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Malcolm Needs

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Everything posted by Malcolm Needs

  1. Hi Mary, As I understand it (from chats with my hospital colleagues) it is just a scaled-up version of what happens with a neonatal exchange transfusion, but with certain differences. Of course, it does not involve a doctor sitting there with a couple of syringes and a three way valve, but a unit is taken off the patient, to be replaced by the donor blood, and then another unit is taken off the patient, to be replaced by more donor blood, and so on. The exchange is not total, but goes on until the HbS level has been brought down to the predetermined desired level.
  2. I don't know whether this will help you, because it is in a BCSH Guideline designed for use in the UK, but it is mentioned in "Guidelines for compatibility procedures in blood transfusion laboratories.". This can be found under References (at the top of this page), Document Library, United Kingdom, BCSH Guidelines. As I say, it probably won't help, but you never know. After all, 60-year-old males are 60-year-old males, wherever they may be in the world!
  3. I agree with you Mabel that one has to identify "low incidence" antigens in your particular area of the world (and, come to that, amongst your own ethnic minorities now that we have a "global village") that are not "low incidence" in your own area (Cw in Latvia, Di(a), as you say in South America and parts of Asia, Mi(a) in parts of Asia, etc) and treat those differently to true low incidence antigens. I would suggest that the ISBT definition of <1% in one's own ethnic admix is a starting place. Incidentally, we would identify an anti-Cob with our panels (in the Reference Laboratory), but only if the antibody has been detected by the referring establishment in the screen/antibody panel in the first place. :)
  4. I think that there is possibility of misinterpretation here. I am not suggesting that coloured labels are the "be all and end all" for identification, and that we should remove the printed ABO and RhD types on the labels (far from it). All I am saying is that standardised coloured labels would act as an extra aid to identification that, in most cases (colour-blind individuals excepted), would be overt. :)
  5. No, maybe not, but others out there will take note and "mark you down". The MHRA are usually happy if you have something in place to investigate a "poor performance" and to see if there are any trends (don't have more than one "poor performance" though, even if the two are totally unrelated), but others, even inside your own organisation (Quality and others) may not be so understanding.
  6. More power to your elbow.
  7. I could not agree more with your suggestion as it is totally logical, but, for that reason alone,the cynic in me says that being logical is precisely the reason the "suits" will not adopt it!!!!!!!!!!!! :devilish::devilish:
  8. I'm prepared to bet somebody else's money that it will not be. Clinically-significant HDNF due to anti-Ce is exceptionally rare. I would just ask though, if you are using r'r' and rr red cells, why the difference between r'r' and rr red cells and R1r red cells. r'r' is "double dose" for both Ce and C. rr is "double dose" for e. R1r is "single dose" for Ce and C, but "double dose" for e. To my mind (such as it is) something doesn't add up. I've got man flu again, so I may not be thinking straight and have missed something. :D
  9. We run the enzyme panel as part of the routine service (i.e. an IAT panel and an enzyme panel gets charged as one panel). I think that your way of charging, other than this, sounds really sensible and fair. :)
  10. Within the NHSBT, we have a simple charge for the use of a single panel (plus a few cells for, say, confirmation of an anti-E present with an anti-c, where we would use an R1Rz). We have a complex charge where we have used more than one panel (and, possibly, some rare cells, such as Kn(a-), McC(a-), U-, Kp(a+b-) etc), but we also have a complex charge (same price, by the way) where we use multiple panels and very rare red cells (such as Oh, Rhnull, MkMk, En(a-), Ko, Er(a-), etc). There is talk tht this latter complex charge may attract a premium, but this is not so at present.
  11. Hi Steve, I'm not sure this really "fits" into "Just For Fun", but... In September 1990, the first NATO Civil/Military Blood Conference was held at the (then) Army Blood Supply Depot in Aldershot. During the conference, a review of the colour coding of blood group labels was undertaken. The attachment shows the different colours used for different blood group labels for certain different countries (wear sun glasses!). Concerns were expressed that , as a result of deployment of multi-national forces, the difference in colour coding of blood group labels could cause confusion. The ISBT suggested a time of five years, after which time standard colour coding could be introduced. During this time, labels would be black and white. Well, there was no agreement within the 5 years, and it is now almost 2010, and the "5 year" experiment is still continuing!!!!!!!!!!!!!!!!!!!!!!!! Strange that. :bonk::bonk: Colours.doc
  12. Well, it is true that there are a small number of patient anti-S samples, and slightly more anti-s samples found that have quite a high proportion of IgM to IgG, and so a lower incubation temperature may well help in identification, but I would recommend putting up two tests, one at 37oC and one at room temperature.
  13. I'm not sure, but this may be more of a role for the IBMS (and, possibly, the RCPath) than BBTS. Certainly though, it should be a role for the Chief Scientific Officer. I'll have a think about this one. :confused::confused:
