Malcolm Needs

She has had one miscarriage before (see post 11 in this thread). :)

True, but then the same would apply if you were disturbed adding serum/plasma last; those first few tubes would have the serum/plasma sensitising the red cells much longer. It is also easier to see where there are no red things in the tubes, rather than where there is no yellow stuff in the tube that has already got red things in it. :confused::confused::confused:

The reason is, if the labels are pre-printed, as opposed to printed at the draw, it is not unusual for another patient's pre-printed label to be stuck on to the sample tube. Makes you go all cold doesn't it!!!!!!!!!!!!!!!!!!?????????????????? :eek::eek:

Quite correct, you would. :):)

And therein lies one of the problems. Some other Departments have lower standards, and people tend to go for the "lowest common denominator". I agree; stick to your guns. :(:(

In the UK, we only accept hand-written specimen tubes for blood transfusion, unless the sticker is produced at the bedside (or wherever the specimen is drawn) and the sticker is produced by bar-code reading the patient's wristband. This was following two papers that showed real problems with the use of pre-printed addressograph labels. Cummins D, Sharp S, Vartanian M, Dawson D, Amin S, Halil O. The BCSH guideline on addressograph labels: experience at a cardiothoracic unit and findings of a telephone survey. Transfusion Medicine 2000; 10: 117-120. Sharp S, Cummins D. The BCSH guideline on addressograph stickers: an update. Transfusion Medicine 2001; 11: 221. :):)

YES, that was it; Seattle. I knew my memory was going! :eek::D:eek:

You can; I looked on the web under "trypsin purchase" and that name came up. :D

Good to see you back Lara. :D:D:D:D

My personal opinion is that whoever set this question must have kinship to Count de Sade, but I'll have a go. In Geoff Daniels book, Human Blood Groups, he quotes 7 studies with anti-Vel. These were as follows: Population Number Tested Number of Negatives Antigen Frequency American 21 000 8 0.9996 British 99 637 25 0.9997 French 10 000 4 0.9996 Australian 5 000 2 0.9996 Finnish 18 920 0 >0.9999 Swedish 91 605 52 0.9994 Norwegian 5 009 4 0.9992 The only published figures I can find immediately to hand (I am at home, rather than at work) concerning anti-Kpb were in the original paper on Kp(, by Fred Allen et al, and in that paper they say, "Only two Kp(b-) individuals were found in tests of 5, 500 unrelated persons, indicating that the gene frequency of KPB is probably in excess of 0.98." These figures would suggest that Kp(a+b-) is very slightly more common than Vel-, BUT, it depends on the ethnic origin of the donor population. The frequency of the KPA gene within the Black population is almost 0 (I have only ever heard of one Black individual who was Kp(a+b-), and she made an anti-Kpb), but in the White population the Kp(a+b-) frequency is often quoted as approximately 0.0015, and that for Kp(a+b+) approximately 2.3%. All of that having been said, our own figures (unpublished as yet) for the period of screening between March 1997 and March 2007 were: 269 491 screened donors, 32 Kp(b-) or 0.012% of the donor population, compared with 268 316 screened donors, 51 Vel-, or 0.019% of the donor population, which suggests that Vel- is slightly more common than Kp(b-) - common, in this case, being a relative term. I know, even before I post this, that this is not going to help much, as the figures are contrary to one another, but I still think that it was something of a vile question to ask in the first place (not your question; the examiners question) and exceptionally badly worded, as it does not take into account ethnic backgrounds. :eek::eek:

Now there is an offer I can't refuse!!!!!!!!!!!!!!!!!!!!!!!!!! I will give you all the answer very soon, but skyanto, in a post on page 2 of this thread, has asked me not to give the answer until next week, and I agreed so to do, unless a lot of people object. :):)

Yes, I am hanging my head in shame! Incidentally, it has just turned into Spring in the UK, but I can't really use that as a valid excuse for my stupidity!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :redface::redface:

I think that what the Managers should realise is that, although all the other Pathology results might well be critical, it is rare for an errant result from the other disciplines to have the capability to kill a patient in a very short space of time. This may sound like I am exaggerating the situation, and, indeed, in most cases I may be, but if an ABO blood type is grouped incorrectly, because the sample is mistaken for another patient, this can, and does, happen. The question is, if this should happen, who would get taken to court? The phlebotomist for not labelling the sample fully, or the person in the Blood Bank for accepting the poorly labelled specimen? I think I already know the answer to that one. I would stick to your guns Brenda. Sex indeed, as an identifier!!!!!!!!!!!!!!!!! :(:(

I have experienced this in the fairly distant past, when they seemed to bung any old plasma/serum into a pool, as long as it had a strong anti-D. We used even to see the odd anti-K. Now, though, I thought that regulations had tightened, and that they only put monospecific plasma containing anti-D into RhIg. Am I wrong (I haven't worked in a Hospital Blood Bank for something just over a decade)? :confused::confused:

I can't say anymore yet (see my earlier posts), otherwise I will start to give the game away. That looks a really useful website, by the way.

Hi LisaM, We repeated the testing in both gel and tube and got identical results. More than that I cannot say as yet, except to say that the lady is healthy, so no recent transfusions. :):)

Oh sorry Anna (and everybody else come to that). The last post was a complete error. She is grouping as an A, and not as a B for the forward group. I will write out 100 times, "I MUST CHECK MY POSTS PROPERLY BEFORE I SUBMIT THEM." Well spotted! Mind you, of course, it does make the case just that little more difficult to work out when I give you duff information!!!!!!!!!! :redface::redface:

Seems to me that your inspector is off the mark. It depends on the patient's idiosyncratic mmHg in the first place, and how much of a range your Pathologist wants to put on this; not what the inspector feels should be the range! I just love these inspectors that come in and make comments like this. :mad::mad::mad::mad::mad:

No, sorry. The patient is grouping as a B, but the reverse group is that of an AB, rather than an O. :o:o

No problem. That's about the size of it!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

Great answer! :D:D:D:D

Hi Heather, All red cells are Pk+, except for the very rare pp red cells. That having been said, in almost all cases, the Pk antigen is expressed so weakly, as to almost appear negative (only about 0.01% of individuals react strongly with anti-Pk). If you like, it is a bit like the situation of the Kell antigens in the more extreme examples of the McLeod phenotype, where the red cells appear to be Ko (but for a different reason entirely). In the case of the Pk antigen, it is a steric hindrance caused by the P antigen. Human anti-Pk is only made by pp individuals, in a mixture of anti-PPkP1, and only in some instances can the anti-Pk be separated. There is a murine monoclonal anti-Pk available. I hope that helps your understanding; if not, ask again and I'll try to explain it in a different way. :):)

Very true Heather, but in this case I am being even more parochial, in that it is National, as in England, rather than the UK, and National, as in the NHSBT, rather than for the Hospitals!!!!!!! :):)

No problem, if everybody else is happy. :confused::confused:

Good point. :)