (probably 70-80% of the time). If those HLA identical platelets are ABO non-identical, they will perform about as badly as non-HLA matched. Thus we try to avoid that or remove incompatible plasma from HLA-matched, plasma incompatible platelets (we wash). It's a good idea to have HPA antibody testing, although not essential, as about 1-2% of refractory patients have HPA antibodies (thus it's rare, but not zero) and this test will also indicate if you have one of the patients who actually have ITP (about 50% of ITP patients have anti-platelet antibodies). There are fairly simple kits available to screen for both HPA and HLA antibodies, although they don't allow for specificity determination.

The reverse cells are normally pooled. So the lady's antibody is probably reacting with some of the cells in the pool and not others. Usually the Rh pheno is the same on all the cells in the pools so it probably is not due to the anti-c unless your provider does not ensure that they are all the same, or one of them is a c-variant. Could easily be an anti-M or Lea or Leb though

Also, the polyclonal (human) reagents will give false pos results in samples with pos DATS. But anyway, finding sufficiently good human antibodies to manufacture reagents from is getting harder and harder. So definitely monoclonal

They should have, or create a policy to replace/reattach the armband. Get your pathologist and QA involved.

David is completely correct. Do not forget, also, the A, B and H antigens are not direct gene products (they cannot be, as they are sugar-residue antigens). The direct gene products are transferase enzymes (proteins). These enzymes are not working at their maximum efficiency at birth (hence the weak antigen expression), but, in addition, the "A transferase" and the "B transferase" are competing against one another. Sometimes the A transferase starts by "beating" the B transferase, in which case the A antigen is expressed more strongly than the B antigen, and, sometimes the reverse is true (as in this case). They eventually "even out", as long as no true subtypes are involved. Test again at about six months.

There was a prominent trauma surgeon who said, "Patients die from the blood they don't get, not the blood they do get".

I have NO idea who are HFAP, but I would say that, whoever they may be, they are complete idiots. Your way of treating the patients as D Negative until proven otherwise (i.e. the patient is D Positive or is Weak D Type 1, 2 or 3) is EXACTLY what is suggested by people who actually know about the subject on both sides of the Atlantic (Daniels G. Variants of RhD – current testing and clinical consequences. British Journal of Haematology 2013; 161: 461-470, and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD. It’s time to phase in RHD genotyping for patients with a serological weak D phenotype. Transfusion 2015; 55: 680-689). I have, as I said above, no idea whether this was an HFAP ruling, or the ruling of a rogue inspector from HFAP, but, either way, I would be appealing against the citation, or changing the organisation who inspects my laboratory, if the appeal is rejected. From my point-of-view (and I have a bit of experience) you have done no wrong, but the inspector/inspectors have not got a clue about the Rh Blood Group System, and, in particular, the vagaries of the RHD gene. My own wife is D Negative, and if this lot forced her to be assigned as D Positive on such minimal reactions, I would be suing immediately. Sorry about the rant!