Malcolm Needs

We would perform an antibody identification every time even if the patient has not been transfused since the last time. The patient has already been shown to be a responder, by the fact that he or she has already produced an alloantibody. What you don't know is whether the patient has produced a second (or more) antibody of a different specificity, but slower than the identified antibody. You should not rely on the cross-match under these circumstances. The red cells in the panel are in a solution designed to preserve the antigen expression, but not necessarily the oxygen carrying capacity. The red cells in the unit are in a solution designed to preserve the oxygen carrying capacity, but not necessarily the antigen expression, and you also may not know the rest of the units phenotype (it may have heterozygous expression of the Kidd antigens, for example, whereas the anti-Jka lurking along with the known antibody may only react in vitro with Jk(a+b-) red cells; but it sure will react with Jk(a+b+) in vivo)! I have, only today, been working on a sickle cell patient who, a week ago, had anti-E+M+Fya+Jkb; he now has an incredibly strong anti-Fy3 as well. :eek:

I couldn't begin to think what you mean Tonyd!!!!!!!!!!!!!!!!!!!!!! :rolleyes::rolleyes:

I forgot to say, there are circumstances when we would not give compatible blood, but would give suitable blood. These cases include such specificities as anti-Ch, anti-Rg, anti-Kna, anti-McCa, etc, but we would make absolutely certain that there were no detectable clinically-significant atypical alloantibodies lurking underneath. On other occasions, where the antibody is known to be clinically significant, but where the antigen is of very low incidence within our population (I am thinking of anti-Wra, anti-Dia, etc) we would also give cross-match compatible, rather than typed antigen negative blood. There, that's got that off my chest! :D

We too would give cross-match compatible random units. We are a little more careful with anti-M, in that we will make certain that it does not react at 37oC. I was on-call about a month ago and had to deal with a patient with a pan-agglutinating auto-antibody and known underlying alloantibodies. Having performed multiple differential alloadsorptions, there were still some extremely strong reactions that did not pattern for the known antibodies. After a couple of hours, and much scratching of the head, I was bale to prove this to have a specificity of anti-M. It was amazing. It reacted 4+ in pre-warmed, warm-washed LISS tube IAT, using a monospecific anti-IgG reagent and, in my opinion, would have been very clinically significant. I've never seen an anti-M like it before. In this particular case I made sure that the units were M-. I wasn't prepared to do an in vivo cross-match on that little blighter!!!!!!!!!!!!!!

Thanks. As for the second bit of your post, there used to be a managerial formula (I think it was invented in Wales, but I'm not sure) that people used to find out how hard a person was working (it wasn't a particular popular formula), but it did have an upper limit, beyond which you were working too hard. I can't remember it myself, but this post might serve to jog the memory of someone else who is not suffering from loss of memory due to extreme old age (thanks Rashmi), who may remember or know where to look for this formula, or something like it.

To be perfectly honest with you, being a pure (well, a bit naughty, but mostly pure) red cell immunohaematologist, I'm not sure about this myself, but in all the books I've read on the subject, the highest platelet count post-transfusion is after 1 hour, because before this the platelets are sequestered in the liver (small amount) and spleen (large amount). I suppose one could extrapolate, therefore, that this is the time when the maximum number of platelets are available for doing what platelets do best; but I am guessing. :confused:

You will let us know the eventual outcome won't you? I am incredibly curious as to how it will pan out (well, incredibly nosy really!!!!!). :confused::confused:

I agree with all of the above. I would really hammer the increase in safety (and the possibility of litigation if they don't provide the money for the change). Break the safety things down into as many bullet points as you possibly can, such as positive sample identification. Play them at their own game, and wear them down. Good luck.

We haven't noticed any problems yet, but I will keep an eye open and also keep you informed.

I presume that this is the titration equivalent of our cut-off point of 0.5 IU/mL for passive anti-D (that amount is brand new, by the way. It used to be 1.0 IU/mL). If the anti-D titre is above 8, or the quant is above 0.5 IU/mL, the anti-D is presumed to be immune.

I would suggest a formal risk assessment. I would, but it would probably be ignored! :rolleyes:

No, you are being perfectly logical. I just thought that I should make the point, otherwise the "science" is not proven.

Our experience during the last several year since switching to plasma has brought me to the conclusion that those strictly "complement-dependent Anti-Kidd antibodies" are far, far less common than I was led to believe during my original training.

A minimum of 2 cell samples expressing presumed homozygosity of the gene, if available. In some cases, of course, this is not possible (for example, we had to group the partner of an Oh pregnant lady the other day. He was H+, but was he HH or Hh? Who knows?). There are also rare occasions when we only have one example of a particularly rare "homozygous" type (such as a Cw+, Cx-, MAR-), but there is nothing else you can do under the circumstances.

