Malcolm Needs

Brain power? Bang goes any chance that I could do it then!!!!!!!!!! :o:o

There ws an editorial, written by Lawrie Petz, a few years ago in Transfusion that may be of interest to people. It is: Petz LD. "Least incompatible" units for transfusion in autoimmune hemolytic anemia: should we eliminate this meaningless term? A commentary for clinicians and transfusion medicine professionals. Transfusion 2003; 43: 1503-1507. The final paragraph should be of particular interest. :)

Our National SOP actually states that we should cross-match with the raw plasma and the adsorbed plasma, if there is sufficient raw plasma available. On average, we deal with about 4 or 5 DAT positive samples a day, most with a panagglutinin giving a 4+ or 5+ reaction across the board. I've never quite seen the point of cross-matching against the raw plasma in such circumstances, knowing before I start that the units will be 4+ or 5+ incompatible. It's a waste of time (1+ or 2+ panagglutinins maybe, but not when they are that strong). You would be amazed just how many times I have insufficient raw plasma left to perform these useless cross-matches! The 50 odd hospitals that we deal with as their Reference Laboratory (from very large London Teaching Hospitals to small Private Hospitals) are a varying lot too. SOme are quite happy to perform an immediate spin cross-match if we detect no atypical alloantibodies following differential adsorption, some will do this if the auto-antibody is 1+ to 2+, but will want us to cross-match if the auto-antibody is strong, or if we identify atypical alloantibodies following differential alloadsorption, whilst others (some quite reasonably sized District General Hospitals) want us to cross-match for them even when the autoantibody results in 2 cells kissing each other in the IAT. This last cohort really annoy us! :mad::mad:

p.s Malcolm.... too much info!!!....my analysers have a strictly professional relationship with the LIMS.

Yes; firstly I would agree with you that, in this particular case, there is insufficient evidence (well, none actually) for the presence of an auto-antibody. Secondly, I agree with you about the antibody characteristics making a difference. Thirdly, I would agree with you that these discussions are wonderful, especially if one can keep a mind open to other people's opinions, which, it would seem, nearly every poster can do. P.S. Thanks for the comment.

Hi Trey, and welcome. If you are as lucky as I have been, you will learn enormously from this site (and in a very short period). There are some wonderfully knowledgable people who post, who are more than willing to share their knowledge. It is great.

In principle, I do agree with you Brenda, but when we detect an underlying atypical alloantibody post-adsorption (say an anti-Fyb for arguement's sake), we do like to cross-match, just to make sure that we are not giving Fy(b+) blood (albeit, the cross-match could easily miss an Fy(a+b+) unit if the anti-Fyb is very weak).

Whilst I hate to admit this, particularly on a worldwide site, I have to agree with you about the knowledge of an antibody screen prior to prophylaxis. This is why, unless we have been told by a hospital that prophylaxis has been given, and we detect an anti-D with a level of 0.5 IU/mL or below, we state that an unspecified anti-D is present. If, however, the level is above 0.5 IU/mL, we are confident that it is an immune anti-D, as extensive tests have shown that, even with a prophylaxis dose of 1, 500 IU (and a BSW {British Standard Woman!]) the level never exceeds 0.5 IU/mL. Of course, if the lady is very petite, or they give the world's supply of anti-D immunoglobulin to a single lady (or, a married lady, come to that, ha!, ha!), then we may be caught out by stating the anti-D to be immune, but then, if we are not told of these circumstances by the hospital, what can we do?

I would agree that, in this case, there are clear cut specificities, and that more cells could be used to rule in and rule out. I would dispute, however, that performing differential alloadsorptions in a case where there are some negative reactions is dangerous. Yes, there is some dilution effect, but a few years ago a colleague of mine deliberately spiked a panagglutinin with a very weak anti-D, and then adsorbed the plasma 8 times with some rr red cells. At the end of this process, the panagglutinin had disappeared, but the anti-D could be readily detected, albeit the reactions were very slightly weaker. The trick is to ensure that the cells used for adsorption are really, really packed, by centrifuging on high for about 10 minutes, and then removing the supernatant and the top layer of cells, and then centrifuging again for another couple of minutes and taking off any residual supernatant and the top layer of cells. After this, the only fluid left to dilute the antibody is, for want of a better way of putting it, "interstitial fluid". I am always more worried when there are NO negative reactions, because then you may be taking out an antibody directed against a high incidence antigen that may be lurking under the auto-antibody. Actually, differential adsorption can be extremely useful when you know that there is no auto-antibody present, but there is a complex mixture of "common" alloantibodies and when there is an alloantibody present directed against a high incidence antigen of known specificity. This can be adsorbed out, leaving any other alloantibodies present in at least one of the plasma samples that have been adsorbed. I have used this method on several occasions with specificities such as anti-U and anti-HrB.

And wedding anniversaries; don't forget they have a very close and intimate relationship with a computer!

You know, I really don't think you're taking this seriously!!!!!!!!! :rolleyes::rolleyes:

Brilliant! :D

Oh how I wish I worked with you or someone similar. In our place the people that work in Quality seem all to have had two "ectomies". The first is a "pragmatismectomy" and the second is a "humourectomy"!

Being a Reference Laboratory, we also perform differential alloadsorptions on such patients (or auto-adsorptions if the patient has not been transfused within the previous 3 months [rare] and if there is sufficient autologous red cells [almost never]). As you may have seen from my posts on threads asking similar (but not identical) questions, I have no problem issuing blood that reacts in vitro with the auto-antibody in the patient's raw palsma, unless the haemolysis is fulimating. When issuing this blood we do not need a doctor's signature, but we would not issue it either as compatible, or as incompatible, but would issue it as "suitable for". In addition, we print a phrase on the bottom of the cross-match form that goes out to the hospitals as follows: "Please note that when suitable blood, rather than compatible blood is provided, observation of the patient during transfusion is of paramount importance." I am almost happy with this, except that the phrase itself seems to imply that observation of the patient during transfusion is not of paramount importance for any other transfusion, which is, of course, complete nonsense! :)

I am entirely sympathetic with your views Lekota40. a) I am glad that I don't have to work for this supervisor. I hope that she never has to deal with me if I need a transfusion (she may think my anti-B is some kind of strange auto-antibody)

Hi Donna, I can see why you are confused, because re-reading my post, I could have been a bit less obscure! It depends what technology is used to perform the typing. In my own Laboratory, we use DiaMed gel for almost all typing. You will note that the Ortho panel (which, I belive is gel, although I'm not entirely sure) gave a 2+ with the patient's own cells. If, therefore, this technology was used to group the patient with any reagents that required an IAT, the results would be unreliable. In such a case, just to be on the safe side, and with knowledge that some antigens may be weakened and others destroyed, we would treat the patient's red cells with chloroquine before grouping, just to be on the safe side. I do totally agree with you that a weak auto-antibody can mimic specificities and that not all cells in the panel will necessarily react by IAT; we'll take that as a given. This is why, however, I feel that a panel of enzyme-treated red cells is essential in this case. A true alloanti-Fya will not react with these panel cells, but an auto-antibody mimicking an anti-Fya may (not will, but may). However, the whole thing is best cleared up by an alloadsorption study, and an auto-adsorption study only serves to muddy the waters. As I say though, I do totally agree with you. A couple of times we have identified an apparently clear cut alloanti-S, but the anti-S was reacting with papain-treated red cells (not unknown, but sufficiently rare to make us suspicious). In both cases, using extremely sensitive serological methods, we were able to demonstrate that the antibody present was, in fact, a very weak auto-anti-U. I do not think, however, indeed, I am certain, that Lekoda40's supervisor has not proved his/her case. I hope that I have made myself a little clearer, but if my ramblings are still confusing you, please do not hesitate so to say, and I'll give it another whorl! :)

Love it John!!!!!!!!!!

I agree with everything you say L106 (especially the bit about us all making mistakes), but one should also ask why, if it is supposedly an auto-antibody reacting with some (but not all) panel cells by IAT, he or she (the supervisor) can rely on the cell typing when some of them must rely on an IAT typing (e.g. the Duffy typing)? Seems strange (= daft) to me.

There! And I thought maru was in bone! Sorry; awful pun!

Reminds me of another story! Joan Powell, who also worked with Race and Sanger, saw a tee-shirt that the IBGRL had made for me with the logo, "I'm Chido Negative" on the front. Not to be outdone, Joan, who was a P1+++++ had one made saying "I've got strong pee"! Ah, the old days before Quality and inspectors made it so boring!

All joking apart, I do think that little stories like these can help enthuse those junior staff members who are already showing some kind of aptitude and enthusiasm for the subject of Blood Confusion!

Well, I think that is very cruel!

Well, the story goes like this. When anti-Sda was first discovered, it was worked on extensively by Rob Race, Ruth Sanger and Patricia Tippett at the Medical Research Council's Blood Group Unit in London. In those days it was not considered unethical to use the staff as "panel cells" and "controls". They discovered that one member of staff's blood, the caretaker, reacted particularly strongly with the original anti-Sda (although he was not as strong as a Cad+). They decided to call the antigen after this staff member, Sid Smith (a delightful chap I might add, as was Rob himself, and Ruth and Pat were delightful "chapesses"; indeed, Patricia still is). Of course, in those days, it was traditional to call the antigen after the first two letters of the surname of the person, but, there was already an Sm antigen (now Sc1 of the Scianna Blood Group System), so they couldn't call it that. In the end, they called it Sid, after the caretaker's first name. As I say, I love stories like that. Swa was called Swann after the Swann of Flanders and Swann fame (who made the song, "Mud, mud, glorious mud" famous, amongst others - at least, famous this side of the pond). I can bore people for hours about this kind of thing!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

Pretty slim. I love stories like that. Do you know how Sd(a) (Sid) got its name?

And a good two cents worth too in my opinion. Where I work, we have to do a root cause analysis if we breathe too noisily (an obvious exaggeration, but not that much of an exaggeration). Quality are scared stiff of the GMP inspectors.