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Malcolm Needs

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Everything posted by Malcolm Needs

  1. Sorry, but I disagree. In most cases of ABO haemolytic transfusion reactions, it is not the ABO antibodies that cause the haemolysis that destroys the incompatible red cells, but activated complement that, in most cases, also causes "innocent bystander haemolysis", whereby the autologous red cells are also haemolysed.
  2. Happy Thanksgiving to all of my USA friends for tomorrow.
  3. This statement is completely true, BUT the fact that NHSBT RCI Laboratories started to use these routine techniques followed a huge amount of work performed by Gordon Burgess when he was the Reference Service Manager at NHSBT-Cambridge Centre (before he became Head of RCI in NHSBT) to show that these were viable techniques that passed prolonged Quality Assessment. To introduce such techniques without such work would not have allowed RCI to pass inspections by our various assessors. I doubt if Clarest would be able to introduce such techniques into Canadian laboratories without similar work.
  4. VERY good point. When I was working at Westminster Hospital (many, many moons ago now), we came across a male Jehovah's Witness patient who swore blind that he had never been transfused, with one of the strongest polyclonal human-derived Fya antibodies I have ever seen.
  5. I've been wracking my brains over this one, but I have hit a brick wall. If it is not an anti-LW, I can see no alternative to an anti-D (possibly caused by a previous pregnancy - if the patient is female [or, these days, possibly a transexual who is now a male], or by one of the donors having a very rare RHD mutation). Somebody will now come up with an explanation that is quite simple, and I really should have thought of immediately!!!!!!!!!!!
  6. Suggests to me that this really is an anti-D then. I'll keep thinking (or trying to think at my age!).
  7. I agree ENTIRELY with the answer given by exlimey. Anti-G usually (not always, but usually) reacts more strongly with the C antigen than the D antigen, so that R1R1 and r'r red cells would give stronger reactions than would R2R2, whereas both anti-D and anti-LW would react more strongly with R2R2 red cells than R1R1 and r'r red cells. I agree that one of the units could express an unusual D type (I was caught out once in a pregnancy case when the dad had the unusual D type of RHD(L214F)-CE(7)-D - which I thought was rather unfair of him!). Have you tried rr cord bloods against the patient's plasma/serum sample? The LW antigen is expressed much more strongly on cord red cells than adult red cells.
  8. I sincerely hope that you would also contact your blood supplier to let them know that there is a high risk of bacterial infection, as there may well be other blood components from the same donor that may yet still be untransfused to a patient, and which should be immediately put into quarantine.
  9. The ONLY way this can be determined accurately is by molecular, rather than serological techniques. The reason I say this is because, although we tend to think in terms of foetal to maternal bleeds (foetal blood into mum's circulation), there is always the chance that the bleed can be maternal to foetus, thus meaning that serological testing can be unreliable at this stage of life.
  10. Until there is a definitive answer, it MUST be D Negative, even though the chances are that, at that stage of life, the baby's immune system would not produce an anti-D if D Positive blood was transfused, BUT it could well be that the baby's immune system could be sensitised to the D antigen. ALWAYS ERR ON THE SAFE SIDE.
  11. Well, you cannot call the baby Weak D+, as there is no such antibody as Anti-Weak-D, but to answer your intended question, it depends on whether or not the baby's red cells are DAT Positive or not, and also on what epitopes your anti-D are designed to detect. It could be that the baby is a Partial D.
  12. Maybe, but RBCs are blood components, rather than blood products.
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