In the UK, the Guidelines state that, as long as it is known for certain that a pregnant lady has been given ant-D immunoglobulin, no further antibody testing is required after 28 weeks gestation (unless, of course, she has a fall or something). Similarly though, if we are tracking an antibody, such as anti-c, through a pregnancy, we would only run a mini panel of 6 cells, including one known c+, with the other 5 covering all the other clinically significant antigens (including an R1Rz to cover the E antigen), and would only perform a full panel if the lady's plasma reacted with 1 or more of the 5 cell samples that we would expect to be negative. We would, of course, also quantify they anti-c.

Hi Tim. I have no doubt whatsoever that you are right. The kind of antibody I was talking about in my post above is disappearingly rare, and I would not want to go back to routine tube IAT for all the tea in China. I am a huge fan of gel. On the other hand, for certain specialised tests performed in my laboratory, LISS tube IAT can be an essential tool.

The problem with the investigation of rare Rh antigens (and, come to that, very common Rh antigens, such as HrB) is that approaching the problem from either the antibody or the panel direction is fraught with difficulty due to the paucity of reagents. If you are really talking about rare Rh antigens (such as, for example Cx) the only real way to address the problem is by using rare antisera (such as anti-Cx). On the other hand, if you are also talking about very common Rh antigens, the problem is somewhat easier, because you can use such antibodies as Rh29 to demonstrate that the high incidence antigen is part of the Rh Blood Group System (assuming, of course, that such a reagent is available for your use - a big assumption, I know). Once you have established that the antigen really is part of the Rh Blood Group System, you can either use specific Rh antibodies to determine whether or not the antigen is expressed on the red cells, or nowadays, it is probably just as easy (if not more so) to obtain genomic DNA from the patient and subject it to sequencing of exons 1 to 9 of the RHD and/or RHCE gene. THat having been said, however, this is not as "easy" as it sounds. THere was a paper published earlier this year (Pham B-N, Peyrard T, Juszczak G, Dubeaux I, Gien D, Blancher A, Cartron J-P, Rouger P, Le Pennec P-Y. Heterogeneous molecular background of the weak C, VS+, hrB-, HrB- phenotype in black persons. Transfusion 2009; 49: 495-504) that showed the molecular background of the weak C, VS+, hrB-, HrB- phenotype to be, quite frankly, a bit of a mess!

Actually, many "warm" are complement binding, but the question was about "cold" antibodies.

I agree downloading from PAS to the LIMS cuts the risk of subsequent mistakes. I have no arguement with that. On the other hand, of course, not correcting a mistake that is on PAS perpetuates the mistake. If John Smith (DoB 01.01.59, blood group AB D Pos) is put on as Jon Smith, and then a real Jon Smith (DoB 01.01.59) comes in, and he is group O, D Neg, where are you then? :confused:

The very best of luck Lara, but from your intelligent posts, luck shouldn't come in to it!

In that case, it's unlikely to be a low incidence antigen, assuming they use exactly the same batch in exactly the same way. We get this occasionally with our hospitals using a DiaMed panel, whilst we use our own NBS panel, which, of course, will not express the same antigens. Also, just ocasionally, it could be due to expression of a Bg antigen that can "disappear" by being soluble. If they wash or resuspend their panel in a different suspension medium (we use Diluent2, most of our hospitals use Alseiver's solution) this too can make a difference. :confused:

I, too, get these telephone calls at all times of the day or night and try to point them in the right direction (mind you, if it is a daft telephone call, instead of pointing them in the right direction, I may well tell them exactly where to go!). Seriously though, I do agree with you that it very often is faster, and cheaper, than querying a software program.

Hi LaraT23, Are you absolutely certain there is nothing in the plasma? The reason I ask is that, very often, if the cell expresses a low incidence antigen (known or unknown to the producer) you will get quite a few apparently spurious positive results. Antibodies directed against low incidence antigens are quite common amongst the general population, more often than not as a "soup" of many specificities. We had an Lu:14 cell on one of our panels not too long ago (we knew about this one) and detected 2 anti-Lu:14's in 2 weeks. I had never detected one before, and have not since. If the Ortho screen cell and cell #2 are expressing low incidence antigens (not necessarily the same low incidence antigen, by the way) this may explain the problem. On the other hand, of course, it may not!

Is that the one that goes: 1. Use a team approach. 2. Describe the problem. 3. Implement and verify interim containment actions 4. Define and verify root causes. 5. Verify the corrective action(s). 6. Implement permanent corrective actions. 7. Prevent problem recurrence. 8. Congratulate the team. ??????? No, never heard of it! Yes, we do use a version of this, but I always get stuck at 7. I can never bring myself to go on to 8!!!!!!!!!!!!!! :rolleyes: