Malcolm Needs

No, this was not done when I was working in a hospital, but I most certainly can see from where they are coming. That having been said, in a real obstetric haemorrhagic emergency, you are going to go through blood like there is no tomorrow. If the lady has made an antibody late in pregnancy, the chances are that you are going to go through any phenotyped blood well before the bleed is stopped. In many cases, it is worthwhile giving random blood during the emergency, and giving the phenotyped blood as the bleeding comes under control (on the grounds that the transfusion reaction will take place on the Labour Ward floor, rather than in the mum). Having some phenotyped blood available is a really good idea though (even if we are only talking about approximately 2 to 5% of mums).

I agree with eric1980 though Rashmi. You do have to take your staff with you (unless, of course, you are as autocratic as your staff tell me you are behind your back)!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

We do the adsorption about twice a week when the patient is being actively transfused, but left often when they are not being transfused. If it were a "normal" patient, we would have to have a sample taken within 24 hours of the next transfusion they are to have, if they have been recently transfused, but patients with WAIHA, like sickle or thalassaemic patients tend either to make no alloantibodies, or every antibody under the sun! The fact that some (much more than the 20% one might expect) do not make alloantibodies is probably because their immune system is affected by their underlying condition. If, however, they do make an alloantibody, we may well do alloadsorption studies more frequently than twice a week.

I would use genuine weak antibodies (not strong antibodies that have been diluted) and test against those antigens that are known to become labile (or, at least, are known to weaken) during storage. These would include, at least, the Lewis and Duffy antigens, but if you are using the cells to exclude or include certain specific antibodies (for instance, if you want to exclude or include the presence of an anti-S) then I would have thought that you would have to ensure that those particular antigens (S and s) are still active. If genuine weak antibodies against the antigen are not available, then you will have no alternative than to use diluted strong antibodies; needs must as the devil drives.

This is a bit late (about 3 and a half years!!!!!!!!!!!!!!!!!!) but have you thought about the possibility that there may be an anti-G present? In such situations, it may be worthwhile splitting the plasma into two, adsorbing one with r'r red cells and then testing this with Ro red cells, and adsorbing the other one with Ro red cells and then testing this with r'r red cells.

Please read AABB Technical Manual 16th edition, page 510, Chapter 17 (Positive DAT and Immune-Mediated Hemolysis), Section, Selection of Blood for Transfusion. Pay particular attention to the sentences, "If the autoantibody has apparent and relatively clear-cut specificity for a single antigen (e.g. anti-e) and there is active ongoing hemolysis, (my bold font throughout this quote) blood lacking that antigen may be selected. There is evidence that, in some patients, such red cells survive better than the patient's own red cells. In the absence of hemolysis, autoantibody specificity is not important, although donor units negative for the antigen may be chosen because this is a simple way to circumvent the autoantibody and detect alloantibodies." In other words, this use of antigen negative blood is not because it will last longer in the patient, but because it will show up serological incompatibility due to alloantibodies. The section goes on to say, "It may be undesirableto expose the patient to Rh antigens absent from the autologous cells, especially D and especially in females who may bear children later, merely to improve serologic compatibility testing with the autoantibody (e.g. when a D- patient has autoanti-e, available e- units will be D+; D-e- units are extremely rare)" They are at a frequency of approximately 1 in 7, 000.

I am afraid, irshadaad, that you are confusing immunogenicity of the antigen with clinical significance of the antibody, but even the results of Mainwaring and Oickles are at odds with those of Greenwalt and Sasaki, and \\\\\\\\\\those quoted by Race and Sanger. The fact that an antigen can readily stimulate an antibody does not mean that the antibody that has been stimulated is clinically significant. I would advise you to read chapter 6, pages 224 and 225 of Mollison's Blood Transfusion in Clinical Medicine (editors Harvey G. Klein and David J. Anstee), 11th edition, where the antigenicity of the Lu(a) antigen is discussed in one section and the clinical significance in another. As far as clinical significance of anti-Lua is concerned, I would also urge you to read page 279 of Human Blood Groups by Geoff Daniels , 2nd edition, pages 674 to 675 of Applied Blood Group Serology by Peter D. Issitt and David J. Anstee, 4th edition, and page 198 of The Blood Group Antigen FactsBook by Marion E. Reid and Christine Lomas-Francis, 2nd edition, all of whom are far better serologists and far more knowledgable than I will ever be. :mad:

Thanks for that tricore, but it is Gamma Immucor that is ceasing production of these kits (at least, over this side of the pond). If they are still producing them elsewhere, I would be really grateful if you could let me know, and we may be able to import. On the other hand, this may act as a "heads up" to you that you may have to source from elsewhere yourself. I really am not sure of the situation. :confused:

We have to enter everything manually, because all of our patients are referred, however, it must be remembered that even the PAS has to be entered manually to start the ball rolling.

Within the Red Cell Immunohaematology Section of the NHSBT (formally National Blood Service) we are suposed to wear gloves whenever we are dealing with samples. However, a lot of people have found that the lose a certain amount of tactile sensitivity when doing so (particularly whe dealing with wet tubes that have been incubating in a water-bth). As a result, we have performed a formal local Risk Assessment and there are now certain times when the staff are allowed to make their own decisions on the subject.

Oh come on John, I'm sure we agree on a lot more things, it's just that it sometimes isn't worth commenting unless we can provoke a discussion! I most certainly have an awful lot of respect for your views. By the way, did you see my post about the PowerPoint concerning quantitation of anti-D and/or anti-c? It's too big to put on the site, but I am more than happy to email it to you if you can let me have an address.

Hi there, It may be that your technician from the company who performs the maintenance should do this (and check the revolutions per minute) with a certified timer (and, in the case of the revolutions, some kind of laser pulsing - also certified). If they so do, they should leave you with an "as found, as left" certificate and a copy of the certificate stating that their own equipment has been certified, when it was certified, how it was certified and against what it was certified. If so, you may not need to do this yourself. I hope so for your sake, as it is a pain to have to do it yourself (particularly as the timing is critical, but is not critical to the nanosecond!).

Nonsense. See my replies to your other posts on the subject of auto-antibodies (and read Petz and Garratty on the subject; you may learn something). :mad::mad::mad:

I am sorry, but this advice is completely against any that I have ever read. If you are giving blood that is antigen negative for an auto-antibody (which is pretty difficult in the case of a warm auto-antibody, as most of these are mimicking specificities, but actually antibodies directed against a high incidence antigen), you will usually be giving blood that is positive for an antigen that the patient does not express. In doing so, not only will you be exposing the patient to sensitisation, resulting (possibly) in the production of an alloantibody, but, if such an antibody is produced, you will be making it far, far more difficult to determine antibody specificity in future. In the case of, for example, an auto-anti-e (or, more probably, an auto-anti-e-like antibody), you will be exposing the patient to the E antigen (homozygous expression) and if they produce an alloanti-E, then what are you going to do? I know that if the auto-anti-e is virulent enough, you may have to switch to e negative blood, but you do not want to do this before you absolutely have to.

I would challenge you to produce ANY reputable paper that suggests that anti-Lua is a clinically significant antibody. The same goes for an awful lot of other antibody specificities. I would suggest you read The Blood Group Antigen FactsBook by Marion Reid and Christine Lomas-Francis before making such sweeping statements.

I'm sorry irshadaad, but your last sentence is totally incorrect. If the antibody titre falls during pregnancy, there are two explanations. The first is that the maternal lymphocytes are no longer producing the auto-antibody at the same rate. The other is that the antibody is being adsorbed onto the apical surface of the placenta. The one thing that it is not is the antibody going through the placenta and sensitising the foetal red cells. This would make no difference to the level of the free maternal antibody in the maternal circulation. Apart from anything else, the maternal antibody, if it is capable of crossing the placenta, is taken over by active transport, and the concentration in the baby is always higher than that found in the maternal circulation, whether or not the foetus is expressing the antigen against which the maternal antibody is directed. In the UK, we do not perform serial antibody titrations when the maternal antibody is an auto-antibody, and have not done so for years now. At worst, the baby may have a positive DAT at birth, but this is not the same as clinically significant haemolytic disease of the newborn. :mad:

Sounds like the General had an excellent army! More power to your elbow Eoin. :D

Whoops! Spelling again! That should be "memento" and not "momento". I think George deserves better than being remembered for only a moment!

Jodi, I've only ever seen these being demonstrated by company reps, and have never used one in anger myself, but I think most of them are a waste of money (which is one of the reasons I've never used one in anger). They are fine if you are using the panel supplied by the people selling you the software and if the antibody is either a simple monospecific or a simple combination, but anything other than that and forget it. SOme allow you to input other panels, but you have to make absolutely certain that you put in each and every antigen correctly (otherwise you end up with rubbish; as in rubbish in, rubbish out) and you then still have the problem that they will only identify a simple monospecific or a simple combination. You will find that, eventually, it is far quicker to teach you staff to read antibody panel sheets than it is to rely on computers. It also gives them an advantage over those who only rely on computers when, and if, they go for a job elsewhere; this skill is transferable. Others, of course, may disagree violently with me! It wouldn't be the first time!!!!!!!!!!!!!!! :)

Over this side of the pond, we require three identifiers. We require a full name (forename and surname, both correctly spelled), a full date of birth (age or year of birth is not sufficient) and hospital number or Accident and Emergency number or Major Incident number oraddress or National Health Service number. You be amazed, given all that choice, how many samples are sent in with the third identifier entirely missing and/or the first two incorrect (particularly as all of our samples at the Reference Laboratory pass through the hands of the Hospital Blood Bank before they are sent to us). The NHS number is, of course, not available in countries other than the UK, I fully acknowledge that, but I do still wonder at the fact that only two identifiers are required. That having been said, I agree with Cliff's comment about how the numbers are assigned.

I know exactly how you feel Brenda. We had an MHRA inspector that was the male mirror image of your female FDA inspector.

Thank you for that really helpful post Rashmi! Actually, you are not too far off the truth! I've been bequeathed some of George Bird's original seed collection, but there is no way I'd use those. They are strictly kept as a momento of the great man. We are getting some lectins looked at by NHSBT Reagents at the moment, but there doesn't seem to be any validated kits about. We are having to use out-of-date kits with strict adherence to controls. We've got a few T-activated cells, Cad+ cells etc frozen down, but they won't last forever, and the dreaded MHRA have invited themselves in on the week beginning 03.08.09; Oh joy! :mad:

The people who make the lectin kits for T activation, etc, used by the NHSBT in the UK have stopped producing it. This has left us with something of a problem (to say the least). Can anyone please help by suggesting where else we can source such kits????? :confused::confused:

When are you on a night next?............I'm sure we will have a DAT pos baby or seven that need eluates performing mega urgently. Malcolm is not really that old, just VERY MUCH older than me!

What you say is true about warm autos being potentially dangerous, but hyperhaemolysis is more so. Hyperhaemolysis can strike whether or not there is a warm auto present and whether or not there is an alloantibody present. It is best to avoid transfusion at all if there is a history of, or worse, an on-going episode of hyperhaemolysis, as it is very often fatal. If transfusion is essential to preserve life, try high-dose IVIG and methylprednisolone.