Malcolm Needs

As a Reference Service Manager (and not yet totally driven insane; despite what Rashmi may say) I would thoroughly recommend not bothering to send in your samples from patients with antibodies directed against low-frequency antigens, and just give cross-match compatible blood! For one thing, identifying the specificity of such an antibody (if it's not something like an anti-Wra) is like looking for a needle in a haystack. For another, such a patient usually makes multiple specificities of antibodies directed against low-frequency antigens, and so a) we would probably never identify all those present, as we do not have access to red cells expressing every low-incidence antigen, and very often, a cell that has been identified as, for example, Li(a+) isn't, because it was identified with an anti-Lia that also had, for example, anti-Bxa in it, but we didn't know that. Lastly, for now (as my rant muscle is running on low) the chances of you cross-matching blood, and then giving a unit that is likely to cause a clinically significant haemolytic transfusion reaction are so low as to be all but zero (just think of the number of patients who have been given blood by electronic issue, some of whom must have antibodies directed against low-incidence antigens, and some of whom have probably been given blood positive for the corresponding low-incidence antigen, and you see what I mean). I shall now go and lie down in a darkened room!!!!!!!!!!!!! :crazy::crazy:

I thought it probably was, but it's worthwhile being on the safe side for the less experienced amongst us.

I am tempted to be facetious and say "What about anti-Leb!", but,actually, that is exactly how I feel about anti-Leb. Anti-Leb has, on very, very rare occasions, caused red cell destruction, but, like anti-Lea, the reaction is self-limiting, and , after initial destruction, most of the red cells transfused are still in circulation many hours after they are transfused (probably because the antigens themselves are soluble and "come off" the red cells pretty quickly, and then block the antibody in vivo). There has only ever been one report of anti-Leb causing HDN, and even then it was sub-clinical HDN (so the case was fairly dubious). I would quite happily ignore the antibody completely and given cross-match compatible blood. :)

Hi Andy. I know how you feel, but try to keep off the mead; it's quite a strong drink you know!!!!! :D:D:D:D

Hi Yanxia, Good question! Sorry, but the totally honest answer is, I don't know. It was a decision made several years ago by the Red Cell Immunohaematology Section of the NHSBT (before I joined) and is does not seem to be 100% logical. I will go back and ask at the next meeting of all the reference Managers (but that will not happen for some time). Perhaps the decision needs to be re-visited, but there may be a logical answer of which I am unaware.

We've had a sample in to test for Weak D. Nothing unusual in that, you may say. Except that the patient is 96-years-old! I mean, for goodness sake, does it blank, blank matter at that age?????????????? :cries::cries:

Yes. The other really useful one is "Pre-op". Does this mean treatment to an in-growing toenail, or does it mean a liver transplant? Very useful if you are using an MSBOS! :):)

Well, as I say, we couldn't prove anything, but...............

I would be quite comfortable giving blood that has been found to be compatible by LISS tube IAT, even if it were found to be incompatible by gel IAT, provided that the people performing the tests are well practiced in the technique (i.e. currently, as opposed to historically, competent in pewrforming the technique). Your Director should remember that, before the gel technique came about, almost all cross-matching was performed by the tube IAT (and earlier than that, we used saline, rather than LISS), and we did not kill every patient with an antibody!

You really shouldn't enourage him adiescast, he will soon become very very unbearable!!!!! I think Jo has definitely taken the prize for managing 3 manuals. I'll try not to mention the 'C' word for the next few weeks, but i'm sure Malcolm will try to remind us, so will need to come up with some suitable insults if I can.

I think that you are thinking along the right lines, but i think it is a combination of SHOT, SABRE (another haemovigilence scheme), CPA and MHRA (the last two being regulatory bodies), and throw in a bit of GMP (good manufacturing practice). I also think that you are thinking along the right lies in that this is the future for the USA. While most of it is welcome, in that it does improve the way we do things, a certain percentage of it is a pain in the ****, with little to show for improvement. :mad::mad::mad:

I would agree entirely with that, except in cases of a stem cell transplant, where it depends on the blood groups of the donor and the recipient, and the length of time after the transplant. You also have to be a bit careful with patients of small stature (particularly neonates).