  14. I agree with everything else you say Rashmi, but in my experience, there have been times when they have been wrong, and they are far, far too arrogant to admit it. This has left Blood Bankers trying to "improve" by doing something they know is wrong. :angered::angered:
  15. I'm sorry irshadaad, but I'm not sure I fully understand your question. You would confirm anti-S and anti-s in the same way that you would confirm any other antibody specificities; in this case using S+s- and S-s+ red cells by IAT to exclude other specificities, and S and s type the patient. I know that various papers and books say that the S and s antigens are variably affected by papain (usually destroyed, but not always) but a paper by Jill Storrey et al a few years ago suggested that "papain-resistant anti-S" is almost always a low-grade auto-anti-U (or, at least, that's how I read it), and certainly, when we've bothered to actually test such antibodies in our lab, this is what we have found (a lot of work for not much return). :confused:
  16. I'm going to be controversial here, and also show my age and reactionary nature, but... I still hanker after the days when each ABO type had its own coloured label, and the print colour of the written RhD type depended on whether it was positive or negative. I know the reasons this was abandoned (no standardisation between countries and, even between civilian and military blood within the same country, and the perception that the colour system discouraged people from checking the units properly), but I never bought these arguments and still don't. I thinki a colour code helped to highlight overt errors. :(:(
  17. Hmm. Sounds like they did neither. Now, where have I heard that before?????????????!!!!!!!!!!!!!!!!!!!!!!!!!!!! :angered:
  18. I agree (except that I m prepared to bet a tidy sum that it was probably foisted upon them too by some "suit" in the background who "thought it was a good idea" and would "improve patient safety", wsithout a thought for those who would have to operate the system). :mad::mad::mad::mad::mad:
  19. Just to be awkward (as ever, some would say!) the NHSBT is doing a study on this kind of thing at the moment (although only for anti-c, anti-E and anti-cE). We are titrating the anti-E (using an R1Rz cell) and the anti-cE (using an r"r cell). In the UK, we do not titre anti-c, but rather perform quantitation by continuous flow, using rr red cells. So, we are, for want of a better way of putting it, "titrating" the anti-c, the anti-E and the anti-cE. There was/is a theory that anti-cE is "virulent" incausing HDN, than a mixture of monospecific anti-c and anti-E. I think I am right in saying that, although the study is not yet complete, there is no proof of the theory being correct. I don't really suppose this answer helps you much, but that is what we are doing. :)
  20. For those of you who have not yet read it, there is a new paper on this subject that strongly agrees with some of the posts above, and suggests that individuals like me can be far more conservative when it comes to performing elutions. It is, Yazer MH, Triulzi DJ. The role of the elution in antibody investigations. Transfusion 2009; 49: 2395-2399. It is a very interesting and thought-provoking paper. :D:D:D:D
  21. Ah, I'm not saying it doesn't have other antibodies present too; I am just saying that the major specificitiy is anti-D.
  22. Sounds a bit like "we are providing the finance, so we also provide the ideas", irrespective of the fact that "they" knew nothing, and yet did not ask the expert on the spot! I sympathise. Sound familiar to anyone else???????????????!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :cool::cool::cool::cool::cool:
  23. I know this is cheeky (and it shouldn't have to be quoted in such a thing), but what did your specification say prior to ordering the fridge? I repeat, though, this kind of thing shouldn't have to be in a specification for a blood fridge (but it is not there, it does give a get out clause for the provider). One has to be so blank, blank careful these days (although I would say that the fridge was not sold as "fit for purpose" anyway).
  24. This answer was written in haste (I had to go and get my son from his Kids' Club!) and is now being somewhat repented at leisure! As I intimated in an earlier post above, the frequency of atypical alloantibodies directed against low-frequency antigens is far higher than the frequency of such antigens themselves. As a result, when one encounters such an antibody, it is very easy to provide antigen negative blood. One has to ask, therefore, is the cost of the primers (which are expensive) in such a situation justifiable, for such a small return (which, if one leaves out the esoteric science of furthering man's knowledge, is virtually nil). I can really only see one situation in which such expense could be justified. This would be in the case of a patient requiring life-saving (but not urgent) surgery, who has an atypical alloantibody directed against a high-frequency antigen (for example, anti-Dib). Searching for Di(a+b-) donors by traditional serological techniques would be extremely expensive in terms of using very rare antisera (either anti-Dia or anti-Dib). To find suitable Di(a+b-) donors could be done by mass genotyping, but even then, it is more likely to be done by use of microarray technology than "traditional" genotyping (if I am justified in using the term "traditional" about a very new technology)! I cannot see the expense being justified in other circumstances; but I could be wrong (again)! :):)

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