Yes (in fact, it was more than one unit - it was a few years ago, so some of the details are a bit hazy, but it may have been as many as three). The patient was under general anaesthetic, and so, of course, only the overt symptoms were seen (generalised bleeding, temperature, etc) by which time it was too late. Of course, the patient could not tell them that he felt unwell. It was a laboratory error. We never did get to the bottom of what he either did or didn't do (which probably saved him from, not only being struck off [as he was], but a jail sentence, because we suspect he was as high as a kite on-call - but could prove nothing). :eek::eek:

jlemmons, you have my sincere sympathy. :comfort::comfort:

Cheek! I knew I shouldn't have agreed with you earlier in this thread!!!!!!!!!!!!!!!! :threaten::threaten:

Quite right too (not that my birthday is on the 23rd mark you, but it is before Christmas)!!!!!!!!!!!!!!!!!!!!!!!! :D:D

Forgot to ask yesterday. Mind like a sieve. No, I was wrong. Apparently, the case I was thinking of was apheresis platelets. :redface::redface:

No, sorry, that isn't what I meant. What I meant was that the group A blood that had been transfused to the unfortunate patient appeared to have been totally cleared from his circulation (as, indeed, had most of his own red cells, as innocent bystanders to the complement cascade), as we could not detect any group A cells in the post-mortem blood sample, but, although the DAT of the post-mortem blood sample was negative, we could still elute anti-A from the few red cells that were left. The original unit that was transfused in error was most certainly a group A, and reacted normally with anti-A. Sorry for any confusion. Having said that, Apae reacts a bit like the scary phenomenon that you describe (but is most unlkely to cause an acute transfusion reaction i a group O patient.

We have just received a sample from one of our hospitals on a pregnant woman. "Antibody detected by enzyme only. ?anti-N??" Even if I'm exsanguinating, please don't send me there!!!!!!!!!!!!!!!!!!!!!!!! It was anti-Le(a+ by the way. :eek::eek:

30 pages! Goodness me, we send ours away to be bound! Bah humbug, by the way. It's not even December yet. There is still a VERY important date to come before 25th December. :mad::mad::mad:

I can see why you would be more than a little aghast at my answer Brenda (particularly concerning the cord bloods), but, as a Reference Laboratory, we only get the odd one or two sent to us, and these are usually listed as for investigation of HDNF. As a result, we are sort of "duty bound" to throw everything at them. I prefer the 1 month time limit. George Garratty and his co-workers wrote a paper concerning auto-adsorptions some time ago, and why they should not be performed on samples from patients who had been transfused within the previous three months. One of the reasons was that the transfused red cells remaining in the circulation could adsorb out a "new" alloantibody, even though there would be very few transfused red cells left. This suggests that the majority of the "new" antibody would be coating the transfused red cells, rather than be free in the plasma (although I am not suggesting that there would be no free "new" antibody in the plasma). These days, however, the elution kits are excellent, making the removal of any antibody much more efficient, and, as a result, the identification of a "new" antibody in the eluate is probably more sensitive than just examining the plasma. I see that you say that you have never performed an adsorption on an eluate. My advice is, DON'T, unless there is a very good reason, you have loads of spare time on your hands and you decide that you do not want to get out more! It is something that we would only do in extremis. :D:D:D:D

I agree with you that the Blood Bank should have a separate Quality Manual; not least, as you say yourself, because many of the other Departments only pay lip-service to GMP. At the very least, there should be a separate "chapter" in the QM devoted to BT, because it is the only Pathology Department that actually gives out a product; and a product that can kill. Within the NHSBT, there is an over arching Quality Manual, but each section and sub-section (e.g. Specialist Services and, within that, Red Cell Immunohaematology) has their own QM; and this works extremely well (and CPA love it). I'm now going for a lie down. Agreeing with you Rashmi has made me feel quite faint!!!!!!!!!!!!! :D:D:D:D

We would perform an eluate on all cord samples with a positive DAT, to make sure that the antibody sensitising the cord cells is not another antibody in the mother's plasma that we hadn't idenified. For example, in group O mum, who is R1R1, K-, and in whose plasma we had identified anti-A, anti-B (+ anti-A,, anti-c, anti-E and anti-K, there could also be, for example, an antibody directed against a low incidence antigen that is actually causing the HDN. Following transfusion, with a de novo DAT+, we would perform an eluate up to 1 month post-transfusion, even if an alloantibody is detected in the plasma, just in case there is a second antibody Lurking in the background that is not detected in the plasma. In a case of a patient with a known +DAT, we would be much more conservative, unless there was a sudden decrease in the time between the requirement for transfusion. In such cases we would perform an eluate, to see if an alloantibody could be identified that reacts more strongly than the auto-antibody. BUT, if the above scenario occurs, and the auto-antibody in the eluate is really strong (and in very rare cases), we will perform alloadsorptions on the eluate to adsorb out the auto-antibody, to see if there is an alloantibody present too. It's a lot of work, but twice now we have discovered just such an alloantibody causing a transfusion reaction. We would NOT expect one of our Hospital Blood Banks to do all this work! :):)